Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
49 Cards in this Set
- Front
- Back
components of the circulatory system
|
-arteries transport blood to tissues under high pressure
-arterioles control valves that regulate local blood flow -capillaries are sites for exchange of oxygen, fluid, nutrients, hormones, wastes, etc. -venules collect blood from capillaries -veins transport blood back to the heart |
|
mechanisms that ensure venous return
|
1) negative pressure in right atrium helps "suck" blood towards the heart
2) smooth muscle constriction in venous wall increases venous pressure 3) most important--combination of venous valves and skeletal muscle contraction creates a "VENOUS PUMP" |
|
primary (essential) hypertension
|
-no identifiable cause
-chronic and progressive -treated but not cured |
|
secondary hypertension
|
-identifiable cause
-possible to treat the cause directly -some individuals can actually be cured |
|
consequences of HTN
|
-heart disease such as heart failure, MI, and angina pectoris
-kidney disease -stroke |
|
antiHTNsive drug therapy
|
-dosage should start low and gradually increase
-lack of adherence is major cause of treatment failure -usually no symptoms -slow progression -treatment is complex and sometimes expensive |
|
METHYLDOPA
|
-drug of choice for pregnant women
-HTN most common complication of pregnancy -chronic hypertension -preeclampsia and eclampsia |
|
RAAS drugs
|
-angiotensin-converting enzyme inhibitors (ACE inhibitors)
-angiotensin II receptor blockers (ARBs) -aldosterone antagonists |
|
ACEI mechanism of action
|
-reduces levels of angiotensin II by inhibition of ACE
-increases level of bradykinin through inhibition of kinase II -vasodilation and blood volume reduction through effects on kidneys |
|
ACEI pharmacokinetics
|
-almost always taken orally (except for Enalaprilat)
-almost all can be administered with food (except for captopril and moexipril) -administered once or twice a day (except for captopril, which is bid or tid) -undergo conversion to active form in small intestine and liver (except for lisinopril) -all excreted renally |
|
ACEI indications
|
-HTN
-heart failure -MI -diabetic neuropathy |
|
RAMIPRIL (Altace)
|
ONLY ACEI approved for prevention of MI, stroke, and death in high-risk cardiac patients
|
|
ACEI side effects
|
-"first dose hypotension"
-COUGH -hyperkalemia -renal failure -angioedema (very rare) -fetal injury (2nd and 3rd trimesters) |
|
ACEI drug interactions
|
-diuretics
-antihypertensives -drugs that raise potassium -lithium -NSAIDs |
|
angiotensin II receptor blockers (ARBs)
|
-decrease influence of angiotensin II by blocking its action, not its production (like ACEIs)
-DO NOT cause cough or hyperkalemia -not interchangeable with ACEIs -usually given to patients who don't tolerate ACEIs |
|
ARB indications and mechanism of action
|
indications:
-HTN -MI -diabetic neuropathy -heart failure mech of axn: vasodilation due to angiotensin II inhibition, less aldosterone so more excretion of water and sodium |
|
ARB pharmacokinetics
|
all taken orally
|
|
LOSARTAN (Cozaar)
|
stroke prevention
|
|
ARB side effects and drug interactions
|
side effects:
-angioedema -fetal harm -renal failure drug interactions: -antihypertensives |
|
EPLERENONE
|
-aldosterone antagonist
-approved in 2002 -indications: HTN and heart failure -administered orally -generally well-tolerated (greatest risk is hyperkalemia) |
|
EPLERENONE drug interactions
|
-erythromycin
-verapamil -fluconazole -ketaconazole |
|
SPIRONOLACTONE
|
-much older than eplerenone
-binds with steroid hormone receptor sites--interferes with hormones |
|
SPIRONOLACTONE side effects
|
-HYPERKALEMIA
-gynecomastia -menstrual irregularities -impotence -hirsutism -deepening of voice |
|
sympatholytics (antiadrenergic drugs)
|
suppress the influence of the sympathetic nervous system on heart, blood vessels, & other structures
|
|
categories of sympatholytics
|
1) beta-adrenergic blockers
2) alpha1 blockers 3) alpha/beta blockers 4) centrally-acting alpha2 agonists 5) adrenergic neuron blockers |
|
beta-adrenergic blockers
|
-less effective in blacks
-most widely-used antihypertensives -exact mechanism of action is unknown |
|
beta-adrenergic blocker mechanism of action
|
-block cardiac beta1 receptors, which causes decreased heart rate and contractility
-suppress reflex tachycardia caused by vasodilators -block beta1 receptors in kidneys so less renin is produced--inhibits RAAS -reduce peripheral vascular resistance |
|
alpha1 blockers
|
-not first-line
-block vascular alpha1 receptors, preventing sympathetically-mediated vasoconstriction -e.g. terazosin, doxazosin, -orthostatic hypotension |
|
alpha/beta blockers
|
-e.g. carvedilol, labetalol
-promote dilation of arteries and veins; decrease heart rate and contractility -can exacerbate asthma and postural hypotension |
|
centrally-acting alpha2 agonists
|
-act in brainstem to reduce sympathetic outflow to heart and blood vessels
-cause vasodilation and reduced cardiac output -SEs: dry mouth and sedation |
|
types of centrally-acting alpha2 agonists
|
-methyldopa (pregnancy)
-clonidine, which can cause rebound hypertension if abruptly discontinued |
|
adrenergic neuron blockers
|
inhibit NE release and decrease sympathetic stimulation of heart and blood vessels
-guanethidine and guanadrel can cause severe orthostatic hypotension -reserpine can cause depression |
|
calcium channel blockers (CCBs)
|
-prevent calcium ions from entering cells, preventing contraction
-help regulate myocardium, SA and AV nodes, beta1 adrenergic receptors -AKA calcium antagonists, slow channel blockers |
|
VERAPAMIL and DILTIAZEM
|
(class IV)
BLOCK CALCIUM CHANNELS AT: 1) peripheral arterioles - dilation and reduction in arterial pressure 2) cardiac arteries and arterioles - increased coronary perfusion 3) SA node - negative chronotropic 4) AV node - decreased AV node conduction 5) myocardium - negative inotropic |
|
VERAPAMIL and DILTIAZEM pharmacokinetics
|
-administered orally or IV
-well absorbed orally, but hepatic metabolism preserves only 20% of dose -effects begin in 30 minutes and peak in 5 hours -elimination is primarily hepatic |
|
VERAPAMIL and DILTIAZEM indications
|
(class IV)
-angina pectoris -essential HTN -supraventricular dysrhythmias such as afib, atrial flutter, and SVT |
|
VERAPAMIL and DILTIAZEM side effects, drug interactions, and toxicity
|
(class IV)
side effects: constipation (verapamil) and cardiac effects, but generally well-tolerated drug interactions: digoxin, beta-adrenergic _______ toxicity: sever hypotension treatment of toxicity: IV calcium gluconate and IV norepinephrine |
|
NIFEDIPINE
|
-very little blockage of calcium channels
-vasodilation and reflex cardiac stimulation -angina and HTN -high doses of rapid-acting can be very dangerous |
|
NIFEDIPINE side effects, drug interactions, toxicity
|
side effects:
-dizziness -flushing -headache -peripheral edema -gingival hyperplasia drug interactions: -beta adrenergic blockers toxicity: loses selectivity, so increased doses can affect heart and blood vessels |
|
vasodilators
|
-differ from one another based on which blood vessels they act on
-selectivity determines hemodynamic effects |
|
vasodilator indications
|
-essential HTN
-hypertensive crisis -angina pectoris -heart failure -MI -PVD -pulmonary arterial hypertension -production of controlled hypotension during surgery |
|
adverse effects related to vasodilation
|
-postural hypotension
-reflex tachycardia -expansion of blood volume |
|
HYDRALAZINE (Apresoline) indications and mechanism of action
|
indications:
-essential HTN -heart failure -hypertensive crisis mechanism of action: -selective dilation of arterioles (exact mech is unknown) |
|
HYDRALAZINE (Apresoline) side effects and drug interactions
|
side effects:
-reflex tachycardia -increased blood volume -systemic lupus erythematosus-like syndrome drug interactions: other antihypertensive agents |
|
MINOXIDIL (Loniten) indication and mechanism of action
|
indication: severe HTN
mechanism of action: selective dilation of arterioles |
|
MINOXIDIL (Loniten) side effects
|
reflex tachycardia
sodium and water retention hypertrichosis pericardial effusion |
|
SODIUM NITROPRUSSIDE (Nitropress)
|
-causes venous and arteriolar dilation
-fastest-acting antiHTNsive agent for HTNsive emergencies -given IV for immediate onset -side effects: excessive hypotension, cyanide poisoning, thiocyanate toxicity |
|
DIAZOXIDE (Hyperstat IV) indication and mechanism of action
|
indication: hypertensive emergency
mechanism of action: selective dilation of arterioles |
|
DIAZOXIDE (Hyperstat IV) side effects and drug interactions
|
side effects:
-reflex tachycardia -salt and water retention -hyperglycemia -hyperuricemia drug interactions: -diuretics -antihypertensive drugs |