Brainscape's Knowledge GenomeTM

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


See full index

Summer pharm 3 > NMB agents > Flashcards

NMB agents Flashcards

1
Q

Drugs that affect skeletal muscle function are grouped as

A
  • Those used during surgery and in ICU for paralysis

- Those used to reduce spasticity in a variety of painful conditions

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

NMB interfere with

A

transmission at the neuromuscular and plate= less CNS activity

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

Adjuncts are used during general anesthesia to

A

optimize surgical conditions, facilitate ET intubation, and ensure adequate ventilation

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

Neuromuscular blocking drugs structurally resemble these agents

A
  1. Depolarizing: succiylcholine
  2. Non-depolarizing isoquinolones: Tubocurarine
  3. Non-depolarizing steroid derivatives: pancuronium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Each subunit of nicotinic Ach receptor contains

A

4 helical domains; M1-M4

-M2 lines the channel pore

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

the N termini of two subunits of a full nACh receptor cooperate to form

A

two distinct binding pockets for ACh, at the a-B and B-a subunit interfaces

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

How do non-depolarizing agents work

A

Prevent opening of the channel when bound to the receptor

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

How do depolarizing agents work

A

Occupy the receptor AND block the channel

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

How are NMB agents administered

A

parenterally!

Rapid initial distribution followed by slow elimination

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

What happens to drugs excreted by the kidneys

A

They have a longer half life= longer duration of action

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

What happens to drugs excreted by the liver

A

They have a shorter half life= shorter duration of action

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

What is the MOA of Succinylcholine (depolarizing NMB)

A
  • nACh receptor agonist= depolarizes and may stimulate receptor
  • 2 molecules must bind to open the ion channels causing depolarization and generation of muscle fasciculations
  • b/c it is not hydrolyzed well, succ. stays at receptor causing sustained local muscle end plate depolarization
  • Na channels remain inactive for a long time
  • Refractory to further release of ACh= flaccid paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Toxicities of succinylcholine include

A

Hyperkalemia
increased intra-abdominal and intra-ocular pressure
post-op muscular pain
Arrhythmias

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

Succinylcholine is a great drug for

A

ET intubation!

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

What are non-depolarizing NMB agents used for

A

facilitating intubation

maintaining skeletal muscle relaxation during surgery

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

What is the MOA of non-depolarizing NMB agents

A

1+ molecule binds to the receptor to competitively inhibit normal channel activation and muscular depolarization
This results in flaccid paralysis

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

Which muscles are affected first with non-depolarizing agents

A

Small rapidly moving muscles first (face and eyes)
Then fingers, toes, extremities, trunk, intercostals
Last: diaphragm
Reverse sequence as paralysis resolves
(same for succinyl choline)

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

How can you shorten duration of NMB drugs

A

Administer cholinesterase inhibitors

This increases the amount of ACh in the synaptic cleft

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

How can you counteract the arrhythmias associated with cardiac muscarinic agonists (non-depolarizing drugs)

A

Give Atropine or Glycopyrolate WITH cholinesterase inhibitors

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

What would reduce the ability of cholinesterase inhibitors to reverse the NMB agents

A

high doses of non-depolarizing agents causing blocked ion channels at the end plate

21
Q

Non-depolarizing agents interact with these drugs

A
  • Aminoglycosides (genta, tobra): inhibit ACh release from nerves by competing w/ calcium AKA they enhance the NMB
  • CCB (verap, dihydro): enhance effects of NMB
22
Q

What is inhalation anesthesia

A

anesthesia induced by inhalation of a drug

23
Q

What is minimum alveolar anesthetic concentration

A

alveolar concentration of an inhaled anesthetic required to prevent a response to standard painful stimulus in 50% of patients

24
Q

What is analgesia

A

State of decreased awareness of pain, sometimes with amnesia

25
Q

What is general anesthesia

A

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

26
Q

What are the stages of anesthesia

A
  1. Analgesia
  2. Disinhibition
  3. Surgical anesthesia
  4. Medullary depression
27
Q

The neurophysiological state produced by general anesthetics is characterized by

A 
unconsciousness 
amnesia
analgesia
inhibited autonomic reflexes 
skeletal muscle relaxation
28
Q

Anesthetic drugs may

A

Enhance inhibitory synaptic activity

Diminish excitatory activity

29
Q

Targets of anesthetics are

A

ACh

GABA

30
Q

What are the inhaled anesthetics

A

-Fluranes

Nitrous oxide

31
Q

How do inhaled anesthetics work

A

facilitates GABA mediated inhibition

Blocks NMDA and ACh-N receptors

32
Q

Inhaled anesthetics cause

A
  • Increased cerebral blood flow
  • Eflurane and halothane decrease cardiac output while others vasodilate
  • Desflurane decreases respiratory functions
  • NO increases ICP (2/2 cerebral blood flow)
33
Q

What are the toxicities of inhaled anesthetics

A

effects on brain, heart, vasculature, and lungs

34
Q

Inhaled anesthetics have a drug interaction with

A

CNS depressing agents, like opioids and sedative hypnotics

35
Q

What is the mechanism by which NO causes increased cerebral blood flow

A

Activates the SNS

In a patient with increased ICP, combine NO with an IV anesthetic or hyperventilation to reduce cerebral blood flow

36
Q

IV anesthetics are used to

A

facilitate rapid induction of anesthesia

They have replaced inhaled as preferred method of inducing anesthesia in everyone EXCEPT kids

37
Q

What are IV anesthetics

A
  • Barbituates: thiopental, thioamylal, methohexital
  • Benzos: Midazolam
  • Dissociative: Ketamine
  • Imidazole: Etomidate
  • Opioids: Fentanyl, Alfentanil, Remifentanil, Morphine
  • Phenols: Propofol, Fospropofol
38
Q

How do barbituates work

A

Facilitate GABA mediates inhibition of GABA-a receptors
Cause circulatory and respiratory depression
decrease ICP

39
Q

Toxicities of barbituates include

A

CNS depression

40
Q

How do benzos work

A

Facilitate GABA mediated inhibition of GABA-a receptors
-Mildly less depressive than barbituates
Slower onset, longer duration

41
Q

Toxicities of benzos include

A

Post-op respiratory depression

*Reversed with Flumazenil

42
Q

How does Ketamine work

A

Blocks excitation by glutamate at NMDA receptors
Analgesia, amnesia, and catatonia- but consciousness is retained
CV stimulation

43
Q

Toxicities of Ketamine include

A

Increased ICP

44
Q

How does etomidate work

A

Facilitates GABA mediated inhibition of GABA-a receptors
Minimally affects CV and respiratory functions
Short duration, no analgesia

45
Q

Toxicities of etomidate include

A

Myoclonus, N/V

46
Q

How do opioids work

A

Interact with u, k, and d opioid receptors

Cause marked analgesia and respiratory depression

47
Q

Toxicities of opioids include

A

Respiratory depression

Reverse with naloxone

48
Q

How do Phenols work

A

Facilitate GABA mediated inhibition of GABA-a receptors
Vasodilate and cause hypotension
Fast onset and fast recovery

49
Q

Toxicities of Phenols include

A

Hypotension during induction

CV depression

Summer pharm 3 (13 decks)

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