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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
Hypertensive crisis
diastolic pressure >120 with evidence of end organ damage goal: decrease DBP 100-105 ASAP can use Nitroprusside, Nitroglycerin, Labetalol, Fenoldapam
26
Alpha antagonists
bind selectively to alpha receptors and interfere with the ability of catecholamines to cause a response
27
Which alpha antagonist binds covalently?
Phenoxybenzamine
28
Which alpha antagonists are competitive?
Phentolamine, Prazosin, Yohimibine
29
Alpha 1 antagonists cause
smooth muscle relaxation, decrease PVR and BP used for HTN and BPH
30
Which alpha antagonists are more selective for alpha 1 over alpha 2 receptors?
prazosin, terazosin, doxazosin, phenoxybenzamine
31
what are our mixed alpha and beta antagonists?
labetalol and carvedilol | B1 = B2 > a1 > a2
32
which beta antagonist is more sensitive to B2 over B1?
Butoxamine
33
Side effect of alpha 1 antagonists?
postural hypotension d/t failure of venous vasoconstriction
34
Phenoxybenzamine
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
Phentolamine
``` 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
Prazosin
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
Yohimibine
alpha 2 selective blocker increases release of norepi from post-synaptic neuron used for orthostatic hypotension, impotence
38
What is our biggest concern if our patient takes terazosin and tamsulosin for BPH?
orthostatic hypotension
39
1st generation non selective beta antagonists
Nadolol, penbutolol, pindolol, propranolol, timolol
40
2nd generative B1 selective antagonists
acebutolol, atenolol, bisoprolol, esmolol, metoprolol
41
3rd generation non selective beta antagonists
carteolol, carvedilol, bucindolol, labetolol
42
4th generation B1 selective antagonists
betaxolol, caliprolol, nebivolol
43
What do beta adrenergic receptor antagonists do?
disallow sympathomimetics from provoking a beta response on the heart, airway, blood vessels, juxtaglomerular cells, and pancreas
44
beta antagonist effects on heart
bradycardia, decreased contractility, decreased conduction velocity, improve O2 supply and demand balance
45
beta antagonist effects on airway
bronchoconstriction and can provoke bronchospasm in those with asthma or COPD
46
beta antagonist effects on blood vessels
vasoconstriction in skeletal muscles, PVD symptoms increase
47
beta antagonist effects on juxtaglomerular cells
decrease renin release - indirect way of decreasing BP
48
beta antagonist effects on pancreas
decreased stimulation of insulin release by epi/norepi at B2 and then masks symptoms of hypoglycemia
49
chronic use of beta blockers is associated with
increase in the number of receptors (up regulation) and need to be continued in the OR
50
clinical uses of beta blockers
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
relative contraindications of beta blockers
pre-existing AV heart block or cardiac failure, reactive airway disease, diabetes mellitus, hypovolemia
52
side effects of beta blockers
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
Propranolol
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
Propranolol pharmacokinetics
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
Metoprolol
``` 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
Atenolol
most selective beta 1 antagonist elimination 1/2 time: 6-7 hours not metabolized in liver, excreted in renal system
57
Esmolol
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
Things to think about with someone taking Timolol eye drops
decreases BP and HR and increases airway resistance
59
What is a good alternative for Timolol for asthmatics with glaucoma?
Betaxolol (less risk of bronchospasm)
60
Labetalol
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
Labetalol uses
decreases systemic BP with attenuated reflex tachycardia | use for intraop HTN and hypertensive crisis, hypotensive technique w/o increase in HR
62
centrally acting agents pharmacokinetics
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
why is it important to wean off of clonidine?
can cause rebound, profound HTN
64
side effects of centrally acting agents
bradycardia, sedation, xerostomia, impaired concentration, nightmares, depression, vertigo, EPS, lactation in men
65
withdrawal syndrome of centrally acting agents
occurs with doses of >1.2 mg/day | occurs 18 hours after acute discontinuation of drug and lasts for 24-72 hours
66
treatment for hypotension
sympathomimetics: ephedrine, phenylephrine, vasopressin, epinephrine, norepinephrine, dopamine, dobutamine

Pharmacology II - CP (12 decks)

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