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

MSK physiology review (Montemayor) Flashcards

(56 cards)

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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

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A

part of actin not overlapping with myosin

no project into A band

24
Q

Z line

Study These Flashcards
A

thin filament attachment

25
what is the thick filament what are its components
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
what are the two binding sites on the myosin heavy chain head
actin binding site (for cross bridge formation) myosin ATPase site (for binding and hydrolyzing ATP)
27
how many actin monomers form 1 helical turn on single strand of filamentous actin
13
28
the thin filament (F-actin) is associated with what 2 important regulatory actin-binding proteins
tropomysin troponin
29
actin (thin filaments) have what important binding site
myosin binding site blocked by tropomyosin at rest
30
what makes up tropomysin
2 alpha helices coiled around eachother regulates binding of myosin heads to myosin binding site on actin
31
troponin T
TnT binds to single tropomysin molecule
32
troponin C
binds Ca2+
33
Troponin I
binds to actin and inhibits contraction
34
what is excitation contraction coupling ?
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
what makes up the triad in skeletal muscle and why is this structure significant ?
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
where do the t tubules penetrate the muscle cell
A and I bands
37
DHP (dihydropyridine receptor)
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
Ryanodine (RyR) receptor
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
what are the steps in EC coupling in skeletal muscle (involving the triad)
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
what is necessary for relaxation of muscle to take place
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
what are the pumps which remove Ca for relaxation
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
what is the role of Ca2+ binding proteins in the SR
- 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
Calsequestrin
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
Tetrodotoxin
inside puffer fish give activated charcoal to bind toxin if ingested blocks Na channels - depolarization is inhibited
45
saxitoxin
in shellfish | blocks Na channels
46
lidocaine, procaine, tetracaine-
block nerve impulse generation and propagation by inhibiting voltage-gated Na channels these are local anesthetics
47
what is malignant hyperthermia
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
which receptor is effected in malignant hyperthermia
RYR located on the SR membrane defect in the RYR1 gene for the ryanodine receptor (Ca2+ release channel)
49
myasthenia gravis
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
why do ice packs work in myasthenia gravis
cooling slows or inhibits AChE activity
51
what is Lambert-Eaton Myasthenic Syndrome (LEMS)
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
synaptotagmin
Ca2+ sensor on the vesicle
53
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?
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
what is the effect of omega - conotoxin
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
clostridium botulinum
peripheral effects flaccid paralylsis inhibition of ACh release at the NMJ
56
With a similar molecular mechanism of action (effect on synaptobrevin), how do you explain the spastic paralysis resulting from tetanus toxin?
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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