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Pharmacology > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

chlorthalidone

A
  • thiazide diuretic
  • distal convoluted tubule: Na/Cl cotransporter; also increases Ca reabsorption
  • 1st line therapy
  • high doses–>more diuresis–> more side effects and not greater at lowering BP
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2
Q

hydrochlorothiazide

A
  • thiazide diuretic
  • distal convoluted tubule: Na/Cl cotransporter; also increases Ca reabsorption
  • 1st line therapy

-high doses–>more diuresis–> more side effects and not greater at lowering BP
(just like chlorthalidone)

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3
Q

furosemide

A
  • loop diuretic
  • loop of henle: inhibits Na/K Cl- transporters
  • pts with reduced renal function; in severe htn when drugs that retain Na are being used
  • short-half-life; don’t work as well as equally potent thiazide dose
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4
Q

ethacrynic acid

A
  • loop diuretic
  • loop of henle: inhibits Na/K Cl- transporters
  • pts with reduced renal function; in severe htn when drugs that retain Na are being used
  • short-half-life; don’t work as well as equally potent thiazide dose

(just like furosemide)

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5
Q

triamterene

A
  • potassium sparing diuretic
  • collecting duct: Na+ channel blocker
  • 2nd line drug; to counteract K+ loss with the loop and thiazide diuretics
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6
Q

amiloride

A
  • potassium sparing diuretic
  • collecting duct: Na+ channel blocker
  • 2nd line drug; to counteract K+ loss with the loop and thiazide diuretics
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7
Q

spirinolactone

A
  • aldosterone antagonist
  • inhibits aldosterone–>diuresis
  • 2nd line drug; to counteract K+ loss with the loop and thiazide diuretics
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8
Q

antihypertensive actions of diuretics: acute effect vs. chronic effect

A

acute: increase Na+ and H2O excretion by kidney–>decrease EC and plasma volume–>decrease preload and CO
chronic: 6-8 wks–>plasma volume and CO return to previous values–> decreased BP due to decreased TPR

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9
Q

verapamil

A
  • non-DHP calcium channel blocker
  • block L-type Ca channels; decreases TPR in smooth m. cell arterioles and can act on heart: decrease HR and CO
  • 1st line therapy, use long acting
  • sinus brady, AV block, exacerbation of HF or pulmonary edema, constipation (due to decreased in sm. m contractility)
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10
Q

diltiazem

A

-non-DHP calcium channel blocker

  • block L-type Ca channels; intermediate effect btw. DHP and verapamil (decrease TPR, and some effect of decreased CO and HR)
  • 1st line therapy, use long acting

-sinus brady, AV block, exacerbation of HF or pulmonary edema, constipation (due to decreased in sm. m contractility)

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11
Q

nifedipine, amlodipine- anything ending in “dipine”

A
  • dihydropiridines
  • block L-type Ca2+ channels: vasodilation–> decrease TPR (does NOT act on heart like non-DHPs)
  • 1st line therapy, use long acting
  • 1st week of therapy: reflex tachycardia, vasodilatory side effects (most vasoeffective): flushing, headache, dizziness, peripheral edema
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12
Q

enalapril, lisinopril, anything ending in “pril”

A
  • ACE inhibitors
  • acts on ACE to decrease Ang II (vasoconstrictor) and increase bradykinin (vasodilator)–>dilates arterioles–>decrease TPR (small effect on HR, CO, and blood volume)
  • 1st line therapy; use in acute and post-MI (reduced mortality), 1st line for heart failure, diabetic and non-diabetic nephropathy (renoprotective)
  • DO NOT use in pts who have functional renal insufficiency due to predisposing conditions: microvascular renal disease, renal artery stenosis, solitary kidney–>reduction in renal blood flow or perfusion pressure–>impairs GFR–>renal insufficiency/failure
  • adverse effects: hypotension, hyperkalemia, hematologic effects, lost of taste/metallic taste, skin rash, angioedema, cough, TERATOGEN
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13
Q

losartan, valsartan, anything ending in “sartan”

A
  • Angiotensin II receptor blocker (ARBs)
  • prevents Ang II from binding to receptor–>dilates arterioles–> decrease TPR (bradykinin not affected)
  • 1st line therapy; much less or no cough/angiodema
  • do not dual blockade RAAS- too many side effects (none listed)
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14
Q

Aliskerin

A
  • renin inhibitor
  • prevents conversion of angiotensinogen–>ang I–>decreases TPR (like ARBs, bradykinin not affected)
  • 2nd line for htn due to side effects (none listed); like ARBs, much less cough and angioedema
  • do not dual blockade RAAS due to side effects (none listed)
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15
Q

propanalol

A

-non-selective B blocker

-B1 on heart: decreased CO
-B1 on kidney: decreased renin–>decreased ang II and aldosterone
-B in CNS: decreased sympathetic discharge
Overall: decreased CO and TPR

  • 2nd line drug; BUT use in HF with reduced EF, and ischemic HD–>reduces mortality of acute and post-MI
  • do not give to pts with: asthma, COPD, diabetes, PVD, HF, symptomatic brady, 2nd or 3rd degree AV block, hyperlipidemia, stable angina
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16
Q

nadalol

A
  • non-selective B blocker

- refer to propanolol

17
Q

timolol

A
  • non-selective B blocker

- refer to propanolol

18
Q

pindolol

A
  • non-selective B blocker

- refer to propanolol

19
Q

carteolol

A
  • non-selective B blocker

- refer to propanolol

20
Q

levobunolol

A
  • non-selective B blocker

- refer to propanolol

21
Q

prazosin, terazosin, doxazosin, ends in “zosin”

A
  • alpha 1 selective blocker
  • acts on alpha 1 receptors of arterioles and veins–> decrease TPR with minimal effect on CO
  • 2nd line therapy for htn, can treat BPH and Reynaud’s dz (can relax arteriolar, prostatic, trigone, and venous smooth m.)
  • reflex tachy, edema, ortho hypotension (1st dose effect), headache, weakness, dizziness
22
Q

metoprolol

A
  • selective B1 blocker
  • refer to propanolol mechanism–>decrease CO and TPR
  • clinical use and adverse effects same as non-selective B blockers
  • all B blockers overall equally effective as antihypertensives

-think BEAM: all B1-selective blockers start with one of these letters

23
Q

atenolol

A
  • selective B1 Blocker
  • refer to propanolol and metoprolol
  • BEAM
24
Q

acebutolol

A
  • selective B1 Blocker
  • refer to propanolol and metoprolol
  • BEAM
25
Q

betaxolol

A
  • selective B1 Blocker
  • refer to propanolol and metoprolol
  • BEAM
26
Q

bisoprolol

A
  • selective B1 Blocker
  • refer to propanolol and metoprolol
  • BEAM
27
Q

esmolol

A
  • selective B1 Blocker
  • refer to propanolol and metoprolol
  • BEAM
28
Q

phentolamine

A
  • non-selective alpha blocker
  • MOA same as alpha 1 selective
  • IV drug for htn emergencies
  • same side effects as alpha 1 selective
29
Q

phenoxybenzamine

A
  • non-selective alpha blocker
  • MOA same as alpha 1 selective
  • PO drug for htn from catecholamine excess (pheochromocytoma)
  • same side effects as alpha 1 selective
30
Q

labetalol

A
  • alpha and beta blocker
  • partial antagonist of B2, full a1 antagonist–>vasodilation–>decrease TPR with little effect on HR and CO from B2 antagonism
  • 2nd line therapy for chronic htn, htn emergencies (IV form)
  • bronchospasm, prolonged/enhanced hypoglycemia, hypotension and ortho hypotension, N/V, sexual dysfunction
31
Q

methyldopa

A
  • centrally acting alpha 2 agonist
  • lipid soluble agents that gain access to CNS–>activate a2 receptors–>decrease symp. outflow–>decrease TPR
  • htn in pregnancy
  • sodium and H2O retention, positive coombs test, hemolytic anemia (rare), hepatotoxicity
32
Q

clonidine

A
  • centrally acting alpha 2 agonist
  • lipid soluble agents that gain access to CNS–>activate a2 receptors–>decrease symp. outflow–>decrease TPR, HR, and CO
  • 2nd line therapy for chronic htn, hypertensive URGENCIES, (transdermal patch better)
  • sedation, dry mouth, depression, impotence, sodium and H2O retention, contact dermatitis (patch), and with abrupt withdrawal–>rebound htn and nervousness, tachy, headache, sweating
33
Q

hydralazine

A
  • direct vasodilator
  • dilate arterioles–>decrease TPR
  • oral: chronic therapy for severe htn (add on drug); IV: hypertensive emergencies
  • general adverse effects: excessive vasodilation and hypotension–>tachy, Na and H2O retention, flushing, dizziness, angina, headache, nausea, sweating (SNS activated)
  • hydralazine specific adverse effects: Lupus-like syndrome, fever, arthralgia, skin rashes
34
Q

minoxidil

A
  • direct vasodilator
  • dilate arterioles–>decrease TPR
  • chronic therapy for severe htn (add on drug)
  • general adverse effects: refer to clonidine
  • minoxidil specific: hypertrichosis (rogaine)
35
Q

nitroprusside

A
  • direct vasodilator
  • sodium nitroprusside–>NO–>increases cGMP–>dilates arterioles and veins–>overall decrease TPR
  • hypertensive emergencies (IV infusion with rapid onset (sec) and short action duration (1-2 min), controlled hypotension during surgery
  • cyanide and thiocyanate toxicity, vasodilation and hypotension–>headache, N/V, dizziness, palpitations

Pharmacology (7 decks)

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