Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CPR II Exam 1 > Drugs for HTN > Flashcards

Drugs for HTN Flashcards

(69 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What organs are critical in controlling BP long term?

A

Kidneys

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main causes of Primary HTN?

A

Low renin

normal renin

high renin

idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is secondary HTN?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some common causes of secondary HTN?

A

Renal parenchymal disease

renovascular disease

primary aldosteronism

OSA

Drugs/ETOH

Pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Thiazide Diuretics

ACEi

ARB

CCB (dihydropyridines and non-dihydropyridines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the toxicities for HCTZ

(thiazide)

A

Low K, Mg, Na

Low Cl, metabolic alkalosis

Sulfa hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the MOA for Furosemide?

(loop diuretic-Lasix)

A

Blocks Na-K-2Cl transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the toxicities of Furosemide?

A

Low K, Na, Ca, Mg, Cl

metabolic alkalosis

HYPERglycemia and Hyperuricemia

OTOTOXICITY

Sulfa hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the benefit of Torsemide over furosemide?

A

Longer 1/2 life, better oral absorption

better for Heart Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the benefit of Bumetanide over Furosemide?

A

more predictable oral absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the benefit of ethacrynic acid?

A

non-sulfanamide

(use for sulfa allergies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the clinical applications for Amiloride?

(K sparing)

A

Counteracts K loss from other diuretics (used in combo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the toxicity concerns with amiloride?

A

HyperKalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the effect of Spironolactone?

A

K-sparing diuretic

Antagonizes pro-fibrotic effects of aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the MOA of losartan?

A

nonpeptide angiotensin II receptor antagonist

(binds 1000x better to AT1R than AT2R)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the benefit of valsartan over losartan? What is the benefit of Candesartan over losartan?
It is not a prodrug relatively irreversible binding
26
What is Aliskiren and why is it not widely used?
Direct renin inhibitor new, expensive, and no obvious benefit with increased risks of adverse effects (lose-lose-lose situation)
27
Drugs that interfere with Angiotensin II have what effects on the kidneys?
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
28
ACEi are contraindicated in which special population?
Pregnant Women Should be discontinued ASAP
29
What is the MOA of Nifedipine? What are is a main effect?
dihydropyridine CCB Frequency-independent, AKA not cardioactive
30
What are the clinical applications for Nifedipine?
HTN ## Footnote **HTN emergency in pregnancy** **Pulmonary HTN**
31
What are toxicities of Nifedipine?
Flushing Peripheral Edema Headache Palpitations gingival hyperplasia
32
Why is amlodipine often used over nifedipine?
limited to CAD and HTN, but very widely used due to long half life (30-50hrs)
33
What is the MOA of Verapamil and Diltiazem? What are there effects?
non-dihydropyridine CCB Frequency-dependent, AKA cardioactive
34
Nifedipine preferentially affects depolarized tissues leading to Verapmil and Diltiazem are use-dependent and target channels that cycle regularly, thus affecting what?
blockade that is voltage dependent in arterial blood vessels myocardium and tachycardic hearts
35
HR and CO are increased by reflex SNS activation with Nifdepine why?
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
Early Alpha Receptor Blockers such as ___ and ____ were not well tolerated due to what effects?
Phentolamine and Phenoxybenzamine due to hypotensive episodes, orthostatic hypotension, arrhythmias, angioedema, miosis
37
What are the clinical applications of prazosin (a1R blocker)
HTN l**ate choice because increases likelihood of stroke and CHF** with doxazosin compared to chlorthalidone
38
What are the toxicities associated with Prazosin?
orthostatic hypotenision "retrograde" ejaculation
39
What is tamsulosin, terazosin and doxasozin marketed for besides HTN?
BPH and passing kidney stones
40
What is the MOA and effects of Clonidine?
A2R antgonist produces a transient increase in BP that then reduces sympathetic outflow from the CNS
41
What are the toxicities for Clonidine?
drowsiness, xerostomia ## Footnote ***REBOUND HTN if dose is missed***
42
What is the MOA and main use of a-methyldopa?
A2R antagonist Drug of choice for gestational hypertension
43
What are some toxicities of a-methyldopa?
can cause a positive Coombs test and SLE-like sx
44
What were some of the issues with SNS and PNS blocker, Hexamethonium?
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
What is the MOA of reserpine? What was the effect? What are the adverse effects?
blocked incorporation of NE into synaptic vesicles mild decrease in BP, no change in CO, RBF, or GFR Severe depression and SI
46
what is the MOA for Guanethidine? What is the adverse effects?
displaces NE from synaptic vesicle decreases CO, TPR, RBF, and GFR Severe orthostatic hypotension, BP slowly increases throughout day
47
What is the MOA of propranolol and who is it contraindicated in?
Nonselective beta blocker can cause cold extremities especially in infants and those with peripheral vascular disease
48
What happens if an a2 agonist or B blocker is stopped abruptly?
**Unmasking the B receptors** leads to excessive c**ardiac 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
Why are beta blockers not used as much now?
Current data suggests that B-blockers **DO NOT** **prevent MI, heart failure or death, as well as other therapies and,** are associated with s**ignificantly higher incident of stroke**
50
What is the MOA of hydralizine and who is it often used in?
direct vasodilator of arteriols Used in hypertensive emergency in pregnancy
51
What are the toxicities of hydralizine? (many)
**Drug induced lupus-like syndrome** cardiovascular CNC Derm GI/GU Hematologic NMS Ocular Resp
52
What is the MOA of nitroprusside?
Venous and arteriolar vasodilation
53
What is the MOA of minoxidil? Concerning Toxicities?
vasodilation of arteriolar smooth muscle ## Footnote **Pericardial effusion with tamponade**
54
What conditions suggest bilateral renovascular hypertension rather than primary HTN?
Flash pulmonary edema progressive renal failure refractory congestive heart failure
55
Why is renal revacularization not done now?
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
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?
B-Blockers, ACEi, ARBs add Dihydropyridine CCBs Add dihydropyridine CCB, thiazide and/or MRAs
57
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?
ACEi Treat with ARB
58
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?
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
How to lower BP in acute spontaneous ICH? (within first 6 hrs)
If BP is 150-220 lower to \<140 if BP is \>220, lower with continuous IV infusion and close BP monitoring
60
Metabolic syndrome is diagnosed with three of the following five
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
What are some ways to increase medication compliance and improve outcomes in treating HTN?
1x day or combination pills behavioural and motivational strategies team-based approach EHR Telehealth strategies performance measures and quality improvement strategies
62
HTN urgency is different from emergency, in that emergency has what?
Emergency has impending or progressing target organ dysfunction Ex: dissecting aortic aneurysms, renal failure, ischemic stroke, eclampsia, etc
63
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?
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
What happens if you drop someone's BP too quickly?
dropping it too far too fast can mean no flow if there is chronic high BP
65
Nicardipine is CI in whom? Clevicipine is CI in whom?
in those with advanced aortic stenosis Soy allergies, egg allergies, defective lipid metabolism
66
Na Nitroprusside should be monitored for what effects? NTG should be used in whom and not used in whom?
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
Hydralizine is unpredictable, thus it is not what? Emsmolol is CI in whom?
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
Labetalol is CI in whom? Phentolamine should be used in whom? FEndolapam is CI in whom? Enalaprilate is CI in whom?
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

CPR II Exam 1 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions