Flashcards in Antihypertensive Meds Deck (38):
What is the definition of stage I hypertension?
SBP btw 140-159
DBP btw 90-99
What is the definition of stage 2 hypertension?
SBP over 160; DBP over 100
What are the 5 potential targets for antihypertensive therapy?
1. Heart (decr. contractility and HR)
2. Arteries/arterioles (decr. TPR)
3. Veins (incr. capacitance, decr. preload)
4.Kidneys (decr. fluid)
5. CNS (regulatory systems)
What class of drug is frequently the first line antihypertensive drug?
What is the general treatment goal for hypertension? What if the pt is diabetic?
diabetic goal: 130/90
Diuretics: what do they all have in common? advantages?
all promote Na and H2O loss
good for elderly, those w chronic renal failure and CHF
good for combo therapy
What is a prototypical loop diuretic?
How do loop diuretics work?
inhibition of the Na-K-2Cl cotransporter in the thick ascending limb (the countercurrent multiplier. this keeps more fluid in the tubule --> more water lost in urine
most are short acting
remember, example of loop diuretic is lasix/furosimide
How do thiazide diuretics work?
inhibit the Na-Cl cotransporter in the distal convoluted tubule. promotes sodium loss. relatively long duration.
What do diuretics of the collecting tubule do?
aka potassium-sparing diuretics
act on the principal cells of the late DCT, collecting tubule and collecting duct.
What are the three key side effects of loop diuretics?
impaired glucose tolerance
What are four main side effects of thiazide diuretics?
imparied glucose tolerance
What are two side effects of potassium sparing/colleting tubule diuretics?
hyperkalemia and gynecomastia
describe the renin/angiotensin cascade.
angiotensinogen converted to angiotensin I by renin from juxtoglomerular cells in kindey that detect low bp.
angiotensin I converted to angiotensin II by ACE (angiotensin converting enzyme)
angiotensin II is a potent chemical that raises bp. these effects are mediated by angiotensin II receptors.
What are the main effects of ACE inhibitors?
decr. angiotensin II-mediated vasoconstriction and resistance. little effect on heart (angiotensin II generated by methods that don't use ACE)
What are some long-term effects of ACE inhibitors?
decr. NE release from peripheral nerves
decr. aldo secretion (less Na and water retention)
incr. renal blood flow (and are sometimes renal protective)
incr. vasodilatory prostaglandins
What is the suffix for an ACE inhibitor drug?
What are some benefits of ACE inhibitors and ARBs?
BP reduction, less LV hypertrophy, less afterload for pts with CHF, good for remodeling after MI, slower progression of DM nephropathy
What are two side effects sometimes seen with ACE inhibitors?
What are the main contraindications for ACE inhibitors and ARBs?
major renal problems (renal artery stenosis, severe renal insufficiency)
What are ARBs?
stand for angiotensin receptor blockers
the are competitive antagonists of angiotensin II at AT1 receptors.
What is the deal with non-selective alpha blockers? What is the main example? How are they used?
PBZ (pnehoxybenzamine) is the main non-selective alpha blocker
it is a noncompetitive oral drug
lots of side effects: basically only used for phenochromocytoma
What is the deal with selective alpha 1 blockers? side effects?
like other classes, they do reduce bp. may also help with cholesterol profile, incr. insulin sensitivity
side effects: very rapid first dose response. can cause syncope, ED
What are the four net effects of beta blockers?
1. decr. contractility
2. decr. HR
3. decr. renin/angiotensin/aldo
4. decr. cardiac output
What is the suffix for a beta blocker?
What are potential benefits of beta blockers? Drawbacks?
benefits: may help with migranes, tremors, situational anxiety, alcohol withdrawal
drawbacks: fatigue, depression, erectile dysfunction
What are some beneficial properites of beta blockers?
helps with PVC
decr Vfib and sudden cardiac death after MI
What are some adverse effects of beta blockers?
Heart block, rebound hypertension, hypoglycemia in DM, asthma, fatigue, ED, depression, glucose intolerance, worse lipid profile
What are CCBs?
calcium channel blockers
inhibit entry of calcium thru channels
relatively selective (for L type Ca channels, which let in Ca in smooth/cardiac muscle over T type which control nodal deopl)
inhibit vascular smooth muscle contraction--> vasodilation, decr. rate/contractility
What are the electrophysiological effects of CCBs (slope of diastolic depol, threshold potential for AP, AP amplitude, duration of AP, AV node refractory period)
threshold potential: incr.
AP amplitude: decr.
duration of AP: decr.
AV node refractory period: incr.
What are some other uses of CCBs? Drawbacks?
arrhythmias (class IV)
drawback: worsens CHF, hypotension, bradycardia, constipation, pedal edema, fatigue,
What is clonidine (class, type)? Side effects
side effects often prohibitive: fatigue, dry mouth, rebound hyertension with non-compliance, constipation
What is the only antihypertensive that is approved for use in pregnant women? Class?
alpha methyl DOPA
centrally acting antihypertensive
What is hydralazine (class)? What are the 2 biggest side effects?
may elicit reflex hypertension, SLE-like side effect (lupus)
What is minoxidil (class/bullet point MOA)? Sides?
direct vasodilator: K channel opener
sides: LV hypertrophy, hair growth (main ingrediant in rogaine)
What is the suffix for an ARB?
What is the use of sodium nitropursside? Main side effect/concern?
immediate onset short duration IV antihypertensive
main concern is cyanide toxicity