Anti-HTN Flashcards

1
Q

What are 3 main strategies for decreasing HTN?

A
  1. Decrease TPR
  2. Decrease CO
  3. Decrease body fluid volume
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2
Q

Decreasing BP may result in homeostatic regulation which involves what potentially unwanted side effects?

A

Reflex tachycardia and edema

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3
Q

Which category of anti-HTN drugs do not result in reflex tachycardia and edema? What side effect will they get instead?

A

Autonomic drugs since they are already working on dampening the sympathetic response. They are more likely to exhibit orthostatic hypotension.

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4
Q

What are clonidine and methyldopa?

A

Alpha 2 agonists

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5
Q

What do alpha 2 agonists do?

A

Decrease in sympathetic outflow –> less NE released –> less activation of alpha 1 and beta 1 –> decreased TPR and decreased HR

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6
Q

What do we use clonidine and methyldopa for?

A

BOTH - mild to moderate hypertension
Just clonidine - opiate withdrawal
Just methyldopa - hypertensive management in pregnancy

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7
Q

Why do we see hemolytic anemia as a potential side effect with methyldopa?

A

Methyldopa binds strongly to plasma proteins (one of the reasons we like to use it as anti-HTN for pregnancy) but that also means it sticks around in the blood increasing the chance of hypersensitivity reaction that leads to hemolytic anemia

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8
Q

What side effects are shared by clonidine and methyldopa?

A

CNS depression and edema

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9
Q

What class of drugs decrease the antihypertensive effects of alpha 2 agonists and why?

A

TCA’s because they work to increase the levels of NE (by inhibiting reuptake) and this is the opposite of alpha 2 agonists trying to decrease NE levels

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10
Q

What does reserpine do?

A

Destroys vesicles - lowers NE, dopamine, and serotonin in CNS (can have side effect of severe depression)

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11
Q

What are 2 side effects of reserpine besides depression?

A
  1. Edema (from upregulating RAA axis from the decrease in blood pressure)
  2. GI secretions (upregulated parasympathetic since we’re blocking sympathetic)
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12
Q

Describe the drug interaction between guanethidine and TCA’s.

A

TCA’s block reuptake and action of guanethidine since guanethidine accumulates in nerve ending via reuptake

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13
Q

What does guanethidine do?

A

Binds to vesicles and inhibits release of NE

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14
Q

What are prazosin, doxazosin, terazosin (“-zosin” drugs)?

A

Alpha 1 blockers

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15
Q

How do alpha 1 blockers lower BP?

A

Decrease arteriolar and venous resistance

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16
Q

What are side effects of alpha 1 blocker?

A

Reflex tachycardia, orthostatic hypotension, urinary incontinence

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17
Q

What do we use alpha 1 blockers for besides lowering BP?

A

BPH

18
Q

What is the main mechanism by which beta blockers decrease hypertension?

A

Decrease renin

19
Q

What are 4 side effects of beta blockers being used as anti-HTN?

A
  1. Cardiac depression
  2. Fatigue
  3. Sexual dysfunction
  4. Increase LDLs and TGs
20
Q

When are beta blockers contraindicated?

A
  1. Asthmatics
  2. Vasospastic disorders
  3. Diabetes (can mask hypoglycemic events)
21
Q

What are 2 antihypertensives that work through NO?

A
  1. Hydralazine

2. Nitroprusside

22
Q

What does it mean that hydralazine is a selective dilator?

A

Works primarily on arteriolar side

23
Q

What is a major side effect of hydralazine and why?

A

SLE-like syndrome because it is highly protein bound (used to treat HTN in pregnant women)

24
Q

Is nitroprusside a selective or nonselective dilator?

A

Nonselective - works on both arterioles and venules

25
Q

What is nitroprusside the drug of choice for?

A

Hypertensive emergencies in the hospital; given IV

26
Q

Why can you not use nitroprusside for more than 24-36 hours?

A

Cyanide toxicity (think PRUSSIDE)

27
Q

How can you decrease the cyanide toxicity of nitroprusside?

A

Coadminister with nitrites and thiosulfate

28
Q

What are minoxidil and diazoxide?

A

AntiHTN drugs that open ATP-dependent K channels causing hyperpolarization of smooth muscle causing arteriolar vasodilation

29
Q

What can minoxidil be used for other than hypertension?

A

Baldness (minoxidil is rogaine)

30
Q

Where are the K channels located that minoxidil and diazoxide act on?

A

Arterioles or the pancreas (causes decreased insulin release by the beta cells which is why hyperglycemia is a side effect of these drugs)

31
Q

Which calcium channel blockers are often used as anti-hypertensives?

A

Dihydropyridines (e.g. nifedipine) - block the L type Ca channels in the heart and blood vessels; acts strongly on the ones in the blood vessels leading to vasodilation

32
Q

Name 2 drugs that give you gingival hyperplasia?

A
  1. Nifedipine

2. Phenytoin

33
Q

What is aliskiren?

A

Renin inhibitor

34
Q

What side effect is present with ACE inhibitors but not with aliskiren?

A

With ACE inhibitors you get cough because you inhibit the inactivation of bradykinin. This doesn’t happen with aliskiren so no cough.

35
Q

What is losartan?

A

Angiotensin 1 receptor blocker (ARB)

36
Q

What do we use ACE inhibitors for?

A
  1. Moderate to mild HTN
  2. Protective against diabetic nephropathy
  3. CHF
37
Q

Why are ACE inhibitors contraindicated in the case of renal artery stenosis?

A

Because you need the effect of renin to get angiotensin II to preferentially constrict the efferent arteriole leading to increased GFR; if you block this with ACE inhibitor then you could cause renal failure

38
Q

Patient with HTN with comorbidities of diabetes and/or heart failure - which antiHTN do we want to use?

A

ACEI’s and ARB’s

39
Q

Patient with HTN and cardiac comorbidity (angina, heart failure, post MI) - which antiHTN do we want to use?

A

Beta blockers

40
Q

Patient with HTN and comorbidities of BPH and dyslipidemia - which antiHTN do we want to use?

A

Alpha blockers