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Pharm II EXAM 2 Deeper dive
Pharmacology II (NUR 354)
Arizona College of Nursing
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PHARM II EXAM 2 Deeper dive Adams Ch. 24 Adams Ch. 26 & 28
Chapter 24: Diuretic Therapy and Drugs for Kidneys Failure
Function of the Kidneys: The primary organs for regulating fluid balance, electrolyte composition, and acid-base balance of body fluids. They also secrete o renin -> regulates blood pressure o erythropoietin -> stimulate RBC production Responsible for production of calcitriol the active form of vitamin D to maintain bone homeostasis Each kidney contains more than 1 million nephrons, the functional units of the kidneys.
Renal reabsorption and Secretion For every 180L of water entering the filtrate each day, approximately 178 Is reabsorbed, leaving only 1 to be excreted as urine. Certain ions and molecules too large to pass through the glomerular capsule may still enter the urine by crossing from the blood to the filtrate in a process called tubular secretion. Acidic drugs secreted in the PCT include penicillin G, ampicillin, sulfisoxazole, nonsteroidal anti- inflammatory drugs and furosemide. 90% of a dose of penicillin enters the urine through secretion.
Kidney Failure: Decrease in the kidneys ability to maintain electrolyte and fluid balance and to excrete waste products. Primary treatment goal is to maintain blood flow through the kidneys and adequate urine output.
Diagnosis and Pharmacotherapy of kidney failure: The most basic test for kidney failure is urinalysis which examines: o Presence of blood cells, proteins, pH, specific gravity, ketones, glucose, and microorganisms. o Can detect proteinuria and albuminuria -> primary measures of structural kidney damage. When kidneys are disease, certain substances accumulate in the blood like serum creatinine and blood urea nitrogen (BUN) Diagnostic imaging such as tomography, sonography, or MRI may be necessary. Kidney biopsy may be performed to examine for scarring or infectious disease. The best marker for estimating kidney function is the glomerular filtration rate (GFR) which is the volume of filtrate passing through the glomerular capsules per minute. Although nephrons die, the remaining healthy nephrons can compensate by increasing their filtration capacity. o Therefore, patients with kidney damage may exhibit no symptoms until 50% or more of the nephrons have become nonfunctional and the GFR falls to less than half its normal value. Acute Kidney Injury (AKI) requires immediate treatment because retention of nitrogenous waste products in the body can result in death if untreated. o Most common cause is hypoperfusion of lack of sufficient blood flow o The cause must be identified and quickly treated to avoid permanent damage o Causes include Heart failure, dysrhythmias, hemorrhage, toxins, and dehydration. Blockage of the urinary tract, blood clots in the kidneys, severe infections, and severe inflammation (glomerulonephritis) Chronic kidney disease (CKD) develops over a period of months or years. o Over half the patients with CKD have a medical history of longstanding hypertension or diabetes. o By the time the disease is diagnosed, impairment may be irreversible. End stage renal disease (ESRD) the kidneys are no longer able to function on their own; thus dialysis and kidney transplantation become treatment options.
Treatment: Depending on the stage of the disease, dietary management may include protein restriction and reduction of sodium, potassium, phosphorus and magnesium intake. For patients with diabetes, control of glucose through insulin therapy may reduce the risk of kidney damage. Administering the “average” dose to a patient in severe kidney disease can have fatal consequences.
Diuretics: A drug that increases the rate of urine flow. Desirable in these conditions:
Factors Responsible for Blood Pressure: Three factors responsible: 1. Cardiac Output (blood pumped per minute) 2. Peripheral resistance 3. Blood volume
Physiological Regulation of Blood Pressure On a minute-to-minute basis, a cluster of neurons in the medulla oblongata called the vasomotor center regulates blood pressure. Receptors in the aorta and the internal carotid artery act as sensors to provide the vasomotor center with vital information on conditions in the vascular system. Baroreceptors have the ability to sense pressure within blood vessels, whereas chemoreceptors recognize levels of oxygen and carbon dioxide and the pH in the blood. With aging or disease such as diabetes, the baroreceptors response may be diminished. Antidiuretic Hormone (ADH) is a potent vasoconstrictor that can also increase blood pressure by raising blood volume. o Available IV as vasopressin
Etiology and Pathogenesis of Hypertension Hypertension having no identifiable cause is called primary hypertension and accounts for 90% of all cases. o Also referred to as essential HTN In 10% of adults a cause can be identified, this is called secondary hypertension. o Disease such as: Cushing’s syndrome, hyperthyroidism, and chronic kidney disease (CKD) cause elevated BP o Some drugs: Systemic corticosteroids, oral contraceptives, alcohol, amphetamines, caffeine, decongestants, and erythropoietin. Four target organs are most often affected by prolonged or improperly controlled HTN: o The heart The most serious consequence is that the heart must work harder to pump blood to the organs and tissues. Excessive cardiac workload can cause the heart to fail and the lungs to fill with fluid, known as heart failure (HF) o The brain o The kidneys o The retina High blood pressure over a prolonged period adversely affects the vascular system. Damage to blood vessels supplying blood and oxygen to the brain can result in transient ischemic attacks and strokes.
Chronic HTN damages arteries in the kidneys leading to progressive development of CKD. Vessels in the retina can rupture or become occluded, resulting in visual impairment and even blindness.
Nonpharmacological Management of Hypertension Greatest importance is maintaining optimal weight because obesity is closely associated with HTN each kg of weight loss correlates to a 1mmHG reduction in blood pressure. It is important that patients attempt to control disease through nonpharmacological means to the greatest extent possible: o Limit alcohol o Restrict sodium consumption and increase potassium intake o Reduce the intake of saturated fat and cholesterol and increase consumption of fresh fruits and vegetables. o Increase physical activity o Discontinue tobacco products. o Reduce stress and learn to implement coping strategies. o Maintain optimal weight
Guidelines for the management of hypertension: Normal o 120/80 or less Elevated o 120-129/less than 80 Hypertension Stage 1 o 130-139/80- Hypertension Stage 2 o 140 and above/ and above
Drugs for treating hypertension Diuretics have been used wince 1950s and are still considered a first line drug.
Treating hypertension with Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers Renin-angiotensin-aldosterone system (RAAS) is one of the primary homeostatic mechanisms controlling blood pressure and fluid balance in the body. o Renin is secreted from the kidneys when blood pressure drops or a decrease of sodium flows through the kidney tubules. o Renin in the blood converts inactive angiotensin to angiotensin I.
Effects of arterial dilation and increased sodium excretion by kidneys are similar to ACE inhibitors. Side effects: o Relatively none but related to hypotension \
Treating Hypertension with Calcium Channel Blockers (CCBs) A group of drugs used to treat angina pectoris, dysrhythmias and HTN. These relax arterial smooth muscle, thus lowering peripheral resistance and decreasing blood pressure. o Nifedipine are selective for calcium channels in arterioles o Think vasodilation, decreased oxygen used by the heart and increase in cardiac output
Treating Hypertension with Adrenergic Antagonists Mechanisms include o Beta1-adrenergic receptors in the heart o Alpha1-adrenergic receptors in the arterioles
Beta-Adrenergic Blockers By decreasing the heart rate and contractility, they reduce cardiac output and lower systemic blood pressure. By decreasing the cardiac workload, beta blockers can ease symptoms of angina pectoris. By slowing conduction through the myocardium, beta blockers are able to treat certain types of dysrhythmias. Side effects: o Predictable based on inhibitions of the fight-or-flight response. o Slow the heart rate, and can cause bronchoconstriction o Caution ins patients with ASTHMA, HEART FAILURE or COPD. o Can cause fatigue and sexual disfunction in males. If stopping abruptly, rebound HTN, angina, and MI can happen.
Alpha1-Adrenergic Blockers Lower blood pressure directly by blocking sympathetic receptors in the arterioles, causing the vessels to dilate. Tend to cause orthostatic hypotension when a person moves quickly from supine to an upright position. Dizziness, nausea, nervousness, and fatigue are also common.
Alpha2-Adrenergic Agonists Decrease the outflow of sympathetic nerve impulses from the central nervous system to the heart and arterioles. o Slowing of the heart rate and conduction velocity and dilation of the arterioles.
o Cause sedation, dizziness and other CNS effects. o Abnormalities in sexual function may occur. o Less common but potentially severe include hemolytic anemia, leukopenia, thrombocytopenia, and lupus.
Treating Hypertension with Direct Vasodilators (hydralazine) Cause direct relaxation of vascular smooth muscle. Highly effective at lowering pressure but they produce too many adverse effects to be a first choice. Produce reflex tachycardia, a non-compensatory response to the sudden decrease in blood pressure caused by the drug o This will cause the heart to work harder and blood pressure to increase counteracting the effects of antihypertensive drugs. o Patients with coronary artery disease could experience acute angina attack o Sodium and water retention can be a serious side effect o Due to vasodilation the angiotensin released does not cause vasoconstriction but does stimulate the release of aldosterone, causing the kidneys to reabsorb sodium and water. Blood volume increases and raises blood pressure canceling the antihypertensive o A diuretic may be administered concurrently to prevent fluid retention
Chapter 28: Drugs for Angina Pectoris and
Myocardial Infarction
Should the blood supply to the myocardium become compromised, cardiovascular function may become impaired, resulting in angina pectoris, myocardial infarction, and possibly death.
Pathogenesis of Coronary Artery Disease: The heart is the hardest working organ in the body, functioning continually during both activity and rest. Coronary Artery Disease (CAD) is the leading cause of death in the United States. The primary defining characteristic of CAD is narrowing or occlusion of a coronary artery. The most common etiology of CAD in adults is atherosclerosis, the presence of plaque- a fatty fibrous material within the wall of the coronary arteries.
Angina Pectoris
Pharmacologic Management of Angina Successful pharmacotherapy should improve exercise tolerance and allow the patient routinely to participate in activities of daily living. There are two categories of antianginal medication o Those that terminate acute angina attacks o Those that decrease the frequency of angina episode The primary way is to reduce the myocardial demand for oxygen. Achieved by: o Slowing the heart rate o Dilating the veins so the heart receives less blood (reduced preload) o Causing the heart to contract with less force (reduced contractility) o Lowering blood pressure, thus offering the heart less resistance when ejecting blood from its chambers (reduced afterload) There are three primary classes: o Organic nitrates Drug of choice for terminating pain o Beta adrenergic antagonists first-line for preventing angina o Calcium channel blockers used when beta blockers aren’t tolerated
Treating Angina with Organic Nitrates Nitric acid a potent vasodilator, in vascular smooth muscle They have the ability to relax both the arterial and venous smooth muscle. o Dilation of veins reduces the amount of blood returning to the heart (preload) o With less blood for the ventricles to pump out cardiac output is reduced and the workload on the heart is decreased thereby lowering myocardial oxygen demand. They have the ability to dilate the coronary arteries. Tolerance is common and a potentially serious problem with the long-acting organic nitrates Daily use often warrants a nitrate free interval. o Transdermal patches should be removed for 6-12 hours a day and oral nitrates should only be dosed to cover a duration of 12-18hours a day.
Treating Angina with Beta Blockers Reduce the cardiac workload by slowing the heart rate and reducing contractility. Tolerance does NOT develop These are a good choice for people who have both HTN and CAD because of their antihypertensive action. o They reduce the incidence of MI They are the preferred drug for prophylaxis of stable angina.
Treating Angina with Calcium Channel Blockers Used in patient with whom initial treatment with beta blockers was unsuccessful. CCB are used for HTN and dysrhythmias Relax the arteriolar smooth muscle, thus lowering blood pressure
The reduction in afterload decreases myocardial oxygen demand. Some also slow conduction velocity through the heart, decreasing rate and contributing to the cardiac workload. They can dilate the coronary arteries and bring more oxygen into the myocardium. o Preferred for Variant angina
Myocardial Infarction (MI) Responsible for a substantial number of deaths o Some die before reaching a medical facility and some die within 48hrs following MI
Diagnosis of Acute Coronary Syndrome General term used to describe conditions in which there is a sudden reduced blood flow to the heart. The two-condition associated are o Unstable angina N-Nitrogen O- Oxygen M- Morphine A -Aspirin o Myocardial infarction The most sensitive and effective biomarker is troponin (protein found in cardiac muscle) ECG can give important clues to the extent and location of the MI When ST segment is elevated (STEMI) the MI must be treated aggressively mortality is high Treatment is different and can be life threatening. MI treatment is: o Restore blood supply to the damaged myocardium as quickly as possible through the use of thrombolytics or PCI o Reduce myocardial oxygen demand with organic nitrates, beta blockers, or angiotensin-converting enzymes (ACE) inhibitors to prevent additional infarctions o Control or prevent MI associated dysrhythmias with beta blockers or other antidysrhythmic o Reduce post MI mortality with aspirin, beta blockers, and ACE inhibitors. o Manage severe MI pain and associated anxiety with narcotic analgesics o Prevent enlargement of the thrombus with anticoagulants and antiplatelet drugs.
Management of Myocardial Infarction
Treating Myocardial Infarction with Thrombolytics (reteplase/Alteplase) Thrombolytic therapy is administered to dissolve clots obstructing the coronary arteries, thus restoring circulation to the myocardium.
Pharm II EXAM 2 Deeper dive
Course: Pharmacology II (NUR 354)
University: Arizona College of Nursing
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