Adrenergic Antagonists- T2 Flashcards Preview

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Flashcards in Adrenergic Antagonists- T2 Deck (50):
1

alpha adrenergic receptor antagonists may be classified as

reversible competitive antagonists and irreversible competitive alpha-adrenergic antagonists

2

phentolamine is a

non-selective (both alpha 1 and 2) reversible competitive alpha-adrenergic receptor antagonists.

3

prazosin, doxazosin, and terazosin are

alpha1 selective reversible competitive alpha-adrenergic receptor antagonists

4

tamsulosin and silodosin (rapaflo) are

alpha1A/D selective reversible competitive alpha-adrenergic receptor antagonists

5

phenoxybenzamine is

a irreversible competitive non selective alpha adrenergic antagonist

6

4 piperazinyl quinazolines

prazosin, terazosin, doxazosin, alfuzosin

7

3 indoles

yohimbine, indoramin, silodosin

8

alpha1 and 2 adrenoceptors are responsible for the

maintenance of TPR and maintain pressure.

9

in many patients with essential HTN, TPR may be abnormally elevated due to

increased alpha-adrenergic receptor stimulation.

10

the 6 alpha-adrenergic receptor subtypes

1a, 1b, 1d, 2a, 2b, 2c

11

agents that antagonize both alpha1 and 2 tend to be

less efficacious in lowering BP than alpha1 selective

12

blockade of alpha2 adrenoceptors will cause

enhanced release of NE at the sympathetic neurons leading to excess adrenoceptor stimulation.

13

alpha2 blockage causes veno___ which leads to__

venodilation leading to a reduction in preload and then reduces SV.

14

why would we want to give a selective alpha antagonist opposed to non selective

giving a selective reduces the peripheral resistance, if it doesn't have selectivity, we won't have effects that come from antagonizing a specific alpha receptor.

15

prazosin and htn tx

a alpha1 selective antagonist that is prone to hepatic metabolism, has the shortest half life and primarily eliminated in the bile. if the patient has renal impairment you would want to use this.

16

doxazosin and terazosin in htn tx.

alpha1 selective antagonists have more renal eliminated of the parent compound and longer half life of elimination, would want to use these if the pt had liver failure.

17

antagonism of alpha1 adrenoceptors result in

dilation of arteries, arterioles, and veins.

18

arteriolar dilation results in

decreased after load (decreased TPR)

19

afterload is

the pressure that the heart has to work against.

20

venous dilation causes

decreased preload

21

decreased preload decreases

myocardial stretch and thus the CO.

22

efferent arteriolar dilation causes

decrease GFR which causes decrease Na in DCT and causes increased renin release.

23

what agents have equivalent BP lowering capacity to alpha1 selective antagonists

Ca channel blockers and thiazides

24

adverse effects of alpha1 selective adrenergic receptor antagonists

hypotension (first dose or orthostatic), dizziness, HA, congestion, impaired ejaculation and miosis

25

the lest well tolerated alpha1 selective antagonist

prazosin

26

alpha1 selective antagonists contraindicated in pts with

right heart failure or cardiac valvular stenosis.

27

how do alpha blockers make right heart failure worse

right HF is the right ventricle not ejecting the right amount of blood, too little filling, not enough stretch. alpha blockers decrease the preload, which makes RHF worse.

28

alternative use for alpha1 selective antagonists other than HTN

benign prostatic hyperplasia

29

tamsulosin is selective for what receptor

alpha1a

30

___ receptors predominate in the vasculature

alpha1b

31

why would you give terazosin for HTN and BPH?

because it isn't subtype selective like flomax is.

32

what is phenoxybenamines MOA and what is its therapeutic use

alkylates alpha 1 &2 adrenoceptors to cause decrease in receptors available for activation by catecholamines. used for pheochromocytoma where excess catecholamine production results in dangerously high BP

33

yohimbine is a selective

alpha2 receptor blocker that produces increase BP via CNS effects.

34

4 non selective b-receptor antagonists

propranolol, nadolol, timolol, pindolol

35

4 b1 receptor selective antagonists

metoprolol, atenolol, esmolol, acebutolol

36

2 beta and alpha1 selective antagonists

labetalol and carvedilol

37

what drug is a beta blocker with additional effects

bystolic, dilates blood vessels by NO release.

38

5 general things that distinguish members of the beta adrenergic receptor antagonist class

b1 vs non selectivity, partial agonism, alpha adrenoceptor blocking, lipid solubility, and inverse agonists.

39

b1 vs non-selectivity

propranolol has equivalent affinities for the 2 receptors while metoprolol, esmolol and atenolol show greater b1 receptor affinity

40

partial agonism with beta adrenergic antagonists

propranolol is an antagonist with no ability to active b-receptors; while pindolol and acebutolol behave more as a partial agonist

41

alpha-adrenoceptor blocking activity in regards to beta-adrenergic antagonist

most agents in this class are relatively b-selective however labetalol and carvedilol have significant alpha1 blocking activity.

42

lipid solubility

more lipophilic agents have greater CNS effects. this is why propranolol can be used for stage fright.

43

generally b-blockade causes

greater decreases in HR and contractility during sympathetic NS activity.

44

major effect of b-blockade

decrease cardiac rate and contractility to decrease Co and thereby MBP

45

initially ___ may rise due to beta2-blockade and/or reflex baroreceptor mechanism to maintain BP

TPR

46

partial agonists or alpha blocking activity may produce less increase in

TPR

47

b-antagonists also ___ renin release..

decrease. causing less circulating angiotensin II.

48

how do mixed antagonists decrease BP

by slpha1 blockage in the vasculature as well as beta-blockade in the heart.

49

partial b-receptor agonists produce smaller decreases in __ and may be preferred in pts with

CO. preferred in pts with bradycardia or decreased cardiac reserve.

50

pharmacological adverse effects of b-adrenergic antagonists

HF, bradycardia, angina after withdrawal, bronchoconstriction in asthmatics, fatigue, insomnia, depression.