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MSK II Exam I > MSK physiology review (Montemayor) > Flashcards

MSK physiology review (Montemayor) Flashcards

1
Q

hyperkalemia effects on membrane potential

A

depolarizes neurons

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2
Q

ECF K affects membrane excitablity. What hormones effect cellular uptake of K +

A

insulin
epinephrine
aldosterone

deficiencies in these may cause hyperkalemia

Resting membrane potential is very sensitive to changes in ECF K+

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3
Q

with increased K+ conductance (K+ efflux) what happens

A

hyperpolarized membrane (becomes more negative)

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4
Q

what happens in hypokalemia (Decreased ECF K+)

A

increased K+ efflux - hyperpolarized

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5
Q

what happens with increased ECF K+ (hyperkalemia)

A

a decrease in K+ efflux (or promotes K+ influx)

membrane becomes less negative, depolarized

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6
Q

what is the NMJ?

A

specialized synapse b/w motor neuron and skeletal muscle fiber

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7
Q

what are some differences b/w a synapse and the NMJ?

A
  • synapse is b/w two neurons. NMJ is b/w a motor neuron and skeletal muscle
  • one-to-one transmission of action potentials occurs at the NMJ wherease one AP in a presynaptic neuron cannot by itself bring about an AP in post-synpatic neuron and requires summation of EPSP’s
  • NMJ is ALWAYS excitatory (an EPP)
  • synapse is either excitatory or inhibitory

-inhibition of skeletal muscles cannot occur at the NMJ- can only occur in the CNS through IPSP’s at dendrites and cell body of the motor neuron

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8
Q

what is the role of acetylcholinesterase

A

terminates synapatic transmission after AP

hydrolyzes ACh to choline and acetate

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9
Q

where is the site of ACh synthesis

A

Nerve terminal

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10
Q

how is ACh made

A

Choline acetyltransferase synthesizes ACh from choline + acetyl CoA

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11
Q

how does ACh uptake occur into synpatic vesicles

A

By the ACH-H+ exchanger

Driven by vesicular proton electrochemical gradient
(ACh influx coupled with H+ efflux; due to positive voltage & low pH inside)

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12
Q

what is synaptobrevin, where is it located, what does it form complexes with ?

A

V-SNARE

this is on the vesicle membrane

essential for transmitter release

Forms complex with SNAP-25 & syntaxin (presynaptic membrane proteins; t-SNAREs)

Helps drive vesicle fusion

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13
Q

synaptotagmin

A

Ca2+ receptor on the vesicle membrane

synaptotagmin detects rise in Ca intracellular and triggers exocytosis of docked vesicles

Ca2+ enters through voltage-gated Ca2+ channels near the active zone of the presynaptic membrane

Triggers vesicle fusion and exocytosis

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14
Q

target of tetanus (endoproteinase)

A

synaptobrevin

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15
Q

botulinum B, D, F, G target (these are endoproteinases)

A

synaptobrevin

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16
Q

Botulinum A/E target

A

cleave SNAP-25 (pre-synaptic protein)

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17
Q

Botulinum C1 target

A

cleaves Syntaxin (pre-synaptic protein)

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18
Q

what is the ACh receptor permeable to

A

cations (Na , K, Ca)

NOT anions

the function of ACh receptor is to raise Vm above threshold (-50 mV –> action potential)

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19
Q

what is the end plate potential and what occurs after this takes place?

A

graded potential of the end plate, small depolarization

as the ACHr channel at the muscle end plate opens, Na and K become equally permeable and the result is an increase in the normally low resting permeabilty of Na relative to K

large movement of Na goes into the muscle cell compared to a smaller movement of K+ outward

local current flow opens voltage gated Na 2+ channels in the adjacent membrane

the resultant Na2+ entry reduces the potential to threshold initiating an AP, which is propagated throughout the muscle fiber

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20
Q

A band

A

Myosin (thick) filaments; Partial overlap with actin (thin) filaments

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21
Q

H zone

A

middle of the A band

part of where actin does not overlap

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22
Q

M line

A

extends vertically down center of A band (myosin thick filaments)

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23
Q

I band

A

part of actin not overlapping with myosin

no project into A band

24
Q

Z line

A

thin filament attachment

25
Q

what is the thick filament

what are its components

A

bipolar assembly of multiple myosin molecules

2 myosin heavy chains (MHC) 
3 regions:
Rod-(tail) alpha helices 
Hinge (arm)
Head- form cross bridges, binding actin on thin filament

4 light chains

  • 2 alkali (essential)
  • 2 regulatory light chains
26
Q

what are the two binding sites on the myosin heavy chain head

A

actin binding site (for cross bridge formation)

myosin ATPase site (for binding and hydrolyzing ATP)

27
Q

how many actin monomers form 1 helical turn on single strand of filamentous actin

A

13

28
Q

the thin filament (F-actin) is associated with what 2 important regulatory actin-binding proteins

A

tropomysin

troponin

29
Q

actin (thin filaments) have what important binding site

A

myosin binding site

blocked by tropomyosin at rest

30
Q

what makes up tropomysin

A

2 alpha helices coiled around eachother

regulates binding of myosin heads to myosin binding site on actin

31
Q

troponin T

A

TnT

binds to single tropomysin molecule

32
Q

troponin C

A

binds Ca2+

33
Q

Troponin I

A

binds to actin and inhibits contraction

34
Q

what is excitation contraction coupling ?

A

Action potential of sarcolemma (excitation) –> Increased [Ca2+]i allowing actin & myosin binding (coupling) –> Power stroke

an increase in Ca intracellularly is a signal to trigger and sustain a contraction (key link b/w excitation and contraction)

AP’s propagate from the sarcolemma to the interior of muscle fibers via transverse tubules

Ca released from SR

Ca binds to troponin allowing cross bridge formation

35
Q

what makes up the triad in skeletal muscle and why is this structure significant ?

A

T tubule and 2 associated cisternae (specialized regions of SR)

Crucial role in linking excitation to contraction
Propagation of AP into T tubules depolarizes triad
Results in Ca2+ release from lateral sacs of the sarcoplasmic reticulum
Two important channels
1. Dihydropyridine receptor
2. Ryanodine receptor

36
Q

where do the t tubules penetrate the muscle cell

A

A and I bands

37
Q

DHP (dihydropyridine receptor)

A

L type voltage gated Ca2+ channels (role is voltage sensor)

associated with T -tubule membrane

they are in clusters of 4

Conformational changes in 4 L-type Ca2+ channels → induces a conformational change in 4 subunits of the Ca2+-release channel

38
Q

Ryanodine (RyR) receptor

A

Ca2+ release Channel

Role: releases stored Ca from the SR

associated with the SR membrane

cluster at the portion of the SR membrane opposite the t tubule

39
Q

what are the steps in EC coupling in skeletal muscle (involving the triad)

A

Depolarization of voltage-sensor L-type Ca2+ channel (Dihydropyridine) on the T-tubule membrane

Mechanical activation of Ca2+-release channel (Ryanodine) in the SR

Ca2+ stored in the SR rapidly leaves through the Ca2+-release channel

40
Q

what is necessary for relaxation of muscle to take place

A

requires reuptake of Ca from sarcoplasm back into SR.

if unregulated, cross bridge cycling would continue until myocyte is depleted of ATP

After an AP, Ca2+ must be removed from the cytoplasm for contraction to cease and for relaxation to occur
When Ca2+ levels decrease, troponin and tropomyosin move back in place and cover myosin-binding site on actin

relaxation is an active process

ATP is required!! for :
Ca pumps

ATPase binding site on myosin head (New atp must be bound for cross-bridge to be broken)

41
Q

what are the pumps which remove Ca for relaxation

A

Na-Ca exchanger and Ca2+ pump

  • MINOR
  • Na in, Ca out
  • Ca out- H+ in

Sarcoplasmic and Endoplasmic Reticulum Ca2+- ATPase (SERCA) type Ca2+ pump

  • Ca2+ reuptake into the SR
  • Ca into SR, H+ out into muscle cytosol
  • MOST IMPORTANT
42
Q

what is the role of Ca2+ binding proteins in the SR

A
  • Calsequestrin
  • Calreticulin- binding protein in smooth muscle

High [Ca2+] in the SR inhibits activity of SERCA (impacts gradient)

Ca2+-binding proteins in the SR lumen can delay inhibition of Ca2+ pump activity

Ca2+-binding proteins buffer increased [Ca2+] during Ca2+ re-uptake and can increase Ca2+ storage capacity of the SR
Ca2+ -binding proteins may have as many as 50 binding sites per molecule

43
Q

Calsequestrin

A

Major Ca2+-binding protein in skeletal muscle

Localized in SR at triad junction
Forms complex with Ca2+-release channel (RYR)
Facilitates muscle relaxation by buffering Ca2+ AND unbinds Ca2+ near Ca2+-release channel

44
Q

Tetrodotoxin

A

inside puffer fish

give activated charcoal to bind toxin if ingested

blocks Na channels - depolarization is inhibited

45
Q

saxitoxin

A

in shellfish

blocks Na channels

46
Q

lidocaine, procaine, tetracaine-

A

block nerve impulse generation and propagation by inhibiting voltage-gated Na channels

these are local anesthetics

47
Q

what is malignant hyperthermia

A

rare, heritable condition
(auto dominant) that can be triggered by volatile anesthetics and some muscle relaxers

block nerve impulse generation and propagation by inhibiting voltage-gated Na channels

What is the cause?
Disorder of Ca2+ regulation in skeletal muscle triggered by volatile anesthetics & some muscle relaxers
Uncontrolled release of Ca2+ from the SR → rigidity, tachycardia, hyperventilation, and hyperthermia
Acute hyper-metabolic state within muscle tissue; prolonged contraction

48
Q

which receptor is effected in malignant hyperthermia

A

RYR located on the SR membrane

defect in the RYR1 gene for the ryanodine receptor (Ca2+ release channel)

49
Q

myasthenia gravis

A

Autoimmune: circulating antibodies directed against nAChR are commonly detected

Immune-mediated destruction or impaired binding of nicotinic ACh receptors
Fewer channels capable of opening in response to ACh: ↓ ability to generate an end-plate potential

weakness and fatigue worsen with increased activity

Neural conduction and sensory and autonomic responses are normal

extraocular m.m. are initially affected (ptosis, diplopia, blurred vision) [small motor units]

Bulbar muscles (speech and swallowing)

Neck muscles

Proximal limb muscles

50
Q

why do ice packs work in myasthenia gravis

A

cooling slows or inhibits AChE activity

51
Q

what is Lambert-Eaton Myasthenic Syndrome (LEMS)

A

paraneoplastic syndrome

Circulating antibodies directed against voltage-gated Ca2+ channels are detected on the pre-synaptic motor nerve terminal

pt’s show proximal weakness and absent tendon reflexes

EMG initially shows a low-amplitude muscle response which significantly increases following repeated activation

a PRE-synaptic disease

52
Q

synaptotagmin

A

Ca2+ sensor on the vesicle

53
Q

Why does repetitive stimulation result in increased contractile strength in this patient with Lambert-Eaton vs. decreased strength after repetitive use in the patient with Myasthenia gravis?

A

Rapid, repetitive stimulation can increase Ca2+ influx via functioning channels

Increase release of ACh

Presynaptic stores of ACh and postsynaptic AChR are intact  the EPP will raise the membrane above threshold and permit generation of muscle AP

54
Q

what is the effect of omega - conotoxin

A

venom of marine coil snake

Blocks N-type voltage-gated Ca2+ channels (on the presynaptic membrane)

Analgesic effect
Other forms of conotoxin block: nicotinic ACh receptors, K+ channels, voltage-gated Na+ channels (activation & inactivation)

55
Q

clostridium botulinum

A

peripheral effects

flaccid paralylsis

inhibition of ACh release at the NMJ

56
Q

With a similar molecular mechanism of action (effect on synaptobrevin), how do you explain the spastic paralysis resulting from tetanus toxin?

A

Central effects
Binds NMJ presynaptic membrane, retroaxonally transported to SC
NT release is blocked
Impact spinal inhibitory interneurons

MSK II Exam I (6 decks)

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