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Year2 MSK exam 1 > MSK phys > Flashcards

MSK phys Flashcards

1
Q

toxin in puffer fish

A

tetrodoxin

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2
Q

what is given to Tx tetrodoxin poisoning

A

activated charcoal to bind it up

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3
Q

how does tetrodoxin work

A

block V Na Channels
inhibits depolarization
AP generation/propagation inhibited

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4
Q

blockage of K leak channels would do what

A

hypopolarize RMP

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5
Q

what toxin is in mamba snakes

A

dendrotoxin

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6
Q

how does dendrotoxin work

A

blocks V K channels so blocks hypopolarization

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7
Q

effects of dendrotoxin on Ach release

A 
inhibit repolarization
prolonging AP
prolonged Ca influx at nerve terminal
enhanced ACh release
hyperexcitability and convulsive Sx
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8
Q

inheritance of malignant hyperthermia

A

autosomal dominant

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9
Q

what can trigger malignant hyperthermia

A

volatile anesthetics and some muscle relaxers

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10
Q

what causes malignant hyperthermia

A

uncontrolled release of Ca from SR leading to tachy, rigidity, hyperventilation and hyperthermia
acute hypermetabolic state in muscle tissue leading to prolonged contraction

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11
Q

what R is affected in malignant hyperthermia

A

RYR1

also could be dihydropyridine R

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12
Q

where is RYR located

A

SR membrane

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13
Q

what are the L type Ca channels and where are they located

A

DHPR

T tubule membrane

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14
Q

role of DHPR

A

voltage sensor

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15
Q

role of Ca in skel mm tension

A

removes regulatory protein tropomyosin from actin so there can be cross bridge formation

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16
Q

what is directly proportional to tension production in skel mm

A

number of cross bridges

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17
Q

what is required for muscle relaxation to occur

A

removal of Ca from sarcoplasm

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18
Q

is ATP needed for muscle relaxation or contraction

A

relaxation

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19
Q

where is the ATPase binding site

A

on myosin head

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20
Q

what is the pump to remove Ca from sarcoplams for skel mm relaxation to occur

A

SERCA the sarcoplasmic and endoplasmic reticulum Ca ATPase

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21
Q

AutoAb are against what in myasthenia gravis

A

nAChrR

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22
Q

initial mm affected in myasthenia gravis

A

extraocular mm
bulbar (speech swallowing)
neck
proximal limb muscles

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23
Q

Ach binding to R on motor end plate cause what

A

opening of ligant gated ion channels

depolarization end plate between Na and K

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24
Q

effect of EPP on adjacent sarcolemma of skel m

A

V Na Channels open and AP generated

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25
Q

enzyme that degrades Ach in NMJ

A

acetylcholinesterase

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26
Q

what enzyme synthesizes Ach

A

choline acetyltransferase

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27
Q

what drives Ach uptake into vesicle

A

vesicular proton elctrochemical gradient (+ voltage and low pH inside)

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28
Q

Where is Ach made

A

nerve terminal

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29
Q

what allows for Ach uptake by vescile

A

ACh- H+ exchanger
in ACh
out H+

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30
Q

endrophonium (tensilon) test

A

give AChEI and see if improve Sx

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31
Q

why does an ice pack help in myasthenia gravis

A

inhibits AChE activity

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32
Q

two major clinical forms of myasthenia gravis in eyes

A

ocular MG: only ocular Sx

general MG: generalized weakness

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33
Q

why does MG attack eyes frist

A

fewer ACh R in eye muscles
high rate firing in eye motor neurons
lower quantal release ACh per event

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34
Q

+ SCC
EMG increase uppon repeated activation
autoAb found against V Ca Ch
Dx

A

lambert eaton myasthenic syndrome

paraneoplastic

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35
Q

where does LEMS attack

A

presynaptic VCaCh

decrease ACh vesicle fusion and exocytosis

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36
Q

Which vesicle protein is a Ca sensor

A

synpatotagmin

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37
Q

conotoxin is from what

A

marine cone snail

38
Q

how does conotoxin work

A

blocks N type VCa ch

analgesic

39
Q

botulism affects what in NMJ

A

impaired ACh vesicle fusion

40
Q

what other toxin (not botulinum) blocks the ACh release

A

tetanus toxin

41
Q

why does botulinum toxicity take a while to reverse after given anti toxin

A 
need synaptobrevin (v SNARE)
and sNAP 25 (t SNARE) to be newly synthesized
42
Q

which botulinum attack SNAP 25

A

A and E

43
Q

which botulinum attack synaptobrevin

A

B D F G

44
Q

what causes spastic paralysis seen in tetanus

A

central effects bind NMJ presynaptic membrane and retroaxonally transported to SC
NT release is blocked
impact spinal INHIBITORY interneurons

45
Q

what type of paralysis does botulinum toxin cause

A

flaccid

46
Q

RMP

A

-70mV

47
Q

what medications promote cellular uptake of K

A

epinephrine, insulinm, aldosterone

48
Q

cell death can result in what metabolic state

A

hyperkalemia

49
Q

what occurs to membrane with highger K efflux

A

hyperpolarization

50
Q

what occurs with a decrease in ECF K

A

more K efflux, hypokalemia

51
Q

what occurs with an increase in ECF K

A

dec K efflux, hyperkalmia

membrane potential less negative aka depolarized

52
Q

RMP most sensitive to what ion [ ]

A

K

53
Q

When is K permeability the highest

A

relative refractory period of Na channels

54
Q

methods of removal of NT from synaptic cleft

A

enzymatic breakdown, cellular uptake, diffusion

55
Q

NMJ are excitatory/inhbitory or both

A

always excitatory EPP

56
Q

how is inhibition of skel mm achieved

A

CNS through IPSPs at dendrites and cell body of motor neuron

57
Q

what are the active zones of NMJ

A

dense spots where synaptic vesicles are clustered

oriented over postjunctional folds

58
Q

what are postjunctional folds

A

extensive invaginations on postsynaptic membranes under nerve terminal
increase SA of muscle plasma membrane

59
Q

what is time delay in impulse transmission with Ach diffusion

A

50 nm

60
Q

What is synaptotagmin

A

Ca R of synaptic vesicles

detect rise in Ca and trigger exocytosis of docked vesicles

61
Q

synaptobrevin forms a complx with what

A

SNAP 25 and syntaxin

62
Q

botulinum toxin C1 blocks what

A

cleaves syntaxin

63
Q

what are sarcomeres

A

actin and myosin units

Z line to Z line

64
Q

What is the A band

A

myosin (thick filament)

65
Q

What is the H zone

A

middle of A band (part where does not overlap with thin actin)

66
Q

what is the M line

A

center of A band

67
Q

what is the I band

A

part of ACtin not overlapping with myosin

68
Q

what is the Z line

A

thin filament attachment

69
Q

what is a thick filament

A

2 myosin heavy chains and 4 light chains

70
Q

what are the regions of the myosin heavy chains

A

rod (tail)
hinge (arm)
head (cross bridges)

71
Q

what are the 4 light chains in thick filament

A 
2 alkali (essential)
2 regulatory
72
Q

What are the binding sites on myosine heavy chains

A

actin binding site for cross bridge formation

myosin ATPase site for hydrolyzing ATP

73
Q

What is F actin

A

filamentous- backbone

double stranded alpha helical polymer of actin molecules

74
Q

what are the actin binding proteins

A

tropomyosin

troponin

75
Q

tropomyosin blocks what at rest

A

myosin binding site on actin

76
Q

tropomyosin interacts with how many actin monomers

A

7

77
Q

tropinin interacts with what

A

1 tropomyosin molecule and actin

78
Q

torponin T

A

binds single tropomyosin molecule

79
Q

troponin C

A

binds Ca

80
Q

troponin I

A

binds actin and inhibits contraction

81
Q

what happens when Ca binds troponin

A

tropomysoin slips away from blocking position allowing for cross bridging to occur

82
Q

how do AP propagate from sarcolemma to interior of muscle fibers

A

transverse tubules

83
Q

What is the triad in skel mm propagation

A

SR cisternae on 2 sides of T tubule that allow for propagation of AP

84
Q

Channels needed to propagate AP

A

DHPR- t tubule

RYR- SR

85
Q

DHPR are found in clusters of how man

A

4 needed for conformational change allowing Ca release

86
Q

do you need Ca release to activate RYR

A

no, mechanical from DHPR

87
Q

high Ca in SR causes what

A

inhibits activity of SERCA

88
Q

what delay inhibition of Ca pump activity

A

Ca binding proteins in SR lumen (increase Ca amount in SR)

89
Q

what are the Ca binding proteins in SR

A

calsequestrin
localized in SR at triad junction
complexes with RYR

90
Q

what is calreticulin

A

Ca binding protein in smooth muscle

Year2 MSK exam 1 (26 decks)

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