Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > 7) Cholinoreceptor Blockers > Flashcards

7) Cholinoreceptor Blockers Flashcards

1
Q

The muscarinic blockers can also be subdivided based on their

A
  • Primary clinical target organs (CNS, eye, bronchi, or GI and genitourinary tracts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Drugs used for their effects on the CNS or the eye must be

A
  • Sufficiently lipid-soluble to cross lipid barriers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Charged (quaternary) amine group in the drug are

A
  • Polar
  • NOT lipophilic
  • Cannot be used for CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Competitive antagonists and their blocking effects can be overcome by

A
  • Increased muscarinic concentrations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Anticholinergic symptoms

A
  • Urinary retention
  • Sedation, dizziness, confusion, hallucinations
  • Dry throat/mouth, constipation
  • Feeling hot, decreased swetting
  • Blurred vision, dry eyes
  • Tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Non selective anti-muscarinic drugs

A
  • Scopolamine
  • Dicyclomine
  • Oxybutinin
  • Atropine
  • Homoatropine
  • Cyclopentolate
  • Tropicamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Selective anti-muscarinic drugs

A
  • Darifenacin
  • Fesoterodine
  • Solifenacin
  • Tolterodine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Scopolamine

A
  • Motion sickness
  • Targets CNS
  • DOA = 2-6 hours
  • Brand = TransdermScop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Dicyclomine

A
  • Intestinal cramping
  • Targets GI
  • DOA = 1 hour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Oxybutinin

A
  • Reduce bladder urgency
  • Targets bladder
  • DOA = 6-10 hours
  • Brand = Oxytrol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Atropine

A
  • Dilates pupils (mydriasis), cramping, hypermotility in diarrhea
  • Targets eye and gut
  • DOA = 2-4 hours (except > 72 hours in eye)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Characteristic of atropine

A
  • Competitive antagonist of all Ms

- Antidote for cholinesterase inhibitors of toxicity

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

Homoatropine

A
  • Dilates pupils (mydriasis)
  • Targets eye
  • DOA > 24 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cyclopentolate

A
  • Dilates pupils (mydriasis)
  • Targets eye
  • DOA = 2-12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tropicamide

A
  • Dilates pupils (mydriasis)
  • Targets eye
  • DOA = 0.5-4 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Darifenacin, fesoterodine, solifenacin, and tolterodine usage

A
  • Urinary urgency/incontinence
  • Overactive bladder
  • Selective for M3 receptors
  • Oral administration
  • DOA = 12-24 hours
  • Excessive parasympatholytic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Ipratorium (Atrovent HFA)

A
  • Short acting muscarinic antagonist (SAMA) in the lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ipratorium (Atrovent HFA) selectivity

A
  • Non-selective antagonist of M1, M2, and M3 muscarinic racetylcholine receptors (mAChRs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ipratorium (Atrovent HFA) effects

A
  • Allows bronchodilation in asthma/COPD
  • OOA = 10 min
  • Peak = 2 hours
  • DOA = 6 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ipratorium (Atrovent HFA) administration route

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

Ipratorium (Atrovent HFA) metabolism

A
  • Partially metabolized to inactive ester hydrolysis products
  • Excreted in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Long acting muscarinic antagonists (LAMA) in lungs

A
  • Aclidinium
  • Glycopyrrolate
  • Tiotropium
  • Umeclidinium
  • MOA for all = reversible antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Aclidinium selectivity

A
  • Non-selective M receptors
  • Similar affinity to all Ms
  • Dissociation half life from subtype M3 = 30 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

LAMA dosage form

A
  • Oral inhalation

- Causes bronchodilation in asthma/COPD

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

Aclidinium brand

A
  • Tudorza

- Pressair

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

Aclidinium peak and DOA

A
  • Peak = 10 min

- DOA = 12 hours

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

Aclidinium metabolism

A
  • Rapid and extensive hydrolysis via plasma esterases
  • Become inactive metabolites
  • Excreted in urine
28
Q

Glycopyrrolate selectivity

A
  • Non-selective, but acts mainly on M3
29
Q

Glycopyrrolate brand

A
  • Seebri

- Neohaler

30
Q

Glycopyrrolate peak and DOA

A
  • Peak = 5 min

- DOA = > 24 hours

31
Q

Glycopyrrolate metabolism

A
  • Hepatic (minimal) then bile excreted
32
Q

Tiotropium selectivity

A
  • Non-selective, but acts mainly on M3

- Has short M2 activity

33
Q

Tiotropium brand

A
  • Spiriva

- Handihaler/Respimat

34
Q

Tiotropium peak and DOA

A
  • Peak = 10 min

- DOA = 24 hours

35
Q

Tiotropium metabolism

A
  • Hepatic (minimal)

- Urine excreted

36
Q

Umeclidinium selectivity

A
  • M3 inhibitor
37
Q

Umeclidinium brand

A
  • Incruse Ellipta
38
Q

Umeclidinium peak and DOA

A
  • Peak = 10 min

- DOA = 24 hours

39
Q

Umeclidinium metabolsim

A
  • Hepatic via CYP2D6

- Excreted in feces

40
Q

Nicotinic antagonists

A
  • Ganglionic blockers

- Neuromuscular blockers

41
Q

Ganglionic blockers

A
  • Competitive antagonists

- Drugs are discontinued because of severe side effects

42
Q

Neuromuscular blockers

A
  • Block transmission at muscle end plate

- Muscle relaxation (required for surgical relaxation, tracheal intubation, and control of ventilation)

43
Q

Neuromuscular blockers structure

A
  • Quaternary amines structurally related to acetylcholine (ACh)
44
Q

Most NMB are

A
  • Antagonists (nondepolarizing type)

- Prototype = tubocurarine

45
Q

Succinylcholine (a neuromuscular blocker)

A
  • Agonist at the nicotinic end plate receptor

- Depolarizing type

46
Q

Neuromuscular blocking drugs are quaternary amines thus they do not enter

A
  • CNS

- No effect on cognition, memory, or sensory input, including perception of pain

47
Q

NMB mechanism of action

A
  • ACh (normal agonist) opens the sodium channel

- Non-depolarizing and depolarizing blockers

48
Q

Non-depolarizing blockers

A
  • Bind to the receptor to prevent opening of the channel
49
Q

Depolarization blockers (Succinylcholine)

A
  • Initial depolarization accompanied by twitching and fasciculations
  • Then persistent depolarization (followed by repolarization) of the channel
  • Leads to muscle relaxation and paralysis
50
Q

All non-depolarizing NMBs are administered

A
  • Parenterally

- Highly polar drugs that can’t cross BBB

51
Q

Rocuronium (non-depolarizing NMB)

A
  • Eliminated in bile
  • DOA = 10-20 min
  • Most rapid onset time (60-120 seconds)
52
Q

Metocurine, pancuronium, pipecuronium, and tubocurarine (non-depolarizing NMBs)

A
  • Eliminated via kidney

- Usually have durations of action of 35–60 min

53
Q

Atracurium (non-depolarizing NMB)

A
  • Hepatic metabolism
  • Clearance forms laudanosine (can cause seizures)
  • Rarely used
54
Q

Cisatracurium (non-depolarizing NMB)

A
  • Stereoisomer of atracurium
  • Inactivated spontaneously but forms less laudanosine
  • One of the most commonly used muscle relaxants in clinical practice
55
Q

Non-depolarizing drugs prevent the action of

A
  • ACh at the skeletal muscle end plate

- Can be overcome by increasing the amount of agonist [ACh] in the synaptic cleft

56
Q

Succinylcholine (depolarizing NMB)

A
  • Duration of action of only a few minutes if given as a single dose
57
Q

Succinylcholine effects

A
  • Stimulates autonomic ganglia

- Stimulates cardiac muscarinic receptors

58
Q

Depolarizing NMB (Succinylcholine) toxicity

A
  • Muscle pain and muscle damage may occur
  • Hyperkalemia, especially in patients with burns or spinal cord injury, peripheral nerve dysfunction, or muscular dystrophy
  • Increases in intragastric pressure caused by fasciculations
59
Q

List of non-depolarizing NMBs

A
  • Atracurium
  • Cisatracurium
  • Rocuronium
  • Pancuronium
  • Tubocuranine
  • Vecuronium
  • Doxacurium
  • Pipecurium
60
Q

Pancuronium effects

A
  • Moderate block of cardiac muscarinic receptors
61
Q

Tubocuranine effects

A
  • Moderate ability to release histamine
62
Q

Non-depolarizing NMBs toxicity

A
  • Respiratory paralysis
63
Q

Cholinesterase generators

A
  • Pralidoxime (2PAM)
64
Q

Pralidoxime (2PAM) use

A
  • Treat exposure to organophosphate AChE inhibitor insecticides (such as parathion) or to nerve gas
65
Q

Pralidoxime (2PAM) structure/MOA

A
  • Oxime that binds to organophosphate inactivated by acetylcholinesterase

Pharmacology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions