Antihypertensives Flashcards

1
Q

Verapamil (what is it, what do we use it for)

A

Non-dihydropyridine (ie binds when L-type is open)

  • Effects are greatest on contractility, blood flow, conduction
  • Use for paroxysmal SVT
  • Use for angina (dec in O2 demand, inc in coronary blood flow)
  • Use for hypertension via reduction of SVR (still causes vasodilation, just not as much as dihydropyridines)
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2
Q

Verapamil side effect

A

Constipation

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3
Q

Diltiazem

A

Non-dihydropyridine

  • Lowest incidence of side effects
  • Effective in treating SVT
  • Not a great antihypertensive drug (verapamil is stronger)
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4
Q

Nifedipine

A

Dihydropyridine (ie works on vasc SMCs and binds when channel is closed)

  • Peripheral vasodilation (effective antihyperT, can use with beta blocker to prevent reflex tachy)
  • ->has no direct effects on the myocardium or nodes, only the coronary arteries
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5
Q

Nifedipine contraindications

A

Post-MI, CHF

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6
Q

Nifedipine side effects

A

facial flushing, headaches, dizziness, palpitations, ankle swelling (think about MOA)

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7
Q

Important hemodynamic response to dihydropyridines in vascular SMCs

A
  • Cause such profound peripheral vasodilation and limited myocardial effects that they can cause compensatory increase in HR and inotropy
  • May produce reflex tachycardia and increase myocardial contractility
  • Compensation increases myocardial workload and has been demonstrated to be detrimental in pts who are at high risk of having an MI
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8
Q

What is Hydralazine?

A

Direct arteriolar dilator (no effects on veins)

  • preferentially effects, renal, peripheral, splanchnic and coronary arteries
  • decrease in PVR leads to dec in BP
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9
Q

What is hydralazine toxicity?

A
  • excessive vasodilation
  • SLE-like syndrome that is reversible when drug is stopped (seen in females with >6mo treatment who are slow acetylators)
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10
Q

When do we use hydralazine?

A
  • HyperT in pregnancy including preeclampsia

- In combo with beta antag to blunt reflex SNS activation

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11
Q

What is minoxidil

A

Direct arteriolar dilator (no effects on veins)

  • MOA: Activates ATP-modulated K+ channels in arteries, allowing for hyperpolarization and relaxation
  • Pharma actions: dec PVR=dec in BP
  • Get reflex SNS activation–>RAAS activation–>BP comes back to baseline (give with beta blocker and diuretics)
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12
Q

Minoxidil side effect

A

Inc hair growth (hypertrichosis)

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13
Q

What is Na Nitroprusside?

A

Direct venous and arteriolar dilator

  • MOA: SMCs metabolize it into NO–>cGMP–>SMC relaxation and vasodilation
  • Leads to dec in afterload and inc in preload (ie venous return)
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14
Q

When do we use nitroprusside?

A

HyperT emergencies (rapid onset of 1-2 min and consistent response)

Easily titrated

initiate with beta blocker prior to discontinuing infusion

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15
Q

How do beta adrenergic antagonists work as antihypertensive drugs?

A

Reduce HR and renin release

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16
Q

What is metoprolol?

A
  • Beta 1 antagonist
  • Lipophilic
  • Short and long duration of action
17
Q

What is atenolol

A
  • Beta 1 antagonist
  • Not lipophilic
  • Short duration of action
18
Q

What is Propanolol

A
  • Beta 1 and 2 antagonist
  • Lipophilic
  • Short and long duration of action
  • ->dont use in pts with lung disease
19
Q

What is prazosin?

A

Alpha 1 and 2 antagonist

20
Q

What are doxazosin and terazosin?

A

Pure alpha 1 antag (third line treatment in hyperT)

21
Q

What are labetolol, carvedilol

A

Combo alpha and beta receptor antagonists (alpha 1, non selective beta)

22
Q

What is clonidine?

A

Centrally acting alpha 2 agonist

  • Stimulates pregang alpha 2 receptors in the medulla to reduce norepi release
  • oral with 12 hr duration or transdermal 1x/wk
  • Results in reduction of sympathetic flow
23
Q

What do we use clonidine for?

A

First line in autonomic neuropathy

24
Q

Adverse effects of clonidine?

A

Due to unopposed vagal tone

  • dry mouth etc
  • rebound hyperT with discontinuation=issue