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FPC2 Exam 8 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What are first line agents for HTN? Second line agents?

A

1st: thiazide diuretics, ACE Is, angiotensin receptor blocker, CCB
2nd: β blockers, centrally acting α 2 agonists, direct vasodilators, α antagonist

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2
Q

Where do thiazide diuretics work?

A
  1. diuretics in the kidney

2. vascular smooth muscle

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3
Q

What are the thiazide and thiazide like diuretics? which are most commonly used

A

Thiazide: hydrochlorothiazide*, chlorothiazide

Thiazide-like: chlorthalidone*, metolazone, indapamide

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4
Q

Thiazide MOA

A

enter PCT through organic anion transporter 1. Inhibit Na+ resorption in DCT (Na+ Cl- symporter)-> increase Na+, H2O, and K+ excretion
Short term: reduce volume in body-> reduce CO
Long term: reduce peripheral resistance by opening K+ channels in SM, increase NO, Ca2+ desensitizaion

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5
Q

Chlorthalidone has a ____ duration of action than hydrochlorothiazide

A

longer. its more potent

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6
Q

Thiazide like diuretics are less effective when GFR is _____

A

<30mL/min

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7
Q

What are adverse effects of thiazide?

A

hypokalemia, hypomagnesemia (more common with chlorthalidone)
Ca2+ respiration enhanced
increased uric acid concentrations (problem with GOUT)

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8
Q

What do ACE-I end in? What do ARBs end in?

A

ACE-I: pril (lisino, enala, benaze, capto)

ARBs: sartan (lo, val, olme, cande, telmi)

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9
Q

What is MOA of ace inhibitors

A

blocks angiotensin II vasoconstriction
increase bradykinin VD
reduce aldosterone secretion
block angiotensin II mediatied LV remodeling and NE from adrenal medulla

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10
Q

Ace inhibitor PK features

A

most are prodrugs (converted hepatic ally)

mostly renal excretion

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11
Q

Renin is excreted in response to

A

low pressure (low Na+ concentration)

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12
Q

Angiotensin II receptor blockers MOA

A

block angiotensin II type 1 receptor

more complete and selective than ACE-I-> no effect on bradykinin (no cough, low angioedema)

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13
Q

When are ARBs used?

A

adverse reactions to ACE-I

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14
Q

How are ARBs excreted?

A

Parent and metabolites excreted in feces

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15
Q

What to monitor for RAAS drugs (ACEI + ARBs)

A

cough (only ACE from Brady)
angioedema (swelling of lips, mouth face)
teratogenic in 2nd and 3rd tri (category D)
acute renal fail
hyperkalemia

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16
Q

Where do CCBs work

A

vascular smooth muscle. non selective reversible block of L-type Ca2+ channels

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17
Q

What are the CCBs? (DHPs and Non-DHPs)

A

DHP (dipine): amlodipine, nifedipine, felodipine, nicardipine (good for HTN)
Non-DHP: diltiazem, verapamil (usually for angina/afib/aflutter)

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18
Q

Should ACEI be combined with ARB

A

no

19
Q

ACEIs are beneficial in chronic kidney disease because

A

reduced intraglomerular capillary pressure

20
Q

What allergy needs to be watched for captopril and why?

A 
sulfa groups (sulfhydryl group on the drug)
skin rash and neutropenia
21
Q

Physiological effect of DHPs

A

reduce systemic vascular resistance + arterial pressure

less cardiac depressant effect than verapamil + diltiazem

22
Q

What are short acting vs long acting DHPs indicated for

A

short acting should not be used for HTN (nifedipine). increase risk of MI and mortality
long acting are good for HTN and they include amlodipine, felodipine, ER nifedipine

23
Q

Specifically MOA of non-DHP (molecular and physiological)

A

Block L-type Ca2+ channels in cardiac muscle cells

reduced isotropy and CO-> avoid HFrEF

24
Q

CCB adverse effects

A

DHP: pedel edema (works at arteriole and non venous-> fluid build up in feet), orthostatic hypotension, flusing
Non-DHP: Bradycradia, sleepiness, constipation

25
Q

Where do β blockers work? and how?

A

work at the <3!
decrease contractility (neg isotropy) and HR (neg chromotropy)
decrease central sympathetic output
some decrease in BP

26
Q

What are the non selective β blockers?

A

Β1 and β2
propanolol
Nadolol

27
Q

What are the selective β blockers? (β1)

A

metoprolol
atenolol
bisoprolol

28
Q

Whare the α blocking activity β blockers (α1, β1, β2)

A

carvedilol, labetalol

29
Q

What are β blocker adverse effects

A

Bradycardia, exercise intolerance/fatigue, bronchospasm, postural hypotension (α blocking), mask hypoglycemia

30
Q

Where do centrally acting α 2 agonists work? what is MOA?

A

Brain! act on presynaptic α 2 receptors in brain-> reduce sympathetic0> increase parasympathetic flow to heart
decreased HR, relaxed veins, reduced peripheral vascular resistance

31
Q

What are the major centrally acting α 2 agonists and what are they used for

A

clonidine (resistant HTN)

methyldopa (HTN in pregnancy)

32
Q

What are adverse effects of centrally acting α 2 agonists

A

sedation, impaired mental concentration, nightmares, vertigo, dry mouth.
Clonidine specific: remind HTN after abrupt cessation

33
Q

MOA of direct vasodilators

A

work at vascular SM
dilation arterioles > veins
Hyperpolarization of cell membranes through opening K+ channels

34
Q

What is the direct vasodilator used? Dosing and AE?

A

hydralazine
low bioavailability + variable among individuals. 3-4 times a day
AE: reflex tachycardia as compensatory for decrease in arteriole resistance

35
Q

What are the α1 antagonists used?

A

“Azosin”

doxazosin, prazosin, terazosin

36
Q

MOA of α 1 antagonists

A

selective block peripheral α 1 post synaptic receptors-> vasodilation of arteries and veins

37
Q

When are α 1 antagonists used?

A

resistant HTN in men with concurrent HTN and benign prostatic hyperplasia (BPH)
also in circulatory conditions, PTSD nightmares (prazosin)

38
Q

AEs of α 1 antagonists

A

postural hypotension -> occasionali syncope

dizziness, reflex tachycardia

39
Q

Initiation of antihypertensive therapy with a single drugs is reasonable in _____

A

adults with stage 1 HTN

40
Q

initiation of antihypertensive therapy with 2 first line agents of different classes is recommended in ______

A

adults with stage 2 HTN (>140/90) and average BP more than 20/10 above target

41
Q

Preferred agents for stable ischemic heart disease

A

BB + ACE1/ARB-> not at goal-> DHP CCB, thiazide, or MRA (mineralocorticoid receptor antagonists)

42
Q

preferred agents in stroke/TIA

A

thiazide, ACE1/ARB or both

43
Q

Preferred agents for DM or CKD with albuminuria

A

ACEI/ARB

FPC2 Exam 8 (5 decks)

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