Brainscape's Knowledge GenomeTM

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


See full index

MJ- P2 E2 > Blocking Drugs - 1 > Flashcards

Blocking Drugs - 1 Flashcards

1
Q

Drugs that affect skeletal muscle function include which two different therapeutic groups?

A

neuromuscular blockers

spasmolytics/antispasmodics

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

used during surgical procedures and in the intensive care unit (ICU) to produce muscle paralysis

Which drug?

A

neuromuscular blockers

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

those used to reduce spasticity in a variety of painful conditions

Which drug?

A

antispasmodics/spasmolytics

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

____________________ interfere with transmission at the neuromuscular end plate and lack central nervous system (CNS) activity

A

neuromuscular blocking drugs

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

How else can neuromuscular blocking drugs be used?

A

Adjuncts during general anesthesia to optimize surgical conditions and to facilitate endotracheal intubation in order to ensure adequate ventilation

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

NMB drugs structurally resemble which neurotransmitter?

A

acetylcholine

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

__________ is a depolarizing agent.

A

Succinylcholine is a depolarizing agent.

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

What are you the 2 major families of nondepolarizing agents and the drugs beneath them?

A
  • Drug class: Isoquinoline
    • tubocuraine
  • Drug class: steroid derivatives
    • pancuronium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which domains on the nicotinic acetylcholine receptror (nAChR) line the channel pore?

A

M2

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

Where do the binding pockets for ACh occur?

A

α-β and the δ-α subunit interfaces

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

This drug occupies the receptor AND blocks the channel.

Normal closure of the channel gate is prevented and the blocker may move rapidly in and out of the pore.

This drug may desensitize the end plate by occupying the receptor and causing persistent depolarization.

Which drug is this?

A

Succinylcholine

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

An additional effect of drugs on the end plate channel may occur through changes in the _____________ surrounding the channel.

General anesthetics and alcohols may impair ________________ by this mechanism

A

An additional effect of drugs on the end plate channel may occur through changes in the lipid environment surrounding the channel.

General anesthetics and alcohols may impair neuromuscular transmission by this mechanism.

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

What are the names of the idoquinoline derivatives?

A

atracurium

cisatracurium

mivacurium

tubocuraine

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

What are the names of the steroid derivatives?

A

pancuronium

rocuronium

vecuronium

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

Which isoquinoline derivative has spontaneous elimination?

A

atracurium

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

Drugs that are excreted by the _________ typically have longer half-lives, leadring to longer durations of action (>35 minutes).

A

Drugs that are excreted by the kidney typically have longer half-lives, leadring to longer durations of action (>35 minutes).

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

Drugs eliminated by the________tend to have shorter half-lives and durations of action.

A

Drugs eliminated by the liver tend to have shorter half-lives and durations of action.

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

Rapid initial distribution phase followed by a slower elimination phase.

PK of which drugs?

A

NBDs

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

What is succinylcholine mainly used for?

A

Used clinically for rapid endotracheal intubation

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

Opens the ion channels causing depolarization and generation of a muscle action potential which results in brief contractions (fasiculations)

Which drug?

A

Succinylcholine

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

This drug is not hydrolyzed efficiently by junctional AChE

Persists at the nAChR resulting in sustained local muscle endplate depolarization

Causes the voltage-gated Na channel to remain in the inactive state for a prolonged period

Becomes refractory to further presynaptic release of Ach, and flaccid paralysis results

Which drug?

A

Succinylcholine

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

MOA: Agonist at nicotinic acetylcholine (ACh) receptors, especially at neuromuscular junctions depolarizes

May stimulate ganglionic nicotinic ACh and cardiac muscarinic ACh receptors

Which drug?

A

Succinylcholine

23
Q

Initial depolarization causes transient contractions, followed by prolonged flaccid paralysis

Depolarization is then followed by repolarization that is also accompanied by paralysis

Effects of which drug?

A

Succinylcholine

24
Q

What are the 2 clinical applications of succinylcholine?

A
  1. placement of endotracheal tube at start of anesthetic procedure
  2. rarely, control of muscle contractions in status epilepticus
25
Q

PK of Succinylcholine

A

Rapid metabolism by plasma cholinesterase: normal duration ~5 minutes

26
Q

What are the 4 toxicities of succinylcholine?

A

arrhythmias

hyperkalemia

transient increased intra-abdominal, intraocular pressure

postoperative muscle pain

27
Q

What are the 2 uses of non-depolarizing neuromuscular blockades Tubocuraine & Pancuronium?

A

Facilitate intubation

maintain skeletal muscle relaxation during surgery

28
Q

competitively inhibit normal channel activation preventing muscle cell depolarization, causing flaccid paralysis

Small rapidly moving muscles of the face and eyes are affected first followed by fingers, toes, extremities, trunk, intercostals and lastly the diaphragm

MOA of which drug?

A

Non-depolarizing neuromuscular blockade: Tubocuraine and Pancuronium

29
Q

How can the action of Tubocuraine and Pancuronium be overcome?

A

By increasing the amount of ACh in the synaptic cleft: administer cholinesterase inhibitors like neostigmine or pyridostigmine to shorten the duration of neuromuscular blockade

30
Q

Which class of drugs are usually co-administered with cholinesterase inhibitors?

What are the names of these drugs?

What is the benefit of this coadministration?

A

Muscarinic receptor antagonists: atropine or glycopyrrolate

Benefit of coadministration: voids the bradydysrhythmias associated with agonism of the cardiac muscarinic receptors

31
Q

T/F: high doses of non-depolarizing agents can block the ion channels of the end plate resulting in increased ability of cholinesterase inhibitors to reverse neuromuscular blockade.

A

False: high doses of non-depolarizing agents can block the ion channels of the end plate resulting in decreased ability of cholinesterase inhibitors to reverse neuromuscular blockade.

32
Q

What are the 2 drug interactions of non-depolarizing neuromuscular blockade?

A

Aminoglycosides: gentamicin and tobramycin

inhibit acetylcholine release from cholinergic nerves by competing with calcium ions. They act synergistically to enhance neuromuscular blockade

Calcium channel blockers: verapamil, and dihydropyrodinesal

enhance the neuromuscular blocking effects of non-depolarizing agents.

33
Q

Competitive antagonist at nACh receptors, especially at neuromuscular junctions

MOA of which drug?

A

d-Tubocurarine

34
Q

Prevents depolarization by ACh, causes flaccid paralysis

Can cause histamine release with hypotension

Weak block of cardiac muscarinic ACh receptors

Effects of which drug?

A

d-Tubocurarine

35
Q

Like tubocurarine but lacks histamine release and antimuscarinic effects

Effects of which drug?

A

Cisatracurium

36
Q

Prolonged relaxation for surgical procedures

Relaxation of respiratory muscles to facilitate mechanical ventilation in intensive care unit

Clinical Applications of which drug?

A

Cisatracurium

37
Q

Prolonged relaxation for surgical procedures

Relaxation of respiratory muscles to facilitate mechanical ventilation in intensive care unit

Clinical Applications for which drug?

A

Cisatracurium

38
Q

Renal excretion: duration: ~40–60 min

Toxicities:

Histamine release

Hypotension

Prolonged apnea

PK, Toxicities and Interactions of which drug?

A

d-Tubocurarine

39
Q

Not dependent on renal or hepatic function

•duration: ~25–45 min

Toxicities:

Prolonged apnea but less toxic than atracurium

PK, toxicities and interactions of which drug?

A

Cisatracurium

40
Q

Hepatic metabolism

duration, ~20–35 min

Toxicities:

Like cisatracurium

A

Rocuronium

41
Q

Anesthesia induced by inhalation of drug

A

Inhalation anesthesia

42
Q

The alveolar concentration of an inhaled anesthetic that is required to prevent a response to a standardized painful stimulus in 50% of patients

A

Minimum alveolar anesthetic concentration (MAC)

43
Q

A state of decreased awareness of pain, sometimes with amnesia

A

Analgesia

44
Q

A state of unconsciousness, analgesia, and amnesia, with skeletal muscle relaxation and loss of reflexes

A

General anesthesia

45
Q

What are the 4 stages of anesthesia?

A

Stage 1: Analgesia

Stage 2: Disinhibition

Stage 3: Surgical Anesthesia

Stage 4: Medullary Depression

46
Q

the patient has decreased awareness of pain, sometimes with amnesia. Consciousness may be impaired but is not lost.

What stage of Anesthesia?

A

Stage 1: Analgesia

47
Q

the patient appears to be delirious and excited. Amnesia occurs, reflexes are enhanced, and respiration is typically irregular; retching and incontinence may occur.

What stage of Anesthesia?

A

Stage 2: Dishinibition

48
Q

the patient is unconscious and has no pain reflexes; respiration is very regular, and blood pressure is maintained

What stage of Anesthesia?

A

Stage 3

49
Q

the patient develops severe respiratory and cardiovascular depression that requires mechanical and pharmacologic support.

What stage of Anesthesia?

A

Stage 4: medullary depression

50
Q

Neurophysiologic state produced by general anesthetics is characterized by what five primary effects

A

uunconsciousness

uamnesia

uanalgesia

uinhibition of autonomic reflexes

uskeletal muscle relaxation

51
Q

Anesthetic drugs may do what 2 things?

A
  1. enhance inhibitory synaptic activity

OR

  1. Diminish excitatory activity
52
Q

What 3 neurotransmitters do anesthetics target?

A

ACh

acetylcholine

GABAa, γ-aminobutyric acid-A

53
Q
A

MJ- P2 E2 (19 decks)

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