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Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Clinically, when we talk about ‘hypertension’ or BP, we are talking about _________ pressures

A

arterial

venous pressures only account for a small fraction of arterial pressure

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2
Q

Normal BP, when correctly measure is

A

< 120/80 mmHg

really should be < 115 mmHg systolic

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3
Q

HTN is defined by

A

sustained (repeated measures) of BP > 140/90 mmHg

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4
Q

Stage 1 HTN

A

systolic BP 140-159 and diastolic BP in the 90’s

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5
Q

Stage 2 HTN

A

systolic BP 160-179 and diastolic BP in the 100-109 range

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6
Q

Stage 3 HTN

A

systolic BP >/= 180 and diastolic BP >/= 110

aka malignant HTN

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7
Q

Recommendation in pt. 60 y/o or older, is to initiate pharmacologic tx at SBP ______ or DBP ______…and treat to a goal of SBP _____ and DBP _______.

A

1) >/= 150 mmHg
2) >/= 90 mmHg
3) < 150 mmHg
4) < 90 mmHg

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8
Q

Recommendation in pt. younger than 60 y/o is to initiate pharmacologic tx at ________, and treat to a goal of ________.

A

1) SBP >/= 140 mmHg
2) SBP < 140 mmHg

(however, Dr. Williams usu. tries to get to < 140 using lifestyle interventions)

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9
Q

Newer evidence is showing that SBP should actually be _________ to lower rates of fatal and nonfatal major CV events

A

< 120 mmHg

instead of < 140 mmHg

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10
Q

What is the best way to avoid stroke?

A

controlling HTN

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11
Q

What other major organ sx besides heart is most threatened by high BP?

A

kidneys

(sustained, elevated BP can chronically damage KD and lead to need for dialysis…#2 cz of dialysis in this country is HTN)

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12
Q

Gold Std is to treat high BP pharmacologically when systolic is

A

> 150 mmHg

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13
Q

Known complications of untx, sustained elevation in BP

A

atherosclerosis (MI, stoke), heart failure, kidney damage

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14
Q

The biggest genetic contribution to HTN involves

A

sodium handling

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15
Q

What are primary non-pharmacolgic interventions for HTN

A

SODIUM RESTRICTION

wt. loss, smoking cessation, stress management

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16
Q

High-output HTN , usu. seen in younger pt. with essential HTN, is best tx with

A

beta-antagonists

b/c these drugs will decrease rate and force of contraction

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17
Q

Vascular resistance-based HTN, usu. seen in elderly, is best tx with

A

thiazide diuretics

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18
Q

What are the four main classes of anti-hypertensive drugs?

A

1) Diuretics
2) Beta-blockers
3) Calcium channel blockers
4) ACE/ARB

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19
Q

Which type(s) of drug(s) will reduce intravascular volume with concomitant vasodilation

A

diuretics

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20
Q

Which type(s) of drug(s) will down-regulate sympathetic tone

A

beta-antagonists
alpha-1-antagonists
central sympatholytics

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21
Q

Which type(s) of drug(s) will modulate vascular smooth muscle tone

A

CCB

K+ channel openers

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22
Q

Which type(s) of drug(s) will inhibit neurohumoral regulators of the circulation

A

renin inhibitors
ACE inhibitors
AT-1 antagonists (angiotensin II type 1 receptor antag.)

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23
Q

Diuretics best work on

A

renal sodium retention

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24
Q

Beta-blockers best work on

A

sympathetic nervous over-excitability (thus reducing CO of heart)

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25
Q

ACE-I/ARB best work on

A

renin-angiotensin excess (the reduce angiotensin II, leading to vasodilation)

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26
Q

CCBs best work on

A

endothelium derived factors to directly relax smooth mm.

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27
Q

Which anti-hypertensive drug class should you start with?

A

It doesn’t seem to matter

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28
Q

Which of the 4 major drug classes have better outcomes data?

A

Diuretics, ACE-I/ARB, and CCB

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29
Q

How long does it take to see maximal effect of each of the four major classes?

A

1 wk: ACE-I/ARB, CCB, B-blockers

2 wks: diuretics

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30
Q

Where do thiazide diuretics act?

A

distal convoluted tubule

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31
Q

Where do loop diuretics act?

A

ascending limb of Henle

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32
Q

What are the MC used thiazide diuretics?

A

1) Chlorothiazide (prototype)
2) Hydrochlorothiazide
3) Chlorothalidone
4) Metolazone

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33
Q

Thiazide diuretic MOA

A

inhibits sodium and chloride reabsorption in the distal tubule –> increased Na+, Cl-, K+, and Mg ++ excretion –> increased urine output and decreased GFR

(also decreases Ca++ excretion)

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34
Q

Thiazide distinguishing characteristics

A

1) orally administered
2) generally poorly absorbed
3) onset of action 1-2 hr, but BP effect takes severals days
4) wide-range of half-lifes (generally longer than loop diuretics and can be dosed just once daily)
5) free drug enters tubules by filtration and organic acid secretion

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35
Q

Thiazide predictable characteristics

A

1) ideal starting agent for HTN, chronic edema, and idiopathic hypercalcuria
2) Better choice of drug for AA pt.
3) MC s/e = hypokalemia and hyponatremia
4) incr. toxicity of digitalis or lithium

36
Q

Thiazide side effects

A

*Hypokalemia
*Hyponatremia
hyperglycemia
decr. insulin secretion
incr. plasma lipids
hyperuricemia
hypercalcemia (can be good if pt. have hx KD stones)

37
Q

Impt. labs when using thiazide diuretics

A

CMP - should do a couple times in the 1st yr of using thiazide diuretics; the first CMP should be done w/in 6 mo. of starting meds

38
Q

MC loop diuretics

A

1) Furosemide (prototype)
2) Bumetanide
3) Torsemide
4) Ethacrynic acid

39
Q

Which type of diuretics is more potent?

A

Loop

40
Q

Loop diuretic MOA

A

1) enters proximal tubule via organic acid transporter
2) inhibits apical Na-K-2Cl transporter in thick ascending loop of henle (really need to pee!!!)
3) competes with Cl- binding
4) enhances Mg++ and Ca++ excretion
5) incr. K+ and H+ excretion in cortical collecting duct
6) inhibits reabsorption of ~25% of glomerular filtrate

41
Q

Loop diuretic distinguishing characteristics

A

1) orally administered
2) rapidly absorbed
3) rapid onset of action for diuresis and BP
4) increases toxicity lithium
5) may have additive toxicity w/ other ototoxic drugs at high doses (IV)

42
Q

Loop diuretic predictable characteristics

A

1) preferred diuretic in pt. w/ moderate-severe chronic renal dz (rapid absorption)
2) Preferred when eGFR < 30 (rapid onset of action)
3) Preferred in malignant HTN
3) potency decreased by inhibitors of organic acid ion transport (NSAID’s)
4) MC s/e = hypokalemia and hyponatremia

43
Q

Side effects of loop diuretics

A

*Hypokalemia
*Hyponatremia
hyperuricemia
metabolic alkalosis
ototoxicity
Mg++ depletion

44
Q

What labs need to be done with loop diuretics?

A

CMP - make sure to do w/in one month of starting drugs

45
Q

What is the use of “Dual RAS blockade”

A

It’s now contraindicated (more hypotension, accelerated renal decline, cz more hyperkalemia)

ppl used to use ACE-I + ARB or Aliskiren + ACE-I/ARB

46
Q

What does ACE-I stand for?

A

angiotensin converting enzyme inhibitors

47
Q

MC used ACE-I

A

1) Lisinopril
2) Enalapril
3) Captopril
4) Ramipril

48
Q

ACE-I MOA

A

inhibits angiotensin converting enzyme in the lung –> reduces synthesis of angiotensin II (potent vasoconstrictor)

suppresses aldosterone –> natriuresis

potentiates other VASODILATORS

49
Q

ACE-I distinguishable characteristics

A

1) Esp. useful in high-renin HTN
2) Preferred drug for HTN pt. with diabetic nephropathy (doesn’t affect glucose levels)
4) First dose hypotension
5) C/I pregnancy

50
Q

ACE-I predictable characteristics

A

1) tx HTN

2) Common s/e: dry cough (MC in AA pt. and even MC in Asian pt.), angioedema (MC in AA), hyperkalemia

51
Q

What does ARB stand for?

A

Angiotensin Receptor Blockers

52
Q

ARB category

A

Vasodilator

53
Q

ACE-I category

A

Vasodilator

54
Q

MC used ARB

A

1) Losartan
2) Irbesartan
3) Valsartan
4) Candesartan

55
Q

ARB MOA

A

antagonist at angiotensin II receptor of vascular muscles

56
Q

ARB distinguishing characteristics

A

1) Best tolerated of anti-HTN drugs (even better tolerated than ACE-I)
2) Less cough and risk for angioedema than ACE-I
3) C/I in pregnancy

57
Q

ARB predictable characteristics

A

1) tx HTN

2) s/e: hypotension, dizziness, hyperkalemia

58
Q

What is paradoxical regarding ACE-I and ARB use in pt. with renal dz?

A

They both can cz small reductions in kidney fn (usu. transient), however, they are the drugs of choice in pt. with HTN and chronic kidney dz and actually improve kd fn many of these pt.

59
Q

What lab(s) do you want to do with ACE-I and ARB?

A

Run a CMP w/in 30 days of starting these drugs

60
Q

If a cough develops in a pt. taking an ACE-I who needs RAS blockage, what should you do?

A

substitute with an ARB

61
Q

What are the three classes of CCBs?

A

1) Phenylakylamines
2) Benzothiazepines
3) 1, 4 - Dihydropyridines

62
Q

Verapamil (Isopten) category

A

CCB - phenylalkylamine

63
Q

Verapamil (Isopten) MOA

A

blocks Ca++ influx, dilates peripheral arterioles, slows AV node, and has alpha adrenergic blocking activity

64
Q

Verapamil (Isopten) distinguishing characteristics

A

1) Reduces frequency of angina and need for nitrates
2) Preferred drug for paroxysmal SVT
3) Slows ventricular response to afib
4) Well absorbed, 80% metabolized in 1st pass
5) 90% protein bound and metabolites are acitve, T1/2 = 5hr (up to 20hr in pt. w/ cirrhosis)

65
Q

Verapamil (Isopten) predictable characteristics

A

1) tx HTN

2) C/I: hypotension, sinus bradycardia, *AV conduction defects, *severe cardiac failure

66
Q

Diltiazem (Cardizem) category

A

CCB - benzothiazepine

67
Q

Diltiazem (Cardizem) MOA

A

dilates peripheral arteries –> reduces afterload

incr. oxygen supply to myocardium by preventing sympathetic-induced coronary a. spasm

68
Q

Diltiazem (Cardizem) distinguishing characteristics

A

1) Less pronounced HR reduction
2) reduces angina episodes and incr. exercise tolerance in stable angina
3) 50% bioavailability after oral dose
4) 75% protein bound and metabolites are active, T1/2 - 3 hr

69
Q

Diltiazem (Cardizem) predictable uses

A

1) tx HTN

2) C/I: hypotension, sinus bradycardia, *AV conduction defects, *severe cardiac failure

70
Q

Nifedipine (Procardia) category

A

CCB - 1,4-dihydropyridines

other drugs in this category all end in -dipine

71
Q

Nifedipine (Procardia) MOA

A
  • potent peripheral vasodilation
  • little depression of nodes
  • fails to dilate coronary aa.
  • cz reflux incr. in HR and output
72
Q

Nifedipine (Procardia) distinguishing characteristics

A

1) No longer used as a single agent d/t toxicity
2) rapid-complete absorption of sublingual dose
3) 98% protein bound and metabolites are inactive, T1/2 = 3 hr
4) May cz MI, peripheral edema, pulmonary edema

73
Q

Nifedipine (Procardia) predictable characteristics

A

1) C/I: *hypotension and severe cardiac failure

74
Q

Which CCB(s) bind to cardiac cells? Which CCB(s) bind to vascular smooth muscle?

A

1) Diltiazem and Verapamil

2) Nifedipine

75
Q

The principal s/e in dihydropyridines is

A

dose-dependent ankle edema

edema appears to be vasogenic d/t vasodilation

76
Q

What is a rare s/e that all CCBs cz?

A

gingival hyperplasia, which is reversible if detected

77
Q

Which CCBs can impair cardiac conduction?

A

verapamil and diltiazem

*esp. in older pt. receiving digoxin, B-blockers, or central sympatholytic agents

78
Q

What is a rare s/e of long-acting dihydropyridine CCBs?

A

flushing and HA

79
Q

Beta-blockers MOA

A

competitive antagonists

generally, they antagonize effects of catecholamines on the heart

80
Q

Beta-blockers distinguishing characteristics

A

1) decrease myocardial oxygen consumption d/t reduced rate and contractility
2) reduce CO and maybe cz a little vasodilation

81
Q

Beta-blockers predictable characteristics

A

1) tx angina

2) hypotensive effect

82
Q

MC cardioselective beta-blocker(s)

relative selectivity for B1 receptor

A 
Metaprolol 
Esmolol 
Acebutolol 
Atenolol 
Betaxolol
83
Q

What happens to MOA of cardioselective beta-blockers at high doses?

A

You lose the selective effects and they can cz bronchoconstriction (bind to B2 receptors)

84
Q

Of the MC cardioselective beta-blockers, only _________ is markedly hydrophilic

A

atenolol

*thus, it’s less preferred in practice

85
Q

MC non-cardioselective beta blocker(s)

bind to B1 and B2 receptors

A

Carvedilol

86
Q

Adverse effects of beta-blockers

A

1) CNS effects - sedation, depression, hallucination
2) May lead to or worsen heart failure when initiated (start low dose)
3) Agg. of bronchospasm (non-selective)
4) Hypoglycemia unawareness in DM (d/t block of adrenergic warning signs)
5) impotence

87
Q

What is the preferred first-line tx for HTN?

A

ACE-I/ARB, CCB, or thiazide diuretics

Pharmacology (14 decks)

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