pharmacology of CV system Flashcards
antihypertensive drugs
diuretics
sympatholytic drugs
vasodilators
inhibition of the renin-angiotensin system
calcium channel blockers
treatment of hyperlipidemia
diuretics
increase the formation and excretion of urine to decrease plasma fluid volume
thiazide diuretics
loop diuretics
potassium-sparing diuretics
adverse effects
thiazide diuretics
act on the early portion of the distal tubule of the nephron
inhibit sodium reabsorption
loop diuretics
act primarily on the ascending limb of the loop of henle
inhibit the reabsorption of sodium and chloride from the nephron
potassium-sparing diretics
prevent the secretion of potassium into the distal tubule
adverse effects of diuretics
fluid depletion and electrolyte imbalance
sympatholytic drugs
decrease sympathetic influence on the heart and/or peripheral vasculature
beta blockers
alpha blockers
presynaptic adrenergic inhibitors
centrally acting agents
ganglionic blockers
beta blockers
slow HR
reduce CO
produce general decrease in sympathetic tone
alpha blockers
decrease vascular resistance in vascular smooth muscle
presynaptic adrenergic inhibitors
depletion of norepinephrine from the presynaptic terminal decreases sympathetic-mediated excitation of the heart and peripheral vasculature
resulting in decreased BP
centrally acting agents
limit sympathetic activity at the brainstem vasomotor center
ganglionic blockers
block synaptic transmission at autonomic ganglia
decreasing systemic sympathetic activity
reducing BP
vasodilators
decreases peripheral vascular resistance
inhibition of renin-angiotensin system
angiotensin converting enzyme (ACE) inhibitors
angiotensin II blockers
ACE inhibitors
decrease the hypertensive effects of angiotensin II by limiting the production of angiotensin II
angiotensin II blockers
block receptor for angiotensin II
blocking effects
calcium channel blockers
limit calcium entry into vascular smooth muscle and cardiac muscle
decrease vascular smooth muscle contraction and myocardial force and rate of contraction
treatment of hyperlipidemia
focus on reducing atherogenic lipoproteins and increasing the beneficial HDLs
HMG-CoA reductase inhibitors (statins)
statins
decrease cholesterol production, especially in liver cells
lipitor
antithrombotic drugs
inhibit the function of platelets
aspirin
others reduce platelet-induced clotting
adverse effects –> increased risk of bleeding
aspirin
suppresses platelet aggregation by inhibiting the synthesis of prostaglandins and thromboxanes
thrombolytic drugs
facilitate the breakdown and dissolution of clots that have already formed
streptokinase and urokinase
anistreplase
reteplase and tenecteplase
adverse effects
streptokinase and urokinase
bring about the activation of plasmin, can be used to successfully resolve acute clot formation in coronary arteries and peripheral vessels
anistreplase
binds to fibrin, where it is chemically activated so that the streptokinase can modify plasminogen and initiate clot breakdown