Endogenous/Drug effects on receptor COPY bottom half/beta blockers

Question 1

Baroceptor response often stay intact if using

Answer 1

clonidine or dexmedetomidine

Question 2

Fenoldopam is

what receptor

Answer 2

D1 receptor agonist

vasodilator for acute treatment of severe HTN

Question 3

Amphetamine and dextroamphetamine

Answer 3

Acts indirectly by releasing biogenic amines
from storage sites in nerve terminals
– Activates RAS
– Can cause psychosis (5-HT mediated)
– Anorectic, locomotor stimulant (DA mediated

Question 4

Phenoxybenzamine
6 things
what is it?
where does it bind? 
causes?
enhanced by what?
Useful in two things?

Answer 4

-Phenoxybenzamine-vasodilator
-Blocks A1 & A2 irreversibly/Antagonists
-Causes decrease in SVR and increase in CO
(reflex)
– Hypotension enhanced with b2 agonists
– Useful in pheochromocytoma and in
-autonomic hyperreflexia, SC injury

Question 5

Phentolamine
5
what is it
use
duration
S/E
contra in who

Answer 5

Phentolamine
Blocks A1 &A2 receptors COMPETITIVELY
– Mainly used in preoperative management of
pheochromocytoma
• Same as phenoxybenzamine, but short-lived (~15
min following IV bolus)
– Causes release of histamine
• Contraindicated in CAD

Question 6

Prazosin

Answer 6

Prazosin/CHF
Potent A1 receptor antagonist/no A2 blockade (no increase in NE release)
• Blocks A1 receptors in arterioles
• Decreases SVR & venous return to heart
– Does not usually cause increase in HR or SV
• half-life 2-3 hours
• Terazosin (Hytrin®) is structural analog of
prazosin
– Also has high specificity for A1 receptors

Question 7

A1-Adrenergic Antagonists
Therapeutic uses
2

Answer 7

A1-Adrenergic Antagonists
Therapeutic uses
-CHF/A1 receptor blockade dilates arteries
• Decrease afterload and preload
-BPH
• A1 receptor antagonists reduce resistance in some
patients
• A1 receptors in bladder trigone and urethra contribute to
blockage
• Essential hypertension & prostatic hypertrophy
(prazosin, doxazosin, terazosin)

Question 8

Yohimbine

inhibits what

Answer 8

Erectile dysfunction (Yohimbine)
• Blockade with selective antagonists
(yohimbine) can increase sympathetic
outflow
A2 receptor antagonist
• Increase SNS activity
• Inhibits the function of monoamine
oxidase enzymes

Question 9

Therapeutic Uses of A Blockers
(Antagonists)
5

Answer 9

• Hypertension
• Pheochromocytoma
• Benign prostatic hyperplasia
• Peripheral vascular disease
• Erectile dysfunction (Yohimbine)

Question 10

Beta Antagonists (B-Blockers) used to treat
4

Answer 10

Used to Tx: CAD, HTN, HF, tachydysrhythmias

Question 11

Cardiac selective (β1 receptor) drugs

Answer 11

Atenolol, metoprolol, esmolol
-Relative selectivity; much less vascular, bronchial smooth
muscle, and metabolic effects

Question 12

Beta blockers Intrinsic sympathomimetic activity (ISA) (partial
agonist activity) drugs

Answer 12

Pindolol, acebutolol
Less slowing of HR at rest; exercise induced ↑ HR still blunted
like non-ISA β-blockers

Question 13

Beta blocker Membrane stabilizing activity (MSA)

Answer 13

Acebutolol, labetalol, metoprolol, pindolol, and

propranolol

Question 14

Beta blocker that vasodilates

Answer 14

Nebivolol vasodilates via endothelial dependent

NO pathway

Question 15

B antagonists block

Answer 15

renin release caused by
SNS stimulation
Reduction in plasma renin activity causes anti-HTN

Question 16

Beta blockers cause these negative effects on the heart

Answer 16

decreased sinus rate, spontaneous &

depolarization of ectopic foci

Question 17

Propranolol is life threating to what patient population? Why

Answer 17

COPD & asthma

blocks B2 receptor

Question 18

Beta blockers cause hypoglycemia. Why ?

4

Answer 18

Beta blockers cause hypoglycemia. Why ?
Metabolic effects
– Catecholamines promote glycogenolysis and mobilize glucose in response to hypoglycemia
-B adrenergic antagonists may block this response
-B2 receptor blockade may inhibit hepatic
response to insulin-induced hypoglycemia
-B3 adrenergic antagonists attenuate the
release of free fatty acids from adipose tissue

Question 19

Propranolol

Answer 19

non selective beta
Interacts with B1& B2 receptors with equal
affinity
Highly lipophilic with large VD
• Crosses BBB
– Lacks intrinsic sympathomimetic activity
– Extensively metabolized
– Propranolol may be administered IV for
management of life-threatening dysrhythmias
or to patients under anesthesia
• 1-3 mg administered slowly
• If bradycardia is profound - atropine may be used

Question 20

Metoprolol

Answer 20

Metoprolol
– β1/β2-receptor affinity (30:1); membrane
stabilizing activity (MSA); no ISA
– Primarily liver metabolism
– ½ as potent as propranolol
– Short elimination half-life 3.5 hrs

Question 21

Atenolol

Answer 21

β1/β2-receptor affinity (30:1); no MSA or ISA
activity
– Primarily excreted via kidneys; no first-pass
metabolism
– Elimination half-life 6.5 hrs, so once daily dosing

Question 22

Pindolol

Answer 22

Nonselective β–blocker that has MSA and

ISA

Question 23

Acebutolol

Answer 23

β1-selective with ISA

Question 24

Esmolol

Answer 24

β1-selective; IV rapid onset and offset
(<10 min.)
– Rapid hydrolysis by non-specific esterases

Question 25

Esmolol

Answer 25

Esmolol • B1 selective adrenergic antagonist with very short duration of action t1/2B 8-9 minutes • Esmolol has an ester linkage (nonspecific esterases – red blood cells) • Rapidly hydrolyzed • Onset (2 minutes) and cessation of B adrenergic blockade are rapid • Peak hemodynamic effect in 10 minutes • Esmolol has little, if any, ISA • Anesthesia uses: – Rapid, brief control of ↑ HR (i.e.: to prevent tachycardia from intubation stimulation) – Infusions can be quickly terminated if needed

Question 26

POISE

Answer 26

Dont hold beta blockers, control rate <80 | beta blocker time out

Question 27

Labetalol Selective ___ and nonselective ___blocker 5x-10x more potent ____ blocker than____ blocker (7:1)

Answer 27

``` Competitive antagonists at A1 and B receptors – Selective a and nonselective b blocker – Racemic mixture with 4 stereoisomers a1 blockade leads to arteriolar dilation b1 blockade leads to decrease in BP by blocking reflex sympathetic stimulation • 5x-10x more potent b blocker than a blocker (7:1) • Extensively metabolized in liver • Elimination half life of 5 hrs • Onset 2-5 minutes, peak 5-15 minutes, and DOA 2-4 hrs • 5-10 mg TTE every 10 minutes ```

Question 28

Adverse Effects of Beta Blockers | 8

Answer 28

``` • Bronchoconstriction • Bradycardia, A-V block, cardiac arrest • Decreased cardiac output • Sudden withdrawal problems • Hypoglycemia problems • Diminished exercise performance • Possible changes in blood lipids • Potential CNS effects ```

Question 29

use__________for bronchial asthma | drug

Answer 29

albuterol

Question 30

use__________for cardiogenic shock | drug

Answer 30

dopamine/dobutamine

Question 31

use__________for rhinitis | drug

Answer 31

phenylephrine

Question 32

use__________for HTN | drug

Answer 32

prazosin

Question 33

use__________for angina pectoris | drug

Answer 33

propranolol

Question 34

use__________for supraventricular arrhythmias | drug

Answer 34

atenolol

Question 35

use__________for BPH | drug

Answer 35

terazosin or prazosin

Question 36

Therapeutic Uses of Beta | Blockers

Answer 36

* Hypertension * Ischemic heart disease * Cardiac arrhythmias * Obstructive cardiomyopathy * Congestive heart failure * Open-angle glaucoma B1 * Migraine headache * Muscle tremor, performance anxiety propranolol

Question 37

Indirect acting irreversible muscarinic?

Answer 37

echothiopate

Question 38

indirect acting reversible muscarinic? | 3

Answer 38

edrophonium, neostigmine, physostigmine

Question 39

Bethanechol

Answer 39

Bethanechol M3 muscarinic agonist Used post-op to treat urinary retention and abdominal distention – Treat neurogenic G.I. atony and megacolon (increase intestinal motility)

Question 40

Pilocarpine

Answer 40

m3 muscarinic agonist Pilocarpine - topical miotic, glaucoma (decrease intraocular pressure

Question 41

Muscarinic Agonists | Clinical Uses

Answer 41

``` Reduces IOP by causing contraction of ciliary body • facilitates aqueous humor outflow • can be treated with cholinergic agonists or cholinesterase inhibitors ```

Question 42

Atropine

Answer 42

CNS effects occur with high doses of atropine – effects from restlessness to somnolence – toxic doses cause more prominent symptoms • disorientation, hallucinations, and delirium – larger (toxic) doses cause depression, circulatory collapse

Question 43

scopolamine

Answer 43

``` Antimuscarinic less likely to change heart depresses RAS – may cause delayed awakening from anesthesia – used for motion-sickness • blocks medullary impulses arising from vestibular overstimulation • transdermal (postauricular) provides sustained blood levels Scopolamine in therapeutic doses may be used for sedation – can be combined with an opioid – drowsiness, amnesia, and fatigue – Intravenous dosing (0.3-0.6 mg ```

Question 44

Glycopyrrolate chem structure doesn't do what why

Answer 44

Glycopyrrolate is a quaternary amine – devoid of sedative effects – does not cross BBB

Question 45

Muscarinic relatively contraindicated

Answer 45

in narrowangle glaucoma • causes flow obstruction • interferes with flow of aqueous humor

Question 46

Scopolamine produces sedation

Answer 46

``` Scopolamine produces sedation by decreasing activity of the RAS (100x more than atropine) – Also effects other areas of brain resulting in amnesia • May have delayed awakening • Physostigmine is effective in reversing restlessness or somnolence from CNS effects of tertiary amine antimuscarinics ```

Question 47

Scopolamine produces sedation by

Answer 47

``` Scopolamine produces sedation by decreasing activity of the RAS (100x more than atropine) – Also effects other areas of brain resulting in amnesia • May have delayed awakening • Physostigmine is effective in reversing restlessness or somnolence from CNS effects of tertiary amine antimuscarinics ```

Question 48

Tiotropium - DOA

Answer 48

>24 hrs

Question 49

Most potent antisialagogue in order order of potency

Answer 49

scopolamine glycopyrrolate atropine

Question 50

Horner Syndrome

Answer 50

``` Stellate ganglion – Superior, middle, and cervicothoracic ganglia – Spinal segments T1-4/5 synapse here – Provide SNS innervation of ↑ ext., head, neck – So? – Horner syndrome • Ptosis • Miosis • Anhidrosis • Enophthalmos • Redness of face and conjunctiva ```

Question 51

Dopamine

Answer 51

Precursor of NE • Effects are mediated through D1 receptors • Low doses primarily activate D1 receptors – Vascular postjunctional D1 receptors in renal and mesenteric blood vessels – 0.5-3.0 mcg/kg/min • Moderate DA dosages act on B1 receptors – 3.0 - 10 mcg/kg/min Higher dosages 10 - 20 mcg/kg/min primarily act at a1 receptors – Leads to vascular vasoconstriction – Low dose increased renal blood flow and GFR – Moderate dose increases myocardial contractility and increase in CO – High dosages vasoconstriction • Benefit to renal perfusion may be lost – Dopamine is an important central neurotransmitter • Peripherally administered dopamine has no central side effects • Substrate for MAO & COMT – Half-life of about a minute

Question 52

Ipatropium/tiotropium

Answer 52

Muscarinic antagonists quaternary compounds used to treat reactive airway disease – used as an inhalant – does not impair mucociliary elevator – toxicity not usually a problem since this compound is poorly absorbed from lungs into circulation

Question 53

Echothipoate

Answer 53

Muscarinic agonist irreversible indirect | glaucoma

Question 54

Carvedilol is similar to ___________and good for

Answer 54

labetalol, chf