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CPR II Exam 1 > Drugs for HTN > Flashcards

Drugs for HTN Flashcards

1
Q

What seems to be the initiating event in chronic hypertension?

A

an initial increase in cardiac output causes a volume overload leading to increased TPR

OR

an increase in TPR can be the initiating event

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2
Q

What organs are critical in controlling BP long term?

A

Kidneys

“slow but ultimate regulator of BP due to their ‘infinite gain’”

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3
Q

What are the main causes of Primary HTN?

A

Low renin

normal renin

high renin

idiopathic

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4
Q

What is secondary HTN?

A

Has a primary cause and can sometimes be cured by treating cause

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5
Q

What are some common causes of secondary HTN?

A

Renal parenchymal disease

renovascular disease

primary aldosteronism

OSA

Drugs/ETOH

Pheochromocytoma

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6
Q

What are the main drug classes of primary agents for treating HTN?

A

Thiazide Diuretics

ACEi

ARB

CCB (dihydropyridines and non-dihydropyridines)

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7
Q

What are the drug classes for secondary agents of HTN?

A

Loop diuretics

K sparing Diuretics

Aldosterone antagonists

B blockers

Renin inhibitors

Alpha-1 and 2 blockers

direct vasodilators

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8
Q

What is the MOA of thiazides?

A

Block Na-Cl cotransporter in the DCT

increases Ca reabsorption in PCT because of volume contraction

Mg and K loss increased

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9
Q

What are the clinical applications for hydrochlorothiazide?

(thiazide)

A

HTN alone or in combo with others

not effective in pt’s with low GFR

used off label for calcium nephrolithiasis

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10
Q

What are the toxicities for HCTZ

(thiazide)

A

Low K, Mg, Na

Low Cl, metabolic alkalosis

Sulfa hypersensitivity

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11
Q

What is the MOA for Furosemide?

(loop diuretic-Lasix)

A

Blocks Na-K-2Cl transporter

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12
Q

What are the clinical applications for Furosemide?

(loop diuretic)

A

edema

heart failure

decreases preload, ECV

relieve dyspnea

HTN (even with low GFR)

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13
Q

What are the toxicities of Furosemide?

A

Low K, Na, Ca, Mg, Cl

metabolic alkalosis

HYPERglycemia and Hyperuricemia

OTOTOXICITY

Sulfa hypersensitivity

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14
Q

What is the benefit of Torsemide over furosemide?

A

Longer 1/2 life, better oral absorption

better for Heart Failure

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15
Q

What is the benefit of Bumetanide over Furosemide?

A

more predictable oral absorption

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16
Q

What is the benefit of ethacrynic acid?

A

non-sulfanamide

(use for sulfa allergies)

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17
Q

What is the MOA for K-sparing diuretics?

A

Amiloride blocks Na channels in collecting duct

Spironolactone blocks aldosterone receptor in collecting duct

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18
Q

What are the clinical applications for Amiloride?

(K sparing)

A

Counteracts K loss from other diuretics (used in combo)

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19
Q

What are the toxicity concerns with amiloride?

A

HyperKalemia

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20
Q

What is the effect of Spironolactone?

A

K-sparing diuretic

Antagonizes pro-fibrotic effects of aldosterone

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21
Q

What are the clinical applications for Spironolactone?

A

counteracts K loss induced by other diuretics especially in treating Heart Failure

Reduce fibrosis in HFrEF and post-MI heart failure

Off label for HFpEF, acne

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22
Q

When GFR decreases due to ACEi, what rises?

A

Creatinine

(helps preserve kidney function, but should be less than 30% increase with no associated hyperkalemia)

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23
Q

What is the MOA of Captopril?

How long is the half life?

What are the main toxicities?

A

ACEi

t1/2 = 1.7hrs, longer if renal impairment

Cough, angioedema

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24
Q

What is the MOA of losartan?

A

nonpeptide angiotensin II receptor antagonist

(binds 1000x better to AT1R than AT2R)

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25
Q

What is the benefit of valsartan over losartan?

What is the benefit of Candesartan over losartan?

A

It is not a prodrug

relatively irreversible binding

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26
Q

What is Aliskiren and why is it not widely used?

A

Direct renin inhibitor

new, expensive, and no obvious benefit with increased risks of adverse effects

(lose-lose-lose situation)

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27
Q

Drugs that interfere with Angiotensin II have what effects on the kidneys?

A

decrease AngII and increase efferent tone

can cause renal failure in pt’s with bilateral renal stenosis

can preserve renal function in DM pt’s

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28
Q

ACEi are contraindicated in which special population?

A

Pregnant Women

Should be discontinued ASAP

29
Q

What is the MOA of Nifedipine?

What are is a main effect?

A

dihydropyridine CCB

Frequency-independent, AKA not cardioactive

30
Q

What are the clinical applications for Nifedipine?

A

HTN

HTN emergency in pregnancy

Pulmonary HTN

31
Q

What are toxicities of Nifedipine?

A

Flushing

Peripheral Edema

Headache

Palpitations

gingival hyperplasia

32
Q

Why is amlodipine often used over nifedipine?

A

limited to CAD and HTN, but very widely used due to long half life (30-50hrs)

33
Q

What is the MOA of Verapamil and Diltiazem?

What are there effects?

A

non-dihydropyridine CCB

Frequency-dependent, AKA cardioactive

34
Q

Nifedipine preferentially affects depolarized tissues leading to

Verapmil and Diltiazem are use-dependent and target channels that cycle regularly, thus affecting what?

A

blockade that is voltage dependent in arterial blood vessels

myocardium and tachycardic hearts

35
Q

HR and CO are increased by reflex SNS activation with Nifdepine why?

A

Because Nifedipine exerts smaller direct inotropic effects and no chronotropic effects with large vasodilatory effects

(thus causing the increased HR and CO due to reflex SNS activation)

36
Q

Early Alpha Receptor Blockers such as ___ and ____ were not well tolerated due to what effects?

A

Phentolamine and Phenoxybenzamine

due to hypotensive episodes, orthostatic hypotension, arrhythmias, angioedema, miosis

37
Q

What are the clinical applications of prazosin

(a1R blocker)

A

HTN

late choice because increases likelihood of stroke and CHF with doxazosin compared to chlorthalidone

38
Q

What are the toxicities associated with Prazosin?

A

orthostatic hypotenision

“retrograde” ejaculation

39
Q

What is tamsulosin, terazosin and doxasozin marketed for besides HTN?

A

BPH and passing kidney stones

40
Q

What is the MOA and effects of Clonidine?

A

A2R antgonist

produces a transient increase in BP that then reduces sympathetic outflow from the CNS

41
Q

What are the toxicities for Clonidine?

A

drowsiness, xerostomia

REBOUND HTN if dose is missed

42
Q

What is the MOA and main use of a-methyldopa?

A

A2R antagonist

Drug of choice for gestational hypertension

43
Q

What are some toxicities of a-methyldopa?

A

can cause a positive Coombs test and SLE-like sx

44
Q

What were some of the issues with SNS and PNS blocker, Hexamethonium?

A

higher resting HR and BP and opposite of SLUDGE

-dry mouth, dry eyes, urinary retention, constipation, mydirasis

Difficulty maintaining CO and BP when upright

45
Q

What is the MOA of reserpine?

What was the effect?

What are the adverse effects?

A

blocked incorporation of NE into synaptic vesicles

mild decrease in BP, no change in CO, RBF, or GFR

Severe depression and SI

46
Q

what is the MOA for Guanethidine?

What is the adverse effects?

A

displaces NE from synaptic vesicle

decreases CO, TPR, RBF, and GFR

Severe orthostatic hypotension,

BP slowly increases throughout day

47
Q

What is the MOA of propranolol and who is it contraindicated in?

A

Nonselective beta blocker

can cause cold extremities especially in infants and those with peripheral vascular disease

48
Q

What happens if an a2 agonist or B blocker is stopped abruptly?

A

Unmasking the B receptors leads to excessive cardiac stimulation in response to normal SNS tone

-leads to tachycardia, HTN, angina, MI, arrhytmia

Suddenly stopping A2 agonists releases CNS brake on SNS tone leading to Rebound HTN (and death)

49
Q

Why are beta blockers not used as much now?

A

Current data suggests that B-blockers DO NOT prevent MI, heart failure or death, as well as other therapies and, are associated with significantly higher incident of stroke

50
Q

What is the MOA of hydralizine and who is it often used in?

A

direct vasodilator of arteriols

Used in hypertensive emergency in pregnancy

51
Q

What are the toxicities of hydralizine?

(many)

A

Drug induced lupus-like syndrome

cardiovascular

CNC

Derm

GI/GU

Hematologic

NMS

Ocular

Resp

52
Q

What is the MOA of nitroprusside?

A

Venous and arteriolar vasodilation

53
Q

What is the MOA of minoxidil?

Concerning Toxicities?

A

vasodilation of arteriolar smooth muscle

Pericardial effusion with tamponade

54
Q

What conditions suggest bilateral renovascular hypertension rather than primary HTN?

A

Flash pulmonary edema

progressive renal failure

refractory congestive heart failure

55
Q

Why is renal revacularization not done now?

A

restoring vessel patency with surgery or stenting fails to materially recover kidney function

IE-no better than drugs to block the RAAS and statin therapy

56
Q

Initial treatment of HTN includes which drug classes?

If this is not enough to lower BP, and chest pain is present, what is the next step?

What if BP goal is not met, but there is no chest pain?

A

B-Blockers, ACEi, ARBs

add Dihydropyridine CCBs

Add dihydropyridine CCB, thiazide and/or MRAs

57
Q

In CKD with goal BP under 130/80 and albuminuria is present, what is the drug class of choice?

what if they are intolerant to that drug class?

A

ACEi

Treat with ARB

58
Q

What is the goal BP to prevent HD in adults with HTN?

What is the goal of treating HTN in those with HFrEF?

What is teh goal of treating HTN in those with HFpEF?

What is the goal of treating HTN after renal transplant?

A

130/80

GDMT (BB) titrated to BP <130/80; nondihydropyridine CCB are not recommended

Diuretics for volume overload and HTN, ACEi or ARBs and BB titrated to SBP 130

BP <130/80 with calcium antagonist to improve GFR and kindey survival

59
Q

How to lower BP in acute spontaneous ICH?

(within first 6 hrs)

A

If BP is 150-220 lower to <140

if BP is >220, lower with continuous IV infusion and close BP monitoring

60
Q

Metabolic syndrome is diagnosed with three of the following five

A

Abdominal obesity

serum triglycerides over 150 or drug treatment for it

serum HDL <40 in men, <50 in women or drug tx for it

BP 130/85 or drug tx for it

fasting plasma glucose >100 or drug tx for it

61
Q

What are some ways to increase medication compliance and improve outcomes in treating HTN?

A

1x day or combination pills

behavioural and motivational strategies

team-based approach

EHR

Telehealth strategies

performance measures and quality improvement strategies

62
Q

HTN urgency is different from emergency, in that emergency has what?

A

Emergency has impending or progressing target organ dysfunction

Ex: dissecting aortic aneurysms, renal failure, ischemic stroke, eclampsia, etc

63
Q

When pt’s present with hypertensive emergency, what is the next step?

If aortic dissection, (pre)-eclampsia, pr pheochromocytoma present, what is the next step?

If there is no dissection, eclampsia, etc, what is the next step?

A

admit to ICU

Reduce BP to <140 in first hour and then to <120 in case of dissection

Reduce BP by max 25% over first hour then to 160/100 over next several hours then to normal over 1-2 days

64
Q

What happens if you drop someone’s BP too quickly?

A

dropping it too far too fast can mean no flow if there is chronic high BP

65
Q

Nicardipine is CI in whom?

Clevicipine is CI in whom?

A

in those with advanced aortic stenosis

Soy allergies, egg allergies, defective lipid metabolism

66
Q

Na Nitroprusside should be monitored for what effects?

NTG should be used in whom and not used in whom?

A

BP “overshoot”, lower doses in elderly, and CN toxicity

USein pts with ACS or acute pulmonary edema only; do not use in volume depleted pts

67
Q

Hydralizine is unpredictable, thus it is not what?

Emsmolol is CI in whom?

A

It is not good for the first-line agent in most patients

Those with concurrent beta-blocker therapy, bradycardia, or decompensated HF; can affect lung function

68
Q

Labetalol is CI in whom?

Phentolamine should be used in whom?

FEndolapam is CI in whom?

Enalaprilate is CI in whom?

A

those with reactive airway disease, or COPD

those with HTN emergencies from catecholamine excess

those at risk for glaucoma or increased IC pressure, sulfite allergies

CI in pregnancy and should not be used in acute MI or renal artery stenosis

69
Q
A

CPR II Exam 1 (25 decks)

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