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PCL469 > Lecture 12: Somatic > Flashcards

Lecture 12: Somatic Flashcards

1
Q

Botulinum toxin (BOTOX)

A

most toxic substance known
prevent quantal release of acetylcholine at presynaptic membrane
inhibit fusion of vesicles with the plasma membrane

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2
Q

Rab proteins, V and T snares

A

Rab binds to GTP and target tethering protein to mediate initial contact between vesicle and target
V and T snares bring membrane close enough with vesicle to initiate fusion
leads to release and diffusion of ACh

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3
Q

Synaptobrevin

A

V-snares

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4
Q

Synaptotagmin

A

Ca sensor

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5
Q

Syntaxin & SNAP-25

A

T-snares

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6
Q

a-latrotoxin

A

promotes ACh release

enhance transmitter release leads to blockade as result of ACh storage depletion

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7
Q

a and b - Bungarotoxins

A

a: irreversibly binds and block nAChR - neuromuscular blockade & skeletal damage
b: prevent release of ACh from motor nerve endings

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8
Q

Curare

A 
active ingredient is D-tubocurarine
competitive antagonist
injection
block receptor so ACh cant bind
excreted in urine
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9
Q

Non-depolarizing neuromuscular blocking drugs (NMBA)

A

D-tubocurarine
compete with ACh for binding site on nicotinic receptor
zero efficacy
no depolarization

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10
Q

Problems with D-tubocurarine

A

small degree of ganglionic blockade lead to respiratory depression
decrease blood pressure caused by release of histamine
onset of action relatively long
cannot use for intubation

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11
Q

How to overcome non-depolarizing block

A 
esterase inhibitor (neostigmine)
increase concentration of ACh to outcompete antagonist

but can also activate muscarinic receptor
block muscarinic effect using atropine

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12
Q

Pancuronium

A

nondepolarizing drug
similar to tubocurarine but no histamine release
m2 ACh receptor antagonism
blocks NE uptake can lead to increase sympathetic tone: increase HR BP

uses:
skeletal muscle relaxant in general anesthesia
facilitate mechanical ventilation

adverse effect:
cardiovascular actions
slow onset (3 min) and duration (86 min)

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13
Q

Vercuronium

A

less potent at m2 ACh receptor than pancuronium

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14
Q

Rocuronium

A

NMBA
competitive antagonist
minimal cardiac effects
rapid onset (1 min) with moderate duration

FASTEST onset can be used for incubation

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15
Q

Sugamadex reversal

A

selectively binds to rocuronium

8 min recovery

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16
Q

Halogenated hydrocarbon anesthetics (Halothane)

A

enhance neuromuscular blockade

17
Q

Aminoglycoside antibiotics (Streptomycin)

A

decrease ACh release from cholinergic fibers by competing with Ca2+
synergy with TUBOCURARINE and other competitive blockers

18
Q

Ca channel blockers

A

increase tubocurarine blockade

19
Q

Depolarizing neuromuscular blocking drugs MOA

A
  1. initially activate nACh receptor leads to depolarization (transient twitch of muscles)
  2. continued binding cause receptor desensitization
  3. endplate remains depolarized while muscle relaxes
  4. endplate repolarizes but muscle is still relaxed and endplate unresponsive to stimulation

FLACCID PARALYSIS

20
Q

Decamethonium

A

depolarizing blocking drug

two quaternary ammonium linked by simple alkyl chain

21
Q

Succinylcholine

A

depolarizing block
two molecules of ACh binds together
cannot be metabolized by acetylcholine esterase but plasma cholinesterase
plasma cholinesterase found in low concentration at NMJ

remains attached to receptor for a long time, constant stimulation and depolarization leads to receptor desensitization

uses:
fast onset but short duration
given by continuous infusion
useful for INCUBATION
electroconvulsive therapy

rare adverse reaction:
malignant hyperthermia: combine use with halothane as anesthetic
leads to large Ca release
treated by dantrolene (DHP receptor antagonist) block release of Ca at SR
dantrolene can reduce heat production and muscle tone

22
Q

Use for neuromuscular block agent

A

surgery (muscle relaxation without CNS depression)
certain anesthetic can only produce relaxation at high doses therefore dangerous

Incubation
maintaining ventilation during surgery and in ICU patients
reduction of muscle tone

23
Q

Organophosphorus derivatives

A

irreversible inactivation of acetylcholine esterase
leads to desensitization of nACh receptor by high level of ACh
neuromuscular blockade - toxic effects

24
Q

3 Therapeutic use of acetylcholine esterase inhibitor at NMJ

A
  1. Antidote for NMDA (tubocurarine and neurotoxins)
  2. Long acting AChase inhibitor can maintain muscular relaxation and avoid respiratory depression following surgery (neostigmine and edrophonium)
  3. Symptomatic treatment for myasthenia gravis (muscle weakness)
25
Q

Myasthenia gravis

A

autoimmune
nACH receptor are destroyed modulated by antibodies
prevent normal activity

symptoms:
muscle fatigue
difficulty in eye motion
throat muscles fatigue (cannot speak properly)

challenge by using acetylcholine esterase
determine between MYASTHENIA GRAVIS or RECEPTOR DESENSITIZATION

26
Q

How does acetylcholine esterase challenge and diagnose myasthenia gravis and receptor desensitization?

A

If myasthenia gravis: burst of ACh can reverse effects of muscle weakness

If receptor desensitization: no or worsen effect because depletion of more ACh, worsen symptoms

27
Q

Myasthenia gravis treatment

A
  1. surgical removal of thymus gland
  2. corticosteroids, immunosuppressive
  3. Pyridostigmine + atropine
28
Q

Ethanol

A

low dose increase ACh release by action potential

higher dose (legally impaired): decrease release of ACh, muscle relaxes

29
Q

Caffeine

A

sensitize muscle so easier to contract
increase intracellular Ca
increase cAMP levels due to PDE inhibiting activity

30
Q

Dantrolene

A

block intracellular Ca release

31
Q

Procaine, tetracaine, lidocaine, bupivacaine

A

esters and amides local anesthetic

tetracaine more potent, lower TI, longer half life

32
Q

Local anesthetic MOA

A

inhibit voltage-gated Na channel
held at inactive conformation at selective tissue
cannot move to open form
decrease pain signalling

PCL469 (10 decks)

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