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Pharm U4 Terms
Unit 4 terms
| Question | Answer |
|---|---|
| Heart failure | clinical syndrome; CO insufficient to meet metabolic demands of body; blood accumulates in heart, lungs, veins of lower extremities (congestion) which can cause clots, pulmonary edema, cardiac arrhythmias |
| Etiology of heart failure | anything that increases plasma volume to such a degree that end diastolic volume stretches the ventricular fibers beyond their optimum length; injury of heart begins cycle of failure by decreasing strength of cardiac contraction |
| Types of heart failure | systolic, diastolic, left-sided, right-sided, acute or chronic |
| Systolic dysfunction | caused by ischemic/idiopathic dilated cardiomyopathy; left vent can’t adequately contract/squeeze out contents, preload increases, SV decreases |
| Diastolic dysfunction | us. Caused by hypertensive, hypertrophic, or restrictive cardiomyopathy; vent relaxation/filling during diastole are impaired; atria & pulmonary vessel increase to cause pulmonary congestion, SV decreases |
| Left sided heart failure | left ventricular SV reduced, blood backs into left side of heart and pulmonary circ which increases pulmonary pressures; fluid overload leads to dyspnea; caused by hypertension, ischemia, or incompetent/stenotic mitral valve |
| Right sided heart failure | right ventricle can’t empty blood/backs up into it from pulmonary circ; either results in blood backing into systemic circulation to cause liver congestion, peripheral edema |
| Acute heart failure | occurs so rapidly body doesn’t have time to activate compensatory mechs to improve cardiac performance |
| Chronic heart failure | develops as a result of inadequate compensatory mechanisms that have been employed over time to improve CO |
| Compensatory mechanisms | activation of Symp NS, activation of RAAS, ventricular remodeling |
| Activation of symp NS compensatory response | body increases catecholamines to increase heart rate, myocardial contractility, and peripheral vasoconstriction |
| Renin-angiotensin-aldosterone system (RAAS) | kidney’s response to decreasing CO2; activation increases concentration of renin, angiotensin II, and aldosterone to increase vascular resistance & Na & H2O absorption |
| Ventricular remodeling | hypertrophy of myocytes; result of prolonged excess activation of the symp NS and RAAS; enlarged and abnormal myocytes can’t contract efficiently; heart muscle mass increases, pump performance impaired |
| Signs of heart failure | cardiomegaly (Hypertrophy), gallop rhythm, hepatomegaly, splenomegaly, peripheral edema, ascites |
| Right sided failure symptoms | anorexia, nausea, pain in upper right quadrant, oliguria during day, polyuria at night |
| Left sided failure (pulmonary congestion) | dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough and wheezing |
| Steps in treatment of chronic heart failure | reduce heart workload, restrict sodium, restrict water, give diuretics, give ACE inhibitors/angiotensin receptor blockers, give digitalis if needed, give beta blockers with stable failure, give vasodilators |
| Chronic heart failure drug therapy | involves use of cardiac glycosides, other positive inotropic agents, diuretics, vasodilator drugs, beta blockers, beta agonists, ACE inhibitors, angiotensin receptor blockers |
| Cardiac glycosides | inhibit NaKATPase pump (Na out, K in) thereby increasing IC Na which in turn releases large amounts of Ca; results in more forceful myocardial contraction, increase in CO, prolongs refractory pd. +ino, -chrono, -dromo |
| Digitalis glycoside toxicity symptoms | may appear as visual alterations i.e. green/yellow vision; very narrow therapeutic window, so toxicity is a danger |
| Digoxin (Lanoxin, Lanoxicaps) | Digitalis antibodies |
| Digitalization | process by which drug is administered PO or IV at doses and intervals that rapidly produce an effective blood level; then daily maintenance doses are lower to maintain a therapeutic level of drug in blood |
| Patient heart rate lower than 60 or higher than 100 | when to hold a dose of digoxin |
| Phosphodiesterase inhibitors | +inotropic; selectively inhibits phosphodiesterase type III, so more Ca becomes available for muscle contractions in heart, more vasodilation. Emergency only. |
| Beta blockers | use is based on idea that excessive tachycardia & adverse effects of high catecholamine lvls on heart lead to further heart failure; used in low doses since it can worsen heart failure if not used correctly |
| Vasodilators | nitrates that pool blood in extremities, thereby reducing blood return or preload and arterial vasodilators that decrease arterial resistance, reducing afterload |
| ACE inhibitors | for left vent systolic dysfunction; decrease peripheral vascular resistance (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance, and secretion of aldosterone; slow rate of vent dilation and delay heart failure onset |
| Antiotensin receptor agonists | produce similar effects to those of ACE inhibitors; clinical trials suggest use only in patients who are tolerant of ACE inhibitors |
| Diuretics | reduce blood volume and edema |
| Beta agonists | used as last resort for CHF to increase myocardial contractility |
| Cardiac dysrhythmias (arrhythmias) | any deviation from the normal rate or rhythm of the heartbeat |
| Disorders in cardiac electrophysiology | result from abnormality in automaticity or abnormality in impulse conduction, or conductivity, or both |
| Vaughn-williams drug classification | all drugs in this group have the ability to suppress automaticity; 4 groups |
| Group I of VW drug class | fast Na blockade in cardiac muscle resulting in increased refractory period; has three subgroups |
| Group IA of VW drug class | bind to Na channels, interfere w/ Na influx during action potential; depresses conduction velocity; widening of QRS complex, prolonged QT interval |
| Group IB of VW class | Na channel blockers; may increase/have no effect on conduction velocity; for acute dysrhythmias; if it works, indicative that damage is in left ventricle |
| Group IC of VW class | Na channel blockers; treats dysrhythmias and prevents supraventricular tachydysrhythmias |
| Group II of VW class—beta adrenergic blocking agents | bind with beta I receptors to block effects of excessive symp nerve activity; slows down heart; -olol drugs |
| Group III of VW | K channel blockers; prolongs effective refractory period by prolonging action potential; terminates dysrhythmias caused by reentry phenomenon |
| Group IV | Ca channel blockers; decrease automaticity in SA node, decrease conduction in AV junction; slows down heart. Prevents/treats ventricular dysrhythmias in pt not responding/tolerating other therapies |
| Adenosine | unclassified antidysrhythmic agent; slows AV node conduction, so slows heart |
| Hypertension (HTN) | persistant elevation of systolic BP > 140 mmHg or diastolic BP > 90 mmHg; diagnosis requires several BP measurements; classified as normal (120/80), pre (120-139/80-89), stage 1 (140-159/90-99), or stage 2 (>160/>100) |
| Primary, essential, idiopathic HTN etiology | 95% sue to unknown etiology; several theories, included hyperactive symp NS; RAAS, defect in natriuresis (Na retention), elevated IC Na |
| Secondary HTN etiology | 5% of cases attributable to secondary causes, i.e. renal disease, hyperaldosteronism, cushing’s, pheochromocytomia, narrowing of aorta, pregnancy |
| Hypertensions signs/symptoms | often no symptoms, “silent killer;” flushing, sweating, suboccipital pulsating headache in morning that improves throughout day, ventricular hypertrophy, oliguria, notcuria, or hematorua; epistaxis (nose bleeds), NV, visual disturbances |
| Baroreceptor reflex (adrenergic, rapid acting) | physiological control of BP; nerve endings in carotid arteries & aortic arch; respond to rapidly to changes in BP by sensing stretching |
| Renin angiotensin aldosterone mechanism (RAAS) | regulates BP by increasing/decreasing blood volume through kidney function; long acting; blood flow to kidneys reduced, renin release, angtiotensin I converted by ACE to angtiotensin II |
| Angiotensin II | most powerful vasoconstrictor in body; widespread peripheral vasoconstriction, which elevates BP |
| Nonpharmacologic treatment of HTN | lifestyle modifications; should be instituted in all patients with this diagnosis; stepped treatment approach. Wt reduction, low Na diet, stop smoking, stop drinking, manage stress, relax/exercise, lipid control |
| Pharmacologic therapy of HTN | instituted in patients with state II or higher of this diagnosis |
| Diuretics | most widely used anti-HTN agent; promote formation and excretion of urin resulting in loss of excess salt, water from body; decrease in volume depresses vascular reactivity to sympathetic stimulation, so lowers BP |
| Beta adrenergic agents | decrease CO and inhibit renin secretion, lowering BP |
| Alpha I adrenergic blocking agents | prevent NE from activating alpha I receptors on vascular smooth muscle, therefore blocking vasoconstriction, facilitating arteriolar dilation, lowering BP |
| Centrally acting alpha 2 adrenergic agonists | stimulate CNS alpha 2 receptors, decrease outflow of NE from brain to blood vessels & heart, lowers BP as result of lower CO, decreased heart rate, decreased peripheral vascular resistance; esp effective w/ diuretics |
| Centrally acting adrenergic inhibitors | act in variety of ways depending on agent to deplete stores of catecholamines in CNS |
| Angiotensin-converting enzyme (ACE) inhibitors | competitively block angtiotensin I converting enzyme necessary for conversion to angtiotensin II (vasoconstrictor); BP decreases, aldosterone release inhibited, resulting in decrease of Na and H20 reabsorption |
| ACE inhibitor side effect | dry, hacking cough; angioedema, hypotension |
| Angiotensin II receptor antagonists | block angiotensin II from binding w/ receptor sites, lowers BP by inhibiting peripheral vasoconstriction |
| Calcium channel blockers/calcium antagonists | inhibit Ca influx through slow Ca channels during membrane depolarization; leads to decrease in vasoconstriction, increase in vasodilation, decrease in BP; -ino, -chrono, -dromo |
| Calcium channel blockers/calcium antagonists | widely effected for most individuals; first line of choice; contraindicated in conduction disorders, CHF |
| Vasodilators | exert direct action on the smooth muscle walls of arterioles and veins, lowering peripheral resistance, BP; relax smooth muscle, increase vasodilation, decrease BP; used in emergencies |
| Ganglionic blocking agents | inhibition of transmission at Nicotinic I receptor sites in ganglia; potent nonselective antihypertensive agent; used in Emergencies only; decreases vasoconstriction, increase vasodilation, decrease BP |
| Aldosterone inhibitors (blockers) | aldosterone binds w/ mineralcoricoid receptors in epithelium; increases BP by inducing Na retention; this agent binds to mineralocorticoid receptors, blocking the effect of aldosterone |
| Renin inhibitors | blocks production of renin in kidneys; decreases vasoconstriction, increases vasodilation; decreases BP |
| Coronary artery disease (CAD)/aka angina pectoris | clinical syndrome result of atherosclerotic changes to coronary vasculature; decreases blood flow through vessels due to sclerosis/vasospasm; tissue ischema + pain due to decrease flow, angina occurs |
| Sclerosis | partial vessel obstruction |
| Ischemia | tissue damage |
| Myocardial infarction | heart attack |
| Etiology of coronary artery disease (cod) | hypertension, tobacco use, high cholesterol, diabetes mellitus, family history, sedentary lifestyle, oral contraceptive use, gender, obesity |
| Types of angina | exertional angina, unstable angina, variant angina |
| Exertional angina (classic, stable, or effort | pain usually associated w/ arteriosclerosis; attack precipitated by exertion/stress, eating; lasts about 15 min and disappears w/ rest or nitrates |
| Unstable angina (crescendo, preinfarction) | progressive form of angina; pain is more frequent, becomes more severe in time; may appear during rest, last longer, less relief w/ antianginal drugs; show signs/symptoms of MI or coronary failure |
| Variant angina (Prinzmetal’s or vasospastic) | occurs only at rest w/out usual precipitating factors; assoc. w/ spasms of coronary arteries (usually R artery); usually in women under 50, early morning, waking pt. from sleep |
| Signs and symptoms of coronary artery disease | very hard to diagnose; chest discomfort, tightness, squeezing, burning, pressure; usually discomfort behind/slightly left of midsternum; radiates left shoulder/upper arm, lower jaw, back of neck; lasts about 15 min. |
| Management/treatment of coronary artery disease acute attack | sublingual/buccal spray nitroglycerin; dose can be repeated 3 times at 5 minute intervals; pain unrelieved after 3 doses is unstable and should be evaluated in ER |
| Prevention of future acute CAD attacks | reduction of risk factors (weight, smoking, exercise); lowering LDL cholesterol; prevention of blood clots (aspirin) |
| IV in hospital for emergencies; lingual aerosol form | administrations of nitroglycerin |
| Relief of exertional angina, prophylactic treatment of exertional angina | uses of nitroglycerin |
| Nitroglycerin side effects | flushing, dizziness, headache, decrease in BP, contraindicated in pt taking Viagra/ED drugs; short shelf life (2 mos) |
| Nitroglycerin usage instructions | angina; sit down, place NTG tab under tongue; allow to dissolve w/out swallowing; relief should occur w/in 5 min; repeat if unrelieved; if unrelieved at that point, seek medical assistance |
| Beta-adrenergic blocking agents | indicated for long-term management of angina by increasing work capacity/exercise tolerance; used in combo w/ nitrates if more than one drug required to control angina |
| Beta-adrenergic blocking agents | antagonize stimulation of sympathetic nervous system of Beta-1 receptors, increasing HR, force of contractions, oxygen consumption |
| Calcium channel blockers (calcium antagonists) | newest class of drugs to treat exertional angina; drug of choice for vasospastic angina; can be used for exertional angina, too |
| Calcium channel blockers (calcium antagonists) | contraction of vascular smooth muscle dependent on Ca influx; agent inhibits influx of Ca, causing vasodilation; decreases venous return, decreases BP, which decreases cardiac work & O2 consumption |
| Acute coronary syndrome | number of clinical presentations that result from progressive atherosclerosis |
| Ischemia | the cellular malfunction of tissues of heart deprived of oxygen; can progress to cell injury and then becomes infarction |
| Infarction | from ischemia to cell injury, if damage still continues without relief, cell death occurs. |
| Penumbra | concept in which ischemia and infarction overlap each other; some cells die, while new cells suffer from ischemia |
| Three I’s of an acute coronary event | myocardial ischemia, injury, infarction |
| Immediate general treatment for acute coronary syndromes | MONA—morphine, oxygen, nitroglycerin SL, ASA; morphine only given after nitro |
| Hematocrit | packed call volume of RBCs; expressed as percentage of total blood volume |
| Blood proteins | albumins, globulins, fibrinogen |
| Albumin | blood protein; responsible for osmotic pressure gradient produced at capillary membrane which prevents plasma fluid from leaving capillaries to enter interstitial space |
| Globulins | blood protein; alpha, beta, gamma; gamma involved in humoral immunity; alpha and beta involved in transport of substances in blood |
| Fibrinogen | plasma protein converted to fibrin by thrombin in presence of Ca ions; necessary for coagulation |
| Thromboplastin produced; thromboplastin converts prothrombin to thrombin; thrombin converts fibrinogen to fibrin | process of coagulation |
| Two mechanisms of thromboplastin production | intrinsic and extrinsic |
| Intrinsic mechanism | mechanism of thromboplastin production; requires many clotting factors and platelets to stimulate production |
| Extrinsic mechanism | mechanisms of thromboplastin production; requires factor VII and tissue extract, a substance released from injured cells |
| Anticoagulants | prevent fibrin clots; heparin—parenteral—IV, SC—in USP units; comes from lungs and GI tract of cattle, pigs; cannot be given orally b/c would be destroyed by gastric acid |
| Anticoagulants | inhibit function of preformed clotting factors; inhibits thrombin activity and thromboplastin activity, thereby preventing clots from forming |
| Anticoagulants | used to prevent thrombi and emboli which might lead to CVA, MI, DVT, or PE; clot suppression prior to blood transfusions and during open heart surgery; clot prevention in indwelling devices; side effect—bleeding, hemorrhage |
| Coumarin derivatives | oral anticoagulants; prevent synthesis of normal clotting factors; discovered as product of spoiled sweet clover |
| Thrombolytic agents | used to treat acute thromboembolic disorders; dissolve clots, used in hospital setting only, “clot busters” |
| Thrombolytic agents | convert plasminogen in blood to plasmin which in turn dissolves fibrin clots wherever they exist; used for AMI, arterial thrombosis, DVT, occlusion of shunts/catheters, and PE |
| Antihemophilic agents | used to treat hemophilia; administration of factor VIII for hemostasis and clotting |
| Hemophilia | hereditary disorder caused by deficiency of one or more plasma protein clotting factors; leads to persistent and uncontrollable hemorrhage after even minor injury |
| Antiplatelet agents | block specific inhibitors of platelet aggregation; used for prevention of arterial thrombi; may be used w/ coumarin anticoagulants; infrequent and mild side effects |
| Antifibrinolytic (hemostatic/coagulant) agents | hasten clots formation to reduce bleeding; purpose of these agents is to control rapid loss of blood; prevents lysis of fibrin; treats excessive bleeding after surgery/massive trauma |
| Anemia | symptom of abnormally low RBC count, quality of hemoglobin, or volume of packed cells which results in a decreased ability of RBCs to carry O2; classified on basis of RBC morphology and amount of pigment they contain; most are deficiency anemias |
| Anemia classifications | RBC morphology—microcytic, macrocytic, normocytic; amount of pigment—hypochromic, normochromic; etiology |
| Antianemic agents | treating deficiency of essential and vitamins and minerals in diet |
| Cyanocobalamin (vitamin B12) deficiency | caused by dietary b12 deficiency, or lack of ability to synthesize intrinsic factor |
| Folic acid deficiency | essential for cell growth, reproduction; available in green leafy veggies and meat |
| Aplastic anemia | anemia caused by defective functioning of the blood-forming organs (blood marrow) |
| Antihyperlipidemic drugs | treatment of hyperlipidemia; treatment based on patient’s cholesterol level and presence of CAD or other risk factors |
| Hyperlipidemia | metablic disorder characterized by increased concentrations of cholesterol & triglycerides |
| VLDLs (very low density lipidproteins | contain large amount of triglycerides and 20 to 30% cholesterol; large and not believed to be involved in atherosclerosis; eventually converted to LDLs |
| LDLs (low-density lipoproteins) | contain major portion of cholesterol in blood, considered most harmful; carry 60-70% total blood cholesterol; elevated level suggest individual have greater chance of developing artherosclerosis |
| HDLs (high density lipoproteins) | smallest, most dense lipoproteins which transport cholesterol from peripheral cells to liver where it is metabolized and excreted; high levels are considered beneficial; prevent accumulation of lipid in arterial walls |
| Bile acid sequestrants | antihyperlipidemic agent; bind bile acids (emulsifiers of fat) in intestine, preventing their absorption, produce insoluble complex excreted; liver compensates by increasing oxidation of cholesterol |
| HMG-CoA enzyme inhibitors | antihyperlipidemic agent; most effective in lowering LDL lvls; competitive inhibitors of HMG-CoA reductase, enzyme necessary for cholesterol biosynthesis (liver enzymes) |
| Cholesterol absorption inhibitor | antihyperlipidemic agent; works in lining of small intestine, inhibits absorption of cholesterol, but does not inhibit cholesterol synthesis; decreases amount of intestinal cholesterol available to liver |
| antihyperlipidemic agent side effects | rhabdomyolysis, hepatotoxicity |
| agents that alter lipid and lipoprotein metabolism | Niacin, fibric acid derivatives, isomer of thyroxine |
| Diuretics | agent interferes with reabsorption of Na, and therefore water, so decreases urine volume |
| Carbonic anhydrase inhibitors (proximal tubule diuretics) | proximal tubule; reduce formation of H and in turn block Na and H20 reabsorption; used to treat glaucoma, edema, seizures, high-altitude sickness |
| Osmotic diuretics | proximal tubules; increase osmotic pressure of glomerular filtrate and pulls water into blood vessels and nephrons producing rapid diuresis; reduce intraocular pressure before/after surgery; interrupt acute attack of glaucoma |
| Loop diuretics | loop of henle diuretics; block reabsorption of Cl and secondarily Na; treats edema associated with CHF, cirrhosis, renal disease, hypertension, acute pulmonary edema; effects—postural hypotension, blurred vision, hypokalemia |
| Thiazide and thiazide type diuretics | inhibit tubular reabsorption of Na and Cl ions; treats hypertension, edema associated w/ CHF, cirrhosis, renal impairment |
| Potassium sparing diuretics | in distal tubule, inhibit reabsorption of Na ions in exchange for K and H ions; prevention and treatment of hypokalemia, edema, hypertension |
| ADH antagonists | inhibit effects of ADH in collecting tubule; investigational only |
Created by:
mbtrimm
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