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Cardiovascular Disorders. Acute Coronary Syndromes

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Acute coronary syndromes (ACSs) include all syndromes compatible with acute myocardial ischemia resulting from imbalance between myocardial oxygen demand and supply. • ACSs are classified according to electrocardiographic (ECG) changes into  (1) ST-segment-elevation (STE) myocardial infarction (MI) or (2) non–ST-segmentelevation (NSTE) ACS, which includes NSTE MI and unstable angina (UA). PATHOPHYSIOLOGY  • Endothelial dysfunction, inflammation, and formation of fatty streaks contribute to development of atherosclerotic coronary artery plaques.  • The cause of ACS in more than 90% of patients is rupture, fissuring, or erosion of an unstable atheromatous plaque. A clot forms on top of the ruptured plaque. Exposure of collagen and tissue factor induces platelet adhesion and activation, which promote release of adenosine diphosphate (ADP) and thromboxane A2 from platelets producing vasoconstriction and platelet activation. A change in the conformation of the glycoprot
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Introduction: principles of drug action

Medical pharmacology is the science of chemicals that interact with the human body. These interactions are divided into two classes: • pharmacodynamics   Effects of the drug on the body • pharmacokinetics  way the body affects the drug with time. A few drugs  act by virtue of their physicochemical properties, and this is called non‐specific drug action. Some drugs act as inhibitors for certain transport systems  or enzymes. However, most drugs produce their effects by acting on specific protein molecules, located in the cell membrane. These proteins are called receptors, and respond to endogenous chemicals in the body. These chemicals are either synaptic transmitter substances or hormones. For example, acetylcholine is a transmitter substance released from motor nerve endings, it activates receptors in skeletal muscle, initiating a sequence of events that results in contraction of the muscle. Chemicals (e.g. acetylcholine) that activate receptors and produce a response are ca
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Hypertension, Pathophysiology, Clinical presentation, Diagnosis & Treatment.

Hypertension  is defined as persistently elevated arterial blood pressure (BP).  • Isolated systolic hypertension is diastolic blood pressure (DBP) values less than 90 mm Hg and systolic blood pressure (SBP) values of 140 mm Hg or more. • Hypertensive crisis (BP >180/120 mm Hg) may be categorized as hypertensive emergency or hypertensive urgency (high BP elevation without acute or progressing target-organ injury). PATHOPHYSIOLOGY • Hypertension may result from a specific cause (secondary hypertension) or from an unknown etiology (primary or essential hypertension). Secondary hypertension(<10% of cases) is usually caused by chronic kidney disease (CKD) or renovascular disease. Other conditions are Cushing syndrome, coarctation of the aorta, obstructive sleep apnea, hyperparathyroidism, pheochromocytoma, primary aldosteronism, and hyperthyroidism. Some drugs that may increase BP include corticosteroids, estrogens, nonsteroidal anti-inflammatory drugs (NSAIDs), amphetami
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Anemias, Pathophysiology, Clinical presentation, Diagnosis & Treatment.

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• Anemias are a group of diseases characterized by a decrease in hemoglobin (Hb) or red blood cells (RBCs), resulting in decreased oxygen-carrying capacity of blood. The World Health Organization defines anemia as Hb less than 13 g/dL (<130 g/L, <8.07 mmol/L) in men or less than 12 g/dL (<120 g/L; <7.45 mmol/L) in women. PATHOPHYSIOLOGY • The functional classification of anemias is found. The most common anemias are included in this chapter.  • Morphologic classifications are based on cell size. Macrocytic cells are larger than normal and are associated with deficiencies of vitamin B12 or folic acid. Microcytic cells are smaller than normal and are associated with iron deficiency, whereas normocytic anemia may be associated with recent blood loss or chronic disease. • Iron-deficiency anemia (IDA) can be caused by inadequate dietary intake, inadequate gastrointestinal (GI) absorption, increased iron demand (eg, pregnancy), blood loss, and chronic diseases. •
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Ischemic Heart Disease, Pathophysiology, Clinical presentation, Diagnosis & Treatment.

Ischemic Heart Disease • Ischemic heart disease (IHD) is defined as lack of oxygen and decreased or no blood flow to the myocardium resulting from coronary artery narrowing or obstruction. It may present as acute coronary syndrome (ACS), which includes unstable angina and non–ST-segment elevation (NSTE) or ST-segment elevation (STE) myocardial infarction (MI), chronic stable exertional angina, ischemia without symptoms, or ischemia due to coronary artery vasospasm (variant or Prinzmetal angina). PA THOPHYSIOLOGY • Major determinants of myocardial oxygen demand (MVo2) are heart rate (HR), contractility, and intramyocardial wall tension during systole. Because the consequences of IHD usually result from increased demand with a fixed oxygen supply, alterations in MVo2 are important in producing ischemia and for interventions intended to alleviate it. • The double product (DP) is the heart rate multiplied by the systolic blood pressure (DP = HR × SBP) and serves as an indirect
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RHEUMATOID ARTHRITIS, PATHOPHYSIOLOGY, CLINICAL PRESENTATION, DIAGNOSIS, TREATMENT

Rheumatoid arthritis • Rheumatoid arthritis (RA) is a chronic, progressive inflammatory disorder of unknown etiology characterized by polyarticular symmetric joint involvement and systemic manifestations. PATHOPHYSIOLOGY • RA results from dysregulation of humoral and cell-mediated immunity. Most patients produce antibodies called rheumatoid factors; these seropositive patients tend to have a more aggressive course than seronegative patients. • Immunoglobulins (Ig) activate the complement system, which amplifies the immune response by enhancing chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells that are then presented to T lymphocytes. Processed antigen is recognized by the major histocompatibility complex proteins on the lymphocyte surface, resulting in activation of T and B cells. • Tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and IL-6 are proinflammatory cytokines important in initiation and continuance of inflammation. • Activated T cells pr
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Dyslipidemia

Dyslipidemia  is elevated total cholesterol, low-density lipoprotein (LDL) cholesterol, or triglycerides; low high-density lipoprotein (HDL) cholesterol; or a combination of these abnormalities. PATHOPHYSIOLOGY • Cholesterol, triglycerides, and phospholipids are transported in blood as complexes of lipids and proteins (lipoproteins). Elevated total and LDL cholesterol and reduced HDL cholesterol are associated with development of coronary heart disease (CHD). • Risk factors such as oxidized LDL, mechanical injury to endothelium, and excessive homocysteine can lead to endothelial dysfunction and cellular interactions culminating in atherosclerosis. Eventual clinical outcomes may include angina, myocardial infarction (MI), arrhythmias, stroke, peripheral arterial disease, abdominal aortic aneurysm, and sudden death. • Atherosclerotic lesions arise from transport and retention of plasma LDL through the endothelial cell layer into the extracellular matrix of the subendothelial
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