RANDOM/PROBABILITY SAMPLING DESIGNS

OBJECTIVES OF THE DISCUSSION

By the end of this discussion, the reader/medical student will be able to;

1.  Differentiate between probability and non-probability sampling designs.

2.  Describe the different random/probability sampling designs

3.  Outline common applications of random sampling designs

INTRODUCTION: For a design to be called random sampling or probability sampling, it is imperative that each element in the population has an equal and independent chance of selection in the sample. Sampling

Equal implies that the probability of selection of each element in the population is the same; that is, the choice of an element in the sample is not influenced by other considerations such as personal preference. Probability

The concept of independence means that the choice of one element is not dependent upon the choice of another element in the sampling; that is, the selection or rejection of one element does not affect the inclusion or exclusion of another. 

To explain these concepts let us take an example. Suppose there are 80 students in the class. Assume 20 of these refuse to participate in your study that is; you have consented them and to respect their rights they won't be able to participate. You want the entire population of 80 students in your study but, as 20 refuse to participate, you can only use a sample of 60 students. 

The 20 students who refuse to participate could have strong feelings about the issues you wish to explore, but your findings will not reflect their opinions. Their exclusion from your study means that each of the 80 students does not have an equal chance of selection. Therefore, your sample does not represent the total class. The same could apply to a community. In a community, in addition to the refusal to participate, let us assume that you are unable to identify all the residents living in the community. If a significant proportion of people cannot be included in the sampling population because they either cannot be identified or refuse to participate, then any sample drawn will not give each element in the sampling population an equal chance of being selected in the sample. Hence, the sample will not be representative of the total community.

THE CONCEPT OF INDEPENDENCE:  To understand the concept of an independent chance of selection, let us assume that there are five students in the class who are extremely close friends. If one of them is selected but refuses to participate because the other four are not chosen, and you are therefore forced to select either the five or none, then your sample will not be considered an independent sample since the selection of one is dependent upon the selection of others. 

The same could happen in the community where a small group says that either all of them or none of them will participate in the study. In these situations where you are forced either to include or to exclude a part of the sampling population, the sample is not considered to be independent, and hence is not representative of the sampling population. However, if the number of refusals is fairly small, in practical terms, it should not make the sample non-representative. In practice there are always some people who do not want to participate in the study but you only need to worry if the number is significantly large.

A sample can only be considered a random/probability sample (and therefore representative of the population under study) if both these conditions are met. Otherwise, bias can be introduced into the study. Bias

There are two main advantages of random/probability samples:

1. As they represent the total sampling population, the inferences drawn from such samples can be generalised to the total sampling population.

2. Some statistical tests based upon the theory of probability can be applied only to data collected from random samples. Some of these tests are important for establishing conclusive correlations.

RELATED;

1.  ACCIDENTAL SAMPLING  

2.  SYSTEMATIC SAMPLING  

3.  SAMPLE SIZE CALCULATION

REFERENCES

WOUND HEALING BY FIRST INTENTION (PRIMARY UNION)

 

INTRODUCTION: Wounds are some of the most common disruptions on the human skin and the leading ports of entry for microbes into the body.  Whether a wound is following a surgical operation, burns or an accidental injury if it is not catered for, it may cause infections from the external environment.  In our discussion here, we are looking at the process through which a surgical and clean wound will take to heal.

This type of healing occurs when there is no contamination of the wound, and the edges of the wound are approximated, thus closing the wound. The best example of this situation is the surgical incision where contamination of the wound is minimized and the wound is closed by suturing, once the wound is sutured, the incision space fills with blood, which contains fibrin and blood cells and which subsequently clots, the surface of this clot becomes dehydrated and forms a scab.

Within 24 hours, neutrophils appear at the edges of the incision and the epithelium at the edges of the incision begins to proliferate, it migrates under the scab and forms a thin continuous epithelial layer.

By 72 hours, macrophages are usually the most numerous inflammatory cells and granulation tissue starts to develop, collagen fibers are present but do not bridge the incision site, the epithelial cells continue to proliferate under the scab and the epidermal covering over the incision becomes thicker.

By day 5, the incision space is filled with granulation tissue and collagen fibers begin to bridge the incision, the epidermis returns to its normal thickness and keratinized architecture.

During the second week, there is continued accumulation of collagen fibers and proliferation of fibroblasts, inflammatory cells, edema disappears, and the process of blanching begins.

By the end of one month, a connective tissue scar is devoid of inflammatory cells and is covered by an intact epidermis.

RELATED;

1. WOUND HEALING BY SECONDARY INTENTION  

2. COMPLICATIONS OF WOUND HEALING  

3. CHRONIC INFLAMMATION

4.  BURNS

REFERENCES

ECHINACEA FOR BOOSTING THE IMMUNE SYSTEM

 

Echinacea purpurea, or purple coneflower, is a popular botanical native to the midwestern United States and central Canada. The flowers, leaves, and stems of this plant are harvested and dried. Preparations include dried powder, tincture, fluid extracts, and teas. No single ingredient seems to be responsible for the herb’s activity; a large number of potentially active chemicals have been identified from the extracts. Echinacea was used by Native Americans to treat various wounds and injuries. Wound healing

Echinacea is believed to boost the immune system by increasing phagocytosis and inhibiting the bacterial enzyme hyaluronidase. Some substances in echinacea appear to have antiviral activity; thus, the herb is sometimes taken to treat the common cold and influenza, an indication for which it has received official approval in Germany. Clinical evidence for the effects of echinacea on upper respiratory tract infections is mixed, with some studies showing no effect and others showing a beneficial effect. In general, echinacea is used as a supportive treatment for any disease involving inflammation and to enhance the immune system. Inflammation: Immunity

Side effects are rare; however, it may interfere with drugs that have immunosuppressant effects.

RELATED;

1.  PASSIVE IMMUNITY  

2.  ACTIVE IMMUNISATION  

3.  SEA VEGETABLES

REFERENCES

GRAPE SEED EXTRACT FOR HYPERTENSION

 

Grapes and grape seeds have been to maintain and improve health used for thousands of years. Their primary use has been for cardiovascular conditions such as hypertension (HTN), high blood cholesterol, and atherosclerosis, and to generally improve circulation. Hypertension: Atherosclerosis

Some claim that grape seed extract improves wound healing, prevents cancer, slows the progression of neurodegenerative diseases, and lowers the risk for the long-term consequences of diabetes. Woundhealing: Diabetes

The grape seeds, usually obtained from winemaking, are crushed and placed into tablet, capsule, or liquid forms. Typical doses are 50 to 300 mg/ day. Grape seed extract has antioxidant properties that have the potential to improve wound healing and repair cellular injury. Grape seed extract is well tolerated in most people, with the most common side effects being dry, itchy scalp; dizziness; headache; hives; indigestion; and nausea. It has few adverse effects but caution should be used if taking anticoagulant drugs because increased bleeding may result.

RELATED;

1.  ARTERIOSCLEROSIS  

2.  GARLIC  

3.  BLOOD PRESSURE CONTROL

4.  TRADITIONAL AND COMPLIMENTARY MEDICATIONS

REFERENCES

HISTAMINE H2 RECEPTOR BLOCKERS

 

INTRODUCTION: Histamine has two types of receptors: H1 and H2. Activation of H1 receptors produces the classic symptoms of inflammation and allergy, whereas the H2 receptors are responsible for increasing acid secretion in the stomach. The H2-receptor antagonists are effective at suppressing the volume and acidity of parietal cell secretions. Duodenal ulcers usually heal in 6 to 8 weeks, and gastric ulcers may require up to 12 weeks of therapy. All of the H2-receptor antagonists are available OTC for the short-term (2 weeks) treatment of GERD.

Prototype Drug: Ranitidine

Therapeutic Class: Antiulcer drug

Pharmacologic Class: H2-receptor antagonist

ACTIONS AND USES: Ranitidine acts by blocking H2 receptors in the stomach to decrease acid production. It has a higher potency than cimetidine, which allows it to be administered once daily, usually at bedtime. Adequate healing of the ulcer takes approximately 4 to 8 weeks, although those at high risk for PUD may continue on drug maintenance for prolonged periods to prevent recurrence. Gastric ulcers require longer therapy for healing to occur. Intravenous (IV) and intramuscular (IM) forms are available for the treatment of acute, stress-induced bleeding ulcers. Ranitidine is available in a dissolving tablet form for treating GERD in children and infants older than 1 month of age. 

ADMINISTRATION ALERT: Administer after meals and monitor liver and renal function.

Pregnancy category B (Read about drug use in relation to pregnancy)

ADVERSE EFFECTS: Adverse effects are uncommon and mild. Ranitidine does not cross the blood–brain barrier to any appreciable extent, so it does not cause the confusion and

CNS depression observed with cimetidine. Although rare, severe reductions in the number of red and white blood cells and platelets are possible; thus, periodic blood counts may be performed. High doses may result in impotence or loss of libido in men.

Contraindications: Contraindications include hypersensitivity to H2-receptor antagonists, acute porphyria, and OTC administration in children less than 12years of age.

INTERACTIONS: Drug–Drug: Ranitidine has fewer drug–drug interactions than cimetidine. Ranitidine may reduce the absorption of cefpodoxime, ketoconazole, and itraconazole. Antacids should not be given within 1 hour of H2-receptor antagonists because the effectiveness may be decreased due to reduced absorption. Smoking decreases the effectiveness of ranitidine.

Lab Tests: Ranitidine may increase the values of serum creatinine, AST, ALT, LDH, alkaline phosphatase, and bilirubin. It may produce false positives for urine protein.

Herbal/Food: Absorption of vitamin B12 depends on an acidic environment; thus, deficiency may occur. Iron is also better absorbed in an acidic environment.

RELATED;

1. PROTON PUMP INHIBITORS  

2. ANTIBIOTICS  

3. PEPTIC ULCER DISEASE

4.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

GARLIC FOR CARDIOVASCULAR HEALTH

 

INTRODUCTION: Garlic also scientifically known as Allium sativum, is one of the best-studied herbs. Several substances, known as alliaceous oils, have been isolated from garlic and shown to have pharmacologic activity.

Dosage forms include eating prepared garlic oil or the fresh bulbs from the plant. Modern claims for garlic uses have focused on the cardiovascular system: treatment of high blood lipid levels, atherosclerosis, and hypertension. Other modern claims are that garlic reduces blood glucose levels and has antibacterial and antiviral properties. Like many other supplements, garlic likely has some health benefits, but controlled, scientific studies are often lacking and the results are mixed. Garlic has been shown to decrease the aggregation or “stickiness” of platelets, thus producing an anticoagulant effect. There is some research to show that the herb has a small effect on lowering blood cholesterol. Evidence on the effects of the herb on blood pressure is mixed. An analysis of the research of the effect of garlic on the common cold concluded that there is insufficient clinical evidence to show any benefit. Garlic is safe for consumption in moderate amounts. Patients taking anticoagulant medications should limit their intake of garlic to avoid bleeding complications. Patients with diabetes should monitor their blood glucose levels closely if taking high doses of garlic.

RELATED;

1.  CARDIOVASCULAR CONDITIONS

REFERENCES

CARDIOGENIC SHOCK

INTRODUCTION: Cardiogenic shock occurs when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues. The causes of cardiogenic shock are known as either coronary or non-coronary. Coronary cardiogenic shock is more common than non-coronary cardiogenic shock and is seen most often in patients with acute myocardial infarction. Non-coronary causes of cardiogenic shock are related to conditions that stress the myocardium (eg, severe hypoxemia, acidosis, hypoglycemia, hypocalcemia, and tension pneumothorax) and conditions that result in ineffective myocardial function (eg, cardiomyopathies, valvular damage, cardiac tamponade, dysrhythmias).

CLINICAL MANIFESTATIONS: Classic signs include low blood pressure (BP), rapid and weak pulse. Dysrhythmias are common. Angina pain may be experienced. Hemodynamic instability. Complaints of fatigue.

MEDICAL MANAGEMENT: Goals of medical treatment include limiting further myocardial damage, preserving the healthy myocardium, and improving cardiac function. It is necessary first to treat the oxygenation needs of the heart muscle, increasing oxygen supply to the heart muscle while reducing oxygen demands. First-line treatment includes administering supplemental oxygen, controlling chest pain, administering fluids, and administering vasoactive medications (eg, dobutamine, nitroglycerin, dopamine) and antiarrhythmic medications. Hemodynamic monitoring and laboratory marker monitoring are performed. 

Mechanical cardiac support may be necessary. Coronary cardiogenic shock may be treated with thrombolytic therapy, a percutaneous coronary intervention, coronary artery bypass graft surgery, and/or intra-aortic balloon pump therapy. Noncoronary cardiogenic shock may be treated with cardiac valve replacement, correction of dysrhythmia, correction of acidosis and electrolyte disturbances, or treatment of the tension pneumothorax.

RELATED;

1. OTHER TYPES OF SHOCK  

2.  HYPERTENTION.  

3.  CONGESTIVE CARDIAC FAILURE

4.  MEDICAL CONDITIONS

REFERENCES

PROTON PUMP INHIBITORS

 

INTRODUCTION: Proton pump inhibitors act by blocking the enzyme responsible for secreting hydrochloric acid in the stomach. They are drugs of choice for the short-term therapy of PUD and GERD. Proton pump inhibitors (PPIs) reduce acid secretion in the stomach by binding irreversibly to K⁺/H⁺ATPase, the enzyme that acts as a pump to release acid (also called H⁺, or protons) onto the surface of the GI mucosa. The PPIs reduce acid secretion to a greater extent than the H2-receptor antagonists and have a longer duration of action.  PPIs heal more than 90% of duodenal ulcers within 4 weeks and about 90% of gastric ulcers in 6 to 8 weeks. Several days of PPI therapy may be needed before patients gain relief from ulcer pain. Beneficial effects continue for 3 to 5 days after the drugs have been stopped. These drugs are used only for the short-term control of peptic ulcers and GERD: Peptic ulcer disease

The typical length of therapy is 4 weeks. Omeprazole and lansoprazole are used concurrently with antibiotics to eradicate H. pylori. Esomeprazole and pantoprazole offer the convenience of once-a-day dosing.

OMEPRAZOLE

Therapeutic Class: Antiulcer drug

Pharmacologic Class: Proton pump inhibitor

ACTIONS AND USES: Omeprazole was the first PPI to be approved for PUD: Both prescription and OTC forms are available. Its pharmacodynamics is discussed in the introduction. Although this drug can take 2 hours to reach therapeutic levels, its effects last up to 72 hours. It is used for the short-term, 4- to 8-week therapy of active peptic ulcers and GERD. Most patients are symptom free after 2 weeks of therapy. It is used for longer periods in patients who have chronic hypersecretion of gastric acid, a condition known as Zollinger–Ellison syndrome.

It is the most effective drug for this syndrome. Omeprazole is available only in oral form.

ADMINISTRATION ALERTS: If possible, administer before breakfast on an empty stomach. It may be administered with antacids. Capsules and tablets should not be chewed, divided, or crushed.

Pregnancy category C. [read about drug use inrelation to pregnancy]

ADVERSE EFFECTS: Adverse effects are generally minor and include headache, nausea, diarrhea, rash, and abdominal pain. Although rare, blood disorders may occur, causing unusual fatigue and weakness. Therapy is generally limited to 2 months. Atrophic gastritis and hypomagnesemia have been reported rarely with prolonged treatment with PPIs.

CONTRAINDICATIONS: The only contraindication is hypersensitivity to the drug. OTC use is not approved for patients under 18 years of age.

INTERACTIONS:

Drug–Drug: Concurrent use with diazepam, phenytoin, and central nervous system (CNS) depressants may cause increased blood levels of these drugs. Concurrent use with warfarin may increase the likelihood of bleeding. Alcohol can aggravate the stomach mucosa and decrease the effectiveness of omeprazole.

Lab Tests: Omeprazole may increase values for ALT, AST, and serum alkaline phosphatase.

Herbal/Food: Ginkgo and St. John’s wort may decrease the plasma concentration of omeprazole.

RELATED;

1. PEPTIC ULCER DISEASE

2.  ANTIACIDS

REFERENCES

PANCREATITIS

 

INTRODUCTION: Pancreatitis (inflammation of the pancreas) is a serious disorder that can range in severity from a relatively mild, selflimiting disorder to a rapidly fatal disease that does not respond to any treatment. Acute pancreatitis is commonly described as an autodigestion of the pancreas by the exocrine enzymes it produces, principally trypsin. [Readabout biochemistry of enzymes]

Eighty percent of patients with acute pancreatitis have biliary tract disease or a history of long-term alcohol abuse. Other less common causes of pancreatitis include bacterial or viral infection, with pancreatitis occasionally developing as a complication of mumps virus.  Many disease processes and conditions have been associated with an increased incidence of pancreatitis, including surgery on or near the pancreas, medications, hypercalcemia, and hyperlipidemia. Up to 10% of cases are idiopathic, and there is a small incidence of hereditary pancreatitis. Mortality is high because of shock, anoxia, hypotension, or fluid and electrolyte imbalances. [Readabout shock]

Attacks of acute pancreatitis may result in complete recovery, may recur without permanent damage, or may progress to chronic pancreatitis.

CLINICAL MANIFESTATIONS: Severe abdominal pain is the major symptom. Pain in the midepigastrium may be accompanied by abdominal distention; a poorly defined, palpable abdominal mass; decreased peristalsis; and vomiting that fails to relieve the pain or nausea. Pain is frequently acute in onset (24 to 48 hours after a heavy meal or alcohol ingestion); may be more severe after meals and unrelieved by antacids. Patient appears acutely ill, Abdominal guarding; rigid or boardlike abdomen (generally an ominous sign, usually indicating peritonitis). Ecchymosis in the flank or around the umbilicus, which may indicate severe hemorrhagic pancreatitis. Nausea and vomiting, fever, jaundice, mental confusion, agitation. Hypotension related to hypovolemia and shock. May develop tachycardia, cyanosis, and cold, clammy skin. Acute renal failure common. Respiratory distress and hypoxia. May develop diffuse pulmonary infiltrates, dyspnea, tachypnea, and abnormal blood gas values. Myocardial depression, hypocalcemia, hyperglycemia, and disseminated intravascular coagulation (DIC).

ASSESSMENT AND DIAGNOSTIC FINDINGS: Diagnosis is based on history of abdominal pain, the presence of known risk factors, physical examination findings, and diagnostic findings (increased urine amylase level and white blood cell [WBC] count; hypocalcemia; transient hyperglycemia; glucosuria and increased serum bilirubin levels in some patients). X-rays of abdomen and chest, ultrasound, and contrast-enhanced computed tomography (CT) scan may be performed. Hematocrit and hemoglobin levels are used to monitor the patient for bleeding. Serum amylase and lipase levels are most indicative (elevated within 24 hours; amylase returns to normal within 48 to 72 hours; lipase remains elevated for longer period). Peritoneal fluid is evaluated for increase in pancreatic enzymes.

MEDICAL MANAGEMENT:

Acute Phase: During the acute phase, management is symptomatic and directed toward preventing or treating complications. Oral intake is withheld to inhibit pancreatic stimulation and secretion of pancreatic enzymes. Parenteral nutrition (PN) is administered to the debilitated patient. Nasogastric suction is used to relieve nausea and vomiting and to decrease painful abdominal distention and paralytic ileus. Histamine-2 (H2) receptor antagonists (cimetidine, ranitidine) or, sometimes, proton pump inhibitors are given to decrease hydrochloric acid secretion.  Adequate pain medication, such as morphine, is administered. Antiemetic agents may be prescribed to prevent vomiting. Correction of fluid, blood loss, and low albumin levels is necessary. Antibiotics are administered if infection is present. Insulin is necessary if significant hyperglycemia occurs. Aggressive respiratory care is provided for pulmonary infiltrates, effusion, and atelectasis. Biliary drainage (drains and stents) results in decreased pain and increased weight gain.  Surgical intervention may be performed for diagnosis, drainage, resection, or debridement.

MEDICAL MANAGEMENT:

Postacute Phase. Antacids are given when the acute episode begins to resolve. Oral feedings low in fat and protein are initiated gradually. Caffeine and alcohol are eliminated. Medications (eg, thiazide diuretics, glucocorticoids, or oral contraceptives) are discontinued.

RELATED;

1. INSULIN  

2. GLUCAGON

3.  THE ENDOCRINE PANCREAS

REFERENCES

LACTOSE INTOLERANCE

 

INTRODUCTION: Lactose intolerance is the most common problem of carbohydrate digestion. It results mainly from the reduction of lactase enzyme activity in adults. Lactase is expressed normally at high levels in the jejunum of neonatal and infant humans and for that reason, this problem is rare in that age group. In many parts of the world, lactase levels are gradually reduced after weaning. However, lactase levels do not decrease significantly in populations in which milk products are an important part of the adult diet. 

Lactase activity is rate limiting for lactose digestion in most adults throughout other regions of the world. If lactase is deficient, non-digested lactose is not absorbed. The non-absorbed lactose retains water in the lumen to maintain the osmolality of chyme equivalent to that of plasma. This fluid retention causes abdominal pain (cramps), nausea, and diarrhea. Bacterial fermentation of lactose in the distal small intestine and colon further exacerbates these symptoms.

RELATED;

1. LACTOSE  

2. CARBOHYDRATES  

3. BIOCHEMISTRY OF ENZYMES

4.  ALLERGY

5.  METABOLISM OF PROTEINS

REFERENCES

ANAPHYLAXIS

 

INTRODUCTION: Anaphylaxis is a clinical response to an immediate (type I hypersensitivity) immunologic reaction between a specific antigen and an antibody. The reaction results from a rapid release of IgE-mediated chemicals, which can induce a severe, life-threatening allergic reaction. Substances that most commonly cause anaphylaxis include foods, medications, insect stings, and latex. Immunoglobulins

Foods that are common causes of anaphylaxis include peanuts, tree nuts, shellfish, fish, milk, eggs, soy, and wheat. Many medications have been implicated in anaphylaxis. Those that are most frequently reported include antibiotics (eg, penicillin), radiocontrast agents, IV anesthetics, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and opioids. Penicillins: Anaesthetic medication: Opioid analgesics  Closely related to anaphylaxis is a nonallergenic anaphylaxis (anaphylactoid) reaction.

Clinical Manifestations: Anaphylactic reactions produce a clinical syndrome that affects multiple organ systems. Reactions may be categorized as mild, moderate, or severe. The severity depends on the degree of allergy and the dose of allergen.  Mild Symptoms include peripheral tingling, a warm sensation, fullness in the mouth and throat, nasal congestion, periorbital swelling, pruritus, sneezing, and tearing eyes. Symptoms begin within 2 hours of exposure. Moderate Symptoms include flushing, warmth, anxiety, and itching in addition to any of the milder symptoms. More serious reactions include bronchospasm and edema of the airways or larynx with dyspnea, cough, and wheezing. The onset of symptoms is the same as for a mild reaction.

Severe: Severe systemic reactions have an abrupt onset with the same signs and symptoms described previously. Symptoms progress rapidly to bronchospasm, laryngeal edema, severe dyspnea, cyanosis, and hypotension.  Dysphagia, abdominal cramping, vomiting, diarrhea, and seizures can also occur.  Cardiac arrest and coma may follow.

Assessment and Diagnostic Methods: Diagnostic evaluation of the patient with allergic disorders commonly includes blood tests (complete blood cell count [CBC] with differential, high total serum IgE levels), smears of body secretions, skin tests, and the radioallergosorbent test (RAST).

Prevention: Prevention by avoidance of allergens is of utmost importance. If avoidance of exposure to allergens is impossible, the patient should be instructed to carry and administer epinephrine to prevent an anaphylactic reaction in the event of exposure to the allergen.  Health care providers should always obtain a careful history of any sensitivities before administering medications. Venom immunotherapy may be given to people who are allergic to insect venom. Insulin-allergic patients with diabetes or penicillin-sensitive patients may require desensitization.

Medical Management: Respiratory and cardiovascular functions are evaluated and cardiopulmonary resuscitation (CPR) is initiated in cases of cardiac arrest. Oxygen is administered in high concentration during CPR or when the patient is cyanotic, dyspneic, or wheezing. Patients with mild reactions need to be educated about the risk for recurrences. Patients with severe reactions need to be observed for 12 to 14 hours.

Pharmacologic Therapy: Epinephrine, antihistamines, and corticosteroids may be given to prevent recurrences of the reaction and to relieve urticaria and angioedema. Corticosteroids.  IV fluids (eg, normal saline solution), volume expanders, and vasopressor agents are administered to maintain blood pressure and normal hemodynamic status; glucagon may be administered. Plasmavolume expanders  Aminophylline and corticosteroids may also be administered to improve airway patency and function.

RELATED;

1. ASTHMA  

2.  ALLERGIC RHINITIS

3.  IMMUNOLOGY

4.  LACTOSE INTOLERANCE

REFERENCES

ANGINA PECTORIS

 

INTRODUCTION: Angina pectoris is a clinical syndrome characterized by paroxysms of pain or a feeling of pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in an inadequate supply of oxygen to meet the myocardial demand. Angina is usually a result of atherosclerotic heart disease and is associated with a significant obstruction of a major coronary artery. Factors affecting anginal pain are physical exertion, exposure to cold, eating a heavy meal, or stress or any emotion-provoking situation that increases blood pressure, heart rate, and myocardial workload. Unstable angina is not associated with the above and may occur at rest.

CLINICAL MANIFESTATIONS: Pain varies from a feeling of indigestion to a choking or heavy sensation in the upper chest ranging from discomfort to agonizing pain. The patient with diabetes mellitus may not experience severe pain with angina. Angina is accompanied by severe apprehension and a feeling of impending death. The pain is usually retrosternal, deep in the chest behind the upper or middle third of the sternum. Discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspect of the upper arms (usually the left arm). A feeling of weakness or numbness in the arms, wrists, and hands, as well as shortness of breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting, may accompany the pain. Anxiety may occur with angina. An important characteristic of anginal pain is that it subsides when the precipitating cause is removed or with nitroglycerin.

ASSESSMENT AND DIAGNOSTIC METHODS: Evaluation of clinical manifestations of pain and patient history. Electrocardiogram changes (12-lead ECG), stress testing, blood tests. Echocardiogram, nuclear scan, or invasive procedures such as cardiac catheterization and coronary angiography.

MEDICAL MANAGEMENT: The objectives of the medical management of angina are to decrease the oxygen demand of the myocardium and to increase the oxygen supply. Medically, these objectives are met through pharmacologic therapy and control of risk factors. Alternatively, reperfusion procedures may be used to restore the blood supply to the myocardium. These include PCI procedures (eg, percutaneous transluminal coronary angioplasty [PTCA], intracoronary stents, and atherectomy) and coronary artery bypass graft (CABG).

PHARMACOLOGIC THERAPY: Nitrates, the mainstay of therapy (nitroglycerin). Beta-adrenergic blockers (metoprolol and atenolol). Calcium channel blockers/calcium ion antagonists (amlodipine and diltiazem). Antiplatelet and anticoagulant medications (aspirin, clopidogrel, heparin, glycoprotein [GP] IIb/IIIa agents [abciximab, tirofiban, eptifibatide]). Oxygen therapy.

RELATED;

1. ARTERIOSCLEROSIS  

2. BETA BLOCKERS  

3. CHAMBERS AND CIRCULATION THROUGH THE HEART

REFERENCES

HYPERTENSION

 

OBJECTIVES OF THE SESSION:  By the end of our discussion here, the learner/reader/medical student will be able to;

1.  Differentiate between the normal and hypertensive blood pressures

2.  Explain the effects of increasing blood pressure on the body organs

3.  Describe the different types and stages of hypertension

INTRODUCTION: Hypertension is defined as a systolic blood pressure greater than 140 mmHg and a diastolic pressure greater than 90 mmHg, based on two or more measurements. Hypertension can be classified as follows:

a) Normal: systolic less than 120 mmHg; diastolic less than 80 mmHg

b) Prehypertension: systolic 120 to 139 mmHg; diastolic 80 to 89 mmHg

c) Stage 1: systolic 140 to 159 mm Hg; diastolic 90 to 99 mmHg

d) Stage 2: systolic 160 mmHg; diastolic 100 mmHg

CONSEQUENCES OF HYPERTENSION: Hypertension is a major risk factor for atherosclerotic cardiovascular disease, HF, stroke, and kidney failure. Hypertension carries the risk for premature morbidity or mortality, which increases as systolic and diastolic pressures rise. Prolonged blood pressure elevation damages blood vessels in target organs (heart, kidneys, brain, and eyes).

Essential (Primary) Hypertension: In the adult population with hypertension, between 90% and 95% have essential (primary) hypertension, which has no identifiable medical cause; it appears to be a multifactorial, polygenic condition. For high blood pressure to occur, an increase in peripheral resistance and/or cardiac output must occur secondary to increased sympathetic stimulation, sodium reabsorption, increased renin–angiotensin–aldosterone system activity, decreased vasodilation of the arterioles, or resistance to insulin action. Hypertensive emergencies and urgencies may occur in patients whose hypertension has been poorly controlled, whose hypertension has been undiagnosed, or in those who have abruptly discontinued their medications.

Secondary Hypertension: Secondary hypertension is characterized by elevations in blood pressure with a specific cause, such as narrowing of the renal arteries, renal parenchymal disease, hyperaldosteronism (mineralocorticoid hypertension), certain medications, pregnancy, and coarctation of the aorta. Hypertension can also be acute, a sign of an underlying condition that causes a change in peripheral resistance or cardiac output.

CLINICAL MANIFESTATIONS: Physical examination may reveal no abnormality other than high blood pressure. Changes in the retinas with hemorrhages, exudates, narrowed arterioles, and cotton–wool spots (small infarctions), and papilledema may be seen in severe hypertension. Symptoms usually indicate vascular damage related to organ systems served by involved vessels. Coronary artery disease with angina or myocardial infarction is the most common consequence. Left ventricular hypertrophy may occur; HF ensues. Pathologic changes may occur in the kidney (nocturia and increased BUN and creatinine levels). Cerebrovascular involvement may occur (stroke or transient ischemic attack [TIA] [ie, alterations in vision or speech, dizziness, weakness, a sudden fall, or transient or permanent hemiplegia]).

ASSESSMENT AND DIAGNOSTIC METHODS: History and physical examination, including retinal examination; laboratory studies for organ damage, including urinalysis, blood chemistry (sodium, potassium, creatinine, fasting glucose, total and high-density lipoprotein); ECG; and echocardiography to assess left ventricular hypertrophy. Additional studies, such as creatinine clearance, renin level, urine tests, and 24-hour urine protein, may be performed.

MEDICAL MANAGEMENT: The goal of any treatment program is to prevent death and complications by achieving and maintaining an arterial blood pressure at or below 140/90 mm Hg (130/80 mm Hg for people with diabetes mellitus or chronic kidney disease), whenever possible. Nonpharmacologic approaches include weight reduction; restriction of alcohol and sodium; regular exercise and relaxation. A DASH (Dietary Approaches to Stop Hypertension) diet high in fruits, vegetables, and low-fat dairy products has been shown to lower elevated pressures. Select a drug class that has the greatest effectiveness, fewest side effects, and best chance of acceptance by patient. Two classes of drugs are available as first-line therapy: diuretics and beta-blockers. Promote compliance by avoiding complicated drug schedules.

RELATED;

1. CONGESTIVE CARDIAC FAILURE  

2. CHAMBERS AND CIRCULATION THROUGH THE HEART  

3. CARDIAC CYCLE AND THE HEART SOUNDS  

4. ARTERIOSCLEROSIS

5.  MEDICAL CONDITIONS

REFERENCES

BACK PAIN

 

INTRODUCTION: Most low back pain is caused by one of many musculoskeletal problems, including acute lumbosacral strain, unstable lumbosacral ligaments and weak muscles, osteoarthritis of the spine, spinal stenosis, intervertebral disk problems, and unequal leg length. Obesity, postural problems, structural problems, stress, overstretching of the spinal supports, and occasionally depression may also result in back pain. Back pain due to musculoskeletal disorders usually is aggravated by activity, whereas pain due to other conditions is not. Older patients may experience back pain associated with osteoporotic vertebral fractures, osteoarthritis of the spine, spinal stenosis, and spondylolisthesis, among other conditions.

CLINICAL MANIFESTATIONS: Acute or chronic back pain (lasting more than 3 months without improvement) and fatigue. Pain that radiates down the leg (radiculopathy, sciatica); presence of this symptom suggests nerve root involvement. Gait, spinal mobility, reflexes, leg length, leg motor strength, and sensory perception may be affected. Paravertebral muscle spasm (greatly increased muscle tone of back postural muscles) occurs with loss of normal lumbar curve and possible spinal deformity.

ASSESSMENT AND DIAGNOSTIC METHODS: Health history and physical examination (back examination, neurologic testing). Spinal x-ray. Bone scan and blood studies. Computed tomography (CT) scan. Magnetic resonance imaging (MRI). Electromyogram and nerve conduction studies. Myelogram, Ultrasound.

MEDICAL MANAGEMENT: Most back pain is self-limited and resolves within 4 weeks with analgesics, rest, and relaxation. Management focuses on relief of pain and discomfort, activity modification, and patient education. Bed rest is recommended for 1 to 2 days, for a maximum of 4 days and only if pain is severe. Other effective nonpharmacologic interventions include the application of superficial heat and spinal manipulation. Cognitive-behavioral therapy (eg, biofeedback), exercise regimens, spinal manipulation, physical therapy, acupuncture, massage, and yoga are all effective nonpharmacologic interventions for treating chronic low back pain but not acute low back pain. Most patients need to alter their activity patterns to avoid aggravating the pain. They should avoid twisting, bending, lifting, and reaching, all of which stress the back. A gradual return to activities and a program of low-stress aerobic exercise are recommended.

PHARMACOLOGIC THERAPY: Acute low back pain: nonprescription analgesics (eg, acetaminophen), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), and prescription muscle relaxants (eg, cyclobenzaprine). Chronic low back pain: tricyclic antidepressants (eg, amitriptyline). Others: opioids (eg, morphine), tramadol (Ultram), benzodiazepines (eg, diazepam [Valium]), and gabapentin (Neurontin).

RELATED;

1. CHRONIC PAIN  

2. INFLAMMATION  

3. OSTEOPOROSIS

4.  MEDICAL CONDITIONS

REFERENCES

THE HUMAN SKIN

THE HUMAN SKIN:  The human skin is one of the largest organs that make up the human body and the outer housing of the entire body with varying thickness in different body parts.  With it's thickness varying in size from the soles of feet to the membranes of the conjunctival sac in the eyes, skin remains the first organ to protect us from the invading microbes and therefore acting as the body's first line of defense or part of the body barriers to invading microbes.  With a multilayered structure and strength, the skin is able to cover the entire human body and naturally protects the rest of the body tissues.  In our next discussions here, we shall be referring to this complex body organ as the integumentary system and the conditions affecting it, as Dermatological conditions, while the drugs used to treat it as dermatological agents.  But skin does not come alone, with it, comes several other structures that are visible with a naked eye including the nails of the feet and fingers, hair, and then microscopic other structures such as sebaceous glands and hair follicles.  In my previous discussions I have tried to look at some of the conditions that affect the skin and below is a list of some of them;

1.  Seborrheic dermatitis

2.  Pruritus

PROPERTIES OF THE HUMAN SKIN

ROLES OF THE HUMAN SKIN

HUMAN SKIN AND IMMUNITY:  To understand the way skin plays a major role in immunity, follow the link below and read about innate immunity.

The innate immune system

RELATED;

1.  THE HUMAN LIVER

2.  SEBORRHEIC DERMATITIS

3.  PRURITUS