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Pharmacology II - CP > Review/Hypertensive Agents (Cardio Lecture II) > Flashcards

Review/Hypertensive Agents (Cardio Lecture II) Flashcards

1
Q

What are the CNS neurotransmitters?

A

epi, norepi, dopamine, serotonin, GABA, acetylcholine

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2
Q

Which are natural catecholamines/endogenous?

A

epi, norepi, dopamine

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3
Q

Which are synthetic catecholamines?

A

isoproterenol, dobutamine

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4
Q

Alpha receptors response in order of potency to epi, norepi, and isoproterenol

A

Norepi > Epi > Isoproterenol

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5
Q

Beta receptors response in order of potency to epi, norepi, and isoproterenol

A

Isoproterenol > Epi > Norepi

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6
Q

Where are alpha 1 receptors found?

A

post-synaptic in the vasculature, heart, glands, and gut

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7
Q

What happens when alpha 1 receptors are activated?

A

vasoconstriction and relaxation of the GI tract

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8
Q

Where are alpha 2 receptors found?

A

pre-synaptic in peripheral vascular smooth muscle, coronaries, brain

post-synaptic in coronaries, CNS

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9
Q

What happens when pre-synaptic alpha 2 receptors are activated?

A

inhibition of norepi release and inhibition of sympathetic outflow = decreased BP and HR and decreased CNS activity

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10
Q

What happens when post-synaptic alpha 2 receptors are activated?

A

constriction and sedation/analgesia

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11
Q

Where are Beta 1 receptors found?

A

heart primarily (myocardium, SA node, ventricular conduction system, coronaries) and kidney

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12
Q

Activation of the Beta 1 receptors causes

A

increase in inotropy, chronotropy, myocardial conduction velocity, coronary relaxation, and renin release

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13
Q

Where are Beta 2 receptors found?

A

lungs primarily

vascular, bronchial, and uterine smooth muscle, smooth muscle in skin, myocardium, coronaries, kidneys, GI tract

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14
Q

Activation of the Beta 2 receptors causes

A

vasodilation, bronchodilation, uterine relaxation, gluconeogenesis, insulin release, potassium uptake

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15
Q

Ephedrine pharmacokinetics

A

usually given in 5 mg increments, DOA 15-60 minutes
indirectly deplete catecholamine stores

repeated doses: tachyphylaxis

will increase HR, inotropy, and BP

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16
Q

Phenylephrine pharmacokinetics

A

DOA 5- 20 minutes
50 - 200 mcg push, 20-100mcg/min infusion
pure alpha = vasoconstriction, reflex bradycardia
can be used in nasal intubation

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17
Q

What kind of receptors are alpha and beta receptors?

A

GPCRs

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18
Q

Drug classes for HTN that work on the SNS

A

beta antagonists, alpha 1 antagonists, mixed alpha and beta antagonists, centrally acting alpha 2 agonists

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19
Q

Drug classes for HTN that work on the RAAS

A

angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, diuretics

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20
Q

Drug classes for HTN that work on the endothelium mediator and/or ion channel modulator

A

direct vasodilators, calcium channel antagonists, potassium channel opener

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21
Q

According to JNC 8 normal blood pressure is

A

<120 systolic and <80 diastolic

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22
Q

If you are age 60 or older goal BP is

A

<150/90 with NO diabetes or kidney disease

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23
Q

What is the first line therapy for HTN (besides lifestyle changes)

A

thiazide diuretic unless this a compelling indication

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24
Q

Hypertensive urgency

A

diastolic pressure >120 without evidence of end organ damage
goal: decrease DBP to 100-105 within 24 hours
can use Clonidine

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25
Q

Hypertensive crisis

A

diastolic pressure >120 with evidence of end organ damage
goal: decrease DBP 100-105 ASAP
can use Nitroprusside, Nitroglycerin, Labetalol, Fenoldapam

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26
Q

Alpha antagonists

A

bind selectively to alpha receptors and interfere with the ability of catecholamines to cause a response

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27
Q

Which alpha antagonist binds covalently?

A

Phenoxybenzamine

28
Q

Which alpha antagonists are competitive?

A

Phentolamine, Prazosin, Yohimibine

29
Q

Alpha 1 antagonists cause

A

smooth muscle relaxation, decrease PVR and BP

used for HTN and BPH

30
Q

Which alpha antagonists are more selective for alpha 1 over alpha 2 receptors?

A

prazosin, terazosin, doxazosin, phenoxybenzamine

31
Q

what are our mixed alpha and beta antagonists?

A

labetalol and carvedilol

B1 = B2 > a1 > a2

32
Q

which beta antagonist is more sensitive to B2 over B1?

A

Butoxamine

33
Q

Side effect of alpha 1 antagonists?

A

postural hypotension d/t failure of venous vasoconstriction

34
Q

Phenoxybenzamine

A

binds covalently
alpha 1 > alpha 2
decreases SVR, vasodilation
pro-drug with 1 hour onset time
long acting
given to pheochromocytoma patients and raynaud’s disease
PO dose: 0.5-1.0 mg/kg (have them start a week or two before surgery)

35
Q

Phentolamine

A 
non selective
peripheral vasodilation and decrease SVR
causes increased HR and CO
used for HTN emergencies (30-70 mcg/kg)
extravascular admin to prevent necrosis (2.5-5 mg)
36
Q

Prazosin

A

selective alpha 1 antagonist
dilates both arterioles and veins
used preop for pheochromocytoma, essential HTN, decreasing afterload in HF, raynaud’s
less reflex tachycardia

37
Q

Yohimibine

A

alpha 2 selective blocker
increases release of norepi from post-synaptic neuron
used for orthostatic hypotension, impotence

38
Q

What is our biggest concern if our patient takes terazosin and tamsulosin for BPH?

A

orthostatic hypotension

39
Q

1st generation non selective beta antagonists

A

Nadolol, penbutolol, pindolol, propranolol, timolol

40
Q

2nd generative B1 selective antagonists

A

acebutolol, atenolol, bisoprolol, esmolol, metoprolol

41
Q

3rd generation non selective beta antagonists

A

carteolol, carvedilol, bucindolol, labetolol

42
Q

4th generation B1 selective antagonists

A

betaxolol, caliprolol, nebivolol

43
Q

What do beta adrenergic receptor antagonists do?

A

disallow sympathomimetics from provoking a beta response on the heart, airway, blood vessels, juxtaglomerular cells, and pancreas

44
Q

beta antagonist effects on heart

A

bradycardia, decreased contractility, decreased conduction velocity, improve O2 supply and demand balance

45
Q

beta antagonist effects on airway

A

bronchoconstriction and can provoke bronchospasm in those with asthma or COPD

46
Q

beta antagonist effects on blood vessels

A

vasoconstriction in skeletal muscles, PVD symptoms increase

47
Q

beta antagonist effects on juxtaglomerular cells

A

decrease renin release - indirect way of decreasing BP

48
Q

beta antagonist effects on pancreas

A

decreased stimulation of insulin release by epi/norepi at B2 and then masks symptoms of hypoglycemia

49
Q

chronic use of beta blockers is associated with

A

increase in the number of receptors (up regulation) and need to be continued in the OR

50
Q

clinical uses of beta blockers

A

HTN, angina, decrease mortality in treatment of post MI pts, used for pts at risk for MI, suppression of tachyarrhythmias, prevent excessive SNS activity

51
Q

relative contraindications of beta blockers

A

pre-existing AV heart block or cardiac failure, reactive airway disease, diabetes mellitus, hypovolemia

52
Q

side effects of beta blockers

A

decrease HR, contractility, BP, exacerbation of peripheral vascular disease, bronchospasm, mask hypoglycemia, inhibit uptake of K+ into skeletal muscle, interact with anesthetics, fatigue, lethargy, N/V/D, reduction in IOP

53
Q

Propranolol

A

non selective
decreased HR and contractility and increased vascular resistance
extensive 1st pass effect
goal: HR 55-60 bpm

concerns: decreased clearance of amide LA, decreased pulmonary clearance of fentanyl

54
Q

Propranolol pharmacokinetics

A

0.05mg/kg IV or 1-10 mg (1 mg slowly over 5 mins)
protein bound
metabolized in liver
elimination 1/2 time: 2-3 hours
risk of systemic toxicity of amide local anesthetics

55
Q

Metoprolol

A 
beta 1 selective
60% goes through 1st pass effect
PO 50-400 mg
IV 1-15 mg
metabolized in the liver
elimination 1/2 time: 3-4 hours
onset 3 minutes (IV)
56
Q

Atenolol

A

most selective beta 1 antagonist
elimination 1/2 time: 6-7 hours
not metabolized in liver, excreted in renal system

57
Q

Esmolol

A

rapid onset and offset (onset -60 seconds, DOA 10-30mintutes)
elimination 1/2 time: 9 minutes
beta 1 selective
metabolized by plasma esterases
useful for: HTN and tachycardia associated with laryngoscopy, pheochromocytoma, thyrotoxicosis, and thyroid storm

58
Q

Things to think about with someone taking Timolol eye drops

A

decreases BP and HR and increases airway resistance

59
Q

What is a good alternative for Timolol for asthmatics with glaucoma?

A

Betaxolol (less risk of bronchospasm)

60
Q

Labetalol

A

non-selective antagonists
metabolism conjugation of glucuronic acid
elimination 1/2 time: 5-8 hours
maximum drop in BP 5-10 minutes after IV dose
dose: 0.1 -0.5 mg/kg
usually give 5mg at a time

61
Q

Labetalol uses

A

decreases systemic BP with attenuated reflex tachycardia

use for intraop HTN and hypertensive crisis, hypotensive technique w/o increase in HR

62
Q

centrally acting agents pharmacokinetics

A

MOA: reduce sympathetic outflow from vasomotor centers in brain stem
site of action: CNS non adrenergic binding sites and a2 receptor agonism
uses: HTN, induce sedation, decrease anesthetic requirements, improve periop hemodynamics, analgesia

63
Q

why is it important to wean off of clonidine?

A

can cause rebound, profound HTN

64
Q

side effects of centrally acting agents

A

bradycardia, sedation, xerostomia, impaired concentration, nightmares, depression, vertigo, EPS, lactation in men

65
Q

withdrawal syndrome of centrally acting agents

A

occurs with doses of >1.2 mg/day

occurs 18 hours after acute discontinuation of drug and lasts for 24-72 hours

66
Q

treatment for hypotension

A

sympathomimetics: ephedrine, phenylephrine, vasopressin, epinephrine, norepinephrine, dopamine, dobutamine

Pharmacology II - CP (12 decks)

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