Exam 2: Cholingerics/Adrenergics Flashcards

(66 cards)

1
Q

Phentolamine

A

Alpha Antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Phenoxybenzamine

A

Long acting alpha antagonist. Used for pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Esters of Choline

A

ACh, succinylcholine, methacholine, carbachol, bethanochol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alkaloids

A

Muscarine, nicotine, pilocarpine, lobeline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Classes of direct acting cholinergics

A

Esters of Choline and Alkaloids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Indirect acting Cholinergics Classes

A

Simple alcohols, carbamic acid esters of alcohol, organic derivatives of phosphoric acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Simple alcohol indirect AChE inhibitor

A

Edrophonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Carbamic acid esters of alcohol AChE inhibitors

A

Carbamate, neostigmine, pyridostigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AChE inhibitor, long acting, covalently bound.

A

Organophosphates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Antimuscarinic drugs

A

Atropine, tropicamide, scopolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Reversal agent for organophosphate

A

2-PAM (Pralidoxine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Neuromuscular junction blocker

A

Succinylcholine and Curare derivatives (pancuronium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Difference between depolarizing and non depolarizing muscle relaxants?

A

Depolarizing bind to ACh receptors, cause depolarization, and do not immediately release from receptor. Not broken down by AChE.

Non depolarizing muscle relaxants bind to ACh receptor and block depolarization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Main side effects of depolarizing muscle relaxants?

A

Malignant hyperthermia and hyperkalemia.

Minor side effects include muscle pain, fasciculation, apnea (expected for intubation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Reversal agent for NMB, muscle relaxants?

A

Neostigmine (many side effects)
Sugammadex (only works with some curare derivatives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Antimuscarinic used for routine eye exam

A

Tropicamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cholingeric used for Dx of Myasthenia Gravis?

A

Edrophonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cholinergic drug used for bladder dysfunction?

A

Bethanocol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cholinergic drug used to decrease IOP?

A

Carbachol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Carbamates are generally associated with what diseases/disorders?

A

Glaucoma, post op ileus, myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Side effects of Atropine

A

BRAND. Blind, red, absence bowels sounds, nuts (AMS), dry.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Meds used for atropine toxicity

A

Physostigmine or neostigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mushroom that does not respond to atropine

A

A. Phalloides. Deadly night cap. Inhibits mRNA. Leads to renal/liver failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What was the plant that atropine was derived from initially used for (Atropa belladona)

A

Pupil dilation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Fatal dose of nicotine? What is treatment for nicotine toxicity?
40 mg. Inducing vomiting.
26
What medications work on organophosphates after the aging process?
None. Important to give pralidoxine any time muscarinic excess is seen in case organophosphate is the cause. Aging strengthens the covalent bond and prevents breakdown.
27
S/s of mycetism (muscarinic excess)
SLUDGE- M Salivation, lacrimation, urination, defecation, GI motility increased, emesis and myosis (pupil construction).
28
Muscarinic used to dx asthma?
Methacholine
29
Direct Adrenergic Agonist
NE, EPI, Dobutamine, dopamine, isoproterenol, phenylephrine, midodrine, clonidine.
30
Indirect acting adrenergic agonist
Amphetamine and cocaine.
31
Catecholamine components
Catechol and amine group
32
What inactivates catecholamines in the gut?
COMT catechol-O-methyltransferase
33
How does substitution at Benzene ring affect metabolism/inactivation?
Non-catecholamines are not broken down in the gut. Therefore their bioavailability is higher and can be given PO.
34
Give an example of a non catecholamine that is given PO and explain its use?
Phenylephrine can be given PO as a nasal decongestant. It constricts vessels in mucous membrane decreasing mucous production.
35
How can you identify the alpha carbon?
Alpha carbon is the Carbon nearest to the amine group.
36
How does altering the alpha carbon affect drug metabolism?
It alters the drug in a way that makes MAO ineffective. Longer during of drug effect.
37
List drugs that possess an alpha carbon substitution
Ephedrine and amphetamines.
38
Irreversible Alpha antagonist? What is the indication for this drug?
Phenoxybenzamine. This drug is used to treat pheochromocytoma, an adrenal medulla tumors that causes over production of epi.
39
List Alpha antagonists
Phentolamine, Phenoxybenzamine, the -zosin drugs.
40
Phentolamine used for
HTN r/t pheochromocytoma. ED although not commonly used d/t direct injection administration
41
Prazosin drug indication
Used for HTN and primarily used for BPH. Alpha 1 selective.
42
Alpha 2 selective antagonist
Yohimbine
43
1st Beta blocker, non selective
Propranolol.
44
What disease processes can non selective beta blockers worsen
Respiratory diseases. Specifically COPD d/t increases airway resistance seen with blocking of Beta 2. Worsen obesity and high cholesterol thru inactivation of beta 3.
45
Beta 1 selective drugs
Metoprolol, atenolol, esmolol, nebivolol.
46
Beta 1 selective agonist
Dobutamine.
47
Pure alpha agonist
Phenylephrine
48
Midodrine used primarily for
Orthostatic hypotension
49
Non catecholamine that crosses BBB
Ephedrine
50
How do cocaine and amphetamines affect NET?
Cocaine blocks the NET, causing NE to remain in synapse longer. Amphetamines reverse the NET and fluid the synapse with increased levels of NE.
51
Sympathomimetic that is found in fermented food
Tyramine
52
How do MAOIs effect blood pressure?
MAOI block the oxidation of catecholamines thru MAO, thereby increasing blood pressure.
53
How is NE formed? How is it stored and released?
1. Tyrosine is transported into presynaptic membrane via an amino acid transporter. (This isn’t a target for drugs as AA are vital to functioning) 2. Tyrosine is converted to NE (via tyrosine hydroxylase…FYI) 3. NE is transported to vesicle via Vesicular Mona amine transporter VMAT. 4. Voltage gated Ca enters presynaptic vesicle and initiates fusion of vesicle to membrane. 5. SNAPS and VAMPS anchor vesicle to membrane.
54
How is NE degraded
NE diffuses away to neighboring cells, is taken back up into presynaptic vesicle via NET. NE does not get degraded in synapse. The degradation can take place inside the presynaptic vesicle via MAO.
55
What drugs target the NE transmission and what steps in NE transmission do they work on? (Not on test?)
Metyrosine acts on the tyrosine hydroxylase step where tyrosine is converted to NE. Reserpine blocks the storage of NE into vesicle, VMAT. Bretylium and guanethidine inhibit NE release.
56
Explain the disease process of myasthenia gravis
Myasthenia Gravis is an autoimmune disease where the body develops antibodies to the ACh receptors. The antibodies bind to the receptor, causing endocytosis of the receptor itself. Over time the amount of ACh receptors diminishes leading to impaired muscle contraction
57
Alpha 1 agonist uses which G Protein and which effect
Gq. Therefore it activates phospholipase C to increase IP3 and DAG.
58
Alpha 2 agonist uses which G Protein and which effect
Gi therefore it decreases cAMP.
59
Beta agonist uses which G Protein and which effect
Gs stimulates increase in cAMP
60
Alpha agonist effects
Increased PVR, decrease heart rate d/t vagal reflex, increased BP
61
Beta agonist effects
Decreased PVR, increased contractility, increased heart rate, blood pressure decreased
62
Alpha 1 locations and effect
Most vascular smooth muscle, prostrate, heart. Effect: contraction.
63
Alpha 2 locations and effect
Adrenergic and cholinergic nerve terminals. Inhibition of transmitter release.
64
Beta 1 location and effect
Heart/juxtaglomerular cells Effect: increased force and rate of contraction. Increased Renin release.
65
Beta 2 location and action
Respiratory, uterine and vascular smooth muscle. Effect: bronchodilator. Smooth muscle relaxation.
66
Dopamine 1 location and effect
Smooth muscle. Effect: dilates renal blood vessels, decreasing blood pressure. Increased doses increased blood pressure.