Hypertension Pharmacology I and II Flashcards

(44 cards)

1
Q

Define Stage I HTN

A

BP: 140-159/90-99

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2
Q

Define Stage II HTN

A

Systolic BP >160; or diastolic BP >100

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3
Q

What is essential HTN

A

no known secondary cause for HTN; accounts for 95% of cases

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4
Q

Causes of Secondary HTN

A

Renal disease, drugs (EtOH, oral contraceptives, NSAIDS, MAOIs), Endocrine (pheochromocytoma, Cushings, hyperaldosteronism, hyper/hypothyroidism), Pulmonary (Obstructive Sleep Apnea)

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5
Q

Clinical Features of Secondary HTN

A

Severe/resistant HTN, onset before puberty, onset before 30 with no fam history or obesity, electrolyte disturbances

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6
Q

Modifiable Risk Factors for HTN

A

sodium intake, obesity, EtOH intake, meds, sedentary lifestyle, stress

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7
Q

Risk factors for aggressive treatment of HTN

A

young age at onset, hyperlipidemia, diabetes, smoking, family history of vascular disease

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8
Q

What is end-organ disease related to?

A

extent of BP elevation and duration of HTN

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9
Q

What are some manifestations of end-organ disease?

A

stroke, CAD, LV hypertrophy, atherosclerosis, nephrosclerosis, aneurysms

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10
Q

Who is more likely to benefit from lowering BP: a 45 y/o male with obesity and BP 145/95, or a 45 y/o female smoker with obesity, diabetes, LV hypertrophy, and BP 145/95

A

45 y/o female-the benefit of lowering BP increases in the setting of end-organ disease

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11
Q

General MOA: Diuretics

A

decrease intravascular volume

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12
Q

General MOA: Angiotensin Blockers

A

inhibit production/action of angiotenisin II->decrease PVR

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13
Q

General MOA: Direct Vasodilators

A

relax smooth muscle to decrease PVR

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14
Q

General MOA: Sympathoplegic agents

A

decrease sympathetic tone -> decrease PVR (ex. beta blockers, alpha blockers)

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15
Q

Which drug classes have no effect on heart rate and cardiac output (5)

A

diuretics, ISA beta blockers, ACEI, ARB, renin inhibitors

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16
Q

Which drug classes have no effect on plasma volume (3)

A

ACEI, ARB, Renin inhibitors

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17
Q

Which type of diuretic is high potency and what is its MOA

A

Loop diuretic; competitively inhibit Na-K-Cl transporter in proximal ascending tubule

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18
Q

Which type of diuretic is medium potency and what is its MOA

A

Thiazides; inhibits exchange of Na-Cl in the distal ascending loop

19
Q

Which type of diuretic is low potency and what is its MOA

A

Potassium sparing; inhibits Na reabsorption in the distal tubule

20
Q

When would you use a loop diuretic

A

severe HTN, CHF, cirrhosis, renal insufficiency (GFR < 30-40 ml/min)

21
Q

Side effects of loop and thiazide diuretics

A

hypokalemia, hypomagnesemia, impaired glucose tolerance, increased lipids, increased uric acid, erectile dysfunction, volume depletion

22
Q

Side effects of potassium sparing drugs

A

gynecomastia, menstrual irregularities, hyperkalemia

23
Q

Most famous loop diuretic

24
Q

MOA of ARBs

A

competitive receptor binding of angiotensin II to vascular endothelium

25
Ending associated with ACEIs
-pril (ex. lisinopril)
26
Ending associated with ARBs
-sartan (ex. losartan)
27
Short acting ACEI
captopril
28
Unique side effect to ACEIs
cough
29
Contraindications to ACEIs and ARBs
renal artery stenosis, hyperkalemia, pregnancy
30
ACEIs/ARBs benefit:
chronic kidney disease and proteinuria, CHF, LV remodeling post-MI, LV hypertrophy
31
Calcium Channel Blockers
Dihydropyridines: Amlopidine, nifedipine | Non-dihydropyridines: Verapamil, diltiazem
32
Which class of Calcium channel blockers has anti-anginal effects
non-dihydropyridines
33
Calcium channel blocker MOA
inhibits contraction of smooth muscle by blocking entry of calcium into cell->decreases PVR
34
Side effects of CCBs
heart failure, block, bradycardia for non-dihydropyridines. reflex tachycardia and angina for dihydropyirdines
35
How do you minimize the side effects of CCBs
use a long-lasting CCB
36
How do beta blockers decrease BP
reduce CO
37
Which beta blocker is used for a hypertensive emergency in the ICU setting
labetolol
38
Which beta blocker is used for acute coronary syndromes or CHF
carvedilol
39
Which beta blocker is administered IV and has a short half life used for AV nodal blocking in unstable patients
Esmolol
40
Ending associated with alpha 1 antagonists
-azosin (terazosin) (doxazosin)
41
Vasodilators (2)
hydralazine, minoxidil
42
Central acting sympathoplegic drugs MOA
stimulate alpha 2 receptors to reduce sympathetic output
43
Only alpha 2 agonist routinely used
clonidine
44
ganglion blocking agents (2) + MOA
Guanethidine: blocks release of NE from post-ganglionic nerve terminals Reserpine: depletes NE, DA, and serotonin; decreases CO and PVR