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 

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.

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by Umaee

Treatment of Diarrhea

Source: pharmacotherapy 7th 

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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.

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by Umaee

Algorithm For Treatment of Peptic Ulcer Disease

Source: Pharmacotherapy 7th

Algorithm for Treatment of Heart Failure

Algorithm for Treatment of Heart Failure - 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. 

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. 

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. 

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.

General Approach to Treatment

Treatment of Stage A Heart Failure

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. 

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
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.

Treatment of Stage B Heart Failure

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.

Treatment of Stage C Heart Failure

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.

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.

Treatment of Stage D Heart Failure

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. 

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by Umaee

Algorithm for Treatment of Heart Failure

Source: Pharmacotherapy 7th

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Algorithm for Treatment of Hypertension

Algorithm for Treatment of Hypertension - 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.

Essential Hypertension

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.

Secondary Hypertension

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.

Classification

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.
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.

Treatment

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.

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).

Nonpharmacologic Therapy

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.

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 :
1. Hypertension is two to three times more likely in overweight than in lean persons.
2. More than 60% of patients with hypertension are overweight.
3. As little as 10 pounds of weight loss can decrease BP significantly in overweight patients.
4. Abdominal obesity is associated with the metabolic syndrome, which is a precursor to diabetes, dyslipidemia, and, ultimately, CV disease.
5. Diets rich in fruits and vegetables and low in saturated fat lower BP in patients with hypertension.
6. Most people experience some degree of SBP reduction with sodium restriction.

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by Umaee

Algorithm for Treatment of Hypertension

Source: Pharmacotherapy 7th 

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Molecular Biological Basis of Personalized Medicine

Molecular Biological Basis of Personalized Medicine. Although several factors are involved in the development of personalized medicine, developments in molecular biology have played an important role. Some basic terms are defined briefly in this section. 

The Human Genome 

The total genetic material of an organism, that is, an organism’s complete DNA sequence is called a genome. The human genome is very complex and contains about 3-billion nucleotides. In 2001, the total number of genes in the human genome was estimated to be 25,000, which was much less than earlier larger estimates by the International Human Genome Sequencing Consortium in 2001.

By 2005, the three members of the International Nucleotide Sequence Database Collaboration (INSDC) − the European Molecular Biology Laboratory (EMBL) Bank, GenBank, and the DNA Data Bank of Japan (DDBJ) − reached a milestone as these databases for DNA and RNA sequences reached 100 gigabases of information. The 100,000,000,000 bases of genetic code, collected since 1982, comprise over 55 million sequence entries from more than 200,000 different organisms. This information was placed in the public domain where it has been freely accessible to the scientific community.

The nucleotide sequence data bases enable researchers to share completed genomes, the genetic makeup of entire ecosystems, and sequences associated with patents. Earlier manual data entry into the repository has been replaced by new automated technology, robotics, and bioinformatics. Combined with decreased cost, these have fostered faster data collection. The gene count of 25,000 came under scrutiny after the publication of the mouse genome in 2002 revealed that many human genes lacked mouse counterparts and vice versa. The possibility that some genes were misidentified was considered. To distinguish such misidentified genes from true ones, a research team at Broad Institute (Cambridge, MA) developed a method that takes advantage of another hallmark of protein-coding genes, i.e., conservation by evolution. 

The genes were considered to be valid if and only if similar sequences could be found in other mammals such as mouse and dog. Application of this technique invalidated a total of approximately 5,000 DNA sequences that had been incorrectly added to the lists of protein-coding genes, reducing the current gene estimate to approximately 20,500 (Clamp et al. 2007). This study suggests that nonconserved open reading frames should be added to the human gene catalog only if there is clear evidence of an encoded protein. It also provides a principled method for evaluating future proposed additions to the human gene catalog.

Chromosomes

Each human chromosome is a long linear double-stranded DNA molecule (except the mitochondrial chromosome) ranging in size from 50 to 250 million base pairs (bp). An average chromosome contains 2,000–5,000 genes within 130 million bp and is equal to about 130 cM of genetic material. A typical microband on a chromosome contains 3–5 million bp and 60–120 genes. There are approximately 400 million nucleotides in a human chromosome, but only about 10% of them actually code for genes; the rest may play different roles such as regulating gene expression.

The complex of DNA and proteins of a chromosome is called chromatin and consists of histones and non-histone proteins. The basic structural unit of chromatin is a nucleosome – a complex of DNA with a core of histones. The amount of DNA associated with each nucleosome is about 200 bp. Nucleosomes are further compacted to solenoids which are packed into loops and each of these contains about 100,000 bps of DNA. The loops are the fundamental units of DNA replication and/or gene transcription. 

A karyotype describes an individual’s chromosome constitution. Each of the 46 human chromosomes can now be counted and characterized by banding techniques. Chromosomes X and Y are the sex chromosomes. Each man carries an X chromosome and a Y chromosome. Every woman carries two X chromosomes. As there are actually few genes on the Y chromosome, men and women each have one active X chromosome that codes most of the information. 

Scientists have determined 99.3% of the euchromatic sequence of the X chromosome (Ross et al. 2005). They found 1,098 genes in the sequence, of which 99 encode proteins expressed in testis and in various tumor types. A disproportionately high number of Mendelian diseases are documented for the X chromosome. Of this number, 168 have been explained by mutations in 113 X-linked genes, which in many cases were characterized with the aid of the DNA sequence. Examples are defects in the gene responsible for Duchenne muscular dystrophy and fragile X mental retardation. As men have only one copy of the X chromosome, it is easier to find mutated genes on that one piece of DNA.

Genes

A gene is a sequence of chromosomal DNA that is required for the production of a functional product: a polypeptide or a functional RNA molecule. Genes range in size from small (1.5 kb for globin gene) to large (approximately 2,000 kb for Duchenne muscular dystrophy gene). A gene includes not only the actual coding sequences but also adjacent nucleotide sequences required for the proper expression of genes − that is, for the production of a normal mRNA molecule.

Mature mRNA is about onetenth the size of the gene from which it is transcribed. The same DNA strand of a gene is always translated into mRNA so that only one kind of mRNA is made for each gene. Transcription is gene in action. Genes are often described as blueprints of life ands transmit inherited traits from one generation to another.

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by Umaee

Source: Personalized medicine

Personalized Medicine

There is no officially recognized definition of personalized medicine. The term “personalized medicine” was used as the title of a monograph in 1998 (Jain 1998a) and started to appear in MEDLINE in 1999, but most of the literature relevant to personalized medicine is still indexed under pharmacogenomics and pharmacogenetics. Various terms that are used to describe the concept of personalized medicine are listed in followong image. Personalized medicine, also referred to as individualized therapy, simply means the prescription of specific treatments and therapeutics best suited for an individual taking into consideration both genetic and environmental factors that influence response to therapy. 

Customized drug therapy
Genomix medicine or genotype-based therapy
Individualized or individual-based therapy
Information-based medicine
Integrated healthcare
Omics-based medicine:pharmacogenomics/pharmacogenetics/pharmacoproteomics
Predictive medicine
Rational drug selection
Systems medicine
Tailored therapy
Translational medicine

The term “genomic medicine” implies that the sequencing of the human genome has enabled the practice of medicine to enter an era in which the individual patient’s genome will help determine the optimal approach to care, whether it is preventive, diagnostic, or therapeutic. Genomic medicine is not an adequate synonym for personalized medicine as other factors are also taken into consideration. Besides genomics, proteomic technologies have facilitated the development of personalized medicines and other technologies such as metabolomics are also contributing to this effort. Personalized medicine is the best way to integrate new biotechnologies into medicine for improving the understanding of pathomechanism of diseases and management of patients.

This process of personalization starts at the development stage of a medicine and is on the basis of pharmacogenomics and pharmacogenetics. The concept of personalized medicine will enable pharmaceutical companies to develop more effective medicines with fewer side effects. Physicians will have access to genetic profiles of their patients that will allow them to use existing medicines more effectively and safely, and individuals will be able to better manage their health on the basis of an understanding of their genetic profile.

In contrast to trial and error approach of some conventional therapies, personalized medicines aim to achieve a better match of drugs to patients so that the right treatments are given to the right patients at the right time. Personalized medicine has become a reality with the sequencing of the human genome, advances in medical genetics, and several technologies including medical diagnostics, single nucleotide polymorphism
(SNP) genotyping, and proteomics.

Some consider the word “personalized” to be somewhat indicative of exclusivity and prefer to use the term integrated healthcare to indicate the integration of diagnostics, screening, prevention, therapy, and treatment monitoring as the future trend in medicine. The problem with the term “integrated healthcare” is that it is already being used to indicate the integration of classical medicine with alternative medicine. Integration of diagnosis and treatment is implied in the development of personalized medicine and the author of this report prefers to use the term “personalized medicine” for the system and to refer to the individual drugs as personalized medicines.

Salam

by Umaee

Source: Personalized Medicine

Image : cisncancer.org

Food and Drug Administration Pregnancy Categories

Food and Drug Administration Pregnancy Categories

A. Controlled studies performed in pregnant women do not demonstrate a risk to the fetus during the first trimester of pregnancy with no evidence of risk in the second or third trimesters. The possibility of fetal harm appears highly unlikely.

B. Either studies in reproducing animals do not demonstrate a fetal risk but there are no controlled studies in pregnant women, or animal reproduction studies have shown adverse effects (other than a decrease in fertility) that were not confirmed in controlled studies in pregnant women in the first trimester and there is no evidence of a risk in later trimesters.

C. Either study in animals has demonstrated adverse effects on the fetus (teratogenic, embryocidal, or other effects) and there are no controlled studies in women, or studies in women and animals are not available. These drugs should be given only if the potential benefits of the drug justify the potential or unknown risk to the fetus.

D. There is positive evidence of human fetal risk, but the benefits from administration in pregnant women may be acceptable despite the risk. For example, if the drug is needed in a life-threatening situation or for a serious disease for which safer drugs cannot be used or are ineffective, administration may be indicated.

X. Animals or human studies have demonstrated fetal abnormalities or there is evidence of risk to the fetus based on human experience, or both. The risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is therefore contraindicated in women who are or may become pregnant.

Salam

by Umaee

source: clinical handbook's of prescriotion drugs (WZFWS95V82ZM)

image: pregnancyandbaby.com

How Drugs Work: Disease Prevention

The design and synthesis of new drugs today is greatly facilitated by scientists’ improved understanding as to how such compounds work in the body. Researchers have long known that most drugs that cure disease do so by killing the microorganisms that cause such diseases. They now have, in many cases, a very detailed and specifi c understanding as to how that process occurs. Research on HIV infection and AIDS (acquired immunodefi ciency syndrome) is a good example. In 1983, two researchers, Luc Montagnier in France and Robert Gallo in the United States, reported that AIDS is caused by a particular type of virus that was later given the name human immunodefi ciency virus (HIV). Over the next decade, teams of researchers in many countries discovered the mechanism by which HIV causes the symptoms of AIDS.

The fi rst step in that process occurs when a person is exposed to HIV (usually through sexual contact or transfer of blood from an infected to a healthy person). HIV travels through the bloodstream until it comes into contact with certain types of white blood cells that contain proteins known as CD4 (cluster designation 4) receptor sites on their surface. The virus then attaches itself to the CD4 receptor and injects a protein (called the p24 protein) into the host cell’s interior. The p24 protein carries the genetic information that
controls reproduction of HIV.

Once installed inside the host cell, the p24 protein attaches itself to and takes over control of the cell’s own DNA. The HIV genetic code begins to function within the host cell, ordering it to produce multiple copies of itself (the virus). The host cell then becomes fi lled with new copies of the HIV, bursts open, releases the viruses into the bloodstream, and dies. Each of the new viruses thus produced then fi nds another CD4 host cell, and the whole process of reproduction is repeated.

Before scientists understood this process, about the only way they had of treating the symptoms of AIDS was a trial-and-error search for chemicals that appeared to have success in curing or slowing down the disease. Once the mechanism of infection was understood, however, they had a more rational method of looking for drugs with which to treat the disease. Their challenge was to fi nd one or more chemicals that would interrupt the series of steps by which the virus operates (attaching itself to the surface of the cell, injecting its p24 protein into the cell, and initiating replication within the host cell).

In fact, various researchers looked for a variety of chemical compounds that acted at one or another of these stages of infection. The best solution that researchers have so far discovered involves the use of a type of drug known as an antiretroviral agent, that is, a chemical that interferes with the process by which the p24 protein takes over the host cell’s own system of replication and reproduction. Many people who are infected with HIV are now able to live reasonably normal lives because they have access to an “AIDS cocktail” that contains some combination of three such antiretroviral substances.

Another example of how drugs kill disease-causing microorganisms is the action of sulfa drugs on bacteria. Normally, a bacterium requires a compound known as para-aminobenzoic acid (PABA) in order to make a second compound, folic acid, as shown in the diagram below. Folic acid, in turn, is used to catalyze the production of nucleic acids that become part of a bacterium’s mechanism for manufacturing new proteins and reproducing its own DNA.

The structure of sulfa drug molecules, however, is very similar to that of the PABA molecule. Compare the structure of sulfanilamide, in part 2 of the diagram, with that of PABA. Notice how easily the sulfanilamide molecule can substitute for the PABA molecule in the synthesis of the bacterium’s folic acid. The problem for the bacterium, however, is that folic acid produced from a sulfa drug molecule is different from one produced from a PABA molecule. The difference is great enough that the altered form of folic acid is unable to catalyze the synthesis of DNA, and the bacterium’s metabolic process is disrupted.

Unable to grow and reproduce, members of the bacterial colony die and the infection that they cause is successfully treated. Understanding the mechanisms by which normal body functions occur, how disease develops, and how drugs fi ght disease is now fundamental to the development of new drugs. This understanding allows researchers to develop new chemical compounds that interfere with biochemical changes that result in disease and death.

Salam

by Umaee

source: chemistry of drug

image: departments.oxy.edu

Approach to the Patient with a Drug Hypersensitivity Reaction – Clinical Perspectives

Drug hypersensitivity reactions are a common clinical problem which may affect a considerable number of the treated patient population. Between 10 and 15% of patients may suffer from an unwanted drug reaction, 2–5% of these have to be hospitalized, and in 1–3% of hospitalized patients mortality may result [1] .

Drug hypersensitivity reactions are systemic reactions which often involve the skin. Cutaneous manifestations may be the only clinically relevant presentation of a drug hypersensitivity, but the skin can also act to herald for example a systemic hypersensitivity reaction such as anaphylaxis or the severe drug hypersensitivity syndrome (drug rash with eosinophilia and systemic symptoms (DHS/DRESS) [2] . 

Particularly the hypersensitivity reactions of type B (bizarre) present with symptoms and signs which are typically not related to pharmacologic doses and effects of the eliciting drugs. Therefore, drug hypersensitivity reactions present a complex challenge for treating physicians and the diagnosing allergologist. To arrive at a useful final diagnosis, a structured stepwise approach is required.

In principle, two steps can be differentiated:
(1) handling the acute drug hypersensitivity reaction: it comprises the classification as well as the definition of the severity of the reaction, its documentation, the choice of an alternative drug, and the symptomatic  treatment, and (2) identification of the eliciting drug(s).

Acute Phase

Drug hypersensitivity reactions can occur during all types of medical treatments, including biologicals [3] , their additives [4, 5] , phytotherapeutic remedies [6] or their adulterated contents [7, 8] . It is of utmost importance that the initial diagnosis is done carefully including some laboratory analysis, in particular an involvement of blood cells, and the affection of internal organs, such as liver and kidneys, should be excluded by appropriate blood tests (differential blood count, liver enzyme analysis, etc.). 

Actually, it is advisable to consult a dermatologist or alternatively to take a photograph of the exanthem and of the particular cutaneous efflorescences, and to note all drugs taken during the last 2 weeks and particularly all newly introduced drugs taken within the last 4 weeks. A skin biopsy for histological examination may be helpful to further differentiate the exanthem. This documentation should give a clue to the severity of the reaction [2] , which is decisive for prognosis, treatment and future pharmacotherapy The morphological differential diagnosis should exclude other causes, the most probably eliciting drugs should be immediately stopped and symptomatic treatment should be started if necessary, particularly when danger signs such as severe anaphylactic symptoms, facial edema with drug treatments causing DHS/DRESS or bullous manifestation, vasculitis or important mucosal signs are present [2] . 

After the complete clearing of the clinical manifestations and normalization of laboratory values, an allergologic investigation is recommended. This should be best done between 3 weeks to 6 months after the incident.

Etiology

The diagnosis of drug hypersensitivity aims, firstly, to define the disease as drug allergy, and, secondly, to identify the eliciting drug or drugs. History and experience (from various textbooks listing drugs and their side effects) are the most widely used and important pillars on which the identification of a potentially eliciting drug is based. Dose, the duration of treatment, the chronology of the appearance of symptoms, and the identification of cofactors such as underlying disorders, for example viral infections, hepatopathy or renal diseases help for the identification of the relevant drug.

The application of a standardized approach, for example with a drug questionnaire, is recommended [12] , in particular for persons less experienced in drug hypersensitivity.

Major Clinical Manifestations

The clinical characteristics of the more common and of some of the severe drug reactions are briefly presented. Some drug-induced syndromes have been proposed to differentiate them from other diseases.

Conclusions

Drugs and drug allergens may elicit a wide variety of clinical manifestations that are based on various pathogenetic mechanisms. However, there still remain many clinical reactions where the pathomechanism is not known and therefore, no validated diagnostic tools are available. The diagnosis of a drug hypersensitivity reaction is based on clinic, history and experience with the drug. In addition, skin [55] and in vitro tests are
available and some rules how to perform them have been published [21, 22, 56] . 

The preparation of drug allergens for skin tests, the performance of in vitro tests [57, 58] , correctly conducted provocation tests [23] and the required validation procedures are time-consuming and cost-intensive. Despite these limitations, an investigation into a drug hypersensitivity reaction is important and useful to prevent recurrences and it may help to select safe drug alternatives in future pharmacological therapies.

Salam

by Umaee

source: Drug Hypersensitivity

image: worldallergy

Examples of Food Synergy

Previews with had talked about principle Understanding Food and Food–Drug Synergy. Now we're talking some Examples of Food Synergy. While the mechanisms involved with each food synergy are not sometimes known, it is possible that foods or food componentsmay act by similar or complementary mechanisms. They may also haveopposing mechanisms, which may negate an undesirable effect of one ormore foods or food components.

Examples of food and/or food components working together to achieve an additive or synergistic effect include those in the:

DASH (Dietary Approaches to Stop Hypertension) diet, characterized by high intakes of fruits, vegetables, and low fat dairy products, in combination with a low sodium diet; results in significant lowering of blood pressure; 

Portfolio diet, containing plant sterols, viscous fibers, and soy protein; demonstrates reductions in serum low-density lipoprotein (LDL) cholesterol similar to traditional statin drugs; 

Mediterranean diet, consisting of a high intake of legumes, grains, fruit, and vegetables, moderate alcohol intake, low to moderate consumption of meats and dairy products, and the use of olive oil for salad dressings and cooking; has been linked to reduced risk of cardiovascular disease.

Other examples abound. The combination of garlic and fish oil has been shown to be beneficial at improving blood lipid profile to a greater extent than garlic or fish oil alone. Garlic attenuates the elevation of LDL cholesterol that occurs with fish oil intervention. With respect to weight loss, consumption of dairy products results in a greater weight reduction than taking calcium alone. This finding suggests that despite the positive effect of calcium on weight loss, additional components in dairy products act synergistically to induce weight loss. Food synergy has been demonstrated with respect to osteoporosis in an animal model. 

Calcium, in combination with soy isoflavones, preserves bone mineral density to a greater extent than either component alone in ovariectomized rodents. In a murine model of lupus, food restriction in combination with fish oil results in increased life span compared to food restriction or fish oil alone, and in another animal modelof inflammation, a diet low in arachidonic acid in combination with fish oil attenuates rheumatoid arthritis.

There are also examples of foods or food components interacting such that a negative effect of a food or food component is attenuated by providing multiple foods, as occurs in vivo . Using an athymic mouse model, flaxseed has been shown to attenuate the late-stage mammary tumor–promoting activity of soy. Similarly, lignans derived from flaxseed have been shown to attenuate the late-stage mammary tumor–promoting activity of genistein, which is abundant in soy.

Salam

by Umaee

source: Food-Drug Sinergy and Safety

image: cricket-crhonicles.blgospot.com

Principles of Family Medicine

Family medicine can be described as a body of knowledge about the problems encountered by family physicians. This is, of course, a tautology, but then so are the descriptions of all applied subjects. As in other practical disciplines, the body of knowledge encompassed by family medicine includes not only factual knowledge but also skills and techniques. Members of a clinical discipline are identifi - able not so much by what they know as by what they do. Surgeons, for example, are identifi able more by their skill in diagnosing and treating “surgical” diseases than by any particular knowledge of anatomy, pathology, or clinical medicine.
What they do is a matter of their mind set, their values and attitudes, and the principles that govern their actions. 

In describing family medicine, therefore, it is best to start with the principles that govern our actions. We will describe nine of them. None is unique to family medicine. Not all family physicians exemplify the whole nine. Nevertheless, when taken together, they do represent a distinctive worldview—a system of values and an approach to problems—that is identifi ably different from that of other disciplines.

1. Family physicians are committed to the person rather than to a particular body of knowledge, group of diseases, or special technique. The commitment is open-ended in two senses. First, it is not limited by the type of health problem. Family physicians are available for any health problem in a person of either sex and of any age. Their practice is not even limited to strictly defi ned health problems: the patient defi nes the problem. This means that a family physician can never say: “I am sorry, but your illness is not in my fi eld.” Any health problem in one of our patients is in our fi eld. We may have to refer the patient for specialized treatment, but we are still responsible for the initial assessment and for coordination and continuity of care. Second, the commitment has no defi ned end point. It is not terminated by cure of an illness, the end of a course of treatment, or the incurability of an illness. In many cases the commitment is made while the person is healthy, before any problem has developed. In other words, family medicine defi nes itself in terms of relationships, making it unique among major fi elds of clinical medicine. 

2. The family physician seeks to understand the context of the illness. “To understand a thing rightly, we need to see it both out of its environment and in it, and to have acquaintance with the whole range of its variations,” wrote the American philosopher William James (1958). Many illnesses cannot be fully understood unless they are seen in their personal, family, and social context. When a patient is admitted to the hospital, much of the context of the illness is removed or obscured. Attention seems to be focused on the
foreground rather than the background, often resulting in a limited picture of the illness.

3. The family physician sees every contact with his or her patients as an opportunity for prevention of disease or promotion of health. Because family physicians, on the average, see each of their patients about four times a year, this is a rich source of opportunities for practicing preventive medicine.

4. The family physician views his or her practice as a “population at risk.” Clinicians think normally in terms of single patients rather than population groups. Family physicians have to think in terms of both. This means that patients who have not attended for such procedures as immunization, papanicolaou smears, or blood pressure test are as much a concern as those who are attending regularly. Electronic records make it very easy to maintain upto- date attendance records of the whole practice population.

5. The family physician sees himself or herself as part of a communitywide network of supportive and health-care agencies. All communities have a network of social supports, offi cial and unoffi cial, formal and informal. The word network suggests a coordinated system. Up to recently this has often not been the case. Too often, family physicians, hospital doctors, medical offi cers of health, home care nurses, social workers, and others have worked in watertight compartments without a grasp of the system as a whole. At the time of writing, many jurisdictions are in the process of reforming general practice as a key link in the network, which will enable patients to benefi t from whichever provider they require.

6. Ideally, family physicians should share the same habitat as their patients. In recent years, this has become less common, except in rural areas. Even here, the commuting doctor has made an appearance. In some communities, notably the central areas of large cities, doctors have virtually disappeared. This has all been part of the recent trend toward the separation of life and work. To Wendell Berry (1978) this is the cause of many modern ills: “If we do not live where we work, and when we work,” he writes, “we are wasting our lives, and our work too.” The Love Canal disaster in Niagara Falls provides a vivid illustration of what can happen when physicians are remote from the environment of their patients. This abandoned canal had been used by a local industry for the disposal of toxic waste products. The canal was then covered over and, some years later, houses were built on the site. During the 1960s, householders began to notice that chemical sludge was seeping into their basements and gardens.

Trees and shrubs died, and the atmosphere became polluted by malodorous fumes. About the same time, residents in the neighborhood began to suffer from illnesses caused by the toxic chemicals. It was not, however, until a local journalist did a health survey in the area that an offi cial health study was done.
This showed rates of illness, miscarriage, and birth defects far in excess of the norm (Brown, 1979). How did the cluster of illnesses in an obviously polluted environment escape the notice of local physicians? One can only assume that they treated patients without seeing them in their home environment. It is difficult to believe that a neighborhood family physician, visiting patients in their homes and interested in their environment, would have remained unaware of the problem for so long. To be fully effective, a family physician still needs to be a visible presence in the neighborhood.

7. The family physician sees patients in their homes. Until modern times, attending physicians in their homes was one of the deepest experiences of family practice. It was in the home that many of the great events of life took place: being born, dying, enduring or recovering from serious illness. Being present with the family at these events gave family doctors much of their knowledge of patients and their families. Knowing the home gave us a tacit understanding of the context or ecology of illness. Ecology, derived from two Greek words, oikos (home) and logos, means literally “study of the home.” The rise of the modern hospital removed much of this experience from the home. There were technical advantages and gains in effi ciency, but the price was some impoverishment of the experience of family practice. The current redefi nition of the hospital’s role is now changing the balance again and we have the opportunity to restore home care as one of the defi ning experiences and essential skills of family medicine. The family physician should be a natural ecologist . At the time of writing, a shortage of general practitioners (GPs) has made it diffi cult for practices to visit their patients in their need. At the same time, there are new reasons for attending housebound patients. Hospitals are dangerous for the elderly, from hospital infections and rapid deterioration from the change of environment. Attending patients with short-term illnesses prevents patients spreading or acquiring diseases in emergency rooms, and doctors’ offi ces. Advances in technology have made diagnosis and therapy much  easier than before.

8. The family physician attaches importance to the subjective aspects of medicine. For many years, medicine has been dominated by a strictly objective and positivistic approach to health problems. For family physicians, this has always had to be reconciled with a sensitivity to feelings and an insight into relationships.
Insight into relationships requires knowledge of emotions, including our own emotions. Hence, family medicine should be a self-refl ective practice 

9. The family physician is a manager of resources. As generalists and fi rst- contact physicians, they have control of large resources and are able, within certain limits, to control admission to hospital, use of investigations, prescription of treatment, and referral to specialists. In all parts of the world, resources are limited, sometimes severely limited. It is, therefore, the responsibility of family physicians to manage these resources for the benefi t of their patients and for the community as a whole. In certain cases, the interests of an individual patient may conflict with those of the community as a whole, and this can raise ethical issues.

Salam

by Umaee

Source: Family Medicine
Image: georgianlondon.com