Clinical Presentation Epilepsy and Seizure

Clinical Presentation of Epilepsy and Seizure - 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.

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.

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.

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.

Clinical Presentation

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.

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.

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.

International Classification of Epileptic Seizures

I. Partial seizures (seizures begin locally)

     A. Simple (without impairment of consciousness)

          1. With motor symptoms

          2. With special sensory or somatosensory symptoms

          3. With psychic symptoms

     B. Complex (with impairment of consciousness)

         1. Simple partial onset followed by impairment of consciousness with or without automatisms

         2. Impaired consciousness at onset with or without automatisms

     C. Secondarily generalized (partial onset evolving to generalized tonic-clonic seizures)

II. Generalized seizures (bilaterally symmetrical and without local onset)

     A. Absence

     B. Myoclonic

     C. Clonic

     D. Tonic

     E. Tonic-clonic

     F. Atonic

     G. Infantile spasms

III. Unclassified seizures

IV. Status epilepticus

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.

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. 

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).

Clinical Presentation of Epilepsy

General

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. 

Symptoms

Symptoms of a specific seizure will depend on seizure type. Although seizures can vary between patients, they tend to be stereotyped within an individual.

• CP seizures can include somatosensory or focal motor features.
• CP seizures are associated with altered consciousness.
• Absence seizures can be almost nondetectable with only very brief (seconds) periods of altered consciousness.
• GTC seizures are major convulsive episodes and are always associated with a loss of consciousness.

Signs

Interictally (between seizure episodes), there are typically no objective or pathognomonic signs

Laboratory Tests

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.

Other Diagnostic Tests

• EEG is very useful in the diagnosis of various seizure disorders.
• An epileptiform EEG is found in only approximately 50% of the patients who have epilepsy.
• 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.
• 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.

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by Umaee

Clinical Presentation of Epilepsy and Seizure

Source: pharmacotherapy 7th

Treatment of Diabetes Mellitus

Treatment of Diabetes Mellitus - General Approach to Treatment ; 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 DM.

Glycemic Goal Setting and The Hemoglobin A1c

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.

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.

Glycemic Goals of Therapy

                 Biochemical Index                             ADA                       ACE and AACE
                 Hemoglobin A1c                               <7%a                            ≤6.5%
                 Preprandial plasma glucose               90–130 mg/dL            <110 mg/dL
                                                                        (5.0–7.2 mmol/L)
                 Postprandial plasma glucose              <180 mg/dLb             <140 mg/dL
                                                                        (<10 mmol/L)

 Monitoring Complications

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.

Self-Monitoring of Blood Glucose

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 insulin injections or pump therapy). The optimal frequency of SMBG for patients with type 2 DM is unresolved.

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.

Nonpharmacologic Therapy

Diet

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. 

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.

Clinical Controversy

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. 

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.

Activity

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.

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.

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by Umaee

Treatment of Diabetes Mellitus

Source: pharmacotherapy 7th

Insulin Algorithm for Type 2 Diabetes Mellitus

Insulin Algorithm for Type 2 Diabetes Mellitus - The primary goals of Diabetes Mellitus 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.

Insulin algorithm for type 2 diabetes mellitus (DM) in children and adults

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by Umaee

Insulin Algorithm for Type 2 Diabetes Mellitus

Source: pharmacotherapy 7th 

Algorithm Treatment of Constipation

Constipation

Algorithm Treatment of Constipation - The patient should be asked about the frequency of bowel movements and the chronicity of constipation. Constipation 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.

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.

Constipation Treatment Algorithm

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.

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.

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.

Nonpharmacologic Therapy

Dietary Modification and Bulk-Forming Agents

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.
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. 

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
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.

Dosage Recommendations for Laxatives and Cathartics

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.

Surgery
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.

Biofeedback
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.

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by Umaee

Algorithm Treatment of Constipation

Source: Pharmacotherapy 7th

Classification & Screening of Diabetes Mellitus

Diabetes Mellitus

Classification and Screening of Diabetes Mellitus - Classification of Diabetes

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).

Etiologic Classification of Diabetes Mellitus

Type 1 Diabetes

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 ketoacidosis, whereas adults often maintain sufficient insulin secretion to prevent ketoacidosis for many years, which is often referred to as LADA.

Type 2 Diabetes

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.

Gestational Diabetes Mellitus

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. 

Other Specific Types of Diabetes

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.

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.

Screening

Type 1 Diabetes Mellitus

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.

Type 2 Diabetes Mellitus

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.

Children and Adolescents

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.

Gestational Diabetes

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

Diagnosis of Gestational Diabetes Mellitus with a
100-g or 75-g Glucose Load

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by Umaee

Classification and Screening of Diabetes Mellitus

Source: Pharmacotherapy 7th

Causes, Signs, and Symptoms of Constipation

Causes, Signs, and Symptoms of Constipation - 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
the general public.

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.

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. 

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. 

Pathophysiology

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.

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.

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. 

An additional contributory mechanism may be an increase in electrolyte
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.

Possible Causes of Constipation

GI disorders 

     Irritable bowel syndrome
     Diverticulitis
     Upper GI tract diseases
     Anal and rectal diseases
     Hemorrhoids
     Anal fissures
     Ulcerative proctitis
     Tumors
     Hernia
     Volvulus of the bowel
     Syphilis
     Tuberculosis
     Helminthic infections
     Lymphogranuloma venereum
     Hirschsprung’s disease

Metabolic and endocrine disorders Diabetes mellitus with neuropathy

     Hypothyroidism
     Panhypopituitarism
     Pheochromocytoma
     Hypercalcemia
     Enteric glucagon excess

Pregnancy

     Depressed gut motility
     Increased fluid absorption from colon
     Decreased physical activity
     Dietary changes
     Inadequate fluid intake
     Low dietary fiber
     Use of iron salts

Neurogenic causes 

     CNS diseases
     Trauma to the brain (particularly the medulla)
     Spinal cord injury
     CNS tumors
     Cerebrovascular accidents
     Parkinson’s disease

Psychogenic causes 

     Ignoring or postponing urge to defecate
     Psychiatric diseases

Drugs Causing Constipation

     Analgesics
     Inhibitors of prostaglandin synthesis
     Opiates
     Anticholinergics
     Antihistamines
     AntiParkinsonian agents (e.g., benztropine or trihexyphenidyl)
     Phenothiazines
     Tricyclic antidepressants
     Antacids containing calcium carbonate or aluminum hydroxide
     Barium sulfate
     Calcium channel blockers
     Clonidine
     Diuretics (non–potassium-sparing)
     Ganglionic blockers
     Iron preparations
     Muscle blockers (D-tubocurarine, succinylcholine)
     Nonsteroidal antiinflammatory agents
     Polystyrene sodium sulfonate

Clinical Presentation of Constipation

Signs and symptoms
• 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. 

• 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.

Laboratory tests
• A series of examinations, including proctoscopy, sigmoidoscopy, colonoscopy, and barium enema, may be necessary to determine the presence of colorectal pathology.
• Thyroid function studies may be performed to determine the presence of metabolic and endocrine disorders

 Salam

by Umaee

Causes, Signs, and Symptoms of Constipation

Source: Pharmacotherapy 7th

Treatment of Diarrhea

Treatment of Diarrhea - To explain "i have diarrhea" you must know diarrhea overall. Prevention ; 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.

Desired Outcome

If prevention is unsuccessful and diarrhea 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.

 Nonpharmacologic Management

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. 

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.

Water and Electrolytes

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. 

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.

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. 

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.

Salam

by Umaee

Treatment of Diarrhea

Source: pharmacotherapy 7th 

Image: ayushveda.com

Signs and Symptoms of Diarrhea

Signs and Symptoms of Diarrhea - 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.

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. 

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.

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.

Physiology

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.

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. 

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.

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.

Clinical Presentation of Diarrhea

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.

General
• Usually, acute diarrheal episodes subside within 72 hours of onset, whereas chronic diarrhea involves frequent attacks over extended time periods.
Signs and symptoms
• Abrupt onset of nausea, vomiting, abdominal pain, headache, fever, chills, and malaise.
• Bowel movements are frequent and never bloody, and diarrhea lasts 12 to 60 hours.
• Intermittent periumbilical or lower right quadrant pain with cramps and audible bowel sounds is characteristic of small intestinal disease.
• 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.
• In chronic diarrhea, a history of previous bouts, weight loss, anorexia, and chronic weakness are important findings.
Physical examination
• Typically demonstrates hyperperistalsis with borborygmi and generalized or local tenderness.
Laboratory tests
• Stool analysis studies include examination for microorganisms, blood, mucus, fat, osmolality, pH, electrolyte and mineral concentration, and cultures.
• Stool test kits are useful for detecting gastrointestinal viruses, particularly rotavirus.
• Antibody serologic testing shows rising titers over a 3- to 6-day period, but this test is not practical and is nonspecific.
• Occasionally, total daily stool volume is also determined.
• Direct endoscopic visualization and biopsy of the colon may be undertaken to assess for the presence of conditions such as colitis or cancer.
• Radiographic studies are helpful in neoplastic and inflammatory conditions.

Drugs Causing Diarrhea

Laxatives
Antacids containing magnesium
Antineoplastics
Auranofin (gold salt)
Antibiotics
Clindamycin
Tetracyclines
Sulfonamides
Any broad-spectrum antibiotic
Antihypertensives
Reserpine
Guanethidine
Methyldopa
Guanabenz
Guanadrel
Angiotensin-converting enzyme inhibitors
Cholinergics
Bethanechol
Neostigmine
Cardiac agents
Quinidine
Digitalis
Digoxin
Nonsteroidal antiinflammatory drugs
Misoprostol
Colchicine
Proton pump inhibitors
H2-receptor blockers

Salam

by Umaee

Sign and Symptoms of Diarrhea

Source: Pharmacotherapy 7th

New Role For Public Health

New Role For Public Health - 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.

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.

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.

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.

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.

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. 

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.

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.

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.

Salam

by Umaee

New Role For Public Health

Source: public health & preventive medicine

Treatment Nausea and Vomiting

Treatment Nausea and Vomiting - Nausea and vomiting 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 pregnancy, or may follow operative procedures or administration of certain medications, such as those used in cancer chemotherapy.

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.

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.

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.

General Approach to Treatment

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. 

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.

Nonpharmacologic Management

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
changes produced by motion may benefit quickly by assuming a stable physical position.

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.

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.

Presentation of Nausea and Vomiting

General
Depending on severity of symptoms, patients may present in mild to severe distress

Symptoms
Simple: Self-limiting, resolves spontaneously and requires only symptomatic therapy
Complex: Not relieved after administration of antiemetics; progressive deterioration of patient secondary to fluid–electrolyte imbalances; usually associated with noxious agents or psychogenic events

Signs
Simple: Patient complaint of queasiness or discomfort 

Complex: Weight loss; fever; abdominal pain

Laboratory tests
Simple: None
Complex: Serum electrolyte concentrations; upper/lower GI evaluation

Other information
Fluid input and output
Medication history
Recent history of behavioral or visual changes, headache, pain, or stress
Family history positive for psychogenic vomiting

Pharmacologic therapy

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.

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.

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.

Salam

by Umaee

Treatment Nausea and Vomiting

Source: Pharmacotherapy 7th

Image:  wikinoticia.com

Algorithm For Treatment of Peptic Ulcer Disease

Algorithm For Treatment of Peptic Ulcer Disease - 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.

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. 

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.

Presentation of Peptic Ulcer Disease

General
• Mild epigastric pain or acute life-threatening upper gastrointestinal complications Symptoms
• Abdominal pain that is often epigastric and described as burning, but may present as vague discomfort, abdominal fullness, or cramping
• A typical nocturnal pain that awakens the patient from sleep (especially between 12 AM and 3 AM)
• 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
• Changes in the character of the pain may suggest the presence of complications
• Heartburn, belching, and bloating often accompany the pain
• 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

Signs
• Weight loss associated with nausea, vomiting, and anorexia
• Complications, including ulcer bleeding, perforation, penetration, or obstruction Laboratory tests
• Gastric acid secretory studies
• Fasting serum gastrin concentrations are only recommended for patients who are unresponsive to therapy, or for those in whom hypersecretory diseases are suspected
• The hematocrit and hemoglobin are low with bleeding, and stool hemoccult tests are positive
• Tests for Helicobacter pylori 

Other diagnostic tests
• 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
• Routine single-barium contrast techniques detect 30% of peptic ulcers; optimal double-contrast radiography detects 60% to 80% of ulcers

General Approach to Treatment

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. 

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.

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.

Nonpharmacologic Therapy

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.

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.

Salam

by Umaee

Algorithm For Treatment of Peptic Ulcer Disease

Source: Pharmacotherapy 7th