Drugs (Midterm I) Flashcards

1
Q

Nicotine, DMPP, TEA

A

Class: Nicotinic Ganglionic Stimulating Receptors
MOA: Activate and desensitize nAChR in ganglionic synapses

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

Muscarine, Pilocarpine

A

Class: Muscarinic Ganglionic Stimulating Drugs
MOA: Stimulate mAChR and stimulates sympathetic nervous system via late EPSP

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

Pentolinium, TEA, Hexamethanonium

A

Class: Ganglionic Blockers
MOA: competitive antagonists and block nAChR

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

Botulinum Toxin

A

MOA: Inhibits ACh by entering the nerve terminal and acts as a protease to prevent neurotransmitter release

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

Gallamine, Curarine, Pancurenium

A

Class: Neuromuscular Blockers (Competitive non-depolarizing blocker)
MOA: Classical competitive antagonists at the nAChRs

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

Decamethonium-C10, Succinyl Choline

A

Class: Neuromuscular Blockers (Depolarizing blocker)
MOA: Partial agonists that bind to the receptors and activate them but antagonize ACh action

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

Edrophonium (a), neostigmine (b), DFP (c), echothiophate (c)

A

Class: Acetylcholinesterase blockers
MOA: Prevents the breakdown of ACh, increasing ACh in the synapse

There are 3 types: a) Reversible, b) Carbamate esters, c) Organophosphates

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

Activate and desensitize nAChR in ganglionic synapses

A

Nicotinic Ganglionic Stimulating Receptors (Nicotine, DMPP, TEA)

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

Stimulate mAChR and stimulates sympathetic nervous system via late EPSP

A

Muscarinic Ganglionic Stimulating Drugs (Muscarine, Pilocarpine)

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

Competitive antagonists and block nAChR

A

Ganglionic Blockers (Pentolinium, TEA, Hexamethanonium)

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

Inhibits ACh by entering the nerve terminal and acts as a protease to prevent neurotransmitter release

A

Botulinum Toxin

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

Classical competitive antagonists at the nAChRs

A

Neuromuscular Blockers (Competitive non-depolarizing blocker: Gallamine, Curarine, Pancurenium)

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

Partial agonists that bind to the receptors and activate them but antagonize ACh action

A

Neuromuscular Blockers (Depolarizing blocker: Decamethonium-C10, Succinyl Choline)

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

Prevents the breakdown of ACh, increasing ACh in the synapse

A

Acetylcholinesterase blockers

There are 3 types: a) Reversible: Edrophonium, b) Carbamate esters: neostigmine, c) Organophosphates: echothiophate, DFP

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

Carbachol, Bethanechol, Bethanecholamine, ACh

A

Class: Choline esters
MOA: mAChR and nAChR agonists (except bethanechol, not an agonist at nAChR)

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

Muscarine, Arecoline, Pilocarpine, Oxotremorine, Aceclidine

A

Class: Cholinomimetic Alkaloids
MOA: Mimics choline esters, relatively selective for mAChRs except arecoline which also activates nAChRs.

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

Belladonna

A

Class: Antimuscarinic drugs
MOA: Reversible inhibition of mAChRs, block parasympathetic stimulation

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

N-methylatropine, Ipratropium, Scopolamine

A

Class: Quaternary Muscarinic Antagonists
MOA: Antagonists to the mAChR and the nAChR

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

Atropine, Diphenhydramine (Benadryl), tricyclics, Scopolamine (anti mAChRs)
Curare, Hexamethonium (anti nAChRs)

A

Class: Anticholinergics
MOA: Competitively inhibit binding of ACh, more commonly in mAChRs, less so in nAChRs

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

Physostigmine, Neostigmine

A

Class: Anticholinesterases
MOA: Cholinometric effects at both nicotinic and muscarinic synapses by inhibiting AChE

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

Albuterol, Ritodrine, Tertbutaline, Salmeterol

A

Class: b2AR agonists
MOA: Mostly selective for b2ARs, will stimulate cAMP and PKA. Relaxation of VSM, bronchodilators, can delay labor (ritodrine), some have cardio effects

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

Dobutamine

A

One isomer is an a1 agonist, the other an a1 antagonist. b1AR antagonist, increases heart rate

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

Fenoldopam

A

Class: D1 agonists
MOA: Activates D1 receptors and increases cAMP levels which can cause vasodilation, lowering BP. No AR activity

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

DOPA, carbidopa

A

Used in treatment of Parkinson’s Disease. Leads to production of dopamine from DOPA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cocaine

A

Blocks vasopressor response to tyramine and potentiates response to NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Methamphetamine, Adderall, Cocaine, Pseudoephedrine

A

Class: Amphetamines
MOA: Blocks the uptake of NE and can stimulate both aARs and bARs causing increase in BP, decrease in HR, elevate cAMP in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

mAChR and nAChR agonists (except _____, not an agonist at nAChR)

A

Choline esters (Carbachol, Bethanechol*, Bethanecholamine, ACh)

*Bethanechol not an agonist at nAchR

28
Q

Mimics choline esters, relatively selective for mAChRs except ______ which also activates nAChRs.

A

Cholinomimetic Alkaloids (Muscarine, Arecoline*, Pilocarpine, Oxotremorine, Aceclidine)

*Arecoline activates mAChRs AND nAChRs

29
Q

Reversible inhibition of mAChRs, block parasympathetic stimulation

A

Antimuscarinic drugs (Belladonna)

30
Q

Antagonists to the mAChR and the nAChR

A

Quaternary Muscarinic Antagonists (N-methylatropine, Ipratropium, Scopolamine)

31
Q

Competitively inhibit binding of ACh, more commonly in mAChRs, less so in nAChRs

A

Anticholinergics (Atropine, Diphenhydramine (Benadryl), tricyclics, Scopolamine (anti mAChRs)
Curare, Hexamethonium (anti nAChRs))

32
Q

Cholinometric effects at both nicotinic and muscarinic synapses by inhibiting AChE

A

Anticholinesterases (Physostigmine, Neostigmine)

33
Q

Mostly selective for b2ARs, will stimulate cAMP and PKA. Relaxation of VSM, bronchodilators, can delay labor (______), some have cardio effects

A

b2AR agonists (Albuterol, Ritodrine*, Tertbutaline, Salmeterol)

*Ritodrine can delay labor

34
Q

One isomer is an a1 agonist, the other an a1 antagonist. b1AR antagonist, increases heart rate

A

Dobutamine

35
Q

Activates D1 receptors and increases cAMP levels which can cause vasodilation, lowering BP. No AR activity

A

Fenoldopam

36
Q

Blocks the uptake of NE and can stimulate both aARs and bARs causing increase in BP, decrease in HR, elevate cAMP in brain

A

Amphetamines (Methamphetamine, Adderall, Cocaine, Pseudoephedrine)

37
Q

Phenoxybenzamine

A

Class: Covalent nonselective aAR antagonists
MOA: Blocks aAR activation, both a1AR (Gaq) and a2AR (Gai)

38
Q

Phentolamine

A

Class: Noncovalent nonselective aAR antagonist
MOA: Blocks aAR activation, both a1AR (Gaq) and a2AR (Gai)

39
Q

Prazosin, terazosin

A

Class: a1AR selective antagonist
MOA: Blocks a1AR activation

40
Q

Yohimbine

A

Class: a2AR selective antagonist
MOA: Stimulates production of NO, causes vasodilation and erections

41
Q

Propranolol, timolol, nadolol

A

Class: Nonselective bAR antagonists
MOA: Blocks bARs in the heart, decreases cardiac output and renin secretion from kidney

42
Q

Atenolol, Metroprolol, Esmolol

A

Class: b1AR selective antagonists
MOA: Blocks b1AR activation

43
Q

Butozamine

A

Class: b2AR selective antagonists
MOA: Blocks b2AR activation

44
Q

Labetalol

A

Class: Mixed AR antagonist
MOA: Nonselective bAR antagonist, a1AR selective antagonist

45
Q

a-Methyldopa

A

Converted in nerve terminal to a-methylnorepinephrine, which is an a2AR agonist and acts in CNS to decrease sympathetic outflow. Used to treat hypertension

46
Q

Hydrochlorothiazide

A

Class: Thiazide
MOA: inhibits the Na+/Cl- cotransporter which decreases Na+/Cl- reabsorption, increase Ca2+ reabsorption, K+ excretion. Can decrease systolic blood pressure, decrease afterload
Toxicity: Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, allergic reactions , ineffective with low GFR

47
Q

Furosemide

A

Class: Loop
MOA: inhibits the Na+/K+/2Cl- transporter by binding Cl- site, preventing salts from being reabsorbed which prevents H2O reabsorption
Toxicity: Hypokalemic metabolic alkalosis, hearing loss/ringing in ears (reversible), hyperuricemia, hypomagnesemia, hyponatremia, allergic reactions

48
Q

Acetazolamide

A

Class: Carbonic anhydrase inhibitor
MOA: Inhibits enzyme carbonic anhydrase, which would decrease bicarbonate reabsorption, increase Cl- excretion
Toxicity: Hyperchloremic metabolic acidosis, Ca2+ renal stones, pins and needles under skin, sulfa allergy, fatigue and drowsiness

49
Q

Mannitol

A

Class: Osmotic
MOA: Increase in osmotic pressure in PT and TDLOH, decrease passive reabsorption of water, increased water and Na+ excretion. Activity dependent on development of osmotic pressure
Toxicity: Pulmonary edema, headache, nausea, vomiting, dehydration

50
Q

Amiloride/Spironolactone

A

Class: K+ sparing
MOA: inhibits Na+ channel in the CD. Spironolactone inhibits aldosterone receptor in the CD, decreasing Na+ pump expression/activity
Toxicity: Antiandrogen effects with spironolactone, hyperkalemia with Na+ channel blockers and aldosterone receptor antagonists

51
Q

Tolvaptan

A

Class: V2R antagonist
MOA: Inhibits V2 vasopressin receptor in DCT and CT, decrease aquaporin-2 insertion into apical membrane, increase water excretion
Toxicity: Nephrogenic diabetes, liver damage with prolonged use

52
Q

Blocks aAR activation, both a1AR (Gaq) and a2AR (Gai)

A

Covalent nonselective aAR antagonists (Phenoxybenzamine)

Noncovalent nonselective aAR antagonist (Phentolamine)

53
Q

Blocks a1AR activation

A

a1AR selective antagonist (Prazosin, terazosin)

54
Q

Stimulates production of NO, causes vasodilation and erections

A

a2AR selective antagonist (Yohimbine)

55
Q

Blocks bARs in the heart, decreases cardiac output and renin secretion from kidney

A

Nonselective bAR antagonists (Propranolol, timolol, nadolol)

56
Q

Blocks b1AR activation

A

b1AR selective antagonists (metoprolol, atenolol, esmolol)

57
Q

Blocks b2AR activation

A

b2AR selective antagonists (Butozamine)

58
Q

Nonselective bAR ntagonist, a1AR selective antagonist

A

Mixed AR antagonist (Labetolol)

59
Q

Converted in nerve terminal to a-methylnorepinephrine, which is an a2AR agonist and acts in CNS to decrease sympathetic outflow. Used to treat hypertension

A

a-Methyldopa

60
Q

Inhibits the Na+/Cl- cotransporter which decreases Na+/Cl- reabsorption, increase Ca2+ reabsorption, K+ excretion. Can decrease systolic blood pressure, decrease afterload

A

Thiazides (Hydrochlorothiazide)

61
Q

Inhibits the Na+/K+/2Cl- transporter by binding Cl- site, preventing salts from being reabsorbed which prevents H2O reabsorption

A

Loop diuretics (Furosemide)

62
Q

Inhibits enzyme carbonic anhydrase, which would decrease bicarbonate reabsorption, increase Cl- excretion

A

Carbonic anhydrase inhibitor (Acetazolamide)

63
Q

Increase in osmotic pressure in PT and TDLOH, decrease passive reabsorption of water, increased water and Na+ excretion. Activity dependent on development of osmotic pressure

A

Osmotic (Mannitol)

64
Q

Inhibits Na+ channel in the CD

Inhibits aldosterone receptor in the CD, decreasing Na+ pump expression/activity

A

K+ sparing (Amiloride, Spironolactone)

65
Q

Inhibits V2 vasopressin receptor in DCT and CT, decrease aquaporin-2 insertion into apical membrane, increase water excretion

A

V2 receptor antagonist (Tolvaptan)