Chapter 4 Cardiovascular and hematology drugs --- general + diuretics/presynpatic adrenergic inhibitors Flashcards
Heart failure
- the heart no longer pum enough blood to meet metabolic demands of body
common cause:
myocardial injury d/t
1) ischemia
2) inflammation
3) chronic inflammation
Angina
- chest pain
- heart’s way of signalling that some of its cell are not getting enough o2 (too little blood flow)
Myocardial infarction happens when o2 started areas of the heart begin dying
Diuretics
- reduce blood pressure and edema by inc urine output
- all diuretics inc water and na+ secretion (but effect of diuretics vary depending on mechanism of action
thiazide diuretics
- inhibit na+ and cl- reabsorption in distal tubule (result in mild diuresis)
- POTASSIUM needed d/t k+ wasting effects
Strategies for HTN
1) diuretics
2) clonidine (a2 receptor agonist, clonidine inihibits further release of sympathetic agonist, NE, and inhibits sympathetic outflow from the brain)
3) atenolol (b1 adrenergic antagonist — reduces HR and myocardial work)
4) prazosin (blocks a1 adrenergic receptors causing vasodilation)
5) nifdeipine (blocks ca++ entry into smooth muscle cells of arterial walls, preventing contraction)
6) hydralazine (relaxes arterioles)
7) captopril (reduce production of angiotensin II – causing vasodilation)
goals — reduce volume overload, reduce sympathetic outflow, block adrenergic receptors, dilate vessels
Strategies for angina
Stable:
1) nitroglycerin – reduce preload by venodilation (markedly reduce venous pressure, venous return to the heart, and cardiac filling pressures
2) atenolol - decreases myocardial work (b1 antagonist)
3) ditilazem (dec BP via vasodilation, by blocking calcium entry + decrease HR => result in dec o2 demand and consumption
Unstable
1) beta blockers - reduce HR and myocardial work
2) aspirin - prevent platelet aggregation in myocardial arteries
3) heparin - inhibit clotting in myocardial arteries
4) nitroglycerin - reduce preload
5) eptifibatide or tirofiban — inhibit platelet aggregation
goals - reduce work of heart and improve cardiac circulation
strategies for myocardial infarction
goal —- reperfuse ischemic tissue
1) streptokinase – converts plasminogen to plasmin (it can digest fibrin and fibrinogen, thus dissolving clots)
2) antianginal agents (nitroglycerin?… not nifedipine which is dangerous for MI)
strategies for heart failure
goal – reduce workload + improve myocardial contractility
1) diuretics (decrease blood volume)
2) natrecor (nesiritide), a BNP analog causes naturesis (process of sodium excretion in the urine through the action of the kidneys), decrease preload and improve cardiac contractility
3) captopril (vasodilation)
4) atenolol (b blocker) — reduce HR and workload
5) nitroglycerin — reduce venous tone => dec preload (also dilates coronary arteries, enchancing blood delivery to heart)
6) hydralyzine and nitroprusside (relax arterioles)
7) diogxin (inc ca++ influx into myocardial cells)
8) amrinone (inhibits cAMP degradation — cAMP is a biochemical messenger that stimulates the heart
9) dobutamine (increase cAMP production by stimulating b1 adrenergic receptors
strategies for arrhythmias
goal – restore synchronous myocardial contraction
table 4.7 A/B
strategies for vascular occulsion
goals — prevent coagulation, prevent platelet aggregation, destory clots that already formed
1) warfarin, heparin
2) direct thrombin inhibitors (bivalirudin)
3) aspirin
4) thienopyridines (clopidogrel)
5) GP IIb/IIa inhibitors (abciximab)
6) tPA
loop diuretics
- more powerful than thiazides and must be used cautiously to avoid dehydration
- may cause hypokalemia, follow this level closely
potassium sparing diuretics
- enhance na+ and h2o excretion while retaining potassium
osmotic diuretics
- draw water into the urine, w/o interfering with ion secretion or absroption in the kidney
o
antiadrenergics
- inc BP by stimulating the heart (b1) and/or constricting peripheral blood vessels (a1 receptors)
- central — prevent sympathetic (adrenergic) outflow from brain by activating inhibitory a2 receptors [parasympathetic predominance]
- peripheral — prevent NE release from peripheral nerve terminals (e.g. such as ones that terminate on the heart); depleting NE stores in nerve terminals
- alpha and beta blockers — compete with endogenous agonists for adrenergic receptors // antagonist occupation of a1 receptors l/t vasoconstriction and occupation of b1 receptors prevents adrenergic stimulation of the heart
selective a1 or b1 blockers replacing nonspecific d/t fewer undesirable effects
* several b blockers have intrinsic sympathomimetic activity (act as weak agonists at some adrnergic receptor)
* these drugs stiulate b2 receptors, which reduces likelihood of rebound HTN (sympathetic reflex to fall in blood pressure) b/c b2 receptors dilate large central arteries which provide a reservoir for blood
hydrochlorothiazide (oretic)
thiazide diuretic
- inhibit na+/cl- reabsorption in distal tube
- loss of K+, na+, and cl- l/t inc urine output
- sodium loss l/t decreased GFR
indication:
* ideal start pt for HTN, chronic edema, idiopathic hypercalcuria
effects
1) hypokalemia
2) hyponatremia
3) hyperglycemia (low potassium, secreted a lot ===> responsible for decreased insulin secretion and/or reduced insulin sensitivity)
4) hyperuricemia (elevated uric) [increase urate reabsorption in the proximal tubule]
5) hypercalcemia (increase renal tubular reabsorption of calcium)
5) oliguria (abnormally small amount of urine)
6) anuria (failure of kidney to produce urine)
7) weakness
8) decreased placental flow
9) sulfonamide allergy
10) GI distress
PO
contraindication
* pregnant women (unless have pathogenic edema)
* anuria
interaction
* inc toxicity of digitalis or lithium
* hypokalemia w/ corticosteroids or ACTH (seceret more K+)
* orthostatic hypotension w/ alcohol, barbiturates or w/ narcotics
* decreases effects of vasopressors
