tag:blogger.com,1999:blog-71137029059715612232024-03-17T15:15:43.752+07:00Umaee FarmMedShare Opinion, News and KnowledgeAnonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.comBlogger60125tag:blogger.com,1999:blog-7113702905971561223.post-69626418106753981012012-04-22T00:28:00.002+07:002012-04-22T00:30:28.043+07:00Clinical Presentation Epilepsy and Seizure<div dir="ltr" style="text-align: left;" trbidi="on">
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/clinical-presentaion-epilepsy.html"><u style="color: #0b5394;"><b>Clinical Presentation of Epilepsy and Seizure</b></u></a><span style="color: #0b5394;"><b> - </b></span>Epilepsy is a disorder that is best viewed as a symptom of disturbed electrical activity in the brain, which may be caused by a wide variety of etiologies. It is a collection of many different types of seizures that vary widely in severity, appearance, cause, consequence, and management. Seizures that are prolonged or repetitive can be life-threatening.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Seizures occur because a group of cortical neurons discharge abnormally in synchrony. Anything that disrupts the normal homeostasis of neurons and their stability can trigger hyperexcitability and seizures. There are thousands of medical conditions that can cause epilepsy, from genetic mutations to traumatic brain injury. A genetic predisposition to seizures has been observed in many forms of primary generalized epilepsy. Patients with mental retardation, cerebral palsy, head injury, or strokes are at an increased risk for seizures and epilepsy. The more profound the degree of mental retardation as measured by the intelligence quotient (IQ), the greater is the incidence of epilepsy. In the elderly, seizures are primarily of partial onset associated with the focal neuronal injury induced by strokes, neuro- degenerative disorders (e.g., Alzheimer disease), and other conditions.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In some cases, if an etiology of seizures can be found and corrected, the patient may not require chronic antiepileptic drug (AED) treatment. Patients can also present with unprovoked seizures that do not have an identifiable cause, and thus by definition have idiopathic or cryptogenic epilepsy. Idiopathic etiology is the term used for suspected primary generalized seizures, whereas cryptogenic etiology is used if no obvious cause is found for partial-onset seizures. The incidence of idiopathic epilepsy is higher in children. Many factors have been shown to precipitate seizures in susceptible individuals. Hyperventilation can precipitate absence seizures.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Sleep, sleep deprivation, sensory stimuli, and emotional stress increase the frequency of seizures. Hormonal changes occurring around the time of menses, puberty, or pregnancy have also been associated with the onset of or an increased frequency of seizures. A careful history should be obtained from patients presenting with seizures because theophylline, alcohol, high-dose phenothiazines, antidepressants (especially maprotiline or bupropion), and street drug use have been associated with provoking seizures. Perinatal injuries and small gestational weight at birth are also risk factors for the development of partial-onset seizures. Immunizations have not been associated with an increased risk of epilepsy.</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<u style="color: #0b5394;"><b>Clinical Presentation</b></u></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The International League Against Epilepsy (ILAE) has proposed two major schemes for the classification of seizures and epilepsies: the International Classification of Epileptic Seizures and the International Classification of the Epilepsies and Epilepsy Syndromes. The International Classification of Epileptic Seizures (Table bellow) combines the clinical description with certain electrophysiologic findings to classify epileptic seizures. Seizures are divided into two main pathophysiologic groups—partial seizures and generalized seizures— by EEG recordings and clinical symptomatology.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Partial (focal) seizures begin in one hemisphere of the brain and— unless they become secondarily generalized—result in an asymmetric motor manifestation. Partial seizures manifest as alterations in motor functions, sensory or somatosensory symptoms, or automatisms. Partial seizures with no loss of consciousness are classified as simple partial (SP). In some cases, patients will describe somatosensory symptoms as a “warning” prior to the development of a GTC seizure. These warnings are in fact simple partial seizures and frequently are termed auras. Partial seizures with an alteration of consciousness are described as complex partial (CP). With CP seizures, the patient can have automatisms, periods of memory loss, or aberrations of behavior. Some patients with CP epilepsy have been mistakenly diagnosed as having psychotic episodes. CP seizures also can progress to GTC seizures.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Patients with CP seizures typically are amnestic to these events. Generalized seizures have clinical manifestations that indicate involvement of both hemispheres. Motor manifestations are bilateral, and there is a loss of consciousness. Generalized seizures can be further subdivided by EEG and clinical manifestations. A partial seizure that becomes generalized is referred to as a secondarily generalized seizure. Generalized absence seizures are manifested by a sudden onset, interruption of ongoing activities, a blank stare, and possibly a brief upward rotation of the eyes. They generally occur in young children through adolescence. It is important to differentiate absence seizures from complex partial seizures.</div>
<div style="text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<u><b>International Classification of Epileptic Seizures</b></u></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
I. Partial seizures (seizures begin locally)</div>
<div style="text-align: justify;">
A. Simple (without impairment of consciousness)</div>
<div style="text-align: justify;">
1. With motor symptoms</div>
<div style="text-align: justify;">
2. With special sensory or somatosensory symptoms</div>
<div style="text-align: justify;">
3. With psychic symptoms</div>
<div style="text-align: justify;">
B. Complex (with impairment of consciousness)</div>
<div style="text-align: justify;">
1. Simple partial onset followed by impairment of consciousness with or without automatisms</div>
<div style="text-align: justify;">
2. Impaired consciousness at onset with or without automatisms</div>
<div style="text-align: justify;">
C. Secondarily generalized (partial onset evolving to generalized tonic-clonic seizures)</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
II. Generalized seizures (bilaterally symmetrical and without local onset)</div>
<div style="text-align: justify;">
A. Absence</div>
<div style="text-align: justify;">
B. Myoclonic</div>
<div style="text-align: justify;">
C. Clonic</div>
<div style="text-align: justify;">
D. Tonic</div>
<div style="text-align: justify;">
E. Tonic-clonic</div>
<div style="text-align: justify;">
F. Atonic</div>
<div style="text-align: justify;">
G. Infantile spasms</div>
<div style="text-align: justify;">
III. Unclassified seizures</div>
<div style="text-align: justify;">
IV. Status epilepticus</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
GTC seizures are what many people think of as epilepsy. The seizure results in a sudden sharp tonic contraction of muscles followed by a period of rigidity and clonic movements. During the seizure, the patient may cry or moan, lose sphincter control, bite the tongue, or develop cyanosis. After the seizure, the patient may have altered consciousness, drowsiness, or confusion for a variable period of time (postictal period) and frequently goes into a deep sleep. Tonic and clonic seizures can occur separately. Brief shock-like muscular contractions of the face, trunk, and extremities are known as myoclonic jerks. They can be isolated events or rapidly repetitive. A sudden loss of muscle tone is known as an atonic seizure. This can be described as a head drop, the dropping of a limb, or a slumping to the ground. These patients often wear protective head ware to prevent trauma.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The International Classification of Epilepsies and Epilepsy Syndromes adds components such as age of onset, intellectual development, findings on neurologic examination, and results of neuroimaging studies to define epilepsy syndromes more fully. Syndromes can include one or many different seizure types (e.g., Lennox-Gastaut syndrome). The syndromic approach includes seizure type(s) and possible etiologic classifications (e.g., idiopathic, symptomatic, or unknown). Idiopathic describes syndromes that are presumably genetic but also those in which no underlying etiology is documented or suspected. A family history of seizures is commonly present, and neurologic function is essentially normal except for the occurrence of seizures. Symptomatic cases involve evidence of brain damage or a known underlying cause. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
A cryptogenic syndrome is assumed to be symptomatic of an underlying condition that cannot be documented. Unknown or undetermined is used when no cause can be identified. This syndromic classification is more important for prognostic determinations than for a classification based simply on seizure type. The syndrome classification scheme requires more information and, in return, provides a more powerful tool for comprehensive clinical management. A patient’s epilepsy is classified based on seizure type (i.e., generalized versus partial) and syndromic type (i.e., idiopathic, symptomatic, or cryptogenic).</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<u style="color: #0b5394;"><b>Clinical Presentation of Epilepsy </b></u></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>General</b></div>
<div style="text-align: justify;">
In most cases, the healthcare provider will not be in a position to witness a seizure. Many patients (particularly those with CP or GTC seizures) are amnestic to the actual seizure event. Obtaining an adequate history and description of the ictal event (including time course) from a third party (e.g., significant other, family member, or witness) is critically important. With treatment the typical clinical presentation of the seizure may change. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Symptoms</b></div>
<div style="text-align: justify;">
Symptoms of a specific seizure will depend on seizure type. Although seizures can vary between patients, they tend to be stereotyped within an individual.</div>
<ul style="text-align: justify;">
<li>CP seizures can include somatosensory or focal motor features.</li>
<li>CP seizures are associated with altered consciousness.</li>
<li>Absence seizures can be almost nondetectable with only very brief (seconds) periods of altered consciousness.</li>
<li>GTC seizures are major convulsive episodes and are always associated with a loss of consciousness.</li>
</ul>
<div style="text-align: justify;">
<b>Signs</b></div>
<div style="text-align: justify;">
Interictally (between seizure episodes), there are typically no objective or pathognomonic signs</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Laboratory Tests</b></div>
<div style="text-align: justify;">
There are currently no diagnostic laboratory tests for epilepsy. In some cases, particularly following GTC (or perhaps CP) seizures, serum prolactin levels can be transiently elevated. Laboratory tests can be done to rule out treatable causes of seizures (e.g., hypoglycemia, altered electrolyte concentrations, infections, etc.) that do not represent epilepsy.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Other Diagnostic Tests</b></div>
<ul style="text-align: left;">
<li>EEG is very useful in the diagnosis of various seizure disorders.</li>
<li style="text-align: justify;">An epileptiform EEG is found in only approximately 50% of the patients who have epilepsy.</li>
<li style="text-align: justify;">A prolactin serum level obtained within 10 to 20 minutes of a tonic-clonic seizure can be useful in differentiating seizure activity from pseudoseizure activity but not from syncope.</li>
<li style="text-align: justify;">Although magnetic resonance imaging (MRI) is very useful (especially imaging of the temporal lobes), a computed tomography (CT) scan typically is not helpful except in the initial evaluation for a brain tumor or cerebral bleeding. </li>
</ul>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/clinical-presentaion-epilepsy.html"><u style="color: #0b5394;"><b>Clinical Presentation of Epilepsy and Seizure</b></u></a></div>
<div style="text-align: left;">
Source: pharmacotherapy 7th </div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com7tag:blogger.com,1999:blog-7113702905971561223.post-76218068557761569252012-04-21T09:49:00.000+07:002012-04-21T10:34:21.584+07:00Treatment of Diabetes Mellitus<div dir="ltr" style="text-align: left;" trbidi="on">
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/04/treatment-of-diabetes-mellitus.html">Treatment of Diabetes Mellitus</a> - General Approach to Treatment ; </b>Appropriate care requires goal setting for glycemia, blood pressure, and lipid levels, regular monitoring for complications, dietary and exercise modifications, medications, appropriate self-monitored blood glucose (SMBG), and laboratory assessment of the aforementioned parameters. Glucose control alone does not sufficiently reduce the risk of macrovascular complications in persons with<a href="http://umaeenews.blogspot.com/2012/04/classification-of-diabetes-mellitus.html"> DM</a>.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Glycemic Goal Setting and The Hemoglobin A1c</b></div>
<div style="text-align: justify;">
<br />
Controlled clinical trials provide ample evidence that glycemic control is paramount in reducing microvascular complications in both type 1 DM and type 2 DM. HbA1c measurements are the gold standard for following long-term glycemic control for the previous 2 to 3 months. Hemoglobinopathies, anemia, and red cell membrane defects can affect HbA1c measurements. Other strategies such as measurement of fructosamine, which measures glycated plasma proteins and correlates to glucose control over the last 2 to 3 weeks, can be necessary to assess diabetes control in these patients.</div>
<div style="text-align: justify;">
<br />
Unless the risk outweighs the benefit (as in elderly patients, patients with advanced complications, and patients with other advanced disease), a HbA1c target of <7% is appropriate (Table bellow), and lower values should be targeted if significant hypoglycemia and/or weight gain can be avoided.</div>
<br />
<div style="text-align: center;">
<b>Glycemic Goals of Therapy</b></div>
<br />
<div style="text-align: left;">
<b>Biochemical Index ADA ACE and AACE</b><br />
Hemoglobin A1c <7%a ≤6.5%<br />
Preprandial plasma glucose 90–130 mg/dL <110 mg/dL<br />
(5.0–7.2 mmol/L)<br />
Postprandial plasma glucose <180 mg/dLb <140 mg/dL<br />
(<10 mmol/L) </div>
<br />
<div style="text-align: justify;">
<b>Monitoring Complications</b></div>
<div style="text-align: justify;">
<br />
The ADA recommends initiation of complications monitoring at the time of diagnosis of DM. Current recommendations continue to advocate yearly dilated eye examinations in type 2 DM, and an initial eye examination in the first 3 to 5 years in type 1 DM, then yearly thereafter. Less frequent testing (every 2 to 3 years) can be implemented on the advice of an eye care specialist. The feet should be examined and the blood pressure assessed at each visit. A urine test for microalbumin once yearly is appropriate. Yearly testing for lipid abnormalities, and more frequently if needed to achieve lipid goals, is recommended.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Self-Monitoring of Blood Glucose</b></div>
<div style="text-align: justify;">
<br />
The advent of SMBG in the early 1980s revolutionized the treatment of DM, enabling patients to know their blood glucose concentration at any moment easily and relatively inexpensively. Frequent SMBG is necessary to achieve near-normal blood glucose concentrations and to assess for hypoglycemia, particularly in patients with type 1 DM.62 The more intense the pharmacologic regimen is, the more intense the SMBG needs to be (four or more times daily in patients on multiple<a href="http://umaeenews.blogspot.com/2012/04/insulin-algorithm-for-diabetes-mellitus.html"> insulin injections</a> or pump therapy). The optimal frequency of SMBG for patients with type 2 DM is unresolved.</div>
<div style="text-align: justify;">
<br />
Frequency of monitoring in type 2 DM should be sufficient to facilitate reaching glucose goals. The role of SMBG in improving glycemic control in type 2 DM patients is controversial but has shown to reduce the HbA1c ~0.4%.63 What is clear is that patients must be empowered to change their therapeutic regimen (lifestyle and medications) in response to test results, or no meaningful glycemic improvement is likely to be effected.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Nonpharmacologic Therapy </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i><b>Diet</b></i></div>
<div style="text-align: justify;">
<br />
Medical nutrition therapy is recommended for all persons with DM. Paramount for all medical nutrition therapy is the attainment of optimal metabolic outcomes and the prevention and treatment of complications. For individuals with type 1 DM, the focus is on regulating insulin administration with a balanced diet to achieve and maintain a healthy body weight. A meal plan that is moderate in carbohydrates and low in saturated fat (<7% of total calories), with a focus on balanced meals is recommended. The amount (grams) and type (via the glycemic index, although controversial) of carbohydrates, whether accounted for by exchanges or carbohydrate counting, should be considered. It is imperative that patients understand the connection between carbohydrate intake and glucose control. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In addition, patients with type 2 DM often require caloric restriction to promote weight loss. Rather than a set diabetic diet, advocate a diet using foods that are within the financial reach and cultural milieu of the patient. As most patients with type 2 DM are overweight or obese, bedtime and between-meal snacks are not needed if pharmacologic management is appropriate.</div>
<div style="text-align: justify;">
<br />
<b>Clinical Controversy </b></div>
<div style="text-align: justify;">
<br />
The recommended daily carbohydrate intake for type 2 DM, and even type 1 DM, has become controversial since low-carbohydrate diets such as the Atkins, South Beach, and Carbohydrate Addict’s Diets have become exceptionally popular. Currently, the ADA recommends that approximately 45% to 65% of daily caloric intake should come from carbohydrates and does not recommend restricting diets to <130 grams of carbohydrate a day. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Many clinicians are trying to increase the monounsaturated fat percentage and decrease the carbohydrate percentage in a patient’s diet to accomplish improved glycemic control. Recent studies have documented short-term success for weight loss on low-carbohydrate diets (~6 months), without deleterious effects on the lipid panel. Weight loss can reduce cardiovascular risk factors in type 2 DM.</div>
<div style="text-align: justify;">
<br />
<i><b>Activity</b></i></div>
<div style="text-align: justify;">
<br />
In general, most patients with DM can benefit from increased activity. Aerobic exercise improves insulin resistance and glycemic control in the majority of individuals, and reduces cardiovascular risk factors, contributes to weight loss or maintenance, and improves well-being. The patient should choose an activity that she or he is likely to continue. Start exercise slowly in previously sedentary patients. Older patients, patients with long-standing disease (age >35 years, or >25 years with DM ≥10 years), patients with multiple cardiovascular risk factors, presence of microvascular disease, and patients with previous evidence of atherosclerotic disease should have a cardiovascular evaluation, probably including an electrocardiogram and graded exercise test with imaging, prior to beginning a moderate to intense exercise regimen. In addition, several complications (autonomic neuropathy, insensate feet, and retinopathy) can require restrictions on the activities recommended.</div>
<div style="text-align: justify;">
<br />
Physical activity goals include at least 150 minutes/week of moderate (50%–70% maximal hear rate) intensity exercise. In addition, resistance training, in patients without retinal contraindications, is recommended for 30 minutes three times per week.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/treatment-of-diabetes-mellitus.html"><b>Treatment of Diabetes Mellitus</b></a></div>
<div style="text-align: left;">
Source: pharmacotherapy 7th</div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com3tag:blogger.com,1999:blog-7113702905971561223.post-12551314574928402962012-04-20T13:17:00.000+07:002012-04-20T13:19:51.203+07:00Insulin Algorithm for Type 2 Diabetes Mellitus<div dir="ltr" style="text-align: left;" trbidi="on">
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/insulin-algorithm-for-diabetes-mellitus.html"><b>Insulin Algorithm for Type 2 Diabetes Mellitus</b></a> - The primary goals of <a href="http://umaeenews.blogspot.com/2012/04/classification-of-diabetes-mellitus.html">Diabetes Mellitus</a> management are to reduce the risk for microvascular and macrovascular disease complications, to ameliorate symptoms, to reduce mortality, and to improve quality of life. Near-normal glycemia will reduce the risk for development of microvascular disease complications, but aggressive management of traditional cardiovascular risk factors (i.e., smoking cessation, treatment of dyslipidemia, intensive blood pressure control, and antiplatelet therapy) are needed to reduce the likelihood of development of macrovascular disease. Following this figure an algorithm for insulin therapy options in type 2 DM.</div>
<div style="text-align: justify;">
<br /></div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-86C3UPAbeTDWUscEm-hqXtkvdNJd8JMu8DD_n_sSyHPzyc9mLtLT4bC_q8eS0tQORgxoRji2NLgTS5KfPhbKTSSfIk3l42R9EOudUdaq5AVPmSXwVqY0BgABMkTfvc9dTSrAKFVgpmI/s1600/Insulin+Algorithm.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="Insulin Algorithm for type 2 Diabetes Mellitus" border="0" height="310" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-86C3UPAbeTDWUscEm-hqXtkvdNJd8JMu8DD_n_sSyHPzyc9mLtLT4bC_q8eS0tQORgxoRji2NLgTS5KfPhbKTSSfIk3l42R9EOudUdaq5AVPmSXwVqY0BgABMkTfvc9dTSrAKFVgpmI/s400/Insulin+Algorithm.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Insulin algorithm for type 2 diabetes mellitus (DM) in children and adults</td></tr>
</tbody></table>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee<br />
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/insulin-algorithm-for-diabetes-mellitus.html"><b>Insulin Algorithm for Type 2 Diabetes Mellitus</b></a></div>
<div style="text-align: left;">
Source: pharmacotherapy 7th<b> </b> </div>
</div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com0tag:blogger.com,1999:blog-7113702905971561223.post-52916074343735047652012-04-19T16:52:00.000+07:002012-04-19T18:09:53.737+07:00Algorithm Treatment of Constipation<div dir="ltr" style="text-align: left;" trbidi="on">
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWvtb5pwgUbK26K3t8vi-TjGdSJrsJgKZZQSFLjsdfGRT1ZIZMN8UuzqIWyDqoNM3jPOSFLAj2SIiBPdlys0Gu-Pqehc2XJ8z14ZRy_V5sLh1CF94gAPXGVj0tKlh-EwwCpybyPEiNIe4/s1600/constipation.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="constipation" border="0" height="211" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWvtb5pwgUbK26K3t8vi-TjGdSJrsJgKZZQSFLjsdfGRT1ZIZMN8UuzqIWyDqoNM3jPOSFLAj2SIiBPdlys0Gu-Pqehc2XJ8z14ZRy_V5sLh1CF94gAPXGVj0tKlh-EwwCpybyPEiNIe4/s320/constipation.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Constipation</td></tr>
</tbody></table>
<b><a href="http://umaeenews.blogspot.com/2012/04/algorithm-treatment-of-constipation.html">Algorithm Treatment of Constipation</a> - </b>The patient should be asked about the frequency of bowel movements and the chronicity of constipation. <a href="http://umaeenews.blogspot.com/2012/04/causes-signs-and-symptoms-of.html">Constipation</a> occurring recently in an adult may indicate significant colon pathology such as malignancy; constipation present since early infancy may be indicative of neurologic disorders. The patient also should be carefully questioned about usual diet and laxative regimens. Does the patient have a diet consistently deficient in high-fiber items and containing mainly highly refined foods? What laxatives or cathartics has the patient used to attempt relief of constipation? The patient should be questioned about other concurrent medications, with interest focused on agents that might cause constipation.</div>
<div style="text-align: justify;">
<br />
For most patients who complain of constipation, a thorough physical examination is not required after it is established that constipation (a) is not a chronic problem, (b) is not accompanied by signs of significant GI disease (e.g., rectal bleeding or anemia), and (c) does not cause severe discomfort. In these circumstances, the patient may be referred directly to the first-line therapies for constipation described in the next section (mainly bulk-forming laxatives and dietary fiber with occasional use of saline or stimulant laxatives). Table bellow presents a general treatment algorithm for the management of constipation.</div>
<div style="text-align: justify;">
<br /></div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1gRth0CMbGgiVdSrAlOXtKzqVnHWYE3K7GtZC9cgjLTwa3HWo0L2VeOXOgPCqoakFDnq-Co47KTVle3t1g0Hz2Z0AeFr3aci4S4XMQbcedmRcdQrV8PD31QC0ZFTXJy1CkkRsDHNVOdU/s1600/Constipation.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="Constipation Treatment Algorithm" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1gRth0CMbGgiVdSrAlOXtKzqVnHWYE3K7GtZC9cgjLTwa3HWo0L2VeOXOgPCqoakFDnq-Co47KTVle3t1g0Hz2Z0AeFr3aci4S4XMQbcedmRcdQrV8PD31QC0ZFTXJy1CkkRsDHNVOdU/s1600/Constipation.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Constipation Treatment Algorithm</td></tr>
</tbody></table>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
The proper management of constipation requires a number of different modalities; however, the basis for therapy should be dietary modification. The major dietary change should be an increase in the amount of fiber consumed daily. In addition to dietary management, patients should be encouraged to alter other aspects of their lifestyles if necessary. Important considerations are to encourage patients to exercise (achieved even by brisk walking after dinner) and to adjust bowel habits so that a regular and adequate time is made to respond to the urge to defecate. Another general measure is to increase fluid intake. This is generally recommended and believed beneficial, although there is little objective evidence to support this measure.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
If an underlying disease is recognized as the cause of constipation, attempts should be made to correct it. GI malignancies may be removed via surgical resection. Endocrine and metabolic derangements should be corrected by the appropriate methods. For example, when hypothyroidism is the cause of constipation, cautious institution of thyroid-replacement therapy is the most important treatment measure. As discussed earlier, many drug substances may cause constipation.</div>
<div style="text-align: justify;">
<br />
If a patient is consuming medications well known to cause constipation, consideration should be given to alternative agents. For some medications (e.g., antacids), nonconstipating alternatives exist. If no reasonable alternatives exist to the medication thought to be responsible for constipation, consideration should be given to lowering the dose. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Nonpharmacologic Therapy </b></div>
<div style="text-align: justify;">
<br />
<i>Dietary Modification and Bulk-Forming Agents</i></div>
<div style="text-align: justify;">
The most important aspect of therapy for constipation for the majority of patients is dietary modification to increase the amount of fiber consumed. Fiber, the portion of vegetable matter not digested in the human GI tract, increases stool bulk, retention of stool water, and rate of transit of stool through the intestine. The result of fiber therapy is an increased frequency of defecation. Also, fiber decreases intraluminal pressures in the colon and rectum, which is thought to be beneficial for diverticular disease and for irritable bowel syndrome.<br />
The specific physiologic effects of fiber are not well understood. Patients should be advised to include at least 10 g of crude fiber in their daily diets.26 Fruits, vegetables, and cereals have the highest fiber content. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Bran, a by-product of milling of wheat, is often added to foods to increase fiber content and contains a high amount of soluble fiber, which may be extremely constipating in larger doses. Raw bran is generally 40% fiber. Medicinal products, often called “bulk-forming agents,” such as psyllium hydrophilic colloids, methylcellulose, or polycarbophil, have properties similar to those of dietary fiber and may be taken as tablets, powders, or granules (Table bellow). A trial of dietary modification with high-fiber content should be<br />
continued for at least 1 month before effects on bowel function are determined. Most patients begin to notice effects on bowel function 3 to 5 days after beginning a high-fiber diet, but some patients may require a considerably longer period of time. Patients should be cautioned that abdominal distension and flatus may be particularly troublesome in the first few weeks of fiber therapy, particularly with high bran consumption. In most cases these problems resolve with continued use.</div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi6CIcVBKKw7JpdDKagi1Zk5b_8FXPfuWdWNbBd8tC3kOdXv8xO5_Lc48K77P2j7ikKA2ER_4KDoBMGrQrdbq1smEnfwJDXikMAOygLVCLSlPIfKVHqbhorsJ20GTM4rnbqe4WgVmNrI_s/s1600/Constipation+1.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="laxatives and Cathartics" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi6CIcVBKKw7JpdDKagi1Zk5b_8FXPfuWdWNbBd8tC3kOdXv8xO5_Lc48K77P2j7ikKA2ER_4KDoBMGrQrdbq1smEnfwJDXikMAOygLVCLSlPIfKVHqbhorsJ20GTM4rnbqe4WgVmNrI_s/s1600/Constipation+1.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Dosage Recommendations for Laxatives and Cathartics</td></tr>
</tbody></table>
<div style="text-align: justify;">
Bulk-forming laxatives have few adverse effects. The only major caution in the use of bulk-forming laxatives is that obstruction of the esophagus, stomach, small intestine, and colon has been reported when the agents have been consumed without sufficient fluid and in patients with intestinal stenosis.</div>
<div style="text-align: justify;">
<i><br />Surgery</i><br />
In a small percentage of patients who present with complaints of constipation, surgical procedures are necessary because of the presence of colonic malignancies or GI obstruction from a number of other causes. In each case, the involved segment of intestine may be resected or revised. Surgery may be required in some endocrine disorders that cause constipation, such as pheochromocytoma, which requires removal of a tumor.</div>
<div style="text-align: justify;">
<br />
<i>Biofeedback</i><br />
The majority of patients with constipation related to pelvic floor dysfunction can benefit from electromyogram-guided biofeedback therapy. The value of biofeedback in children with chronic constipation has not been well demonstrated.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-treatment-of-constipation.html"><b>Algorithm Treatment of Constipation</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com2tag:blogger.com,1999:blog-7113702905971561223.post-18159655720668352372012-04-19T16:21:00.000+07:002012-04-22T00:38:29.997+07:00Classification & Screening of Diabetes Mellitus<div dir="ltr" style="text-align: left;" trbidi="on">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQKmEO_3Np2WV_LHfHwACNwg4numupCLFBxtmnF9NcdrL3fD4a8S0nxfdZugeLu6MZmcOddK1C6d-0-p3qyUWtTLTUZlD67F8N_rOqrO69nz22qgZo3rb4bgkkTg3tWdy5BnwgeDATWpA/s1600/diabetic.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="211" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQKmEO_3Np2WV_LHfHwACNwg4numupCLFBxtmnF9NcdrL3fD4a8S0nxfdZugeLu6MZmcOddK1C6d-0-p3qyUWtTLTUZlD67F8N_rOqrO69nz22qgZo3rb4bgkkTg3tWdy5BnwgeDATWpA/s320/diabetic.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Diabetes Mellitus</td></tr>
</tbody></table>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/04/classification-of-diabetes-mellitus.html">Classification and Screening of Diabetes Mellitus</a> -<span style="color: #0b5394;"> </span></b><u style="color: #0b5394;"><b>Classification of Diabetes</b></u></div>
<div style="text-align: justify;">
<br />
Diabetes is a metabolic disorder characterized by resistance to the action of insulin, insufficient insulin secretion, or both. The clinical manifestation of these disorders is hyperglycemia. The vast majority of diabetic patients are classified into one of two broad categories: type 1 diabetes caused by an absolute deficiency of insulin, or type 2 diabetes defined by the presence of insulin resistance with an inadequate compensatory increase in insulin secretion. Women who develop diabetes because of the stress of pregnancy are classified as having gestational diabetes. Finally, uncommon types of diabetes caused by infections, drugs, endocrinopathies, pancreatic destruction, and known genetic defects are classified separately (Table).</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<br /></div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZmz3uL5FEDN2AUORjow9rJq_r23SoYr2pEhEKyiL6MzSlEIvddfw2AyVNo0wTg460hO4YgoHOaI15-YN-d_Smw0RV0qY6S4xHydahOIOcn1xEril-6rswK9sLsgPLbR7ciNpaXSsY5mY/s1600/DM.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="332" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZmz3uL5FEDN2AUORjow9rJq_r23SoYr2pEhEKyiL6MzSlEIvddfw2AyVNo0wTg460hO4YgoHOaI15-YN-d_Smw0RV0qY6S4xHydahOIOcn1xEril-6rswK9sLsgPLbR7ciNpaXSsY5mY/s400/DM.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Etiologic Classification of Diabetes Mellitus</td></tr>
</tbody></table>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
</div>
<div style="color: #0b5394; text-align: justify;">
<u><b>Type 1 Diabetes</b></u></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
This form of diabetes results from autoimmune destruction of the β cells of the pancreas. Markers of immune destruction of the β cell are present at the time of diagnosis in 90% of individuals and include islet cell antibodies, antibodies to glutamic acid decarboxylase, and antibodies to insulin. Although this form of diabetes usually occurs in children and adolescents, it can occur at any age. Younger individuals typically have a rapid rate of β-cell destruction and present with <a href="http://umaeenews.blogspot.com/2012/03/diabetic-ketoacidosis-and-hyperosmolar.html">ketoacidosis</a>, whereas adults often maintain sufficient insulin secretion to prevent ketoacidosis for many years, which is often referred to as LADA.</div>
<div style="text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<u><b>Type 2 Diabetes</b></u></div>
<div style="text-align: justify;">
<br />
This form of diabetes is characterized by insulin resistance and a relative lack of insulin secretion, with progressively lower insulin secretion over time. Most individuals with type 2 diabetes exhibit abdominal obesity, which itself causes insulin resistance. In addition, hypertension, dyslipidemia (high triglyceride levels and low HDL-cholesterol levels), and elevated plasminogen activator inhibitor type 1 (PAI-1) levels are often present in these individuals. This clustering of abnormalities is referred to as the insulin resistance syndrome or the metabolic syndrome. Because of these abnormalities, patients with type 2 diabetes are at increased risk of developing macrovascular complications. Type 2 diabetes has a strong genetic predisposition and is more common in all ethnic groups other than those of European ancestry. At this point the genetic cause of most cases of type 2 diabetes is not well defined.</div>
<div style="color: #0b5394; text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<u><b>Gestational Diabetes Mellitus</b></u></div>
<div style="text-align: justify;">
<br />
GDM is defined as glucose intolerance that is first recognized during pregnancy. Gestational diabetes complicates approximately 7% of all pregnancies. Clinical detection is important, as therapy will reduce perinatal morbidity and mortality. </div>
<div style="text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<u><b>Other Specific Types of Diabetes</b></u></div>
<div style="text-align: justify;">
<br />
Genetic Defects MODY is characterized by impaired insulin secretion with minimal or no insulin resistance. Patients typically exhibit mild hyperglycemia at an early age. The disease is inherited in an autosomal dominant pattern with at least six different loci identified to date. Genetic inability to convert proinsulin to insulin results in mild hyperglycemia and is inherited in an autosomal dominant pattern. Similarly, the production of mutant insulin molecules has been identified in a few families and results in mild glucose intolerance.</div>
<div style="text-align: justify;">
<br />
Several genetic mutations have been described in the insulin receptor and are associated with insulin resistance. Type A insulin resistance refers to the clinical syndrome of acanthosis nigricans, virilization in women, polycystic ovaries, and hyperinsulinemia. In contrast, type B insulin resistance is caused by autoantibodies to the insulin receptor. Leprechaunism is a pediatric syndrome with specific facial features and severe insulin resistance because of a defect in the insulin receptor gene. Lipoatrophic diabetes probably results from postreceptor defects in insulin signaling. </div>
<div style="text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<u><b>Screening</b></u></div>
<div style="text-align: justify;">
<br />
<div style="color: #0b5394;">
<b>Type 1 Diabetes Mellitus</b></div>
</div>
<div style="text-align: justify;">
<br />
There is still a low prevalence of type 1 DM in the general population and because of the acuteness of symptoms, screening for type 1 DM is not recommended.</div>
<div style="text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<b>Type 2 Diabetes Mellitus</b></div>
<div style="text-align: justify;">
<br />
Based on expert opinion, and not uniformly accepted by all guidance organizations, the American Diabetes Association (ADA) recommends screening for type 2 DM every 3 years in all adults beginning at age 45 years. Testing should be considered at an earlier age and more frequently in individuals with risk factors. The recommended screening test is the fasting plasma glucose (FPG). An oral glucose tolerance test (OGTT) (more costly, less convenient, less reproducible) can be performed alternatively or in addition to FPG when a high index of suspicion for the disease is present.</div>
<div style="text-align: justify;">
<br /></div>
<div style="color: #0b5394; text-align: justify;">
<b>Children and Adolescents</b></div>
<div style="text-align: justify;">
<br />
Despite a lack of clinical evidence to support widespread testing of children for type 2 DM, it is clear that more children and adolescents are developing type 2 DM. The ADA, by expert opinion, recommends that overweight (defined as BMI >85th percentile for age and sex, weight for height >85th percentile, or weight >120% of ideal [50th percentile] for height) youths with at least two of the following risk factors: a family history of type 2 diabetes in first- and second-degree relatives; Native Americans, African Americans, Hispanic Americans, and Asians/South Pacific Islanders; and those with signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, or polycystic ovary syndrome) be screened. Testing should be done every 2 years starting at 10 years of age or at the onset of puberty if it occurs at a younger age.</div>
<div style="color: #0b5394; text-align: justify;">
<br />
<b>Gestational Diabetes</b></div>
<div style="text-align: justify;">
<br />
Risk assessment for GDM should occur at the first prenatal visit. Women at high risk (positive family history, history of GDM, marked obesity, or member of a high-risk ethnic group) should be screened as soon as feasible. If the initial screening is negative, they should undergo retesting at 24 to 28 weeks of gestation, as should all other pregnant women with the possible exception of low-risk primigravidas. Evaluation for GDM can be done in one of two ways. The one-step approach involves a 3-hour, 100 gram-OGTT and can be cost-effective in high-risk patient populations. The two-step approach uses a screening test to measure plasma or serum glucose concentration 1 hour after a 50 gram oral glucose load (glucose challenge test), followed by a diagnostic 3-hour OGTT on the subset of women exceeding a glucose threshold of either ≥140 mg/dL (80% sensitive) or ≥130 mg/dL (90% sensitive). The diagnosis of GDM is based on a 75-gram (not as well validated) or 100-gram OGTT. Criteria for diagnosis of GDM based on the OGTT are summarized in Table bellow</div>
<div style="text-align: justify;">
<br /></div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgOe527ztsRngyg1ohaU_xbgxmIvsoOJDZXN_spGJa_CEmikmkhlZIhooJNTYhFBeNHvNS5-9CvbxrBxCsVspN811Y3UV7KTSeIotDsTI4jHtYVcsMLsg13FdCRsDAcJP2qqF-6YNBFjHc/s1600/DM+1.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="221" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgOe527ztsRngyg1ohaU_xbgxmIvsoOJDZXN_spGJa_CEmikmkhlZIhooJNTYhFBeNHvNS5-9CvbxrBxCsVspN811Y3UV7KTSeIotDsTI4jHtYVcsMLsg13FdCRsDAcJP2qqF-6YNBFjHc/s400/DM+1.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Diagnosis of Gestational Diabetes Mellitus with a<br />
100-g or 75-g Glucose Load</td></tr>
</tbody></table>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/classification-of-diabetes-mellitus.html"><b>Classification and Screening of Diabetes Mellitus</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com2tag:blogger.com,1999:blog-7113702905971561223.post-58044533382220408202012-04-18T17:44:00.001+07:002012-04-18T17:45:44.508+07:00Causes, Signs, and Symptoms of Constipation<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiWVmbhZVIOSvTwj2xiTCaaIwPYam2JIKz21x63tev3McOfwtjoohH9T8QEo4mAVigwRfHPFo-2cCcaJfR1oNofSaa6UMBXzroDr_qI2M1WgNvRJyyKe-eNsDJ0dy3OVZmSXFKWrrSeQks/s1600/constipation.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="212" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiWVmbhZVIOSvTwj2xiTCaaIwPYam2JIKz21x63tev3McOfwtjoohH9T8QEo4mAVigwRfHPFo-2cCcaJfR1oNofSaa6UMBXzroDr_qI2M1WgNvRJyyKe-eNsDJ0dy3OVZmSXFKWrrSeQks/s320/constipation.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/04/causes-signs-and-symptoms-of.html">Causes, Signs, and Symptoms of Constipation </a>- </b>Constipation is a commonly encountered medical condition in the United States for which many patients initiate self-treatment. One reason constipation continues to be a frequent problem in this country is lack of adequate dietary fiber. Another unfortunate problem is that many people have misconceptions about normal bowel function, and think that daily bowel movements are required for health and well being. Others believe that the lack of a daily bowel movement contributes to the accumulation of toxic substances or is associated with various somatic complaints. These misconceptions often lead to the inappropriate use of laxatives by<br />
the general public.</div>
<div style="text-align: justify;">
<br />
Constipation does not have a single, generally agreed upon definition. When using the term, the lay public or healthcare professional may be referring to several difficult-to-quantify variables: bowel movement frequency, stool size or consistency, and such symptoms as the sensation of incomplete defecation. Stool frequency is most often used to describe constipation; however, the frequency of bowel movements used to define constipation is not well established.</div>
<div style="text-align: justify;">
<br />
Normal people pass at least 3 stools per week. Some of the definitions of constipation used in clinical studies include (a) less than 3 stools per week for women and 5 stools per week for men despite a high-residue diet, or a period of more than 3 days without a bowel movement; (b) straining at stool greater than 25% of the time and/or 2 or fewer stools per week; or (c) straining at defecation and less than 1 stool daily with minimal effort. These varying definitions demonstrate the difficulty in characterizing this problem. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
An international committee defined and classified constipation on the basis of stool frequency, consistency, and difficulty of defecation. Functional constipation is defined as two or more of the following complaints present for at least 12 months in the absence of laxative use: (a) straining at least 25% of the time; (b) lumpy or hard stools at least 25% of the time; (c) a feeling of incomplete evacuation at least 25% of the time; or (d) two or fewer bowel movements in a week. Rectal outlet delay is defined as anal blockage more than 25% of the time and prolonged defecation or manual disimpaction when necessary. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Pathophysiology </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Constipation is not a disease, but a symptom of an underlying disease or problem. Approaches to the treatment of constipation should begin with attempts to determine its cause. Disorders of the GI tract (irritable bowel syndrome or diverticulitis), metabolic disorders (diabetes), or endocrine disorders (hypothyroidism) may be involved. Constipation commonly results from a diet low in fiber or from use of constipating drugs such as opiates. Finally, constipation may sometimes be psychogenic in origin.24 Each of these causes is discussed in the following sections.</div>
<div style="text-align: justify;">
<br />
Constipation is a frequently reported problem in the elderly, probably the result of improper diets (low in fiber and liquids), diminished abdominal wall muscular strength, and possibly diminished physical activity. However, as previously stated, the frequency of bowel movements is not decreased with normal aging. In addition, diseases that may cause constipation, such as colon cancer and diverticulitis, are more common with increasing age. </div>
<div style="text-align: justify;">
<br />
The majority of cases of drug-induced constipation are caused by opiates, various agents with anticholinergic properties, and antacids containing aluminum or calcium. The inhibitory effects on bowel function are dose dependent, with larger doses clearly causing constipation more frequently. Opiates have effects on all segments of the bowel, but effects are most pronounced on the colon. The major mechanism by which opiates produce constipation has been proposed to be prolongation of intestinal transit time by causing spastic, nonpropulsive contractions. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
An additional contributory mechanism may be an increase in electrolyte<br />
absorption. All opiate derivatives are associated with constipation, but the degree of intestinal inhibitory effects seems to differ between agents. Orally administered opiates appear to have greater inhibitory effects than parenterally administered products. Orally administered enkephalins (endogenous opiate-like polypeptides) are recognized to have antimotility properties.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Possible Causes of Constipation</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>GI disorders </i></div>
<div style="text-align: justify;">
Irritable bowel syndrome<br />
Diverticulitis<br />
Upper GI tract diseases<br />
Anal and rectal diseases<br />
Hemorrhoids<br />
Anal fissures<br />
Ulcerative proctitis<br />
Tumors<br />
Hernia<br />
Volvulus of the bowel<br />
Syphilis<br />
Tuberculosis<br />
Helminthic infections<br />
Lymphogranuloma venereum<br />
Hirschsprung’s disease</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Metabolic and endocrine disorders Diabetes mellitus with neuropathy</i></div>
<div style="text-align: justify;">
Hypothyroidism<br />
Panhypopituitarism<br />
Pheochromocytoma<br />
Hypercalcemia<br />
Enteric glucagon excess</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Pregnancy</i></div>
<div style="text-align: justify;">
Depressed gut motility<br />
Increased fluid absorption from colon<br />
Decreased physical activity<br />
Dietary changes<br />
Inadequate fluid intake<br />
Low dietary fiber<br />
Use of iron salts</div>
<div style="text-align: justify;">
<br />
<i>Neurogenic causes </i></div>
<div style="text-align: justify;">
CNS diseases<br />
Trauma to the brain (particularly the medulla)<br />
Spinal cord injury<br />
CNS tumors<br />
Cerebrovascular accidents<br />
Parkinson’s disease</div>
<div style="text-align: justify;">
<br />
<i>Psychogenic causes </i></div>
<div style="text-align: justify;">
Ignoring or postponing urge to defecate<br />
Psychiatric diseases</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<i>Drugs Causing Constipation</i></div>
<div style="text-align: justify;">
Analgesics<br />
Inhibitors of prostaglandin synthesis<br />
Opiates<br />
Anticholinergics<br />
Antihistamines<br />
AntiParkinsonian agents (e.g., benztropine or trihexyphenidyl)<br />
Phenothiazines<br />
Tricyclic antidepressants<br />
Antacids containing calcium carbonate or aluminum hydroxide<br />
Barium sulfate<br />
Calcium channel blockers<br />
Clonidine<br />
Diuretics (non–potassium-sparing)<br />
Ganglionic blockers<br />
Iron preparations<br />
Muscle blockers (D-tubocurarine, succinylcholine)<br />
Nonsteroidal antiinflammatory agents<br />
Polystyrene sodium sulfonate</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Clinical Presentation of Constipation</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Signs and symptoms</i><br />
• It is important to ascertain whether the patient perceives the problem as infrequent bowel movements, stools of insufficient size, a feeling of fullness, or difficulty and pain on passing stool. </div>
<div style="text-align: justify;">
• Signs and symptoms include hard, small, or dry stools, bloated stomach, cramping abdominal pain and discomfort, straining or grunting, sensation of blockade, fatigue, headache, and nausea and vomiting.</div>
<div style="text-align: justify;">
<br />
<i>Laboratory tests</i><br />
• A series of examinations, including proctoscopy, sigmoidoscopy, colonoscopy, and barium enema, may be necessary to determine the presence of colorectal pathology.<br />
• Thyroid function studies may be performed to determine the presence of metabolic and endocrine disorders</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/causes-signs-and-symptoms-of.html"><b>Causes, Signs, and Symptoms of Constipation</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com1tag:blogger.com,1999:blog-7113702905971561223.post-2276842664082443492012-04-18T14:46:00.000+07:002012-04-18T16:50:33.638+07:00Treatment of Diarrhea<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWQU_pVsR_zZ6UWnZrcNhx4JrL83_BC8rQwyZdFzNaLb24vfWt54I8D8-3rc_DyubTGdhOJbVFy9HoH2eLgFvLFcLnFgch_at87c7DvLe3axi4YQNeebZg3kgIJIeCR7uQM3hJ8kAj_ik/s1600/Diarrhea.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWQU_pVsR_zZ6UWnZrcNhx4JrL83_BC8rQwyZdFzNaLb24vfWt54I8D8-3rc_DyubTGdhOJbVFy9HoH2eLgFvLFcLnFgch_at87c7DvLe3axi4YQNeebZg3kgIJIeCR7uQM3hJ8kAj_ik/s1600/Diarrhea.jpg" /></a></div>
<b><a href="http://umaeenews.blogspot.com/2012/04/treatment-of-diarrhea.html">Treatment of Diarrhea</a> - </b>To explain<b> </b>"<b>i have diarrhea</b>"<b> </b>you must know diarrhea overall.<b> Prevention ; </b>Acute viral diarrheal illness often occurs in daycare centers and nursing homes. As person-to-person contact is the mechanism by which viral disease spreads, isolation techniques must be initiated, For bacterial, parasite, and protozoal infections, strict food handling, sanitation, water, and other environmental hygiene practices can prevent transmission. If diarrhea is secondary to another illness, controlling the primary condition is necessary. Antibiotics and bismuth subsalicylate are advocated to prevent traveler’s diarrhea, in conjunction with treatment of drinking water and caution with consumption of fresh vegetables.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Desired Outcome</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
If prevention is unsuccessful and <a href="http://umaeenews.blogspot.com/2012/04/signs-and-symptoms-of-diarrhea.html">diarrhea</a> occurs, therapeutic goals are to (a) manage the diet; (b) prevent excessive water, electrolyte, and acid–base disturbances; (c) provide symptomatic relief; (d) treat curable causes; and (e) manage secondary disorders causing diarrhea (Figs. 38–1 and 38–2). Clinicians must clearly understand that diarrhea, like a cough, may be a body defense mechanism for ridding itself of harmful substances or pathogens. The correct therapeutic response is not necessarily to stop diarrhea at all costs.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgD5yGJ8FD210u02KovIde9i5_vkVthCfTwaVMD0GhuNhSnGSFtWjKhUZX9n4bm2iPitg473UWBPqfilcLj7V4a_gGZxW189A8SCRBalYE38ueSPVc2U1Xjer1d-196Qv5my7R4GhSoiX4/s1600/Diarrhea.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="338" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgD5yGJ8FD210u02KovIde9i5_vkVthCfTwaVMD0GhuNhSnGSFtWjKhUZX9n4bm2iPitg473UWBPqfilcLj7V4a_gGZxW189A8SCRBalYE38ueSPVc2U1Xjer1d-196Qv5my7R4GhSoiX4/s400/Diarrhea.jpg" width="400" /></a></div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiWqS5jjeZrz3ycKcquxkikSZ1KRBIbtuGaPf8xldKfXTMmimh2Kp1bH_aLq0PwbVenSz1DxWr-U2DbOUiV79rZ7s1sfFmSXrWU7uCO5wNb-AdRWy4zrBFl8w5XHa8josxsGtsIWg25cRE/s1600/Diarrhea1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiWqS5jjeZrz3ycKcquxkikSZ1KRBIbtuGaPf8xldKfXTMmimh2Kp1bH_aLq0PwbVenSz1DxWr-U2DbOUiV79rZ7s1sfFmSXrWU7uCO5wNb-AdRWy4zrBFl8w5XHa8josxsGtsIWg25cRE/s640/Diarrhea1.jpg" width="376" /></a></div>
<b> Nonpharmacologic Management</b></div>
<div style="text-align: justify;">
<br />
Dietary management is a first priority in the treatment of diarrhea. Most clinicians recommend discontinuing consumption of solid foods and dairy products for 24 hours. However, fasting is of questionable value, as this treatment modality has not been extensively studied. In osmotic diarrhea, these maneuvers control the problem. If the mechanism is secretory, diarrhea persists. For patients who are experiencing nausea and/or vomiting, a mild, digestible, low-residue diet should be administered for 24 hours. If vomiting is present and uncontrollable with antiemetics, nothing is taken by mouth. As bowel movements decrease, a bland diet is begun. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Feeding should continue in children with acute bacterial diarrhea. Fed children have less morbidity and mortality, whether or not they receive oral rehydration fluids. Studies are not available in the elderly or in other high-risk groups to determine the value of continued feeding in bacterial diarrhea.</div>
<div style="text-align: justify;">
<br />
<i>Water and Electrolytes</i></div>
<div style="text-align: justify;">
<br />
Rehydration and maintenance of water and electrolytes are primary treatment goals until the diarrheal episode ends. If the patient is volume depleted, rehydration should be directed at replacing water and electrolytes to normal body composition. Then water and electrolyte composition are maintained by replacing losses. Many patients will not develop volume depletion and therefore will only require maintenance fluid and electrolyte therapy. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Parenteral and enteral routes may be used for supplying water and electrolytes. If vomiting and dehydration are not severe, enteral feeding is the less costly and preferred method. In the United States, many commercial oral rehydration preparations are available (Table 38–3). Because of concerns about hypernatremia, physicians continue to hospitalize patients and intravenously correct fluid and electrolyte deficits in severe dehydration. Oral solutions are strongly recommended. In developing countries, the World Health Organization Oral Rehydration Solution (WHO-ORS) saves the lives of millions of children annually.</div>
<div style="text-align: justify;">
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisuw8tlotuYz1S8DEEd4C2xXn7Y6FSJe5CHr-tTq18qJ2RII1r92oAMxcW7lzKYRhmvg823uPEbIspNL1gjYyGnMTBb0_j29gZqfAk_yPpDIiYz6STWbmEPRAHgw38RflFATxbkGTNzBY/s1600/Diarrhea2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="243" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisuw8tlotuYz1S8DEEd4C2xXn7Y6FSJe5CHr-tTq18qJ2RII1r92oAMxcW7lzKYRhmvg823uPEbIspNL1gjYyGnMTBb0_j29gZqfAk_yPpDIiYz6STWbmEPRAHgw38RflFATxbkGTNzBY/s640/Diarrhea2.jpg" width="640" /></a></div>
During diarrhea, the small intestine retains its ability to actively transport monosaccharides such as glucose. Glucose actively carries sodium with water and other electrolytes. Because the WHO-ORS has a high sodium concentration, physicians have been reluctant to use it in well-nourished children. Yet controlled comparative studies describe more favorable results with the WHO-ORS than with parenteral fluids. The recommended WHO-ORS (see Table 38–3) has now been reformulated to have a lower osmolarity, sodium content, and glucose load. Rice-based oral solution is also a hyposmotically active substrate that elutes glucose without increasing stool or urine outflows. Rehydration of infants with acute diarrhea using a rice-based solution is effective.9 Decreased stool output and greater absorption and retention of fluid and electrolytes also results. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In summary, oral rehydration solution is a lifesaving treatment for millions afflicted in developing countries. Acceptance in developed countries is less enthusiastic; however, the advantage of this product in reducing hospitalizations may prove its use as a cost-effective.<br />
<br />
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/treatment-of-diarrhea.html"><b>Treatment of Diarrhea</b></a></div>
<div style="text-align: left;">
Source: pharmacotherapy 7th<b> </b></div>
<div style="text-align: left;">
Image: ayushveda.com<b> </b></div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com3tag:blogger.com,1999:blog-7113702905971561223.post-70452939078901000662012-04-18T11:25:00.000+07:002012-04-18T11:27:06.790+07:00Signs and Symptoms of Diarrhea<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/signs-and-symptoms-of-diarrhea.html"><b>Signs and Symptoms of Diarrhea</b></a> - Diarrhea is a troublesome discomfort that affects most individuals in the United States at some point in their lives and can be thought of as both a symptom and a sign. Usually diarrheal episodes begin abruptly and subside within 1 or 2 days without treatment. Acute diarrhea is commonly defined as <14 days’ duration, persistent diarrhea as more than 14 days’ duration, and chronic diarrhea as more than 30 days’ duration.</div>
<div style="text-align: justify;">
<br />
To understand diarrhea, one must have a reasonable definition of the condition; unfortunately, the literature is extremely variable on this. Simply put, diarrhea is an increased frequency and decreased consistency of fecal discharge as compared to an individual’s normal bowel pattern. Frequency and consistency are variable within and between individuals. For example, some individuals defecate as often as three times per day, whereas others defecate only two or three times per week. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
A Western diet usually produces a daily stool weighing between 100 and 300 g, depending on the amount of nonabsorbable materials (mainly carbohydrates) consumed. Patients with serious diarrhea may have a daily stool weight in excess of 300 g; however, a subset of patients experience frequent small, watery passages. Additionally, vegetable fiber-rich diets, such as those consumed in some Eastern cultures, such as those in Africa, produce stools weighing more than 300 g/day.</div>
<div style="text-align: justify;">
<br />
Diarrhea may be associated with a specific disease of the intestines or secondary to a disease outside the intestines. For instance, bacillary dysentery directly affects the gut, whereas diabetes mellitus causes neuropathic diarrheal episodes. Furthermore, diarrhea can be considered as acute or chronic disease. Infectious diarrhea is often acute; diabetic diarrhea is chronic. Congenital disorders in gastrointestinal ion-transport mechanisms are another cause of chronic diarrhea. Whether acute or chronic, diarrhea has the same pathophysiologic causes that help identification of specific treatments.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Physiology</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In the fasting state, 9 L of fluid enters the proximal small intestine each day. Of this fluid, 2 L are ingested through diet, while the remainder consists of internal secretions. Because of meal content, duodenal chyme is usually hypertonic. When chyme reaches the ileum, the osmolality adjusts to that of plasma, with most dietary fat, carbohydrate, and protein being absorbed. The volume of ileal chyme decreases to about 1 L/day upon entering the colon, which is further reduced by colonic absorption to 100 mL daily. If the small intestine water absorption capacity is exceeded, chyme overloads the colon, resulting in diarrhea. In humans, the colon absorptive capacity is about 5 L daily.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Colonic fluid transport is critical to water and electrolyte balance. Absorption from the intestines back into the blood occurs by three mechanisms: active transport, diffusion, and solvent drag. Active transport and diffusion are the mechanisms of sodium transport. Because of the high luminal sodium concentration (142 mEq/L), sodium diffuses from the sodium-rich gut into epithelial cells, where it is actively pumped into the blood and exchanged with chloride to maintain an isoelectric condition across the epithelial membrane. Hydrogen ions are transported by an indirect mechanism in the upper small intestine. As sodium is absorbed, hydrogen ions are secreted into the gut. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Hydrogen ions then combine with bicarbonate ions to form carbonic acid, which then dissociates into carbon dioxide and water. Carbon dioxide readily diffuses into the blood for expiration through the lung. The water remains in the chyme. Paracellular pathways are major routes of ion movement. As ions, monosaccharides, and amino acids are actively transported, an osmotic pressure is created, drawing water and electrolytes across the intestinal wall. This pathway accounts for significant amounts of ion transport, especially sodium. Sodium plays an important role in stimulating glucose absorption. Glucose and amino acids are actively transported into the blood via a sodium dependent cotransport mechanism. Cotransport absorption mechanisms of glucose-sodium and amino acid-sodium are extremely important for treating diarrhea.</div>
<div style="text-align: justify;">
<br />
Gut motility influences absorption and secretion. The amount of time in which luminal content is in contact with the epithelium is under neural and hormonal control. Neurohormonal substances, such as angiotensin, vasopressin, glucocorticoid, aldosterone, and neurotransmitters also regulate ion transport<b>. </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Clinical Presentation of Diarrhea</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
A medication history is extremely important in identifying drug-induced diarrhea. Many agents, including antibiotics and other drugs, cause diarrhea or, less commonly, pseudomembranous colitis. Self-inflicted laxative abuse for weight loss is popular. Most acute diarrhea is self-limiting, subsiding within 72 hours. However, infants, young children, the elderly, and debilitated persons are at risk for morbid and mortal events in prolonged or voluminous diarrhea. These groups are at risk for water, electrolyte, and acid–base disturbances, and potentially cardiovascular collapse and death. The prognosis for chronic diarrhea depends on the cause; for example, diarrhea secondary to diabetes mellitus waxes and wanes throughout life.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>General</i><br />
• Usually, acute diarrheal episodes subside within 72 hours of onset, whereas chronic diarrhea involves frequent attacks over extended time periods.<br />
<b><i>Signs and symptoms</i></b><br />
• Abrupt onset of nausea, vomiting, abdominal pain, headache, fever, chills, and malaise.<br />
• Bowel movements are frequent and never bloody, and diarrhea lasts 12 to 60 hours.<br />
• Intermittent periumbilical or lower right quadrant pain with cramps and audible bowel sounds is characteristic of small intestinal disease.<br />
• When pain is present in large intestinal diarrhea, it is a gripping, aching sensation with tenesmus (straining, ineffective, and painful stooling). Pain localizes to the hypogastric region, right or left lower quadrant, or sacral region.<br />
• In chronic diarrhea, a history of previous bouts, weight loss, anorexia, and chronic weakness are important findings.<br />
<i>Physical examination</i><br />
• Typically demonstrates hyperperistalsis with borborygmi and generalized or local tenderness.<br />
<i>Laboratory tests</i><br />
• Stool analysis studies include examination for microorganisms, blood, mucus, fat, osmolality, pH, electrolyte and mineral concentration, and cultures.<br />
• Stool test kits are useful for detecting gastrointestinal viruses, particularly rotavirus.<br />
• Antibody serologic testing shows rising titers over a 3- to 6-day period, but this test is not practical and is nonspecific.<br />
• Occasionally, total daily stool volume is also determined.<br />
• Direct endoscopic visualization and biopsy of the colon may be undertaken to assess for the presence of conditions such as colitis or cancer.<br />
• Radiographic studies are helpful in neoplastic and inflammatory conditions.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Drugs Causing Diarrhea</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Laxatives<br />
Antacids containing magnesium<br />
Antineoplastics<br />
Auranofin (gold salt)<br />
Antibiotics<br />
Clindamycin<br />
Tetracyclines<br />
Sulfonamides<br />
Any broad-spectrum antibiotic<br />
Antihypertensives<br />
Reserpine<br />
Guanethidine<br />
Methyldopa<br />
Guanabenz<br />
Guanadrel<br />
Angiotensin-converting enzyme inhibitors<br />
Cholinergics<br />
Bethanechol<br />
Neostigmine<br />
Cardiac agents<br />
Quinidine<br />
Digitalis<br />
Digoxin<br />
Nonsteroidal antiinflammatory drugs<br />
Misoprostol<br />
Colchicine<br />
Proton pump inhibitors<br />
H2-receptor blockers </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/signs-and-symptoms-of-diarrhea.html"><b>Sign and Symptoms of Diarrhea</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com1tag:blogger.com,1999:blog-7113702905971561223.post-22359886194545101222012-04-17T13:38:00.000+07:002012-04-17T13:56:42.114+07:00New Role For Public Health<div class="separator" style="clear: both; text-align: center;">
</div>
<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
</div>
<div class="separator" style="clear: both; text-align: center;">
</div>
<div class="separator" style="clear: both; text-align: center;">
</div>
<br />
<b><a href="http://umaeenews.blogspot.com/2012/04/new-role-for-public-health.html">New Role For Public Health</a> </b>- With the spiraling costs of medical care and the corresponding interest in cost containment and accountability, it is reasonable to avoid duplications. We need a closer link of clinical and public health disciplines and activities.<br />
<br />
A recent example of the control of a new epidemic by the collaborative efforts of the World Health Organization (WHO), basic scientists and clinicians followed the outbreak of SARS—Severe Acute Respiratory Syndrome. WHO forcefully assumed international leadership, coordinated scientific investigations, and quickly reported all new advances from the laboratory and field epidemiological studies to clinicians. In medical schools it is propitious for these disciplines jointly to develop curricula and research projects.</div>
<div style="text-align: justify;">
<br />
In the health service arena, closer ties between clinicians and public health officials will be efficient and effective for the good of the population. A special role for public health officials could be to “translate” important epidemiological data for clinicians giving primary care. This could be particularly important and useful in enhancing prevention. Examples of useful data would be the risk ratios for becoming an alcohol abuser for persons with and without a family history of abuse; cigarette smoking for the smoker, those nearby, and the unborn fetus; and for fatal versus nonfatal injury in persons driving with and without a seat belt.</div>
<div style="text-align: justify;">
<br />
<div class="separator" style="clear: both; text-align: center;">
</div>
</div>
<div style="text-align: justify;">
In the field of communicable diseases it is useful to know the risk of AIDS in those practicing intravenous drug abuse or unprotected sexual activities, the relative risk of Lyme disease in those using effective insect repellents versus those not using such agents, and the relative risk of hepatitis B in healthcare workers who have received the vaccine and those who have not. In 2006, a key role for a public health-clinicians partnership is the continual education of the public about the real risks of avian (H5N1) influenza and the progress toward its prevention and control. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
An epidemiological approach to community-wide education about local health risks, perhaps with a well-designed periodical, would further link the clinician and public health official. The Centers for Disease Control and Prevention (CDC) has done this successfully with Morbidity and Mortality Weekly Report. A community-wide modification for consumption by local practitioners would be helpful. Such networking is feasible and desirable.</div>
<div style="text-align: justify;">
<br />
Networking with schools, businesses, health clubs, and senior citizen groups might increase compliance with behavior designed to enhance resistance to environmental hazards. Fundamentals of general and dental hygiene, nutrition, exercise, and stress control would be essential components. It would be reasonable to reinforce such basic principles as maintaining immunizations and proper use of antibiotics. In summary, we need a proactive and integrative role in education, one that involves networking with clinicians and the public directly. Improving environmental safety has been the focus and strength of public health. Essentially, the goal has been to reduce the microbial hazards to humans. For the most part, this is carried out by systematic measurement or a series of inspections of the environment. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Good general sanitation and safe air, water, and food are hallmarks of public health. Environmental activist groups have heightened interest in environmental safety. This is an opportune time to build a coalition between informed public health officials and interested and energetic activists genuinely concerned with improving the environment. From infectious diseases point of view, an important goal would be to reduce the degree of exposure while preserving the vitality of the ecosystem. The government of Brazil was reported to have instituted a $200 million program to control malaria in the Amazon region by spraying dichlorodiphenyltrichloroethane (DDT) in thousands of rain forest huts. As McCoy pointed out, however, the chemical has been banned in over 40 countries because of its lethal effect on birds and fish.</div>
<div style="text-align: justify;">
<br />
Moreover, in India, although it had a remarkable short-term effect initially (75 million annual cases of malaria reduced in the 1950s to 50,000), the number of cases rose to 65 million by 1976, the result of resistance in mosquito vectors. Moreover, bottled milk sampled in India in April 1990 had 10 times the permissible limit of DDT. DDT is fat soluble and has been carried in food chains to countries all over the world. The lesson we have learned from the Russian nuclear accident at Chernobyl, the AIDS epidemic, and the DDT experience and the SARS epidemic is that radiation, viruses, and pollutants respect no national borders.</div>
<div style="text-align: justify;">
<br />
The response to such lessons needs to be an enhanced commitment by individuals, communities, and nations to solve the problems of others and to view the world as a global village. Limiting the survival of important infection agents, their animal reservoirs, or hosts requires careful examination of the implications of such approaches in collaboration with veterinarians, entomologists, and toxicologists.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
</div>
<div class="separator" style="clear: both; text-align: center;">
</div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<br /></div>
<div style="text-align: left;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/new-role-for-public-health.html"><b>New Role For Public Health </b></a></div>
<div style="text-align: left;">
Source: public health & preventive medicine</div>
<div style="text-align: left;">
</div>
<div style="text-align: right;">
<br /></div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com0tag:blogger.com,1999:blog-7113702905971561223.post-38221959888258437812012-04-13T15:03:00.001+07:002012-04-13T15:04:56.178+07:00Treatment Nausea and Vomiting<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjMBnvy2hyR0JtktHoGBaBS8ZLIS3_gsChl50A9P_Ev4VBRK7ZY5NVWMNwHqe2BIRjrqAEEua5QFU0u1x7CPN95iziU3Y_En8ulQd_ic6F9cG4rTpueR2xcStpy2s1LYaDh-zU-t35ER4U/s1600/nausea+and+vomiting+2.gif" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjMBnvy2hyR0JtktHoGBaBS8ZLIS3_gsChl50A9P_Ev4VBRK7ZY5NVWMNwHqe2BIRjrqAEEua5QFU0u1x7CPN95iziU3Y_En8ulQd_ic6F9cG4rTpueR2xcStpy2s1LYaDh-zU-t35ER4U/s320/nausea+and+vomiting+2.gif" width="264" /></a></div>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/04/treatment-nausea-and-vomiting.html">Treatment Nausea and Vomiting</a> </b>- <b>Nausea and vomiting</b> are common complaints among many individuals with gastrointestinal (GI) disorders. However, because of the variable etiologies of these problems, management can be quite simple or detailed and complex, essentially innocuous or associated with therapy-induced adverse reactions. This chapter provides an overview of nausea and vomiting, two multifaceted problems. Nausea and vomiting may be associated with a variety of clinical presentations. In addition to GI diseases, either or both may accompany cardiovascular, infectious, neurologic, or metabolic disease processes. Nausea and vomiting may be a feature of such conditions as <a href="http://umaeenews.blogspot.com/2012/02/food-and-drug-administration-pregnancy.html">pregnancy</a>, or may follow operative procedures or administration of certain medications, such as those used in cancer chemotherapy.</div>
<div style="text-align: justify;">
<br />
Psychogenic etiologies of these symptoms may be present, especially in young women with an underlying emotional disturbance. Anticipatory etiologies may be involved, such as in patients who have previously received cytotoxic chemotherapy. Table below lists specific etiologies associated with nausea and vomiting. In addition to identifying conditions associated with nausea and vomiting, it is important to address the specific causative medical problems. For example, nausea and vomiting may occur in as many as 70% of patients with inferior myocardial infarction or diabetic ketoacidosis. Eighty percent to 90% of patients with an Addisonian crisis, acute pancreatitis, or acute appendicitis may present with nausea and vomiting.</div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqKpmOzZ_IVmaeX-cOFtrNotmzX_UJASE965DA5ne7fyj8_RP1o6G21FBox4735BiGWikt5sgcqnsIY-tKQpqxK8xFlzycjvW24e-MhGR-ql2gBvBMsxRNLnqMtUvzEi_-NaF-SjV-v0U/s1600/Nausea+and+Vomiting.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqKpmOzZ_IVmaeX-cOFtrNotmzX_UJASE965DA5ne7fyj8_RP1o6G21FBox4735BiGWikt5sgcqnsIY-tKQpqxK8xFlzycjvW24e-MhGR-ql2gBvBMsxRNLnqMtUvzEi_-NaF-SjV-v0U/s1600/Nausea+and+Vomiting.jpg" /></a></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The etiology of nausea and vomiting may vary with the age of the patient. For example, vomiting in the newborn during the first day of life suggests upper digestive tract obstruction or an increase in intracranial pressure. Other illnesses associated with vomiting in children include pyloric stenosis, duodenal ulcer, stress ulcer, adrenal insufficiency, septicemia, and diseases of the pancreas, liver, or biliary tree. Also, the hepatocellular failure seen in Reye syndrome may lead to profound cerebral edema followed by persistent emesis.</div>
<div style="text-align: justify;">
<br />
A common etiology of vomiting in children is viral gastroenteritis caused by rotavirus. Vomiting in infants may be associated with something as simple as overfeeding, rapid feeding, inadequate burping, or lying down too soon after feeding. These types of vomiting are usually indicative of minor problems and may be altered by changing the approach to feeding.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>General Approach to Treatment </b></div>
<div style="text-align: justify;">
<br />
Treatment options for nausea and vomiting include drug and nondrug modalities. The treatment of nausea and vomiting is quite varied depending on the associated medical situation. Even though a number of potentially effective measures are available, most patients receive a medication at some point in their care. For simple nausea and vomiting, patients may choose to do nothing or to select from a variety of nonprescription drugs. As symptoms become worse or are associated with more serious medical problems, patients are more likely to benefit from prescription antiemetic drugs. When prescribed according to reliable clinical information, these agents often provide acceptable relief; however, some patients will never be totally free of symptoms. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
This lack of relief is most disabling when it is associated with an unresolved medical problem or when the necessary therapy for this condition is the cause of the nausea or vomiting, as in the case of patients who are receiving chemotherapy of moderate or high emetic risk.</div>
<div style="text-align: justify;">
<br />
<b>Nonpharmacologic Management </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Nonpharmacologic management of nausea and vomiting may include a variety of dietary, physical, or psychological changes consistent with the etiology of symptoms. For patients with simple complaints, perhaps resulting from excessive or disagreeable food or beverage consumption, avoidance or moderation in dietary intake may be preferable. Patients suffering symptoms of systemic illness may improve dramatically as their underlying condition resolves. Finally, patients in whom these symptoms result from labyrinthine<br />
changes produced by motion may benefit quickly by assuming a stable physical position.</div>
<div style="text-align: justify;">
<br />
Cancer patients who are undergoing chemotherapy may experience nausea and/or vomiting despite receiving prophylactic antiemetics. Anticipatory nausea or vomiting rarely occurs unless the patient has previously experienced posttreatment nausea or vomiting, suggesting that the mechanism for anticipatory nausea and vomiting is a learned process involving elements of classic conditioning. This conditioning model may also be important in understanding the development of pregnancy-related nausea. Nonpharmacologic interventions are classified as behavioral interventions and include relaxation, biofeedback, self-hypnosis, cognitive distraction, guided imagery, and systematic desensitization.</div>
<div style="text-align: justify;">
<br />
The management of psychogenic vomiting is greatly dependent on psychological intervention. However, because the underlying problems are so complex and intertwined in personal relationships, psychological therapy may require lengthy, in-depth treatment. Pharmacologic therapy offers only minimal benefit in these patients. Surgery, such as gastroenterostomy, is of no value.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Presentation of Nausea and Vomiting</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>General</i><br />
Depending on severity of symptoms, patients may present in mild to severe distress<br />
</div>
<div style="text-align: justify;">
<i>Symptoms</i><br />
Simple: Self-limiting, resolves spontaneously and requires only symptomatic therapy<br />
Complex: Not relieved after administration of antiemetics; progressive deterioration of patient secondary to fluid–electrolyte imbalances; usually associated with noxious agents or psychogenic events<br />
</div>
<div style="text-align: justify;">
<i>Signs</i><br />
Simple: Patient complaint of queasiness or discomfort </div>
<div style="text-align: justify;">
Complex: Weight loss; fever; abdominal pain<br />
</div>
<div style="text-align: justify;">
<i>Laboratory tests</i><br />
Simple: None<br />
Complex: Serum electrolyte concentrations; upper/lower GI evaluation<br />
</div>
<div style="text-align: justify;">
<i>Other information</i><br />
Fluid input and output<br />
Medication history<br />
Recent history of behavioral or visual changes, headache, pain, or stress<br />
Family history positive for psychogenic vomiting </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<b>Pharmacologic therapy</b> </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Although many approaches to the treatment of nausea and vomiting have been suggested, antiemetic drugs (nonprescription and prescription) are most often recommended. These agents represent a variety of pharmacologic and chemical classes, as well as dosage regimens and routes of administration. With so many treatment possibilities available, factors that enable the clinician to discriminate among various choices include (a) the suspected etiology of the symptoms; (b) the frequency, duration, and severity of the episodes; (c) the ability of the patient to use oral, rectal, injectable, or transdermal medications; and (d) the success of previous antiemetic medications. Table below gives information concerning commonly available antiemetic preparations.</div>
<div style="text-align: justify;">
</div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjylhJfC02Qm2mDsv7tbd1y9h_m7sShzpgCh6KE7G7x7yIXt9YBMZHGAgqD5eNFZEErdVlwSC5yutPa3pOFPZ4PDHHDjnXgSofT50JP7UDGqObbkUpmeGAcNO-XTT8mWKOY3FVy-zwD98g/s1600/Nausea+and+Vomiting+1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="332" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjylhJfC02Qm2mDsv7tbd1y9h_m7sShzpgCh6KE7G7x7yIXt9YBMZHGAgqD5eNFZEErdVlwSC5yutPa3pOFPZ4PDHHDjnXgSofT50JP7UDGqObbkUpmeGAcNO-XTT8mWKOY3FVy-zwD98g/s400/Nausea+and+Vomiting+1.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The treatment of simple nausea and vomiting usually requires minimal therapy. For these symptoms, patients may choose from a lengthy list of nonprescription products. Both nonprescription and prescription drugs useful in the treatment of simple nausea and vomiting are usually effective in small, infrequently administered doses. Side effects and toxic effects in these settings are also usually minimal. Although suitable for occasional simple nausea and vomiting, nonprescription agents are often abandoned by the patient as symptoms continue or become progressively worse. As the patient’s condition warrants, prescription medications may be chosen, either as single-agent therapy or in combination.</div>
<div style="text-align: justify;">
<br />
The management of complex nausea and vomiting, for example, in patients who are receiving cytotoxic chemotherapy, may require combination therapy. In combination regimens, the goal is to achieve symptomatic control through administration of agents with different pharmacologic mechanisms of action.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/treatment-nausea-and-vomiting.html"><b>Treatment Nausea and Vomiting</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>
<div style="text-align: left;">
Image: wikinoticia.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com0tag:blogger.com,1999:blog-7113702905971561223.post-72170170945548065412012-04-05T20:37:00.000+07:002012-04-07T18:41:34.405+07:00Algorithm For Treatment of Peptic Ulcer Disease<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhuzretUAvB4EUVH0uwTSEZY4shOxX35V8yIICQcNSVyFHyaAyDURNEMbEzkvaGr0lplAovBezlDS3hHCfk9CtIHLdZ5GJzEOA7-1_O7ABzplUA9FlXmqwUjXvp-SSXB4FJ5DgWumeZSIA/s1600/peptic+ulcer.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="202" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhuzretUAvB4EUVH0uwTSEZY4shOxX35V8yIICQcNSVyFHyaAyDURNEMbEzkvaGr0lplAovBezlDS3hHCfk9CtIHLdZ5GJzEOA7-1_O7ABzplUA9FlXmqwUjXvp-SSXB4FJ5DgWumeZSIA/s320/peptic+ulcer.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-for-treatment-of-peptic-ulcer.html"><b>Algorithm For Treatment of Peptic Ulcer Disease</b></a> - The clinical presentation of PUD varies depending on the severity of epigastric pain and the presence of complications (presentation of peptic ulcer disease). Ulcer-related pain in duodenal ulcer often occurs 1 to 3 hours after meals and is usually relieved by food, but this is variable. In gastric ulcer, food may precipitate or accentuate ulcer pain. Antacids usually provide immediate pain relief in most ulcer patients. Pain usually diminishes or disappears during treatment; however, recurrence of epigastric pain after healing often suggests an unhealed or recurrent ulcer.</div>
<div style="text-align: justify;">
<br />
Epigastric pain does not define an ulcer. The absence of pain does not preclude the diagnosis especially in the elderly who may present with “silent” ulcer complications. The reasons for this are unclear, but may relate to differences in the way the elderly perceive pain or the analgesic effect of NSAIDs. Dyspepsia in itself is of little clinical value when assessing subsets of patients who are most likely to have an ulcer. Patients taking NSAIDs often report dyspepsia, but dyspeptic symptoms do not directly correlate with an ulcer. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Patients with dyspeptic symptoms may have either uninvestigated (no upper endoscopy) or investigated (underwent upper endoscopy) dyspepsia. If an ulcer is not confirmed in a patient with ulcer-like symptoms at the time of endoscopy, the disorder is referred to as nonulcer dyspepsia. Ulcer-like symptoms may occur in the absence of peptic ulceration in association with H. pylori gastritis or duodenitis. There is no one sign or symptom that differentiates between H. pylori-associated and NSAID-induced ulcer.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Presentation of Peptic Ulcer Disease</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>General</i><br />
• Mild epigastric pain or acute life-threatening upper gastrointestinal complications Symptoms<br />
• Abdominal pain that is often epigastric and described as burning, but may present as vague discomfort, abdominal fullness, or cramping<br />
• A typical nocturnal pain that awakens the patient from sleep (especially between 12 AM and 3 AM)<br />
• The severity of ulcer pain varies from patient to patient, and may be seasonal, occurring more frequently in the spring or fall; episodes of discomfort usually occur in clusters, lasting up to a few weeks and followed by a pain-free period or remission lasting from weeks to years<br />
• Changes in the character of the pain may suggest the presence of complications<br />
• Heartburn, belching, and bloating often accompany the pain<br />
• Nausea, vomiting, and anorexia, are more common in patients with gastric ulcer than with duodenal ulcer, but may also be signs of an ulcer-related complication</div>
<div style="text-align: justify;">
<br />
<i>Signs</i><br />
• Weight loss associated with nausea, vomiting, and anorexia<br />
• Complications, including ulcer bleeding, perforation, penetration, or obstruction Laboratory tests<br />
• Gastric acid secretory studies<br />
• Fasting serum gastrin concentrations are only recommended for patients who are unresponsive to therapy, or for those in whom hypersecretory diseases are suspected<br />
• The hematocrit and hemoglobin are low with bleeding, and stool hemoccult tests are positive<br />
• Tests for Helicobacter pylori </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Other diagnostic tests</i><br />
• Fiberoptic upper endoscopy (esophagogastroduodenoscopy) detects more than 90% of peptic ulcers and permits direct inspection, biopsy, visualization of superficial erosions, and sites of active bleeding<br />
• Routine single-barium contrast techniques detect 30% of peptic ulcers; optimal double-contrast radiography detects 60% to 80% of ulcers</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>General Approach to Treatment </b></div>
<div style="text-align: justify;">
<br />
The treatment of PUD centers on healing the ulcer and reducing the risk of ulcer recurrence and related complications. Drug regimens containing antimicrobials such as clarithromycin, metronidazole, amoxicillin, and bismuth salts and antisecretory drugs (PPIs or H2RAs) relieve ulcer symptoms, heal the ulcer, and eradicate H. pylori infection. Successful eradication will alter the natural history of PUD and cure the disease. PPIs are preferred to H2RAs or sucralfate for healing H. pylori-negative NSAID ulcers because they accelerate ulcer healing and provide more effective relief of symptoms. Treatment with a PPI should be extended to 8 to 12 weeks if the NSAID must be continued. A PPI-based H. pylori eradication regimen is recommended in H. pylori-positive patients with an active ulcer who are also taking an NSAID. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Prophylactic cotherapy with either a PPI or miso-prostol decreases ulcer risk and upper GI complications in patients taking nonselective NSAIDs. A COX-2 inhibitor may be used as an alternative to a nonselective NSAID, but the risk of adverse cardiovascular effects must be weighted against the gastroprotective benefits in each patient. The optimal therapeutic strategy for patients at very high risk of NSAID-related GI events is not known, but selected patients may benefit from the use of a COX-2 inhibitor and a PPI.</div>
<div style="text-align: justify;">
<br />
Dietary modifications are important for patients who are unable to tolerate certain foods and beverages. Lifestyle modifications such as reducing stress and decreasing or stopping cigarette smoking is encouraged. Some patients may require radiographic or endoscopic procedures for a definitive diagnosis or for complications such as bleeding. Surgery may be necessary in patients with ulcer-related complications.</div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
</div>
<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhsrCEok9EXwqVfV-DEcJORa6KDOMNDBZ-6SWffTtN6NfBK6VV04PnLdgzQBDMZ9rvFKtQBQTayDH3S-ljvT1dr_xgPjhyETwJsdB0euCTxtPEcK-KQ15dpNtt-gqsrRbs7OTJMMeaA6TY/s1600/Algorithm+of+Peptic+Ulcer+Disease.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhsrCEok9EXwqVfV-DEcJORa6KDOMNDBZ-6SWffTtN6NfBK6VV04PnLdgzQBDMZ9rvFKtQBQTayDH3S-ljvT1dr_xgPjhyETwJsdB0euCTxtPEcK-KQ15dpNtt-gqsrRbs7OTJMMeaA6TY/s400/Algorithm+of+Peptic+Ulcer+Disease.jpg" width="380" /></a></div>
<br />
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<b>Nonpharmacologic Therapy </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Patients with PUD should eliminate or reduce psychological stress, cigarette smoking, and the use of nonselective NSAIDs (including aspirin). Although there is no “antiulcer diet,” the patient should avoid foods and beverages (e.g., spicy foods, caffeine, and alcohol) that cause dyspepsia or that exacerbate ulcer symptoms. If possible, alternative agents such as acetaminophen, nonacetylated salicylate (e.g., salsalate), or COX-2 inhibitors should be used for relief of pain. Elective surgery for PUD is rarely performed today because of highly effective medical management such as the eradication of H. pylori and the use of potent acid inhibitors. A subset of patients, however, may require emergency surgery for bleeding, perforation, or obstruction. In the past, surgical procedures were performed for medical treatment failures and included vagotomy with pyloroplasty or vagotomy with antrectomy.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Vagotomy (truncal, selective, or parietal cell) inhibits vagal stimulation of gastric acid. A truncal or selective vagotomy frequently results in postoperative gastric dysfunction and requires a pyloroplasty or antrectomy to facilitate gastric drainage. When an antrectomy is performed, the remaining stomach is anastomosed with the duodenum (Billroth I) or with the jejunum (Billroth II). A vagotomy is unnecessary when an antrectomy is performed for gastric ulcer. The postoperative consequences associated with these procedures include postvagotomy diarrhea, dumping syndrome, anemia, and recurrent ulceration.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-for-treatment-of-peptic-ulcer.html"><b>Algorithm For Treatment of Peptic Ulcer Disease </b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com3tag:blogger.com,1999:blog-7113702905971561223.post-83051059608525264262012-04-05T14:12:00.001+07:002012-04-05T14:13:29.824+07:00Severe Asthma Attack<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgFk-IaEsJV1EGmHDDfb59gbKLl-zetnxiM1fbX06uc0xD2nGmG8Vr6vxrl0INE8alGxo07Q2g0PErl-fWf9vnGTdSI7Rft_76p7Q5E0O-qTNi-Og07TA4CVsBs0MzIw1JOcrGwqNGznl8/s1600/asthma.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="214" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgFk-IaEsJV1EGmHDDfb59gbKLl-zetnxiM1fbX06uc0xD2nGmG8Vr6vxrl0INE8alGxo07Q2g0PErl-fWf9vnGTdSI7Rft_76p7Q5E0O-qTNi-Og07TA4CVsBs0MzIw1JOcrGwqNGznl8/s320/asthma.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/severe-asthma-attack.html"><b>Severe Asthma Attack</b></a> - Uncontrolled asthma, with its inherent variability, can progress to an acute state where inflammation, airways edema, excessive accumulation of mucus, and severe bronchospasm result in a profound airways narrowing that is poorly responsive to usual bronchodilator therapy (see Clinical Presentation: Severe Acute Asthma). Although this progression is the most common scenario, some patients experience rapid onset or hyperacute attacks.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Hyperacute attacks are associated with neutrophilic as opposed to eosinophilic infiltration and resolve rapidly with bronchodilator therapy, suggesting that smooth muscle spasm is the major pathogenic mechanism. In most cases, emergency department visits for severe acute asthma represent the failure of an adequate therapeutic regimen for persistent asthma. Underuse of antiinflammatory drugs and excessive reliance on short-acting inhaled β2-agonists are the major risk factors for severe exacerbations. A blunted perception of airway obstruction may predispose certain individuals to fatal <b>asthma attacks</b>.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Clinical Presentation </b></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>General</i></div>
<div style="text-align: justify;">
■ An episode can progress over several days or hours (usual scenario) or can progress rapidly over 1 to 2 hours.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Symptoms</i></div>
<div style="text-align: justify;">
■ The patient is anxious in acute distress and complains of severe dyspnea, shortness of breath, chest tightness, or burning. The patient is only able to say a few words with each breath. Symptoms are unresponsive to usual measures (inhaled shortacting β2-agonist administration).</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Signs</i></div>
<div style="text-align: justify;">
■ Signs include expiratory and inspiratory wheezing on auscultation (breath sounds may be diminished with very severe obstruction), dry hacking cough, tachypnea, tachycardia, pale or cyanotic skin, hyperinflated chest with intercostal and supraclavicular retractions, and hypoxic seizures if very severe.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Laboratory</i></div>
<div style="text-align: justify;">
■ PEF and/or FEV1 less than 50% of normal predicted values. Decreased arterial oxygen (PaO2), and O2 saturations by pulse oximetry (SaO2 less than 90% on room air is severe). Decreased arterial or capillary CO2 if mild, but in the normal range or increased in moderate to severe obstruction.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Other Diagnostic Tests</i></div>
<div style="text-align: justify;">
■ Blood gases to assess metabolic acidosis (lactic acidosis) in severe obstruction. Complete blood count if there are signs of infection (fever and purulent sputum). Serum electrolytes as therapy with β2-agonist and corticosteroids can lower serum potassium and magnesium and increase glucose.Chest radiograph if signs of consolidation on auscultation.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Factors Contributing to Asthma Severity </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<i>Viral Respiratory Infections</i> </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Viral respiratory infections are primarily responsible for exacerbations of asthma, particularly in children younger than age 10 years. Infants are particularly susceptible to airways obstruction and wheezing with viral infections because of their small airways. The most common cause of exacerbations in both children and adults is the common rhinovirus. Other viruses isolated include respiratory syncytial virus, parainfluenza virus, coronavirus, and influenza viruses. The inflammatory response to viral infection is thought to be associated directly with the increasing BHR. Certain viruses (respiratory syncytial virus and parainfluenza virus) are capable of inducing specific IgE antibodies, and rhinovirus can activate eosinophils directly in asthmatics.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The increase in asthma symptoms and BHR that occurs may last for days or weeks following resolution of the symptoms of the viral infection. Recent evidence does not support a beneficial effect of influenza vaccine for preventing asthma exacerbations from subsequent influenza infections.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Envirenmental And Occupational </i></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Table below lists the agents, events, and mechanisms that are known to trigger asthma. The general mechanisms are unknown but presumably are the result of epithelial damage and inflammation in the airway mucosa. Ozone and sulfur dioxide, common components of air pollution, have been used to induce BHR in animals. Exposure to 0.2 parts per million ozone for 2 to 3 hours can induce bronchoconstriction and increase BHR in asthmatics. Sulfur dioxide in the ambient atmosphere is highly irritating. It presumably induces bronchoconstriction through mast cell or irritantreceptor involvement. </div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhnGUaoSRuU78VZU62ZsJfJQ_RJI_a9zXCb8Spz_8Y9TtuP1Pdk-W4ohJv4-wHqYwmvQvMmiVXC2Y_NLZIWdCd9y7tyx80fZUPbS7FOXJpCtzuJbVQOlgjRXJL2IxKsMZqelRBMtzYLVo4/s1600/Agents+of+Ashtma.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="340" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhnGUaoSRuU78VZU62ZsJfJQ_RJI_a9zXCb8Spz_8Y9TtuP1Pdk-W4ohJv4-wHqYwmvQvMmiVXC2Y_NLZIWdCd9y7tyx80fZUPbS7FOXJpCtzuJbVQOlgjRXJL2IxKsMZqelRBMtzYLVo4/s400/Agents+of+Ashtma.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Asthma produced by repeated prolonged exposure to industrial inhalants is a significant health problem. It has been estimated that occupational asthma accounts for 2% of all asthmatic persons. Persons with occupational asthma have the typical symptoms of asthma with cough, dyspnea, and wheeze. Typically, the symptoms are related to work and improve on weekends and during vacations. In some instances, symptoms may persist even after termination of exposure.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Stress, Depression, And Psychosocial </i></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Observational studies demonstrate an association between increased stress and worsening asthma, but the role is not clearly defined. Bronchoconstriction from psychological factors appears to be mediated primarily through excess parasympathetic input. Atropine has been shown to block experimental psychogenic bronchoconstriction. It is most important to emphasize to both patients and parents that asthma is not an emotional disease; however, coping skills may benefit the patient who becomes emotionally distraught during an asthma attack.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Rhinitis And Sinusitis</i></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Disorders of the upper respiratory tract, particularly rhinitis and sinusitis, have been linked with asthma for many years. As many as 40% to 50% of asthmatics have abnormal sinus radiographs. However, chronic sinusitis may just represent a nonbacterial coexisting condition with allergic asthmatics because the histologic changes in the paranasal sinuses are similar to those seen in the lung and nose. Treatment of upper airway disease may optimize overall asthma control. The mechanism by which sinusitis aggravates asthma is unknown. The treatment of allergic rhinitis with inhaled corticosteroids and cromolyn but not antihistamines will reduce BHR in asthmatic patients. It has been postulated that transport of mucus chemotactic factors and inflammatory mediators from nasal passages during allergic rhinitis into the lung may accentuate BHR.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Gastroesophageal Reflux Disease </i></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Symptoms of gastroesophageal reflux disease are common in both children and adults who have asthma. Nocturnal asthma may be associated with nighttime reflux. Reflux of acidic gastric contents into the esophagus is thought to initiate a vagally mediated reflex bronchoconstriction. Also of concern is that most medications that decrease airways smooth muscle tone also have a relaxant effect on gastroesophageal sphincter tone. Although a systematic review concluded there was no significant improvement in asthma symptoms from medical management of gastroesophageal reflux disease, the standard approach is to initiate standard antireflux therapy in those patients who are exhibiting symptoms of reflux (particularly with nocturnal asthma) and observe the asthma symptoms.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Female Hormones And Asthma</i></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Premenstrual worsening of asthma has been reported in as many as 30% to 40% of women in some studies, whereas worsening of pulmonary functions has been reported even in women who are unaware of worsening symptoms. The pathophysiology is uncertain because estrogen replacement in postmenopausal women worsens asthma, whereas estradiol and progesterone administration have been variably reported to improve or have no effect on asthma in women with premenstrual asthma. The clinical significance of menstruation-related asthma is still unclear because some studies report that up to 50% of emergency department visits by women were premenstrual, whereas others report no association with menstrual phase. Studies indicate that, in general, BHR and symptoms improve in asthmatics during pregnancy.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Treatment</b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The primary goal is prevention of life-threatening asthma by early recognition of signs of deterioration and early intervention. As such, the principal goals of treatment include</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
• Correction of significant hypoxemia.</div>
<div style="text-align: justify;">
• Rapid reversal of airflow obstruction</div>
<div style="text-align: justify;">
• Reduction of the likelihood of relapse of the exacerbation or future recurrence of severe airflow obstruction</div>
<div style="text-align: justify;">
• Development of a written asthma action plan in case of a further exacerbation</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
These goals are best achieved by early initiation or intensification of treatment and close monitoring of objective measures of oxygen-ation and lung function. Early response to treatment as measured by the improvement in FEV1 at 30 minutes following inhaled β2-agonists is the best predictor of outcome. Providing adequate oxygen supplementation to maintain oxygen (O2) saturations above 90% (or above 95% in pregnant women and those who have coexistent heart disease) is essential. In children younger than 6 years of age, in whom lung function measures are difficult to obtain, a combination of objective (e.g., oxygen saturation, capillary CO2, respiratory rate, and heart rate) and subjective measures may be used to assess severity.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/severe-asthma-attack.html"><b>Severe Asthma Attack </b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>
<div style="text-align: left;">
Image: babble.com </div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com5tag:blogger.com,1999:blog-7113702905971561223.post-29223917589146646612012-04-04T12:05:00.000+07:002012-04-04T12:06:08.631+07:00How to Treatment Gastric Reflux<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhRBC2JIP71_B9GnjVoN3A-ATKAGRYOvFRBlQHMTepbFbBIQLG1QJ0tN6w4MSSK88_eH7rlAlwXJziPkoqObsLdmYbHkdV9VYsUjmgN_v3YEVA41wyH23AHD9XaKoIZ88cRVPdWW-TRFTY/s1600/Gastric.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhRBC2JIP71_B9GnjVoN3A-ATKAGRYOvFRBlQHMTepbFbBIQLG1QJ0tN6w4MSSK88_eH7rlAlwXJziPkoqObsLdmYbHkdV9VYsUjmgN_v3YEVA41wyH23AHD9XaKoIZ88cRVPdWW-TRFTY/s1600/Gastric.jpg" /></a></div>
<a href="http://umaeenews.blogspot.com/2012/04/how-to-treatment-gastric-reflux.html"><b>How to Treatment Gastric Reflux</b></a> - Patients with GERD (Gastroesophageal Reflux Disease) may display symptoms described as (a) typical, (b) atypical, or (c) alarm. Table 34–2 summarizes each of these clinical presentations of GERD. The severity of the symptoms of gastroesophageal reflux does not always correlate with the degree of esophagitis, but it does correlate with the duration of reflux. Patients with nonerosive disease may have symptoms as severe as those with endoscopic findings. It is important to distinguish GERD symptoms from those of other diseases, especially when chest pain or pulmonary symptoms are present. Interestingly, close to half of patients presenting with chest pain who have a normal electrocardiogram have GERD. Similarly, approximately half of patients with asthma have GERD.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhP0d1Y-ZL74fVG3tIp3YL-5_yUWO1ofzwyOlTk-9OUylCtxXADpD_yXw-QwOnmwoxtCvAA-7bdRnNfYa85vAN17mrIgQpsC9D4ydeKlECgPPXpLsd-f1FPwWDNBV0o5FtzBu3vm9UFf4s/s1600/GERD+2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="397" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhP0d1Y-ZL74fVG3tIp3YL-5_yUWO1ofzwyOlTk-9OUylCtxXADpD_yXw-QwOnmwoxtCvAA-7bdRnNfYa85vAN17mrIgQpsC9D4ydeKlECgPPXpLsd-f1FPwWDNBV0o5FtzBu3vm9UFf4s/s400/GERD+2.jpg" width="400" /></a></div>
</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Patients presenting with asthma (especially nocturnal asthma) that is poorly responsive to standard medical therapies should be evaluated to determine if GERD contributes to their symptoms. Pulmonary symptoms result from either direct irritation of the vagus nerve when refluxed acid comes in contact with the esophageal mucosa, causing bronchospasm (the reflex theory) or, less commonly, from aspiration of the refluxate into the lungs, causing chemical irritation that manifests as pneumonia or pulmonary fibrosis (the reflux theory). As previously mentioned, patients who are inadequately treated for GERD may go on to develop complications from long-term acid exposure.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Long-term, recurrent reflux symptoms that are not ade quately treated may lead to the development of Barrett’s esophagus and may be an independent risk factor for the development of esophageal adenocarcinoma. Esophageal strictures may be present in patients presenting with dysphagia. However, these symptoms may occur in other esophageal disorders such as esophageal diverticulum, achalasia, obstruction, esophageal spasm, esophageal infections, scleroderma, and malignancy. The presence of alarm symptoms should be further investigated to differentiate other diseases as the cause.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The most useful tool in the diagnosis of gastroesophageal reflux is the clinical history, including both presenting symptoms and associated risk factors. Patients presenting with mild, typical symptoms of reflux (heartburn and regurgitation) do not usually require invasive esophageal evaluation. These patients generally benefit from an initial empiric trial of acid-suppression therapy. A clinical diagnosis of GERD can be assumed in patients who respond to appropriate therapy.1 Further diagnostic evaluation should be performed in those patients do not respond to therapy, for those who present with alarm symptoms (e.g., dysphagia, weight loss), and in those with long-standing GERD symptoms. Alarm symptoms may indicate more complicated disease and long-standing GERD symptoms increase the risk for Barrett’s esophagus.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Useful tests in diagnosing GERD include endoscopy, ambulatory reflux monitoring, and manometry. Endoscopy is the preferred technique for assessing the mucosa for esophagitis, identifying Barrett’s esophagus and diagnosing complications. It enables visualization and biopsy of the esophageal mucosa. Although endoscopy is a highly specific test, it is not extremely sensitive. In mild cases of GERD, the esophageal mucosa may appear relatively normal. In addition, noninflammatory GERD and major motor disorders may be missed by endoscopy. A camera-containing capsule swallowed by the patient offers the newest technology for visualizing the esophageal mucosa. The PillCam ESO is less invasive and takes less than 15 minutes to perform in the clinician’s office. Images of the esophagus are downloaded through sensors placed on the patient’s chest that are connected to a data collector. The camera-containing capsule is passed in the stool.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Although less expensive than endoscopy, barium radiography lacks the sensitivity and specificity needed to accurately determine the presence of mucosal injury or to distinguish between Barrett’s esophagus and esophagitis. For these reasons, barium radiography has limited use in the routine diagnosis of GERD. Unfortunately, the presence or absence of mucosal damage does not prove the patient’s symptoms are reflux related; for that, ambulatory reflux monitoring is useful.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Ambulatory pH testing identifies patients with excessive esophageal acid exposure and helps determine if symptoms, both typical and atypical, are acid related. However, pH monitoring may be less reliable in confirming laryngopharyngeal reflux. Interestingly, patients may have severe symptoms, including esophagitis, even when total acid exposure is considered normal.1 Ambulatory pH testing may also be useful in patients who are on what is considered adequate therapy, but whose symptoms are not improving. However, GERD that is truly refractory to medical therapy is uncommon. Ambulatory pH testing can be performed by passing a small pH probe transnasally and placing it approximately 5 cm above the LES. Patients are asked to keep a diary of symptoms that later are correlated with the pH measurement corresponding to the time the symptom was reported. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In addition to correlating symptoms to abnormal esophageal acid exposure, ambulatory pH testing also documents the percentage of time the intraesophageal pH is below 4 and determines the frequency and severity of reflux. Two recent developments related to ambulatory reflux monitoring include (a) the use of combined impedance and acid testing and (b) the use of a tubeless method of acid monitoring. Whereas ambulatory pH testing only measures acid reflux, combined impedance and acid testing measures both acid and nonacid reflux. This may be useful when evaluating patients on acid suppression therapy.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The second method involves the attachment of a radiotelemetry capsule to the esophageal mucosa. The advantages of this method are that a longer period of monitoring is possible (48 hours) and it is more comfortable for the patient because a nasogastric tube is unnecessary. The empiric use of standard- or even double-dose proton pump inhibitor (specifically omeprazole) as a therapeutic trial for diagnosing the presence of GERD may be useful in patients with atypical symptoms. This approach is less expensive, more convenient, and more readily available than ambulatory reflux monitoring. Problems with using a proton pump inhibitor as a diagnostic tool include lack of a standardized dosing regimen and duration of the diagnostic trial.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Esophageal manometry may be used to ensure the proper placement of esophageal pH probes and to evaluate esophageal peristalsis and motility prior to antireflux surgery. To perform manometry, a multilumen pressure sensing tube is passed into the stomach and the pressures are measured as the tube is pulled back across the lower esophageal sphincter, esophagus, and pharynx. The recent advancement of the tubeless pH monitoring system using endoscopic landmarks for placement may negate the need for manometry</div>
<div style="text-align: justify;">
for ensuring proper placement of esophageal pH probes.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>General Approach to Treatment</b> <br />
<br /></div>
<div style="text-align: justify;">
The treatment of GERD is categorized into one of the following modalities: (a) lifestyle modifications and patient-directed therapy with antacids, nonprescription H2-receptor antagonists, and/or nonprescription proton pump inhibitors; (b) pharmacologic intervention with prescription-strength acid suppression therapy; (c) and interventional therapies (antireflux surgery or endoscopic therapies; Table 34–3). The initial therapeutic modality used is in part dependent on the patient’s condition (frequency of symptoms, degree of esophagitis, and presence of complications).</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEinY4Cssl_N-La4jDRxX8PR-3MUAyR-50bFuT6J07YkEQiGZ__g1dLMvAfH953UsInRvrao0pMd1j9QW1pMFp8slvglgJZ3hJ13fPNdXSf81ua-s-rJngFsYrAmCTAzhHi72D9A7yRHuSI/s1600/GERD+1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEinY4Cssl_N-La4jDRxX8PR-3MUAyR-50bFuT6J07YkEQiGZ__g1dLMvAfH953UsInRvrao0pMd1j9QW1pMFp8slvglgJZ3hJ13fPNdXSf81ua-s-rJngFsYrAmCTAzhHi72D9A7yRHuSI/s640/GERD+1.jpg" width="300" /></a></div>
<br />
<br />
Historically, a step-up approach was used, starting with noninvasive lifestyle modifications and patient-directed therapy, and progressing to pharmacologic management or interventional approaches (Table 34–4). A step-down approach, starting with a proton pump inhibitor given once or twice daily instead of an H2-receptor antagonist, and then stepping down to the lowest degree of acid suppression needed to control symptoms, is also effective. Neither the “step-up” nor the “step-down” approach has superior efficacy over the other.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjjfnSkNh0WKCjUQX_itYqZOpkikrBLkCKOIU5KcdGA8OHnyeSYjCk9W1dh2IHx0y9IVdFOzLywqrktOa0oPKZCLQg2g2u6AbIprZdsFqrLIh2QqTCxkaaDIjEqKhukXlAICetBpT5Z0pM/s1600/GERD+3.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjjfnSkNh0WKCjUQX_itYqZOpkikrBLkCKOIU5KcdGA8OHnyeSYjCk9W1dh2IHx0y9IVdFOzLywqrktOa0oPKZCLQg2g2u6AbIprZdsFqrLIh2QqTCxkaaDIjEqKhukXlAICetBpT5Z0pM/s400/GERD+3.jpg" width="391" /></a></div>
<br />
<br />
The clinician should determine the most appropriate approach for the individual patient. Every attempt should be made to aggressively control symptoms and to prevent relapses early in the course of the patient’s disease in order to prevent the complications that are seen with long-standing symptomatic GERD. In patients with moderate to severe GERD, especially those with erosive disease, starting with a proton pump inhibitor as initial therapy is advocated because of its superior efficacy over H2-receptor antagonists. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Dietary and lifestyle modifications with education about factors that may worsen GERD symptoms is reasonable to discuss with the patient even though they are unlikely to control the patient’s symptoms in most cases. Table 34–5 lists many of the lifestyle modifications that can be recommended. Although most patients do not respond to lifestyle changes alone, education about their potential benefits should be stressed on a routine basis. Patients with mild or infrequent symptoms may see improvement with the inexpensive nonprescription H2- receptor antagonists, proton pump inhibitors, antacids, or alginic acid.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Patients who do not respond to lifestyle modifications and patientdirected therapy after 2 weeks should seek medical attention and are generally started on empiric therapy consisting of an acid-suppression agent. Acid-suppression therapy with proton pump inhibitors or H2- receptor antagonists is the mainstay of GERD treatment. Patients presenting with moderate to severe symptoms (with or without esophageal erosions) should be started on a proton pump inhibitor as initial therapy because it provides the most rapid symptomatic relief and healing in the highest percentage of patients. H2-receptor antagonists in divided doses are effective in patients with mild GERD. Standard H2-receptor antagonist doses may be increased to 2 to 4 times the normal dose in patients who do not respond to standard doses. However, if this is necessary, it is more cost-effective to switch to a proton pump inhibitor.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Promotility agents are not as effective as acid-suppression agents. Combining promotility agents with acid-suppression drugs offers only modest improvements in symptoms over standard doses of H2- receptor antagonists and should not be routinely recommended. In addition, the availability of a promotility agent that has an acceptable adverse effect profile is lacking. Mucosal protectants, such as sucralfate, have a very limited role in the treatment of GERD. Maintenance therapy is generally necessary to control symptoms and to prevent complications. In patients with more severe symptoms (with or without esophageal erosions), or in patients with other complications, maintenance therapy with a proton pump inhibitor is most effective.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Routine use of combination therapy has no role in maintenance therapy of GERD. GERD that is refractory to adequate acid suppression is rare. In these cases, the diagnosis should be confirmed through further diagnostic tests before longterm, high-dose therapy or interventional approaches (antireflux surgery or endoscopic therapies) are considered.<br />
<br />
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/how-to-treatment-gastric-reflux.html"><b>How to Treatment Gastric Reflux</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>
<div style="text-align: left;">
image: realresultswsl.com </div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com2tag:blogger.com,1999:blog-7113702905971561223.post-90958475789330018072012-04-02T21:19:00.001+07:002012-04-02T21:20:26.076+07:00Algorithm for Treatment of Heart Failure<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj065-ehOWGY2fThWyI0hLzaJd5SA6mCu1e2cnaFML-wR26cJ8IxshaHySqMLWiptfR7bB5YCEW0_aNPfCXGeFKG6-AAn9zysk3dNjUnC2dqCW6ykNurqlUFpes_y6xaOQVVND_OT7kMw4/s1600/Algorithm+of+Hearth+Failure.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj065-ehOWGY2fThWyI0hLzaJd5SA6mCu1e2cnaFML-wR26cJ8IxshaHySqMLWiptfR7bB5YCEW0_aNPfCXGeFKG6-AAn9zysk3dNjUnC2dqCW6ykNurqlUFpes_y6xaOQVVND_OT7kMw4/s1600/Algorithm+of+Hearth+Failure.jpg" /></a></div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-for-treatment-of-heart.html"><b>Algorithm for Treatment of Heart Failure</b></a> - Heart failure can result from any disorder that affects the ability of the heart to contract (systolic function) and/or relax (diastolic dysfunction); Table 16–1 lists the common causes of heart failure. Heart failure with impaired systolic function (i.e., reduced LVEF) is the classic, more familiar form of the disorder, but current estimates suggest up to 50% of patients with heart failure have preserved left ventricular systolic function with presumed diastolic dysfunction. </div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg8B-_5UODQX0Wp-wwsboOGmqy8whzdfFPdgDgQdy4aXYk8ml8Xe7ngo2Bxhyphenhypheng1-JlUNTYXzoTvlY6HmeFqtcFrWvcK6Hr1YbHcbt5L2lPjTRSxA8F4mnCIKMGwbDRRNkMqWU7BGruaXlw/s1600/Heart+Failure.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="343" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg8B-_5UODQX0Wp-wwsboOGmqy8whzdfFPdgDgQdy4aXYk8ml8Xe7ngo2Bxhyphenhypheng1-JlUNTYXzoTvlY6HmeFqtcFrWvcK6Hr1YbHcbt5L2lPjTRSxA8F4mnCIKMGwbDRRNkMqWU7BGruaXlw/s400/Heart+Failure.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In contrast to systolic heart failure that is usually caused by previous myocardial infarction (MI), patients with preserved LVEF typically are elderly, female, obese, and have hypertension, atrial fibrillation, or diabetes. Recent data indicate that survival is similar in patients with impaired or preserved LVEF. Frequently, systolic and diastolic dysfunction coexist. The common cardiovascular diseases, such as MI and hypertension, can cause both systolic and diastolic dysfunction; thus many patients have heart failure as a result of reduced myocardial contractility and abnormal ventricular filling. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Coronary artery disease is the most common cause of systolic heart failure, accounting for nearly 70% of cases. Myocardial infarction leads to reduction in muscle mass as a consequence of death of affected myocardial cells. The degree to which contractility is impaired will depend on the size of the infarction. In an attempt to maintain cardiac output, the surviving myocardium undergoes a compensatory remodeling, thus beginning the maladaptive process that initiates the heart failure syndrome and leads to further injury to the heart. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Myocardial ischemia and infarction also affect the diastolic properties of the heart by increasing ventricular stiffness and slowing ventricular relaxation. Thus, myocardial infarction frequently results in systolic and diastolic dysfunction. Impaired systolic function is a cardinal feature of dilated cardiomyopathies. Although the cause of reduced contractility frequently is unknown, abnormalities such as interstitial fibrosis, cellular infiltrates, cellular hypertrophy, and myocardial cell degeneration are seen commonly on histologic examination. Genetic causes of dilated cardiomyopathies may also occur.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>General Approach to Treatment </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<i>Treatment of Stage A Heart Failure</i><br />
<br />
Patients in stage A do not have structural heart disease or heart failure symptoms but are at high risk for developing heart failure because of the presence of risk factors. The emphasis here is on identification and modification of these risk factors to prevent the development of structural heart disease and subsequent heart failure. Commonly encountered risk factors include hypertension, diabetes, obesity, metabolic syndrome, smoking, and coronary artery disease. Although each of these disorders individually increases risk, they frequently coexist in many patients and act synergistically to foster the development of heart failure. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Effective control of blood pressure reduces the risk of developing heart failure by approximately 50%, thus current hypertension treatment guidelines should be followed. Control of hyperglycemia reduces the risk of end-organ damage and the risk of developing heart failure. Appropriate management of coronary disease<br />
and its associated risk factors is also important, including treatment of hyperlipidemia according to published guidelines and smoking cessation. Although treatment must be individualized, ACE inhibitors or ARBs should be strongly considered for antihypertensive therapy in patients with multiple vascular risk factors. Diuretics and β-blockers may also useful in this setting.</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<br />
<i>Treatment of Stage B Heart Failure</i><br />
<br />
Patients in stage B have structural heart disease, but do not have heart failure symptoms. This group includes patients with left ventricular hypertrophy, recent or remote MI, valvular disease, or reduced LVEF (less than 40%). These individuals are at risk for developing heart failure and treatment is targeted at minimizing additional injury and preventing or slowing the remodeling process. In addition to the treatment measures outlined in stage A, ACE inhibitors and β-blockers are important components of therapy. Patients with a previous MI should receive both ACE inhibitors and β-blockers, regardless of the LVEF.1 Similarly, patients with a reduced LVEF should also receive both these agents, whether or not they have had a MI. ARBs are an effective alternative in patients intolerant to ACE inhibitors.</div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj5RYsYHKnQizhOPXqf6yNjB-B-5kLWdwWNO4uVxuYz7hdSSVDBdCc5ytO48RMn_rP8UMXnSFJHaK5bVt5oPkwZu_P5m2DZ774nBMtfgMjUAuJLX8Qm8EBtKldhPSa-j_QD9dnwuNIfB3E/s1600/Heart+Failure+1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="336" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj5RYsYHKnQizhOPXqf6yNjB-B-5kLWdwWNO4uVxuYz7hdSSVDBdCc5ytO48RMn_rP8UMXnSFJHaK5bVt5oPkwZu_P5m2DZ774nBMtfgMjUAuJLX8Qm8EBtKldhPSa-j_QD9dnwuNIfB3E/s400/Heart+Failure+1.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<i>Treatment of Stage C Heart Failure</i></div>
<div style="text-align: justify;">
<br />
Patients with structural heart disease and previous or current heart failure symptoms are classified in stage C. In addition to treatments in stages A and B, most patients in stage C should be routinely treated with three medications: a diuretic, an ACE inhibitor, and a β-blocker (see Drug Therapies for Routine Use below). The benefits of these medications on slowing heart failure progression, reducing morbidity and mortality, and improving symptoms are clearly established. Aldosterone receptor antagonists, ARBs, digoxin, and hydralazine-isosorbide dinitrate are also useful in selected patients.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Nonpharmacologic therapy with devices such as an implantable cardiac-defibrillator (ICD) or cardiac resynchroni zation therapy (CRT) with a biventricular pacemaker is also indicated in certain patients in stage C (see Nonpharmacologic Therapy below). Other general measures are also important, including moderate sodium restriction, daily weight measurement, immunization against influenza and pneumococcus, modest physical activity, and avoidance of medications that can exacerbate heart failure. Recent evidence suggests that careful followup and patient education that reinforces dietary and medication compliance can prevent clinical deterioration and reduce hospitalization.</div>
<div style="text-align: justify;">
<br />
<i>Treatment of Stage D Heart Failure</i></div>
<div style="text-align: justify;">
<br />
Stage D heart failure includes patients with symptoms at rest that are refractory despite maximal medical therapy. This includes patients who undergo recurrent hospitalizations or who cannot be discharged from the hospital without special interventions. These individuals have the most advanced form of heart failure and should be considered for specialized therapies including mechanical circulatory support, continuous intravenous positive inotropic therapy, cardiac transplantation, or hospice care. </div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiIv0dcYSSC-dJQZjAZYMNdtO3DuUH1GxZ0ZeCtt59fw0M3KmQPeI_-jLvm6OZRogNzFwIJjrjIYX6zGOT03rzeVZm8wOH7fgp8MJrDC0-AVydrDkY9oowcL9e3mCzkueBknj6SjpxJTCc/s1600/Heart+Failure+2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="382" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiIv0dcYSSC-dJQZjAZYMNdtO3DuUH1GxZ0ZeCtt59fw0M3KmQPeI_-jLvm6OZRogNzFwIJjrjIYX6zGOT03rzeVZm8wOH7fgp8MJrDC0-AVydrDkY9oowcL9e3mCzkueBknj6SjpxJTCc/s400/Heart+Failure+2.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-for-treatment-of-heart.html"><b>Algorithm for Treatment of Heart Failure</b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th</div>
<div style="text-align: left;">
Image: zeenews.india.com </div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com4tag:blogger.com,1999:blog-7113702905971561223.post-8604904302002626742012-04-02T12:51:00.000+07:002012-04-20T13:48:01.201+07:00Algorithm for Treatment of Hypertension<div dir="ltr" style="text-align: left;" trbidi="on">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjOrTDS886ShSWkEEAzNc3rUIaIm_9Q1nCsekkDKsnDdn7kq1lWR_EcaTUz-BAe3kZUBU0_FOcEvd_YimfWgiNkMqD0oLmVsljHOk1RBYmE48TSNlWFMV0htOXHduhbNpntbbjNE47Cm_Q/s1600/hypertension.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="hypertension" border="0" height="298" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjOrTDS886ShSWkEEAzNc3rUIaIm_9Q1nCsekkDKsnDdn7kq1lWR_EcaTUz-BAe3kZUBU0_FOcEvd_YimfWgiNkMqD0oLmVsljHOk1RBYmE48TSNlWFMV0htOXHduhbNpntbbjNE47Cm_Q/s320/hypertension.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-for-treantment-of.html"><b>Algorithm for Treatment of Hypertension</b> </a>- In most patients, hypertension results from an unknown pathophysiologic etiology (essential or primary hypertension). This form of hypertension cannot be cured, but it can be controlled. A small percentage of patients have a specific cause of their hypertension (secondary hypertension). There are many potential secondary causes that are either concurrent medical conditions or are endogenously induced. If the cause can be identified, hypertension in these patients has the potential to be cured.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Essential Hypertension</b> </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
More than 90% of individuals with hypertension have essential hypertension. Numerous mechanisms have been identified that may contribute to the pathogenesis of this form of hypertension, so identifying the exact underlying abnormality is not possible. Genetic factors may play an important role in the development of essential hypertension. There are monogenic and polygenic forms of BP dysregulation that may be responsible for essential hypertension. Many of these genetic traits feature genes that affect sodium balance, but genetic mutations altering urinary kallikrein excretion, nitric oxide release, and excretion of aldosterone, other adrenal steroids, and angiotensinogen are also documented. In the future, identifying individuals with these genetic traits could lead to alternative approaches to preventing or treating hypertension; however, this is not currently recommended.</div>
<div style="text-align: justify;">
<br />
<b>Secondary Hypertension</b> </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Fewer than 10% of patients have secondary hypertension where either a comorbid disease or drug is responsible for elevating BP (Figure 15–1), In most of these cases, renal dysfunction resulting from severe chronic kidney disease or renovascular disease is the most common secondary cause. Certain drugs, either directly or indirectly, can cause hypertension or exacerbate hypertension by increasing BP. When a secondary cause is identified, removing the offending agent (when feasible) or treating/correcting the underlying comorbid condition should be the first step in management.</div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcnfG2KjWXc5D1nY-ioF62rp7UFonRRE0CloY5meYcAnNrLX_6aXprj9FuHf5TA83tpRvqtHdeBw1JCsjigF7WkpKr1sFMtkDNJ9GET6DlnYh9FQqjr9IT0bLp0rNLJtMJiwaBmaVaH2s/s1600/Algorithm+of+Hypertension+1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="algorithm of hypertension" border="0" height="342" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcnfG2KjWXc5D1nY-ioF62rp7UFonRRE0CloY5meYcAnNrLX_6aXprj9FuHf5TA83tpRvqtHdeBw1JCsjigF7WkpKr1sFMtkDNJ9GET6DlnYh9FQqjr9IT0bLp0rNLJtMJiwaBmaVaH2s/s400/Algorithm+of+Hypertension+1.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Classification</b></div>
<div style="text-align: justify;">
<br />
The JNC7 classification of BP in adults (age ≥18 years) is based on the average of two or more properly measured BP readings from two or more clinical encounters (Table 15–3). It includes four categories: normal, prehypertension, stage 1 hypertension, and stage 2 hypertension. Prehypertension is not considered a disease category, but identifies patients whose BP is likely to increase into the classification of hypertension in the future. Hypertensive crises are clinical situations where BP values are very elevated, typically greater than 180/120 mm Hg. They are categorized as either a hypertensive emergency or hypertensive urgency.<br />
Hypertensive emergencies are extreme elevations in BP that are accompanied by acute or progressing target-organ damage. Hypertensive urgencies are high elevations in BP without acute or progressing target-organ injury.</div>
<div style="text-align: justify;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjOFf7Yyq1LeQNZ60h7ZbX4je1Z08KE8NXTcm7dFd8wvPfCKw5AFsSp1DwZcoTEqMOEszIN-_n1xwwd4YxL4YxiP54cXaBx8isXKdzAaFs8ybbHAcI83mDN04KwP6EyjkQlp_5meKiB8wU/s1600/Algorithm+of+hypertension+2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="algorithm of hypertension1" border="0" height="287" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjOFf7Yyq1LeQNZ60h7ZbX4je1Z08KE8NXTcm7dFd8wvPfCKw5AFsSp1DwZcoTEqMOEszIN-_n1xwwd4YxL4YxiP54cXaBx8isXKdzAaFs8ybbHAcI83mDN04KwP6EyjkQlp_5meKiB8wU/s400/Algorithm+of+hypertension+2.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Treatment</b></div>
<div style="text-align: justify;">
<br />
After a definitive diagnosis of hypertension is made, most patients should be placed on both lifestyle modifications and drug therapy concurrently. Lifestyle modification alone is considered appropriate therapy for patients with prehypertension. However, lifestyle modi fications alone are not considered adequate for patients with hypertension and additional Cardiovascular (CV) risk factors, especially patients with BP goals of less than 130/80 mm Hg (e.g., diabetes, coronary artery disease, chronic kidney disease) or less than 120/80 mm Hg (i.e., left ventricular dysfunction), who have not attained this goal BP.</div>
<div style="text-align: justify;">
<br />
The choice of initial drug therapy depends on the degree of BP elevation and presence of compelling indications (see Patients with Compelling Indications section). Most patients with stage 1 hypertension should be initially treated with a thiazide-type diuretic, ACE inhibitor, ARB, or CCB. For patients with more severe BP elevation (stage 2 hypertension), combination drug therapy, with one of the agents being preferably a thiazide type-diuretic, is recommended. Figure 15–2 outlines this general approach. There are six compelling indications where specific antihypertensive drug classes have evidence showing unique benefits in patients with the compelling indication (Fig. 15–3).<b></b></div>
<div style="text-align: justify;">
<b><br /></b></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgvWB7bYr0btZ9GHeqmfonKOY0GERZ5Kep5Ksjz-gbcbRA9OjjXVH48ZcXWBZat7uxbTF31tMWeulcJb8J_UI2-BiWJGoA2LRDMNly6wAy6LZgiRmxDb3tRpIL_pTsA1lk1krmfbdMjSK4/s1600/Algorithm+of+Hypertension.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="185" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgvWB7bYr0btZ9GHeqmfonKOY0GERZ5Kep5Ksjz-gbcbRA9OjjXVH48ZcXWBZat7uxbTF31tMWeulcJb8J_UI2-BiWJGoA2LRDMNly6wAy6LZgiRmxDb3tRpIL_pTsA1lk1krmfbdMjSK4/s400/Algorithm+of+Hypertension.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<b><br /></b></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhXFBtJQT8Y-mJmjZ4g2hX9bZnthhtrSIHJyhAFKG5cDNh0HjwwzirlXilscKGKarakJIdI2EZRaZhuY0XjGYklJTOLrghIVdFyTwf3B9gpXl3buKT8fENrjBQJAocBPnzxm5tITaNf3l4/s1600/Algorithm+of+hypertension+3.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="algorithm ot hypertension2" border="0" height="385" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhXFBtJQT8Y-mJmjZ4g2hX9bZnthhtrSIHJyhAFKG5cDNh0HjwwzirlXilscKGKarakJIdI2EZRaZhuY0XjGYklJTOLrghIVdFyTwf3B9gpXl3buKT8fENrjBQJAocBPnzxm5tITaNf3l4/s400/Algorithm+of+hypertension+3.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<b><br /></b></div>
<div style="text-align: justify;">
<b><br /></b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Nonpharmacologic Therapy</b></div>
<br />
<div style="text-align: justify;">
All patients with prehypertension and hypertension should be prescribed lifestyle modifications. Table 15–4 lists modifications that lower BP. These approaches are recommended by the JNC7 (Seventh report of Joint Nasional of committe of Prevention ) and the AHA (American Heart Association). They can provide small to moderate reductions in SBP. Aside from lowering BP in patients with known hypertension, lifestyle modification can decrease the progression to hypertension in patients with prehypertension BP values. In a portion of patients with hypertension that have relatively good BP control while on single antihypertensive drug therapy, sodium reduction and weight loss may allow withdrawal of drug therapy. A sensible dietary program is one that is designed to reduce weight gradually, for overweight and obese patients, and one that restricts sodium intake with only moderate alcohol consumption.</div>
<div style="text-align: justify;">
Successful implementation of dietary lifestyle modifications by clinicians requires aggressive promotion through reasonable patient education, encouragement, and continued reinforcement. Patients may better understand the rationale for dietary intervention in hypertension if they are provided the following observations and facts :<br />
1. Hypertension is two to three times more likely in overweight than in lean persons.<br />
2. More than 60% of patients with hypertension are overweight.<br />
3. As little as 10 pounds of weight loss can decrease BP significantly in overweight patients.<br />
4. Abdominal obesity is associated with the metabolic syndrome, which is a precursor to diabetes, dyslipidemia, and, ultimately, CV disease.<br />
5. Diets rich in fruits and vegetables and low in saturated fat lower BP in patients with hypertension.<br />
6. Most people experience some degree of SBP reduction with sodium restriction.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/04/algorithm-for-treantment-of.html"><b>Algorithm for Treatment of Hypertension </b></a></div>
<div style="text-align: left;">
Source: Pharmacotherapy 7th </div>
<div style="text-align: left;">
Image: ayushveda.com </div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<br /></div>
</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com47tag:blogger.com,1999:blog-7113702905971561223.post-14379511049037778552012-03-24T12:23:00.004+07:002012-03-24T12:26:27.107+07:00Sport Nutrition of Macronutrient Demands<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj4NgohPI14usI8ZZhfB4AwXvCkeAyRpyECU9fp6p92WAEZm8jvVt2bxxfuLbqFFL9EgWSpOH-76OtGPL2Xi45S7mKVbQMZFr5-t1r3Iyl00whcxdpTOl_eoTY0AO6Dbd2agthQVESNfBc/s1600/Macronutrient.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="192" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj4NgohPI14usI8ZZhfB4AwXvCkeAyRpyECU9fp6p92WAEZm8jvVt2bxxfuLbqFFL9EgWSpOH-76OtGPL2Xi45S7mKVbQMZFr5-t1r3Iyl00whcxdpTOl_eoTY0AO6Dbd2agthQVESNfBc/s320/Macronutrient.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<b>Protein</b></div>
<div style="text-align: justify;">
<br />
The idea that protein requirements are increased by physical activity is intuitively attractive, and highprotein diets are a common feature of the diets of sportsmen and women. The available evidence shows an increased rate of oxidation of the carbon skeletons of amino acids during exercise, especially when carbohydrate availability is low. Protein contributes only about 5% of total energy demand in endurance exercise, but the absolute rate of protein breakdown is higher than at rest (where protein contributes about the same fraction as the protein content of the diet, i.e., typically about 12–16%) because of the higher energy turnover. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
It is often recommended that athletes engaged in endurance activities on a daily basis should aim to achieve a protein intake of about 1.2–1.4 g kg-1 day-1, whereas athletes engaged in strength and power <a href="http://umaeenews.blogspot.com/2012/03/nutrition-for-training.html"><b>training</b></a> may need as much as 1.6–1.7 g kg-1 day-1. Those who take no exercise have an estimated average requirement of about 0.6 g kg-1 day and the recommended intake for these individuals is about 0.8– 1.0 g kg-1 day.</div>
<div style="text-align: justify;">
<br />
In strength and power sports such as weightlifting, sprinting and bodybuilding, the use of high-protein diets and protein supplements is especially prevalent, and daily intakes in excess of 2–4 g-1 kg-1 are not unusual. Scientific support for such high intakes is generally lacking, but those involved in these sports are adamant that such high levels of intake are necessary, not only to increase muscle mass but also to maintain muscle mass. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
This apparent inconsistency may be explained by Millward’s adaptive metabolic demand model, which proposes that the body adapts to either high or low levels of intake, and that this adjustment to changes in intake occurs only very slowly. This means that individuals such as strength and power athletes who consume a highprotein diet over many years will find that any reduction in protein intake will result in a loss of muscle mass. This is because of an upregulation of the activity of the enzymes involved in protein oxidation to cope with the high intake: activity of these enzymes remains high when there is a sudden decrease in intake, leading to a net catabolic effect.</div>
<div style="text-align: justify;">
<br />
Protein synthesis and degradation are both enhanced for some hours after exercise, and the net effect on muscle mass will depend on the relative magnitude and duration of these effects. Several recent studies have shown that ingestion of small amounts of protein (typically about 35–40 g) or essential amino acids (about 6 g) either before or immediately after exercise will result in net protein synthesis in the hours after exercise, whereas net negative protein balance is observed if no source of amino acids is consumed. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
These observations have led to recommendations that protein should be consumed immediately after exercise, but the control condition in most of these studies has involved a relatively prolonged (6–12 h) period of fasting, and this does not reflect normal behavior. Individuals who consume foods containing carbohydrate and proteins in the hour or two before exercise may not further increase protein synthesis if additional amino acids or proteins are ingested immediately before, during, or after exercise.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Various high (30%) protein, high (30%) fat, low (40%) carbohydrate diets have been promoted for weight loss, and some diets even suggest almost complete elimination of carbohydrate from the diet. Some of these diets have been specifically targeted at athletes, accompanied by impressive claims and celebrity endorsements. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Proposed mechanisms of action of these diets include reduced circulating insulin levels, increased fat catabolism, and altered prostaglandin metabolism, but it seems more likely that these diets achieve weight loss simply by restricting dietary choice. These diets can be effective in promoting short-term weight loss, primarily by restricting energy intake (typically to 1000–2000 kcal day-1). There is no evidence to support improvements in exercise performance, and what evidence there is does not support the<br />
concept.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Carbohydrate</b></div>
<div style="text-align: justify;">
<br />
Carbohydrate is an essential fuel for the brain, red blood cells, and a few other tissues. Fat and carbohydrate<br />
are the main fuels used for energy supply in muscle during exercise. In low-intensity exercise, most of the energy demand can be met by fat oxidation, but the contribution of carbohydrate, and especially of the muscle glycogen, increases as the rate of energy demand increases. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Carbohydrate oxidation rates of 3–4 g min-1 may be sustained for several hours by athletes in training or competition. When the glycogen content of the exercising muscles reaches very low levels, the work rate must be reduced to a level that can be accommodated by fat oxidation. In high-intensity exercise, essentially all of the energy demand is met by carbohydrate metabolism. Therefore, repeated short sprints place high demands on the muscle carbohydrate store, most of which can be converted to lactate within a few minutes.</div>
<div style="text-align: justify;">
<br />
Carbohydrate is stored in the body in the form of glycogen, primarily in the liver (about 70–100 g in the fed state) and in the skeletal muscles (about 300–500 g, depending on muscle mass and preceding diet). These stores are small relative to the body’s requirements for carbohydrate. Carbohydrate supplies about 45% of the energy in the typical Western diet. This amounts to about 200–300 g day-1 for the average sedentary individual, and is adequate for normal daily activities. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In an hour of hard exercise, however, up to 200 g of carbohydrate can be used, and sufficient carbohydrate must be supplied by the diet to replace the amount used. Replacement of the glycogen stores is an essential part of the recovery process after exercise: if the muscle glycogen content is not replaced, the quality of training must be reduced, and the risks of illness and injury are increased. Low muscle glycogen levels are associated with an increased secretion of cortisol during exercise, with consequent negative implications for immune function.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
</div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjCarKXcVGeGO6oTA2Is_KLvV8vnzvqoqW9IneXQihPt5G8WaNAt7GOraY49fjeHZkwEXmMnvmDI0bwUeydIhsSnPIZ_LbhGeQIM1UCmsVVCe055iWb8uwmZ7BDIEGG6Uu0pemGnBKsz7E/s1600/Carbohydrat.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="156" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjCarKXcVGeGO6oTA2Is_KLvV8vnzvqoqW9IneXQihPt5G8WaNAt7GOraY49fjeHZkwEXmMnvmDI0bwUeydIhsSnPIZ_LbhGeQIM1UCmsVVCe055iWb8uwmZ7BDIEGG6Uu0pemGnBKsz7E/s400/Carbohydrat.jpg" width="400" /></a></div>
<div style="text-align: justify;">
<br />
When rapid recovery is a priority, replacement of carbohydrate should begin as soon as possible after exercise with carbohydrate foods that are convenient and appealing. Thereafter, the diet should supply sufficient carbohydrate to replace the amount used in training and to meet ongoing demands of other tissues. Some recommendations for carbohydrate intake after training or competition are shown in Table. For athletes preparing for competition, a reduction in the training load and the consumption of a high-carbohydrate diet in the last few days are recommended. This maximizes the body’s carbohydrate stores and should ensure optimum performance, not only in endurance activities, but also in events involving short-duration high-intensity exercise and in field games involving multiple sprints.</div>
<div style="text-align: justify;">
<br />
The high-carbohydrate diet recommended for the physically active individual coincides with the recommendations of various expert committees that a healthy diet is one that is high in carbohydrate (at least 55% of energy) and low in fat (less than 30% of energy). However, where energy intake is either very high or very low, it may be inappropriate to express the carbohydrate requirement as a fraction of energy intake. With low total energy intakes, the fraction of carbohydrate in the diet must be high, but the endurance athlete with a very highenergy intake may be able to tolerate a higher fat intake. Recommendations, as in Table, should be framed in absolute amounts relative to body mass, i.e., grams of carbohydrate per kilogram body mass. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
The type of carbohydrate eaten is less important than the amount. It is valuable to choose nutrientrich carbohydrates and to add other foods to recovery meals and snacks to provide a good source of protein and other nutrients. The presence of small amounts of protein in recovery meals may promote additional glycogen recovery when carbohydrate intake is less than optimal or when frequent snacking is not possible. Protein taken at this time may also stimulate protein synthesis in muscles, as described above. Carbohydrate-rich foods with a moderate to high glycemic index (GI) provide a readily available source of carbohydrate for glycogen synthesis, and should be the major fuel choices in recovery meals.</div>
<div style="text-align: justify;">
<br />
<b>Fat</b></div>
<div style="text-align: justify;">
<br />
Fat is an important metabolic fuel in prolonged exercise, especially when the availability of carbohydrate is low. One of the primary adaptations to endurance training is an enhanced capacity to oxidize fat, thus sparing the body’s limited carbohydrate stores. Studies where subjects have trained on high-fat diets, however, have shown that a highcarbohydrate diet during a period of training brings about greater improvements in performance. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Even Table Suggested carbohydrate intakes for athletes in training Immediate postexercise recovery (0–4 h): 1 g per kg body mass per h, consisting of several small snacks Daily recovery (moderate duration/low intensity training): 5–7 g kg-1 day-1 Daily recovery (moderate–heavy endurance training): 7–12 g kg-1 day-1 Daily recovery (extreme training: 4–6 h or more per day): 10–12 g kg-1 day-1 when a high-carbohydrate diet is fed for a few days to allow normalization of the muscle glycogen stores before exercise performance is measured, the exercise capacity remains less after training on a high fat diet. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
It must be recognized, though, that these shortterm training studies usually involve relatively untrained individuals and may not reflect the situation of the highly trained elite endurance athlete where the capacity of the muscle for oxidation of fatty acids will be much higher. For the athlete with very high levels of energy expenditure in training, the exercise intensity will inevitably be reduced to a level where fatty acid oxidation will make a significant contribution to energy supply and fat will provide an important energy source in the diet. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Once the requirements for protein and carbohydrate are met, the balance of energy intake can be in the form<br />
of fat. Fat also serves other important functions in the diet. As well as providing essential fatty acids, it acts as a vehicle for the transport of fat-soluble nutrients. Some athletes try to minimize their fat intake, but this is not wise.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/03/sport-nutrition-of-macronutrient.html"><b>Sport Nutrition of Macronutrient Demads</b></a></div>
<div style="text-align: justify;">
Source: Nutritional Supplement</div>
<div style="text-align: justify;">
Image:Studentrecentre.wvu.edu</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com2tag:blogger.com,1999:blog-7113702905971561223.post-78206699060153065952012-03-23T20:26:00.000+07:002012-03-23T20:27:10.105+07:00Nutrition For Training<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg_BWbzouGSwjeSmDfPbr3Kf2HqVx7MRrS_0bKKQPhqVavrk0irWUHvoCpBYb6e3tPIeYepPtK_cPYr2mUtOeEOuXrcCD17DXjINKPyPO0VSf-sVjwZAfE6LmYZCtMjrnyJSWacLdlrBeg/s1600/Training.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="207" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg_BWbzouGSwjeSmDfPbr3Kf2HqVx7MRrS_0bKKQPhqVavrk0irWUHvoCpBYb6e3tPIeYepPtK_cPYr2mUtOeEOuXrcCD17DXjINKPyPO0VSf-sVjwZAfE6LmYZCtMjrnyJSWacLdlrBeg/s320/Training.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/03/nutrition-for-training.html">The training</a> </b>load of athletes varies greatly between individuals, depending on the nature of the sport and the level of competition, and it also varies over time in relation to the competitive season. Training may consist of high-intensity resistance training, brief but intense sprints, prolonged moderate intensity efforts, or technical work. Each places different demands on the muscles, cardiovascular system, and other tissues, and each has different energy requirements. The aim of training is to induce changes in body tissues and organs that will improve exercise performance, but different adaptations are required in different sports. Increasing muscle mass, strength, and power is a key objective in many sports, but in other sports, these changes would hinder, rather than help, performance. The training stimulus, therefore, must be specific to the objectives of the event. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Within limits, the greater the training stimulus – consisting of the intensity, duration and frequency of individual training sessions – the greater the adaptation that takes place. As mentioned above, nutrition is important in promoting recovery between training sessions to allow an increase in the training load that can be sustained without succumbing to illness and injury, and also in allowing more effective adaptations to each bout of training. This may be important in complex sports such as soccer, where different training objectives must be achieved and where the training must also accommodate practice of a variety of skills.</div>
<div style="text-align: justify;">
<br />
Influence of Exercise Training on Energy Balance Energy must be supplied by the diet to meet immediate energy needs (body functions, energy for activity, and growth) and for the maintenance of body energy stores. Energy stores, consisting primarily of fat, but including the key carbohydrate stores in liver and muscle, play a number of important roles related to exercise performance, since they contribute to size and function (e.g., muscle mass) as well as providing fuel for exercise. Athletes try to manipulate these factors towards the characteristics that offer advantages to their sport: this may mean a change in body mass, a change (usually a reduction) in body fat, a change (usually an increase) in muscle mass, and optimization of muscle and liver carbohydrate stores.</div>
<div style="text-align: justify;">
<br />
Not all athletes are able to correctly identify goals that are suitable for their sport and for their individual make-up. This can lead to various problems, including excessive restriction of energy intake in an attempt to achieve an unrealistically low body mass. If energy intake is too low, and especially if carbohydrate intake is inadequate, it may not be possible to sustain the training load without the risk of chronic fatigue, injury and illness. If an energy deficit is incurred, it may lead to changes in metabolic and hormonal function, which affect performance, growth and health. One outcome of low energy availability in female athletes is a disturbance of reproductive function and menstrual regularity. Other problems are likely to occur in male athletes. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
There is a real danger that the focus on achieving a specific body mass and body composition, may become more important than achieving success in competition. Monitoring of body mass can provide a useful index of energy balance in some situations, but other biomarkers are generally better. Measurement of body fat stores, usually by measurement of skinfold thickness, can be helpful in setting targets and in monitoring progress. Other markers, such as measurement of urinary ketone levels, can identify athletes who are failing to achieve an adequate carbohydrate intake. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Problems are most likely to occur when the energy expenditure is either very high or very low. Athletes with very high energy demands are likely to be training at least twice per day, leaving limited opportunities for eating the large amounts of foods that are necessary. Athletes with low energy demands and who must restrict energy intake to achieve a low body mass have two main problems: they must cope with constant hunger and they must also be careful in their selection of foods to ensure that they achieve an adequate intake of essential nutrients. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
An athlete’s energy requirements are set primarily by the training load and by body mass, although there is also a large interindividual variability even when these factors are constant. Measurements of oxygen uptake, heart rate, and other variables made after exercise show that the metabolic rate may remain elevated for at least 12 h and possibly up to 24 h if the exercise is prolonged and close to the maximum intensity that can be sustained. After more moderate exercise, the metabolic rate quickly returns to baseline level. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Therefore, it seems likely that the athlete training at near to the maximum sustainable level and who already has a very high energy demand will find this increased further by the elevation of postexercise metabolic rate: this will increase the difficulties that many of these athletes have in meeting their energy demand. The recreational exerciser, for whom the primary stimulus to exercise is often to control body mass or reduce body fat content, will not exercise hard enough or long enough to experience substantial elevations of metabolic rate after exercise.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/nutrition-for-training.html"><b>Nutritional For Training </b></a></div>
<div style="text-align: left;">
Source: Nutritional Supplements</div>
<div style="text-align: left;">
Image: bodyhealthnfitness.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com1tag:blogger.com,1999:blog-7113702905971561223.post-15291871743210038602012-03-22T18:03:00.001+07:002012-04-01T13:20:40.365+07:00Role in Management of Hyperlipidemia<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjw8HvsdoyZica8WizMBvZxMugSG0uieirxyOISZ41bM_71IMEPrfhpqFetbR809Keb-I4N3_G1D9MlMrFBIL9Xd90KAHQCPHAn-i5u8JZXRCu4pMrb53lA96pSO30svez033f4kNHxF6A/s1600/Hyperlipidemia.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjw8HvsdoyZica8WizMBvZxMugSG0uieirxyOISZ41bM_71IMEPrfhpqFetbR809Keb-I4N3_G1D9MlMrFBIL9Xd90KAHQCPHAn-i5u8JZXRCu4pMrb53lA96pSO30svez033f4kNHxF6A/s320/Hyperlipidemia.jpg" width="237" /></a></div>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/03/role-in-management-of-hyperlipidemia.html">Role in Management of Hyperlipidemia</a>.</b> Some forms of <b>dietary fiber </b>lower blood lipids, notably total cholesterol and low-density lipoprotein (LDL) cholesterol. The earliest observations on fiber preparations and blood lipids date from the mid 1930s when there was a fairly extensive investigation of the effects of pectin (polygalacturonic acid). The next period of investigation dates from 1974 when extracted and purified dietary fiber preparations such as guar gum – a glucomannan – were tested in normal subjects, diabetics, and <b>hyperlipidemic</b> subjects and were found to lower blood cholesterol when given in sufficient quantities. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In very large doses these materials increase fecal excretion of fat and sterol compounds and would be expected to reduce the body bile salt pool. Subsequent work has shown that at lower doses preparations of soluble <a href="http://umaeenews.blogspot.com/2012/03/sources-and-types-of-dietary-fiber.html"><b>dietary fiber</b></a> have a mild cholestyramine-like effect: they bind bile salts rendering them unavailable for reabsorption in the terminal ileum, thus interfering with the normal entero-hepatic cycle of bile salts and depleting the bile salt pool. Total and LDL cholesterol fall as cholesterol is diverted for the resynthesis of lost bile salts. There have been few direct clinical applications of the early experimental work on pectin and guar gum. No pectin compounds have been developed commercially, but there are a few pharmaceutical preparations of guar gum presented primarily as adjuncts to dietary therapy in diabetes rather than for lipid lowering. Dietetic food products containing guar gum have been developed, again for use in controlling diabetes.</div>
<div style="text-align: justify;">
<br />
Preparations of soluble dietary fiber have been shown to lower blood cholesterol whereas most preparations of predominantly insoluble fiber, such as wheat bran, have little or no effect. The major food sources of soluble fiber are oats, beans, lentils, rye, and barley, and these foods have naturally become the subject of investigations. The addition of oats to the diet in normolipidemic and hyperlipidemic subjects following either their normal diets or where pretreated with low-fat diets has been the subject of extensive research. In sufficient quantity oats, oat products, and oat Beta-glucan (providing at least 3 g oat beta glucan per day) lower blood total cholesterol and LDL cholesterol (usually by 5–10%) while leaving triglycerides and HDL cholesterol largely unchanged. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
A sufficiently large number of good-quality studies have now been done on oats that the Food and Drug Administration (FDA) has allowed the first ever food-specific health claim: ‘‘Soluble fiber from oatmeal, as part of a low saturated fat, low cholesterol diet, may reduce the risk of heart disease.’’ Products that are labeled with this claim must provide at least 0.75 g of soluble fiber (as Beta-glucan) per serving. When considering the above claim the FDA reviewed 37 studies and found that a sufficient number provided convincing evidence of efficacy. An earlier metaanalysis of some of those trials had shown that the efficacy of oats and oat products was influenced by the initial values of blood cholesterol in the subjects: patients with high starting values (over 6.7 mmol per liter total cholesterol) showed the greatest reductions when treated with oats, while healthy young subjects with low–normal starting values showed little response. There was a dose effect: food products providing more than 3 g soluble fiber per day had a greater blood cholesterol lowering effect than diets that provided less than 3 g per day.</div>
<div style="text-align: justify;">
<br />
Other soluble fiber-containing products have been shown to lower blood cholesterol. Recent extensive studies on psyllium (Plantago ovata) presented both as a pharmaceutical preparation and as a food product (a ready to eat breakfast cereal) have shown blood cholesterol-lowering properties where the dose–effect relationship is such that a useful additional therapeutically meaningful lipid-lowering effect can be achieved by prescribing a daily portion of psyllium-fortified breakfast cereal. Products of this type are now marketed in the US and Australia, and the US FDA has now allowed a food specific health claim for psyllium.</div>
<div style="text-align: justify;">
<br />
There is also a small literature on the effects of beans on blood lipids and the findings of a blood cholesterol-lowering effect are as expected. Virtually all of the reports of the effects of soluble fiber products on blood lipids report lowering effects on total cholesterol and LDL cholesterol without any effect on HDL cholesterol or triglycerides – this contrasts with the effects of some drugs that may cause slight rises of triglycerides and falls of HDL cholesterol. The relationship between lowering of blood cholesterol and lowering of risk of heart disease is now generally accepted and a proven lipid-lowering effect is taken to mean a beneficial effect on risk of coronary heart disease. This means that in clinical practice it is perfectly reasonable to include advice on use of foods high in soluble dietary fiber in a lipid-lowering diet, and perfectly proper to emphasize the benefits of oats and oat products. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Generally, a high-soluble-fiber diet is more acceptable when the soluble fiber is drawn from smaller quantities of a larger range of foods; thus the diet includes beans, lentils, rye breads, and barley as well as generous use of oats. A range of foods containing mycoprotein and fungal mycelial cell walls (chitin) may also help to lower blood cholesterol. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/role-in-management-of-hyperlipidemia.html"><b>Role in Management of Hiperlipidemia </b></a></div>
<div style="text-align: left;">
Source: Nutritional Supplements</div>
<div style="text-align: left;">
Image: Shannonassosiate.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com1tag:blogger.com,1999:blog-7113702905971561223.post-59411414939016309242012-03-22T15:22:00.000+07:002012-04-01T13:20:19.189+07:00Role in Nutritional Management of Diabetes<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-SEtRgYnr8J2Fl3djoCRyPtkBXguRir28jU04QFdC864y-5zWQ9l18AnfP00kkmePAcbBvl-TJIfE-FdNrQDtKBc-FNrvl9AFZoXJ2C4hFAoUnsCjPoDbiA67sub1iPEdoNeN4DBkXqA/s1600/Diabetes.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="287" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-SEtRgYnr8J2Fl3djoCRyPtkBXguRir28jU04QFdC864y-5zWQ9l18AnfP00kkmePAcbBvl-TJIfE-FdNrQDtKBc-FNrvl9AFZoXJ2C4hFAoUnsCjPoDbiA67sub1iPEdoNeN4DBkXqA/s320/Diabetes.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/03/role-in-nutritional-management-of.html">Diabetes mellitus</a> </b>is characterized by either an absolute or relative lack of insulin, which has short-term and long-term consequences. <b>Diabetic</b> people may develop both microvascular complications (mainly affecting the eyes, kidneys, and nerves) and macrovascular complications (essentially accelerated development of atherosclerosis presenting mainly as heart attack and peripheral vascular disease). Medical management aims to replace the insulin, or modulate its production or efficacy using oral (hypoglycemic) drugs, in a metabolic environment enhanced by good control of diet and body composition. Medical management also aims to achieve early detection of complications and other risk factors for cardiovascular disease by regular testing of blood and urine biochemical variables and blood pressure and by regular physical examination of the eyes, neurological, and cardiovascular systems.</div>
<div style="text-align: justify;">
<br />
Control of dietary energy intake (in relation to the varying demands for growth, maintenance, physical activity, etc.) remains the key feature of dietary control affecting metabolic fluxes, blood glucose levels, and body weight. Views on the appropriate proportional sources of energy from fat, carbohydrate, and protein have changed enormously over the last century from seriously energy-restricted high-fat diets (with percentage energy from fat as high as 70% raising some doubts about the level of compliance) through to very high-carbohydrate diets (sometimes 60–65% energy from carbohydrate) used in specialist centers in the US. Today, for most diabetic patients in most countries the target is to achieve 50–55% energy from carbohydrate sources. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Prior to the 1970s, when the move towards high-carbohydrate diets began, the high fat content of the diet along with less tight blood glucose (and urine glucose) control than is customary today was partly responsible for the high relative mortality from cardiovascular disease seen among diabetic patients. At that time young male diabetics were up to nine times more likely to die from heart attack than matched nondiabetic individuals. Reduction of fat in the diet and achievement of an optimal distribution from saturated, monounsaturated, and polyunsaturated sources (<10%, 10–20%, and no more than 10%, respectively, for patients with diabetes in the UK) remain a major aspect of dietary management of diabetic people in order to reduce the risk of developing coronary heart disease.</div>
<div style="text-align: justify;">
<br />
Control of blood glucose is critical in order to achieve avoidance of prolonged periods of hyperglycemia, which is associated with glycation of proteins and the risk of development of microvascular complications, and avoidance of hypoglycemia with its attendant risks of coma. In day-to-day practice, the avoidance of hypoglycemia is very important to patients and any new method of achieving normalization of blood glucose profiles is an advance. Dietary fiber offered such an advance from the mid 1970s when some forms (notably isolated polysaccharides such as guar gum, a glucomannan, and pectin, polygalacturonic acid) were shown to reduce the area under the blood glucose and insulin curves after acute test meals. Subsequent long-term<br />
(6-week) clinical trials showed that diets high in foods containing soluble dietary fiber, such as beans, oats, and barley, were more effective in reducing the area under the 24-h blood glucose profiles than diets containing more <a href="http://umaeenews.blogspot.com/2012/03/sources-and-types-of-dietary-fiber.html">high-fiber foods</a> based on wheat products.</div>
<div style="text-align: justify;">
<br />
Research in this area led David Jenkins to describe (in 1981) the concept of the ‘glycemic index’ (GI) which is a numerical expression of the ability of a food to raise blood glucose levels. In practice it is measured by comparing the blood glucose response to a 50-g carbohydrate portion of food with the response to 50 g glucose (in some papers the comparison is with a 50-g carbohydrate portion of bread). The dietary fiber (especially soluble fiber) content of a food slows down the rate of digestion and absorption of starch in foods giving flatter blood glucose responses and a lower GI; however, the structure of the starch (whether amylose or amylopectin) influences its rate of degradation and the extent to which the starch granules are hydrated by processing (including cooking) is also important.</div>
<div style="text-align: justify;">
The physical structure of the food (particularly the extent to which plant cells are intact), the presence of fat, which may slow gastric emptying, and the presence of some ‘antinutrient’ substances may all influence the GI. Low-GI diets have been shown in many clinical trials to improve important variables that are secondary indicators of blood glucose control, and to reduce blood lipids. Low-GI diets may be particularly helpful to patients who are frequently troubled by episodes of hypoglycemia though adequate proof of this is still awaited. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Low-GI diets are not just relevant to treatment of <b>diabetes </b>but have been shown in two large-scale epidemiological surveys published in 1997 to result in a significant reduction in the risk of development of maturity onset (type 2) diabetes in middle-aged American men and women. Thus, there is good reason to believe that there should be greater emphasis on the GI of diabetic diets and the fiber content, as well as emphasis on GI for those at risk of developing diabetes, especially the older obese person. Expert committees in many developed countries of the world have set target values for dietary fiber intake for diabetic patients (e.., the American Diabetes Association (ADA) recommends 20–35 g day-1 total dietary fiber by the AOAC method) and many, especially the Australian Diabetes Association and with the notable exception of the ADA, have recommended an increase in low-GI foods.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
In 2003 even <a href="http://umaeenews.blogspot.com/2012/03/diabetic-ketoacidosis-and-hyperosmolar.html"><b>Diabetes</b></a> UK (the UK Diabetes Association) noted that there might be merit in taking account of GI in dietary management for those with diabetes. Some physicians believe that the GI of foods is too complex an issue for patients to grasp, but in essence simply requires a partial substitution of bread and potatoes with pasta products, an increased use of high-fiber breakfast cereals including oats, increased use of beans and lentils, and emphasis on the use of temperate fruits (e.g., apples and pears).</div>
<div style="text-align: justify;">
Obesity (body mass index (weight in kilograms divided by height in meters squared) in excess of 30 kgm-2) is becoming more prevalent in developing countries and attracts an increased risk of the development of diabetes mellitus; a high proportion of established type 2 diabetics are obese and overweight. In the popular diet book ‘The F-Plan Diet,’ published in 1982, Audrey Eyton claimed that dietary fiber would help people lose weight by a number of mechanisms including reducing the efficiency of dietary energy absorption and by making people feel full for longer after meals thus having an overall effect on reducing food intake. At the time of publication these ideas were hypothetical - subsequent investigation has shown that increasing fiber intake two- or threefold by a variety of dietary changes can increase fecal energy losses by 75–100 kcal day-1. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Studies on the effects of dietary fiber on postprandial satiety where experimental meals are carefully designed to differ little except for fiber content have given variable results. However, there is a clear effect of fiber on chewing (the number of chews necessary to eat the same energy equivalent of food) where high- and low-fiber types of commonly consumed foods are eaten and this may have an important satiating effect. Clinical trials of highfiber weight loss regimens have given variable results. Double-blind placebo-controlled trials using pressed barley fiber and pectin tablets compared to a starch control have been undertaken in Scandinavia and have demonstrated statistically significantly greater weight losses in the fiber-treated groups up to 26 weeks of treatment. It seems reasonable to conclude that under some conditions the right kind of high-fiber diet can facilitate weight loss, but may not always do so.</div>
<div style="text-align: justify;">
<br />
<b>Diabetic</b> people are more likely to have dyslipidemia than nondiabetic people. When control of <b>diabetes</b> is lost, patients may demonstrate gross hypertriglyceridemia due to increased production of very-low-density lipoprotein (VLDL) particles in the liver as a consequence of the increased flux of free fatty acids from the peripheral tissues. At the same time total and LDL cholesterol may be raised. Improvement in diabetic control often achieves normalization of blood lipids, but where hyperlipidemia persists there may be a place for use of dietary fiber, especially soluble fiber, and especially oat Beta-glucan-containing foods as an adjunct to dietary and pharmacological therapy (see above).</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/role-in-nutritional-management-of.html"><b>Role in Nutritional Management of Diabetes </b></a></div>
<div style="text-align: left;">
Source: Nutritional Supplement</div>
<div style="text-align: left;">
Image: diabetes-ok.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com0tag:blogger.com,1999:blog-7113702905971561223.post-42305373752761494422012-03-22T01:43:00.002+07:002012-03-22T14:11:33.921+07:00Acute Pulmonary Edema<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiLxceVuCH_7DQRaTOuYS7H2qNVUWENhUIeSRwOCQP0f32mJMOqwLxf-5w-wzkvhP2kchjdwcR4CPMChAAyk0hmSJdrNxk4eUKBQ3lgPr52IWIGEuXZEFkyMyFNdKfTRtOlUep5-Ll5T4s/s1600/pulmonary.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="280" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiLxceVuCH_7DQRaTOuYS7H2qNVUWENhUIeSRwOCQP0f32mJMOqwLxf-5w-wzkvhP2kchjdwcR4CPMChAAyk0hmSJdrNxk4eUKBQ3lgPr52IWIGEuXZEFkyMyFNdKfTRtOlUep5-Ll5T4s/s320/pulmonary.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/03/acute-pulmonary-edema.html"><b>Acute Pulmonary Edema</b></a>.<b> </b>Life-threatening, acute development of alveolar lung edema often due to:<br />
• Elevation of hydrostatic pressure in the <b>pulmonary </b>capillaries (left heart failure, mitral stenosis)<br />
• Specific precipitants (Table), resulting in cardiogenic pulmonary edema in pts with previously compensated CHF or without previous cardiac history<br />
• Increased permeability of <b>pulmonary</b> alveolar-capillary membrane</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Physical Findings </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Patient appears severely ill, sitting bolt upright, tachypneic, dyspneic, with marked perspiration; cyanosis may be present. Bilateral <b>pulmonary </b>rales; third heart sound may be present. Frothy and blood-tinged sputum.</div>
<div style="text-align: justify;">
<b>Laboratory</b></div>
<div style="text-align: justify;">
Early ABGs show reductions of both PaO2; and PaCO2<br />
• Later, withprogressive respiratory failure, hypercapnia develops with progressive acidemia.<br />
• CXR shows pulmonary vascular redistribution, diffuse haziness in lung fields withperih ilar “butterfly” appearance. </div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1wj4Tur4ojrtUCqIu7qtLndbwc7rg3yGmPFcYUWnlfEiaOAICRK2DWJacnCikzzz-JAXM9lrhIe8oP5a0mCEm2OiaCvacx3sHIur0MknjlM3C2mtEwjVBnw4WNwLnxM6Vd7AxF6-FYlE/s1600/Pulmonary.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="156" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1wj4Tur4ojrtUCqIu7qtLndbwc7rg3yGmPFcYUWnlfEiaOAICRK2DWJacnCikzzz-JAXM9lrhIe8oP5a0mCEm2OiaCvacx3sHIur0MknjlM3C2mtEwjVBnw4WNwLnxM6Vd7AxF6-FYlE/s400/Pulmonary.jpg" width="400" /></a></div>
<br />
<br />
<div style="text-align: justify;">
<b>Treatment</b></div>
<div style="text-align: justify;">
<br />
Immediate, aggressive therapy is mandatory for survival. The following measures should be instituted nearly simultaneously:<br />
• Seat pt upright to reduce venous return.<br />
• Administer 100% O2 by mask to achieve PaO2 > 60 mmHg; in pts who 2 can tolerate it, continuous positive airway pressure (10 cmH2O pressure) by mask improves outcome. Assisted ventilation by mask or endotracheal tube is frequently necessary.<br />
• Intravenous loop diuretic (furosemide, 40–100 mg, or bumetanide, 1 mg); use lower dose if pt does not take diuretics chronically.<br />
• Morphine 2–4 mg IV (repetitively); assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects of morphine if necessary.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Additional therapy may be required if rapid improvement does not ensue:<br />
• The precipitating cause of pulmonary edema (Table 16-1) should be sought and treated, particularly acute arrhythmias or infection. </div>
<div style="text-align: justify;">
• Several noncardiogenic conditions may result in pulmonary edema in the absence of left heart dysfunction; therapy is directed toward the primary condition.<br />
• Inotropic agents, e.g., dobutamine, in cardiogenic pulmonary edema withsh ock.<br />
• Reduce intravascular volume by phlebotomy (removal of ~250 mL through antecubital vein) if rapid diuresis does not follow diuretic administration.<br />
• Nitroglycerin (sublingual 0.4 mg x 3 q5min) followed by 5 to 10 mug/min IV. Alternatively, nesiritide [2-mug/kg bolus IV followed by 0.01 (mug/kg)/min] may be used.<br />
• For refractory pulmonary edema associated withpersistent cardiac ischemia, early coronary revascularization may be life-saving.</div>
<br />
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/acute-pulmonary-edema.html"><b>Acute Pulmonary Edema</b></a></div>
<div style="text-align: left;">
source: Manual of Medicine</div>
<div style="text-align: left;">
Image: eccpn.aibarra.org</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com1tag:blogger.com,1999:blog-7113702905971561223.post-35890091472690168792012-03-21T13:55:00.003+07:002012-03-22T14:08:52.635+07:00Diabetic Ketoacidosis and Hyperosmolar Coma<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQKmEO_3Np2WV_LHfHwACNwg4numupCLFBxtmnF9NcdrL3fD4a8S0nxfdZugeLu6MZmcOddK1C6d-0-p3qyUWtTLTUZlD67F8N_rOqrO69nz22qgZo3rb4bgkkTg3tWdy5BnwgeDATWpA/s1600/diabetic.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="212" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQKmEO_3Np2WV_LHfHwACNwg4numupCLFBxtmnF9NcdrL3fD4a8S0nxfdZugeLu6MZmcOddK1C6d-0-p3qyUWtTLTUZlD67F8N_rOqrO69nz22qgZo3rb4bgkkTg3tWdy5BnwgeDATWpA/s320/diabetic.jpg" width="320" /></a></div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/03/diabetic-ketoacidosis-and-hyperosmolar.html"><b>Diabetic ketoacidosis </b></a>(DKA) and <b>hyperglycemic hyperosmolar</b> state (HHS) are acute complications of diabetes mellitus (DM). DKA is seen primarily in individuals withtype 1 DM and HHS in individuals withtype 2 DM. Both disorders are associated withabsolute or relative insulin deficiency, volume depletion, and altered mental status. The metabolic similarities and differences in DKA and HHS are summarized in Table 24-1.</div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEipXqF-yMlcqUomPdj-uxCSdFk6t34TunrqL5v-IEvkSV4ztO2cBvSIrmFsry_V2Jt1ZdR2kflP95QUWC5_FpTMtkxl4qhrKfmh3KvUCNEccd_yLENE0gatMjq38uVULc-8B0vZXftzW0g/s1600/Diabetic.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="352" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEipXqF-yMlcqUomPdj-uxCSdFk6t34TunrqL5v-IEvkSV4ztO2cBvSIrmFsry_V2Jt1ZdR2kflP95QUWC5_FpTMtkxl4qhrKfmh3KvUCNEccd_yLENE0gatMjq38uVULc-8B0vZXftzW0g/s400/Diabetic.jpg" width="400" /></a></div>
<br />
<br />
<br />
<div style="text-align: justify;">
<b>Diabetic Ketoacidosis</b></div>
<div style="text-align: justify;">
<br />
<i>Etiology DKA</i> results from insulin deficiency witha relative or absolute increase in glucagon and may be caused by inadequate insulin administration, infection (pneumonia, UTI, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), surgery, drugs (cocaine), or pregnancy.</div>
<div style="text-align: justify;">
<br />
<i>Clinical Features</i> The initial symptoms of DKA include anorexia, nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function, or frank coma may ensue. Classic signs of DKA include Kussmaul respirations and an acetone odor on the pt’s breath. Volume depletion can lead to dry mucous membranes, tachycardia, and hypotension. Fever and abdominal tenderness may also be present. Laboratory evaluation reveals hyperglycemia, ketosis (Beta-hydroxybutyrate > acetoacetate), and metabolic acidosis (arterial pH 6.8–7.3) withan increased anion gap (Table 24-1). The fluid deficit is often 3–5 L.</div>
<div style="text-align: justify;">
<br />
Despite a total-body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are common. Hyperamylasemia is usually of salivary origin but may suggest a diagnosis of pancreatitis. The measured serum sodium is reduced as a consequence of hyperglycemia (1.6-meq reduction for each100-mg/dL rise in the serum glucose).</div>
<div style="text-align: justify;">
<br />
<b>Treatment </b><br />
The management of DKA is outlined in Table 24-2.</div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1oE1jAMfn_6IcD9_d5jZsZ3g2mdtGNepAlYzPUJQlu2FGkgbZTFE-4Dpzulr-4dx87UKKB2PYKanyapTqU2LFYWbpj-j4IY9GODV2afmd-C_3O6xoNbsQnbI3VpY8zmA-STe-IwNpK0E/s1600/Diabetic1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1oE1jAMfn_6IcD9_d5jZsZ3g2mdtGNepAlYzPUJQlu2FGkgbZTFE-4Dpzulr-4dx87UKKB2PYKanyapTqU2LFYWbpj-j4IY9GODV2afmd-C_3O6xoNbsQnbI3VpY8zmA-STe-IwNpK0E/s640/Diabetic1.jpg" width="498" /></a></div>
<br />
<br />
<b>Hyperglicemic Hyperosmolar State </b><br />
<br />
<div style="text-align: justify;">
<i>Etiology</i> Relative insulin deficiency and inadequate fluid intake are the underlying causes of HHS. Hyperglycemia induces an osmotic diuresis that leads to profound intravascular volume depletion. HHS is often precipitated by a serious, concurrent illness suchas myocardial infarction or sepsis and compounded by conditions that impede access to water.</div>
<div style="text-align: justify;">
<br />
<i>Clinical Features</i> Presenting symptoms include polyuria, thirst, and altered mental state, ranging from lethargy to coma. Notably absent are symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA. The prototypical pt is an elderly individual with a several week history of polyuria, weight loss, and diminished oral intake. The laboratory features are summarized in Table 24-1. In contrast to DKA, acidosis and ketonemia are usually not found; however, a small anion gap may be due to lactic acidosis, and moderate ketonuria may occur from starvation. Though the measured serum sodium may be normal or slightly low, the corrected serum sodium is usually increased (add 1.6 meq to measured sodium for each100- mg/dL rise in the serum glucose).</div>
<div style="text-align: justify;">
<br />
<b>Treatment</b></div>
<div style="text-align: justify;">
<br />
The precipitating problem should be sought and treated. Sufficient IV fluids (1–3 L of 0.9% normal saline over the first 2–3 h) must be given to stabilize the hemodynamic status. The calculated free water deficit (usually 8–10 L) should be reversed over the next 1–2 days, using 0.45% saline initially then 5% dextrose in water. Potassium repletion is usually necessary. The plasma glucose may drop precipitously with hydration alone, though insulin therapy withan intravenous bolus of 5–10 units followed by a constant infusion rate (3–7 units/h) is usually required. Glucose should be added to intravenous fluid when the plasma glucose falls to 13.9 mmol/L (250 mg/dL). The insulin infusion should be continued until the patient has resumed eating and can be transitioned to a subcutaneous insulin regimen.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
by Umaee</div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/diabetic-ketoacidosis-and-hyperosmolar.html"><b></b></a><b><a href="http://www.blogger.com/blogger.g?blogID=7113702905971561223">Diabetic Ketoacidosis and Hyperosmolar Coma</a> </b></div>
<div style="text-align: left;">
Source: Medical of Medicine</div>
<div style="text-align: left;">
Image: ucdmc.edu</div>
<div style="text-align: right;">
<br /></div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com3tag:blogger.com,1999:blog-7113702905971561223.post-7198226602281989962012-03-21T13:12:00.000+07:002012-03-22T14:04:07.118+07:00Cardiovascular Collapse and Sudden Death<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi4OOeuzCThgmY0pQ0QcZeLtKp4OjctbfWiiFsTZRAZT4C1YweDcQywaX-tVv1S9mcabetBYy72tvY6FwnvO2s0w46NhHSrIyd5__yUkJhCVfwz1mSGRpP9fFwY6QEfEsIXQBddM2Z7w94/s1600/emerge.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi4OOeuzCThgmY0pQ0QcZeLtKp4OjctbfWiiFsTZRAZT4C1YweDcQywaX-tVv1S9mcabetBYy72tvY6FwnvO2s0w46NhHSrIyd5__yUkJhCVfwz1mSGRpP9fFwY6QEfEsIXQBddM2Z7w94/s320/emerge.jpg" width="256" /></a></div>
<div style="text-align: justify;">
Unexpected <a href="http://umaeenews.blogspot.com/2012/03/cardiovascular-collapse-and-sudden.html"><b>cardiovascular collapse</b></a> and death most often result from ventricular fibrillation in pts withunderlying coronary artery disease, with or without acute MI. Other common causes are listed in Table. The arrhythmic causes may be provoked by electrolyte disorders (primarily hypokalemia), hypoxemia, acidosis, or massive sympathetic discharge, as may occur in CNS injury. Immediate institution of cardiopulmonary resuscitation (CPR) followed by advanced life support measures (see below) are mandatory. Ventricular fibrillation, or asystole, without institution of CPR within 4–6 min usually causes death.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiQw5NvClTW-fl1JKdq1k2wbK3a3hKFwQwaCtyxEjIc43iHS-6oQ1jmacM0RKBbkL_By78rqxWS63F5kKadNYdBmaWis3rq-i6Y2_nHnaW8xjwIsWFgr71grkid3kBg4QtQRuEMnsueJE8/s1600/Cardiovascular.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="278" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiQw5NvClTW-fl1JKdq1k2wbK3a3hKFwQwaCtyxEjIc43iHS-6oQ1jmacM0RKBbkL_By78rqxWS63F5kKadNYdBmaWis3rq-i6Y2_nHnaW8xjwIsWFgr71grkid3kBg4QtQRuEMnsueJE8/s400/Cardiovascular.jpg" width="400" /></a></div>
<br />
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<b>Management of Cardiac Arrest </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Basic life support (BLS) must commence immediately (Fig. 13-1):<br />
• Open mouthof patient and remove visible debris or dentures. If there is respiratory stridor, consider aspiration of a foreign body and perform Heimlich maneuver.<br />
• Tilt head backward, lift chin, and begin mouth-to-mouth respiration if rescue equipment is not available (pocket mask is preferable to prevent transmission of infection). The lungs should be inflated twice in rapid succession for every 15 chest compressions.<br />
• If carotid pulse is absent, perform chest compressions (depressing sternum 3–5 cm) at rate of 80–100 per min. For one rescuer, 15 compressions are performed before returning to ventilating twice.<br />
• As soon as resuscitation equipment is available, begin advanced life support withcontinued chest compressions and ventilation.<br />
• Although performed as simultaneously as possible, defibrillation takes highest priority (Fig. 13-2A), followed by placement of intravenous access and in tubation. 100% O2 should be administered by endotracheal tube or, if rapid intubation cannot be accomplished, by bag-valve-mask device; respirations should not be interrupted for more than 30 s while attempting to intubate.<br />
• Initial intravenous access should be through the antecubital vein, but if drug administration is ineffective, a central line (internal jugular or subclavian) should be placed. Intravenous NaHCO3 should be administered only if there is persistent severe acidosis (pH < 7.15) despite adequate ventilation. Calcium is not routinely administered but should be given to pts with known hypocalcemia, those who have received toxic doses of calcium channel antagonists, or if acute hyperkalemia is thought to be the triggering event for resistant ventricular fibrillation.<br />
• The approach to cardiovascular collapse caused by bradyarrhythmias, asystole, or pulseless electrical activity is shown in Fig. 13-2B.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzPpKrtdvFEAy_hrP7XLCltlc-fQu0jvgA_rPxZ9dwylDhPLsDdA_Avz-llwFMhpTq0aXThCPMLKFZDDa71zDNVoBOuvOAC-OwNA-2x8VwDVo_iQR0yA67ak1sWYTFUNJsB8-9pemcqnc/s1600/Cardiovascular1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzPpKrtdvFEAy_hrP7XLCltlc-fQu0jvgA_rPxZ9dwylDhPLsDdA_Avz-llwFMhpTq0aXThCPMLKFZDDa71zDNVoBOuvOAC-OwNA-2x8VwDVo_iQR0yA67ak1sWYTFUNJsB8-9pemcqnc/s640/Cardiovascular1.jpg" width="426" /></a></div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh5UYNwK3lvfuPjqm9Rn4qGH7rFX6BEsmwzvEXwIHSyLB7ghwnKKvPHmEaj1yQjbZr1HuTkWwBt8ydunXek9_I51Flf7DEzEnYQ01FPqSwDXOYo95gPZpEARqvMhubVPW-sbulUqq8TCYk/s1600/Cardiovascular2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh5UYNwK3lvfuPjqm9Rn4qGH7rFX6BEsmwzvEXwIHSyLB7ghwnKKvPHmEaj1yQjbZr1HuTkWwBt8ydunXek9_I51Flf7DEzEnYQ01FPqSwDXOYo95gPZpEARqvMhubVPW-sbulUqq8TCYk/s640/Cardiovascular2.jpg" width="500" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhhR21Z2EvsLX_yfA2GO7vQQ-UxAsOyevlme2zTMW8uNwgGgtUFkZ4wj0xNrgEnpSS__W_T7vAvNX61_nfQyK3bpIxWvxks9xS2-4exEfX2Ae6KI3ILDZpHw8iKzCw1QBh1AFYZzPbuHAQ/s1600/Cardiovascular2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><br /></a></div>
<br />
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
</div>
<div style="text-align: justify;">
<b>Follow-up</b></div>
<div style="text-align: justify;">
<br />
If cardiac arrest was due to ventricular fibrillation in initial hours of an acute MI, follow-up is standard post-MI care. For other survivors of a ventricular fibrillation arrest, extensive assessment, including evaluation of coronary anatomy, left ventricular function, and invasive electrophysiologic testing, is often recommended. In absence of a transient or reversible cause, ICD placement usually indicated.</div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg2nTPfgj-ESbGhYZYFyhLycq5X_iV_pj-aXqWXXvxxirpzEDQbJS-RWATRvbGpizdX3d40dwwCCDuT-y9BYSnPBpzP2-34BsZMhlu0Nrxzk-iv6v1Ss_O-6LtAxdfzJBxmpy6Gg01RVE0/s1600/Cardiovascular3.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg2nTPfgj-ESbGhYZYFyhLycq5X_iV_pj-aXqWXXvxxirpzEDQbJS-RWATRvbGpizdX3d40dwwCCDuT-y9BYSnPBpzP2-34BsZMhlu0Nrxzk-iv6v1Ss_O-6LtAxdfzJBxmpy6Gg01RVE0/s400/Cardiovascular3.jpg" width="382" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
</div>
<br />
<br />
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/cardiovascular-collapse-and-sudden.html"><b>Cardiovascular Collapse and Sudden Death </b></a></div>
<div style="text-align: left;">
Source: Manual of Medicine</div>
<div style="text-align: left;">
Image: hana.com</div>
<br />
<br />Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com0tag:blogger.com,1999:blog-7113702905971561223.post-16789224408280422652012-03-21T12:03:00.000+07:002012-03-21T12:04:38.562+07:00Diagnostic Imaging in Internal Medicine<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhYCbqoP4fO0nHcz0Mh2VIsaqxn6UDKKrqju-fdcaUYB1KGoqXEx5k8x0502CXHyrL0I3fQWr7oycxssFHBliRsnLhEziDXJKVBj-rQ7cGu2iuyznVqiEn7AeoBlK1iitFRjixzulLP1t4/s1600/internal+medicine.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhYCbqoP4fO0nHcz0Mh2VIsaqxn6UDKKrqju-fdcaUYB1KGoqXEx5k8x0502CXHyrL0I3fQWr7oycxssFHBliRsnLhEziDXJKVBj-rQ7cGu2iuyznVqiEn7AeoBlK1iitFRjixzulLP1t4/s1600/internal+medicine.jpg" /></a></div>
<div style="text-align: justify;">
<b><a href="http://umaeenews.blogspot.com/2012/03/diagnostic-imaging-in-internal-medicine.html">Diagnostic Imaging in Internal Medicine</a>. </b>Clinicians have a wide array of radiologic modalities at their disposal to aid them in noninvasive diagnosis. Despite the introduction of highly specialized imaging modalities, radiologic tests such as chest radiographs and ultrasound continue to serve a vital role in the diagnostic approach to patient care. At most institutions, computed tomography (CT) is available on an emergent basis and is invaluable for initial evaluation of patients with trauma, stroke, suspected CNS hemorrhage, or ischemic stroke. Magnetic resonance imaging (MRI) and related techniques (MR angiography, functional MRI, MR spectroscopy) are providing remarkable resolution of many tissues including the brain, vascular system, joints, and most large organs.</div>
<div style="text-align: justify;">
<br />
This Article will review the indications and utility of the most commonly utilized radiologic studies used by internists.</div>
<div style="text-align: justify;">
<br />
<b>Chest Radiography</b></div>
<div style="text-align: justify;">
<br />
• Can be obtained quickly and should be part of the standard evaluation for patients with cardiopulmonary complaints.<br />
• Is able to identify life-threatening conditions such as pneumothorax, intraperitoneal air, pulmonary edema, and aortic dissection.</div>
<div style="text-align: justify;">
• Is most often normal in a patient with an acute pulmonary embolus.<br />
• Should be repeated in 4–6 weeks in a patient with an acute pneumonic process to document resolution of the radiographic infiltrate.<br />
• Is used in conjunction with the physical exam to support the diagnosis of congestive heart failure.Radiographic findings supporting the diagnosis of heart failure include cardiomegaly, cephalization, Kerley B lines, and pleural effusions.<br />
• Should be obtained daily in intubated patients to examine endotracheal tube position and the possibility of barotrauma.<br />
• Helps to identify alveolar or airspace disease.Radiographic features of such diseases include inhomogeneous, patchy opacities and air-bronchograms.<br />
• Helps to document the free-flowing nature of pleural effusions.Decubitus views should be obtained to exclude loculated pleural fluid prior to attempts to extract such fluid.</div>
<div style="text-align: justify;">
<br />
<b>Abdominal Radiography</b></div>
<div style="text-align: justify;">
<br />
• Should be the initial imaging modality in a patient with suspected bowel obstruction.Signs of small-bowel obstruction on plain radiographs include multiple air-fluid levels, absence of colonic distention, and a “stepladder” appearance of small-bowel loops.<br />
• Should not be performed with barium enhancement when perforated bowel, portal venous gas, or toxic megacolon is suspected.<br />
• Is used to evaluate the size of bowel:<br />
1.Normal small bowel is < 3 cm in diameter.<br />
2.Normal caliber of the cecum is up to 9 cm, with the rest of the large bowel up to 6 cm in diameter.</div>
<div style="text-align: justify;">
<b>Ultrasound</b></div>
<div style="text-align: justify;">
• Is more sensitive and specific than CT scanning in evaluating for the presence of gallstone disease.</div>
<div style="text-align: justify;">
• Can readily identify the size of the kidneys in a patient with renal insufficiency and can exclude the presence of hydronephrosis.<br />
• Can expeditiously evaluate for the presence of peritoneal fluid in a patient with blunt abdominal trauma.<br />
• Is used in conjunction with doppler studies to evaluate for the presence of arterial atherosclerotic disease.<br />
• Is used to evaluate cardiac valves and wall motion.<br />
• Should be used to localize loculated pleural and peritoneal fluid prior to draining such fluid.<br />
• Can determine the size of thyroid nodules and guide fine-needle aspiration biopsy.<br />
• Is the modality of choice for assessing known or suspected scrotal pathology.<br />
• Should be the first imaging modality utilized when evaluating the ovaries.</div>
<div style="text-align: justify;">
<br />
<b>Computed Tomography</b></div>
<div style="text-align: justify;">
<br />
• CT of the brain should be initial radiographic modality in evaluating a patient with a potential stroke.<br />
• Is highly sensitive for diagnosing an acute subarachnoid hemorrhage and in the acute setting is more sensitive than MRI.<br />
• CT of the brain is an essential test in evaluating a patient with mental status changes to exclude entities such as intracranial bleeding, mass effect, subdural or epidural hematomas, and hydrocephalus.<br />
• Is better than MRI for evaluating osseous lesions of the skull and spine.<br />
• CT of the chest should be considered in the evaluation of a patient with chest pain to rule out entities such as pulmonary embolus or aortic dissection.<br />
• CT of the chest is essential for evaluating lung nodules to assess for the presence of thoracic lymphadenopathy.<br />
• CT with high-resolution cuts through the lungs is the imaging modality of choice for evaluating the lung interstitium in a patient with interstitial lung disease.<br />
• Can be used to evaluate for presence of pleural and pericardial fluid and to localize loculated effusions.<br />
• Is an essential test in a patient with unexplained abdominal pain to evaluate for conditions such as appendicitis, mesenteric ischemia or infarction, diverticulitis, or pancreatitis.<br />
• CT of the abdomen is also the test of choice for evaluating for nephrolithiasis in a patient with renal colic.<br />
• Is the test of choice for evaluating for the presence of an abscess in the chest or abdomen.<br />
• In conjunction with abdominal radiography, CT is part of the evaluation of a patient with a bowel obstruction and can help identify the cause of such an obstruction.<br />
• Can identify abdominal conditions such as intussusception and volvulus in a patient with abdominal pain.<br />
• Is the imaging modality of choice for evaluating the retroperitoneum.<br />
• Should be obtained expeditiously in a patient with abdominal trauma to evaluate for the presence of intraabdominal hemorrhage and to assess injury to abdominal organs.</div>
<div style="text-align: justify;">
<br />
<b>Magnetic Resonance Imaging</b></div>
<div style="text-align: justify;">
<br />
• Is more useful than CT in the evaluation of ischemic infarction, dementia, mass lesions, demyelinating diseases, and most nonosseous spinal disorders.</div>
<div style="text-align: justify;">
• Provides excellent imaging of large joints including the knee, hip, and shoulder.<br />
• Can be used, often with CT or angiography, to assess possible dissecting</div>
<div style="text-align: justify;">
• Can be used, often with CT or angiography, to assess possible dissecting aortic aneurysms and congenital anomalies of the cardiovascular system.</div>
<div style="text-align: justify;">
• Cardiac MRI is proving useful to evaluate cardiac wall motion and for assessing cardiac muscle viability in ischemic heart disease.<br />
• Is preferable to CT for evaluating adrenal masses such as pheochromocytoma and for helping to distinguish benign and malignant adrenal masses.</div>
<br />
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/diagnostic-imaging-in-internal-medicine.html"><b>Diagnostic Imaging in Internal Medicine </b></a></div>
<div style="text-align: left;">
Source: Manual of Medicine</div>
<div style="text-align: left;">
Image:exammaster.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com2tag:blogger.com,1999:blog-7113702905971561223.post-44147137870423118122012-03-21T10:54:00.000+07:002012-04-17T12:48:59.500+07:00Pain and Its Management<div class="separator" style="clear: both; text-align: center;">
</div>
<div style="text-align: justify;">
<a href="http://umaeenews.blogspot.com/2012/03/pain-and-its-management.html"><b>Pain</b></a> is the most common symptom of disease.Management depends on determining its cause, alleviating triggering and potentiating factors, and providing rapid relief whenever possible.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Organization of </b><b>Pain Pathways </b></div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Pain-producing (nociceptive) sensory stimuli in skin and viscera activate peripheral nerve endings of primary afferent neurons, which synapse on secondorder neurons in cord or medulla.These second-order neurons form crossed ascending pathways that reach the thalamus and are projected to somatosensory cortex. Parallel ascending neurons connect with brainstem nuclei and ventrocaudal and medial thalamic nuclei.These parallel pathways project to the limbic system and underlie the emotional aspect of pain.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEio-ltPgWyudGsJiJ3qiRnn0xvz1FP2IS2tHb1Uq4tjVTBEOHGjrvTR9b5XCfJzRX110BXlkSuWCPTqIEWQFMZKAZoOaN6c16Qc7rQXJbYvgob0LxYT9ND626mFgKa_2Tzpu1wTw58xn54/s1600/Pain2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="235" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEio-ltPgWyudGsJiJ3qiRnn0xvz1FP2IS2tHb1Uq4tjVTBEOHGjrvTR9b5XCfJzRX110BXlkSuWCPTqIEWQFMZKAZoOaN6c16Qc7rQXJbYvgob0LxYT9ND626mFgKa_2Tzpu1wTw58xn54/s320/Pain2.jpg" width="320" /></a></div>
<br />
<br />
<b>Pain</b> transmission is regulated at the dorsal horn level by descending bulbospinal pathways that contain serotonin, norepinephrine, and several neuropeptides. Agents that modify pain perception may act to reduce tissue inflammation (NSAIDs, prostaglandin synthesis inhibitors), to interfere with pain transmission (narcotics), or to enhance descending modulation (narcotics and antidepressants). Anticonvulsants (gabapentin, carbamazepine) may be effective for aberrant pain sensations arising from peripheral nerve injury.</div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
<b>Evaluation</b></div>
<div style="text-align: justify;">
<br />
<b>Pain</b> may be of somatic (skin, joints, muscles), visceral, or neuropathic (injury to nerves, spinal cord pathways, or thalamus) origin. Characteristics of each are summarized in Table the following.</div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiKJAJw2BviLNCEJzUBlJufpqh7wwRC4RqV4OWiVNizYSG_0n67ezewmfeN79xH5TEk3YGrhJyV22_9T2iBuFkwkBt8IKQQCzAbipTINR09jCCPKA0CXLDLbx45k1nTw-bAmZv1lhlPsew/s1600/Pains.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="250" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiKJAJw2BviLNCEJzUBlJufpqh7wwRC4RqV4OWiVNizYSG_0n67ezewmfeN79xH5TEk3YGrhJyV22_9T2iBuFkwkBt8IKQQCzAbipTINR09jCCPKA0CXLDLbx45k1nTw-bAmZv1lhlPsew/s400/Pains.jpg" width="400" /></a></div>
<br />
<br />
<div style="text-align: justify;">
Neuropathic <b>pain</b> definitions: neuralgia: pain in the distribution of a single nerve, as in trigeminal neuralgia; dysesthesia: spontaneous, unpleasant, abnormal sensations; hyperalgesia and hyperesthesia: exaggerated responses to nociceptive or touch stimulus, respectively; allodynia: perception of light mechanical stimuli as painful, as when vibration evokes painful sensation.Reduced pain perception is called hypalgesia or, when absent, analgesia. Causalgia is continuous severe burning pain with indistinct boundaries and accompanying sympathetic nervous system dysfunction (sweating; vascular, skin, and hair changes—sympathetic dystrophy) that occurs after injury to a peripheral nerve. </div>
<div style="text-align: justify;">
<br /></div>
<div style="text-align: justify;">
Sensitization refers to a lowered threshold for activating primary nociceptors following repeated stimulation in damaged or inflamed tissues; inflammatory mediators play a role.Sensitization contributes to tenderness, soreness, and hyperalgesia (as in sunburn). Referred pain results from the convergence of sensory inputs from skin and viscera on single spinal neurons that transmit pain signals to the brain.Because of this convergence, input from deep structures is mislocalized to a region of skin innervated by the same spinal segment.</div>
<div style="text-align: justify;">
<i>Treatment</i></div>
<div style="text-align: justify;">
<br />
Acute Somatic Pain If moderate, it can usually be treated effectively with nonnarcotic analgesics, e.g., aspirin, acetaminophen, and NSAIDs (Table 8-2).All inhibit cyclooxygenase (COX) and, except for acetaminophen, all have anti-inflammatory actions, especially at high dosages.For subacute musculoskeletal pain and arthritis, selective COX-2 inhibitors such as celecoxib are useful, especially if the pt is at risk for upper gastrointestinal ulceration or bleeding.Narcotic analgesics are usually required for relief of severe pain; the dose should be titrated to produce effective analgesia.</div>
<div style="text-align: justify;">
<b><br />Chronic Pain</b></div>
<div style="text-align: justify;">
<br />
The problem is often difficult to diagnose, and pts may appear emotionally distraught.Psychological evaluation and behaviorally based treatment paradigms are frequently helpful, particularly in a multidisciplinary pain management center.<br />
Several factors can cause, perpetuate, or exacerbate chronic pain: (1) painful disease for which there is no cure (e.g., arthritis, cancer, migraine headaches, diabetic neuropathy); (2) neural factors initiated by a bodily disease that persist after the disease has resolved (e.g., damaged sensory or sympathetic nerves); (3) psychological conditions. Pay special attention to the medical history and to depression.Major depression is common, treatable, and potentially fatal (suicide).</div>
<div style="text-align: justify;">
<br />
<i>Treatment</i></div>
<div style="text-align: justify;">
<br />
After evaluation, an explicit treatment plan should be developed, including specific and realistic goals for therapy, e.g., getting a good night’s sleep, being able to go shopping, or returning to work.A multidisciplinary approach that utilizes medications, counseling, physical therapy, nerve blocks, and even surgery may be required to improve the pt’s quality of life.Some pts may require referral to a pain clinic; for others, pharmacologic management alone can provide significant help.The tricyclic antidepressants are useful in management of chronic pain from many causes, including headache, diabetic neuropathy, postherpetic neuralgia, atypical facial pain, chronic low back pain, and post-stroke pain.Anticonvulsants or antiarrhythmics benefit pts with neuropathic pain and little or no evidence of sympathetic dysfunction (e.g., diabetic neuropathy, trigeminal neuralgia).The combination of the anticonvulsant gabapentin and an antidepressant such as nortriptyline may be effective for chronic neuropathic pain.</div>
<div style="text-align: justify;">
<br />
The long-term use of opioids is accepted for pain due to malignant disease but is controversial for chronic pain of nonmalignant origin.When other approaches fail, long-acting opioid compounds such as levorphanol, methadone, sustained-release morphine, or transdermal fentanyl may be considered for these pts (Table 8-2).</div>
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgfQaF__DmlNFzPuvMqyhA3IoMeIpEL2YijDy1CIYSL295UC01rqzwE42WqJWBiEfSgFk40IQkHNKAr3MhuX8ZjUSTpDYhxxXKQygJOTa_7Ns2W4gnU03KfVARSlVpfS0iU_wzmVWSpYqU/s1600/Pain.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="180" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgfQaF__DmlNFzPuvMqyhA3IoMeIpEL2YijDy1CIYSL295UC01rqzwE42WqJWBiEfSgFk40IQkHNKAr3MhuX8ZjUSTpDYhxxXKQygJOTa_7Ns2W4gnU03KfVARSlVpfS0iU_wzmVWSpYqU/s400/Pain.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><br /></td></tr>
</tbody></table>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjxLRcBhQ0X9SRfTHDH1BEuHHnB8_yMAmpv4NItys2wA1ZAYNj3JM6WK59bcfnVY_5Co-YcKyDIaW0OHaNt-RGtDtbjLZkx0iE7vQ78L3n9lutgGurn6b_DwCzf4oQtOz3FnEhuCB_G54A/s1600/Pain1.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="180" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjxLRcBhQ0X9SRfTHDH1BEuHHnB8_yMAmpv4NItys2wA1ZAYNj3JM6WK59bcfnVY_5Co-YcKyDIaW0OHaNt-RGtDtbjLZkx0iE7vQ78L3n9lutgGurn6b_DwCzf4oQtOz3FnEhuCB_G54A/s400/Pain1.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><br /></td></tr>
</tbody></table>
<div style="text-align: right;">
</div>
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/pain-and-its-management.html"><b>Pain and Its Management </b></a></div>
<div style="text-align: left;">
Source: Manual of Medicine</div>
<div style="text-align: left;">
Image: dicakila.wp.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com3tag:blogger.com,1999:blog-7113702905971561223.post-16527183898008045702012-03-20T17:07:00.002+07:002012-03-20T17:08:56.784+07:00Respiratory Failure<div style="text-align: justify;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjVF9KA8gHCQ0LUt2c8wf0dEMD8ZkdBnFQ9Q9cl0B5_HzdDHygk_T-0yEzZoq9h3x0tyWh4a_SrQgu1ZUKQoXrY3BP1AGKGTDNoznFKo0Xx6BtYe0A-jAHmLrle3pPeMYbq4DgBYBytC_E/s1600/respiratory.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjVF9KA8gHCQ0LUt2c8wf0dEMD8ZkdBnFQ9Q9cl0B5_HzdDHygk_T-0yEzZoq9h3x0tyWh4a_SrQgu1ZUKQoXrY3BP1AGKGTDNoznFKo0Xx6BtYe0A-jAHmLrle3pPeMYbq4DgBYBytC_E/s320/respiratory.jpg" width="277" /></a></div>
<b>Definition and Classification <a href="http://umaeenews.blogspot.com/2012/03/respiratory-failure.html">Respiratory Failure</a></b></div>
<div style="text-align: justify;">
<br />
• Defined as failure of gas exchange due to inadequate function of one or more of the essential components of the respiratory system.<br />
• Classified as hypoxemic (PaO < 60 mmHg), hypercarbic (PaCO < 45 2 2 mmHg), or combined.<br />
• Also classified in terms of acuity—acute respiratory failure reflects a sudden catastrophic deterioration, chronic respiratory failure reflects long-standing respiratory insufficiency, and acute or chronic respiratory failure is an acute deterioration in a patient with chronic respiratory failure, usually due to chronic obstructive lung disease.</div>
<div style="text-align: justify;">
<br />
<b>Pathophysiology</b></div>
<div style="text-align: justify;">
<br />
<b>Respiratory failure</b> occurs when one or more components of the respiratory system fails.<br />
• Disorders due to failure of the central control system can be thought of as controller dysfunction, or central apnea.<br />
• Failure of the respiratory pump—the diaphragm and intercostal muscles that move the chest wall—is termed pump dysfunction.<br />
• Respiratory insufficiency attributable to narrowing, collapse, spasm, or plugging of the large or small airways can be termed airway system dysfunction.<br />
• Respiratory failure due to collapse or flooding of or injury to the alveolar network can be considered alveolar network dysfunction.<br />
• Disease resulting from obstruction, inflammation, or hypertrophy of the pulmonary capillary vessels can be termed pulmonary vascular dysfunction.<br />
Many processes will involve more than one of these components of the respiratory system, but assessment of each compartment can provide a basis for differential diagnosis.</div>
<div style="text-align: justify;">
<br />
<b>Clinical Evaluation</b></div>
<div style="text-align: justify;">
<br />
Initial inspection should assess upper airway patency and signs of distress such as nasal flaring, intercostal retractions, diaphoresis, level of consciousness.Use of sternocleidomastoid muscles and pulsus paradoxus in a patient who is wheezing suggest severe asthma.Asymmetric breath sounds may indicate pneumothorax, atelectasis, or pneumonia.Oximetry permits rapid assessment of oxy CO2 level and acid-base status.Because of the potential for rapid, possibly fatal, deterioration, therapy may need to be initiated without a definite diagnosis.<br />
• Controller dysfunction is suggested by medication history, the absence of tachypnea (respiratory rate < 12 breaths/min) in a patient with hypercarbia, altered level of consciousness.<br />
• Pump dysfunction is suggested by supine abdominal paradox (diaphragmatic paralysis), peripheral muscle weakness, reduced maximal inspiratory pressure generation.<br />
• Upper airway dysfunction is suggested by stridor, and lower airways dysfunction by wheezing.In ventilated patients obstruction can be deduced by inspection of the flow:time curve as displayed on most current ventilators. Auto PEEP (positive end-expiratory pressure), a sign of delayed emptying of the lungs in ventilated patients, is another sign of obstruction.<br />
• Alveolar compartment dysfunction is evident when there are signs of consolidation on auscultation, with tubular breath sounds and dullness.Since alveolar flooding effectively increases the stiffness of the lung, respiratory compliance, as measured on the ventilator [VT/(end-inspiratory plateau pressure - PEEP)], is reduced to < 30 mL/cmH2O.<br />
• Pulmonary vascular dysfunction is reflected indirectly by signs of right heart failure on exam (qP2,qJVP, right-sided heave). </div>
<div style="text-align: justify;">
<b><br /></b></div>
<div style="text-align: justify;">
<b>Treatment</b></div>
<div style="text-align: justify;">
• First priority is always to establish adequate oxygenation.If hypercarbia and acidosis coexist, mechanical ventilation should be strongly considered.<br />
• Attention must always be paid to establishing airway patency, even if another cause of respiratory failure is present.This may mean removal of a foreign body, suctioning, or simply a jaw lift.<br />
• With respiratory failure due to alveolar dysfunction, increasing end-expiratory lung volume with extrinsic PEEP may substantially improve arterial oxygenation.</div>
<br />
<div style="text-align: right;">
Salam</div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<a href="http://umaeenews.blogspot.com/">by Umaee</a></div>
<div style="text-align: left;">
<a href="http://umaeenews.blogspot.com/2012/03/respiratory-failure.html"><b>Respiratory Failure</b></a> <br />
Source: Manual of Medicine</div>
<div style="text-align: left;">
Image:sciencephoto.com</div>Anonymoushttp://www.blogger.com/profile/01782455722878344805noreply@blogger.com0