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Flashcards in L4 Deck (31):
1

What are the uses of neuromuscular blockers?

Muscle relaxants - intubation, surgery
Muscle paralysis - botox
Ortho

2

Describe the structure of the NMJ

Pre-synapse w/ active zones
Basal lamina w/ AChE
Post-synapse w/ dense nAChR
Peri-jxnal Na+ channels deep in synaptic folds

3

What are the 2 forms of botulinum toxin?

Both work to disrupt the SNARE proteins for vesicle fusion to release ACh at NMJ
BoNT A = botox, cleaves SNAP 25
BoNT B = myobloc, cleaves synaptobrevin

4

4 clinical uses of botulinum toxins

1. Strabismus = misaligned eyes
2. Excessive sweating
3. Cervical dystonia (head twisting)
4. Cosmetic

5

What is the structure of AChR?

Ion channel - Na/K
5 subunits: 2 alpha, beta, delta, gamma or epsilon (development)
ACh binds alpha subunit - need 2 AChs
Therefore blockers that bind 1 alpha inactivate the entire receptor

6

5 non-depol NM blockers

1. d-Tubocurarine
2. Pancuronium
3. Vecuronium
4. Cisatracurium
5. Rocuronium

7

1 depolarizing NM blocker & metabolism

Succinyl choline
Hydrolyzed (aka metabolized) by BChE

8

Mechanism of non-depol NM blockers

Works by competitively blocking nAChR
See:
- ↓mepp & epp - proportionally

9

Why are non-depol NM blockers competitive blockers?

With repeated stimulation, see temporal summation
- ↑ACh in synapse yields larger and large depol - adds with each release to eventually reach threshold

10

Mechanism of depol NM blockers

Na channel inactivation
Binds nAChR - causing depol - then inactivates it
- Add drug slowly to suppress initial depol from happening all at once
If stim nerve, still get epps but don't reach threshold b/c not opening any channels

11

What is the train of 4 stimulation

Tests depth of NM block
Fade = muscle twitch starts high then fades in correlation to the degree to which the non-depol is blocking

12

What does recovery from an NM block look like?

Looks like a train of 4
Starts high - goes low
See net amplitude grow with recovery until all twitches return to same baseline amplitude

13

NM blocker toxicity - what are 3 things you're worried about

1. Breathing - toxic level will arrest diaphragm muscle too
2. Stimulating histamine release
3. Inducing malignant hyperthermia

14

Can NM blockers cross BBB?

No - all charged
Also why can't give PO - poor tissue penetration
Give IV

15

Babies response to NM blockers

More sen to ND blockers (use less)
Less sen D
B/c of how NMJ matures

16

Hypothermic response to NM blockers

Less sen to ND blocker
More sen to D
Lower temp = less efficient ATPase = membrane potential is more positive than normal (closer to threshold)

17

Genetic variant that would dictate NM blocker response

BChE variants for succinylcholine metabolism

18

Which electrolytes should you be aware of affecting the NMJ/NM blockers?

Ca2+
K

19

Hypokalemia response to NM blockers

Hyperpolarized
More sen to ND
Less sen to D

20

Hyperkalemia response to NM blocker

Closer to threshold
Less sen to ND
More sen to D

21

Which pts might be hypovolemic? How does this effect NM blockers?

Burn & trauma
Artificial hyperkalemia
DON'T use succinylcholine

22

How do MG pts respond to NM blockers?

Fewer nAChR there b/c autoimmune attack
BUT whatever is there is hypersensitized
VERY sen to ND blockers (acts directly on receptor)

23

How do pts with small cell (bronchiogenic) carcinoma respond to NM blockers?

No Ca2+ channels on pre-synaptic side
Less vesicle fusion --> less ACh release
Sen to BOTH ND and D

24

How do pts with liver disease respond to NM blockers? Which 3 NM blocker are specifically effected?

Liver makes less BChE
Decrease SuCh, vecuronium, rocuronium metab

25

What is malignant hyperthermia?

@ muscle: rapid release SR Ca2+ for no reason
Heat production via ATP - rapid rise body temp

26

Which NM blocker can induce underlying malignant hyperthermia?

SuCh

27

What is the difference between neurotransmission at the NMJ vs ganglia

NMJ = 1:1
Ganglia = temporal & spatial summation

28

Which receptors create fast EPSP

nAChR

29

Which receptors create slow IPSPs

mAChR

30

2 ganglionic blocking agents

Mecamylamine
Trimethaphan

31

What happens with ganglionic blockade?

Reverse the dominant autonomic tone of that organ - opposite of normal baseline
Ex: heart becomes tachycardic w/ ↑CO (baseline = para)