Muscle Tissue (Histology) Oct30 M3 COPY Flashcards

1
Q

shape of the SR in striated muscle

A

regular. has tubules (segments of SR) and cisternae (lateral sacs of SR)

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2
Q

T-tubule def

A

invagination of the plasmalema that goes very deep in cell

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3
Q

SR cisternae name near T-tubule

A

terminal cisternae

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4
Q

Triad def.

A

cisterna-T tubule-cisterna combination

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5
Q

what is found between adjacent cisternae (SR component)

A

connecting tubules of SR

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6
Q

location of triad in SKM

A

at junction of A and I band.

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7
Q

location of triad in cardiac muscle

A

near Z line

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8
Q

what is found at the terminal cisternae + function

A

Calcium ATPase (Ca pump) pumps Ca in the SR

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9
Q

What makes the Ca release from the SR

A

depolarization of the membrane due to membrane potential coming from outside, via the T tubule

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10
Q

perimysium appearance on cross section

A

appears enlarged (histology artefact) bc tissue was put on hot plate for it to spread

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11
Q

On EM, what we see between adjacent myofibrils within the cytoplasm

A

mitochondria and glycogen molecules that appear as dark dots

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12
Q

T-F: axon myelinated in SKM NMJ + explan.

A

True. Myelinated by Schwann cells that form myelin sheaths

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13
Q

appearance of postsynaptic membrane (sarcolema) in NMJ

A

is folded.

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14
Q

space name between pre and post synaptic membrane at NMJ

A

synaptic cleft

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15
Q

other name for NMJ

A

terminal button

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16
Q

NMJ neurotransmitter

A

ACh

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17
Q

cardiac muscle NMJ neurotransmitter

A

Ach if PSS

NE if SS

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18
Q

SKM NMJ postsyn. receptor nd function

A

AchR, binds Ach. Makes Na+ flow in and K+ flow out

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19
Q

AchR type of receptor and conformation

A

ligand-gated. 5 subunits: two alpha, 1 gama, 1 beta, 1 delta encoded by diff genes

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20
Q

Why do we say that the AchR at the NMJ is immunologically protected

A

No Abs normally produced against it

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21
Q

Myastenia gravis cause (autoimmune disease)

A

Ab produce against AchR at NMJ

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22
Q

AChE function at the synaptic cleft

A

splits ACh into acetate and choline, both recycled by presynaptic neuron

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23
Q

location of BM at NMJ

A

BM of striated muscle is continuous with BM of Schwann cells (which wraps around axon) and doesn’t enter T tubules. Also no BM between Schwann and axon

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24
Q

heart layers from outside to inside (not only heart wall)

A

fibrous pericardium, serous pericardium (parietal lamina and visceral lamina or epicardium), myocardium, endocardium

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25
Q

three layers forming the wall of the heart

A

epicardium (visceral lamina of serous pericardium), myocardium, endocardium

26
Q

fibrous pericardium charact.

A

CT around the heart (external capsule)

27
Q

epicardium charact.

A

covers the heart and part of the blood vessels

28
Q

myocardium charact.

A

thickest part of heart wall. made of cardiac muscle fibers (cells)

29
Q

endocardium charact.

A

thin membrane of endothelium, CT and SM tissue

30
Q

percardial cavity separates what layers

A

parietal lamina of serous peric. and visceral lamina (epicardium) of serous peric.

31
Q

what muscle type has cells that sometimes branch

A

cardiac

32
Q

what muscle type has highest density of capillaries

A

cardiac muscle

33
Q

what is the BM at intercalated disks

A

is in fact two BMs that attach

34
Q

two portions of intercalated disks

A

north south portion and east west (or west east) portion

35
Q

3 junction zones at ICs and which part of IC they’re in

A

Zonula adherens and macula adherens (desmosome) in north south

Gap junction in east west portion

36
Q

Zonula adherens charact

A

'’Z line like’’: alpha actinin at the plasmalema anchors F-actin

37
Q

Desmosome (macula adherens) charact

A

plaque with proteins called plaquoglobins and intermediate filaments anchoring there

38
Q

Gap junction charact.

A

The 2 BMs become very close. Interaction between them bc have pores there

39
Q

Gap junction pores names and components

A

connexons. each has 6 connexin molecules

40
Q

heart: type of connexin molecule and consequence of mutation

A

connexin 48. mutation is lethal.

41
Q

gap junction function

A

allow passage of ions of calcium

42
Q

why gap junctions necessary in cardiac muscle

A

Ca flows between the cells so available everywhere. as in Ca available to all the troponin in SKM

43
Q

cardiac muscle: why SR is complex

A
  • sometimes have terminal cisternae, sometines not

- sometimes have triad at level of Z line, sometimes not

44
Q

cardiac muscle SR similarities with SKM SR

A

T tubules, calcium pump

45
Q

why difficult to see myofibrils in SM

A

mainly actin there and not much myosin. + not organized in sarcomeres

46
Q

something special happening in SM at contraction

A

shape of nucleus changes

47
Q

special structure at sarcolema of SM

A

vesicles that don’t detach called caveoles (that could do function of T tubules?)

48
Q

what do we see outside SM cells near them (equivalent to endomysium)

A

reticular fibers

49
Q

Dense bodies on SM cells plasma membrane: what they are

A

contain alpha actinin like proteins achoring the actin filaments (are rich in alpha actinin) (Z line like)

50
Q

SM mechanism of contraction: what Ca does

A

binds myosin light chain kinase (MLCK)

51
Q

SM mechanism of contraction: what MLCK does

A

phosphorylates the light chains of the myosin to displace the head previously attached to the tail. Head can bind acin

52
Q

SM mechanism of contraction: how close myosin is to actin and how myosin is organized in SM cell

A

myosin close to actin b4 contraction but doesn’t bind. Myosin is as individual molecules

53
Q

SM speed of contraction and what this makes it good for

A

slow. makes it good for peristaltic movement, lumen contraction of blood vessels.

54
Q

how SM shape changes from before to after contraction

A

more elongated to more round and less elongated

55
Q

SM relaxation: how

A

Ca levels decreased, inactivation of MLCK.

56
Q

Ehlers-Danlos syndrome affects what + consequence

A

affects CT, joints and vessel walls. Severe form called vascular Ehlers-Danlos causes walls of blood vessels, intestines or uterus to rupture

57
Q

Ehlers-Danlos syndrome cause

A

mutation of reticular fibers. causes wall ruptures (in aorta, digestive system, etc.)

58
Q

Myasthenia gravis: symptoms and explanation

A

fluctuating muscle weakness and fatigue. The Ab binding to AchR inhibits the excitatory effect of Ach on AchR at the NMJ

59
Q

Muscular dystrophy: give two types

A

Duschenne and Becker

60
Q

Muscular dystrophy: two mutations that can give that

A

mutation in laminin or dystrophin

61
Q

what dystrophin does + associated diseases

A

DMD. BMD. is at muscle fiber membrane. links actin to dystroglycans in sarcolemma which are linked to laminin.

62
Q

what laminin does

A

Are part of the basement membrane. interacts with dystroglycans at the sarcolemma