Histology - Muscle Tissues Flashcards

1
Q

degrades ACh in synaptic cleft.

A

ACh esterase (AChE)

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2
Q

a protein complex that connects the cytoskeleton of a muscle fiber to the surrounding extracellular matrix through the cell membrane.

A

dystrophin

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3
Q

dervied from mesoderm, striated, capilaries in intercellular spaces. Slow and fast fiber types.

A

skeletal muscle

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3
Q

aggregate at top of junctional folds

A

ACh receptors (AChRs)

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3
Q

associated with sweat glands, contain both actin and myosin. contraction mechanism similar to smooth muscle cells, but ectoderm derived.

A

myoepithelial cells

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4
Q

Contains the entire length of a single thick filament.

A

A-band

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5
Q

Dense bodies (where actin attatches) instead of Z disks as in skeletal muscle; have noncontractile intermediate filaments (along w/dense bodies, form intracellular cytoskeleton); has slower contraction speed than skeletal.

A

Difference in Smooth and Skeletal Muscles

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6
Q

calcium interacts with calmodulin, causing interaction between actin and myosin

A

Ca2+ in smooth muscle

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7
Q

presynaptic element

A

lower motor neuron (LMN)

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8
Q

cylinder-shaped, paralell, multinucleated, periferal nuclei. Mitochondria and myoglobin in high quantity.

A

skeletal muscle fibers structure

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9
Q

great capacity for hyperplasia and hypertrophy, (ex: uterus in pregnancy)

A

smooth muscle regenration

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10
Q

fast glycolitic muscle fibers, anaerobic respiration.

A

type II skeletal muscle

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10
Q

type III collagen are located external to the basal lamina. Hugh compnent of endomesium fround smooth muscle.

A

reticular fibers

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11
Q

calcium storage and release

A

Sarcoplasmic reticulum

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11
Q

Purkinje fibers

A

Purkinje fibers

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12
Q

receptors on t-tubule and SR interact to release calcium

A

depolarization down t-tubule

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13
Q

On perfery of muscle fibers, can undergo hyperplasia (mitosis) and hypertrophy by fusing with other skeletal muscles.

A

satellite cells

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14
Q

is the zone of thin filaments that is not superimposed by thick filaments.

A

I-band

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14
Q

Autoimmune disorder. Autoantibodies bind acetylcholine receptors in skeletal muscle, causing muscle weakness and potential death. Treatment includes AChE inhibitors

A

myasthenia gravis

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14
Q

branched, layered, mononucleated, central nucleus. Intercalcated discs with gap junctions, high mitochondria and myoglobin. diad at the Z disc.

A

structure of cms

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16
Q

enzyme that aids in active calcium reuptake by SR after contraction.

A

calsequestrin

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17
Q

A paler region within the A-band, zone of the thick filaments that is not superimposed by the thin filaments.

A

H-zone

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17
Q

Stain dark and lie just inside sarcolema. Interaction between them and reticular fibers that harnesses the force of contraction of the myofilaments, like wringining a sponge, Causes “corkscrew nucleus”.

A

dense bodies

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18
Q

Autonomic nervous system, Purkinje fibers (modified cardiac muscle cells), gap junctions.

A

cardiac muscle innervation

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19
Q

indentations in surface of sarcolemma, may act like T tubules and sarcoplasmic reticulum of skeletal muscle

A

Caveolae of Smooth Muscle

21
Q

a layer of connective tissue, which ensheaths the entire muscle. dense irregular connective tissue, continuous with fascia.

A

epimysium

22
Q

derived from mesoderm, striated, rich capillary beds in intracellular connective tissue, located in proximal portion of heart and pulmonary vessels.

A

cardiac muscle

24
Q

a wispy layer of areolar connective tissue that ensheaths each individual muscle fiber. It also contains capillaries andnerves. It overlies the muscle fiber’s cell membrane: thesarcolemma.

A

endomysium

25
Q

(from the German “Mittelscheibe”, the disc in the middle of the sarcomere) formed of cross-connecting elements of the cytoskeleton.

A

M-line

26
Q

anchors thin myofilaments to Z disc.

A

a-actinin

27
Q

two chains of F-actin, tropomyosin and troponin associate. Ca2+ causes conformational change.

A

thin myofilaments

29
Q

two Z discs are brought closer together as myofilaments slide past each other.

A

Huxley’s sliding filament theory

29
Q

Dystrophin or sarcolemma molecules absent or reduced causing muscle weakness and potential death. Treatment controls symptoms to maximize quality of life.

A

muscular dystrophies

31
Q

fusiform-shaped, often in perpendicular layers, surrounded by basal lamina.

A

structure of smooth muscle fibers

32
Q

new myofibrils form to increase fiber diameter

A

hypertrophy of skeletal muscle fibers

34
Q

200-300 myosin molecules, 2 heavy and 2 light chains per myosin.

A

thick myofilaments

36
Q

Ca2+ required to initiate contractions, binds to calmodulin (no troponin is smooth muscle) which regulates myosin kinase (transfers P+ group from ATP to light myosin on heads), cross-bridging occurs(enzymes are slower than skeletal, so slower formation)

A

Chemical Reaction of Smooth Muscle

37
Q

Occurs following death because the lack of ATP preventing the dissassociation of actin and myosin. ATP important for relaxing muscle, dissociation of thin and thick myofilaments.

A

rigor mortis

39
Q

prominent in wound contraction and tooth eruption deriving from connective tisues.

A

myofibroblasts

40
Q

lower motor neuron (LMN) + muscle fibers

A

motor unit

41
Q

They connect heart muscle cells, allowing them to work as a single functional organ. Have lateral and transverse portions. Lateral has gap junctions, and faces less stress in contraction. Transverse region contains adherens junctions.

A

Intercalated discs

42
Q

Functional units of muscle fiber. Defined by Z lines.

A

sarcomere

43
Q

anchors thick myofilaments to Z discs

A

titin

44
Q

triad of structures at A-I junction, t-tubule, terminal cisternal of SR.

A

triad of structures at A-I junction

45
Q

monitors length and changes in length of muscle, and participates in stretch reflexes. In OMM, an important target for effective treatment, i.e. counter-strain technique.

A

muscle spindle

46
Q

slow oxidative muscle fibers, aerobic respiration

A

type I skeletal muscle

47
Q

indicating the contracted state of the cell

A

“cork-screw” nucleus

48
Q

a sheath ofconnective tissue that groupsmuscle fibers into bundles (anywhere between 10 to 100 or more) or fascicles.

A

Perimysium

49
Q

mononucleate, central nucleus
no striations or sarcomeres
no t-tubules, but have caveolae
involuntary control by ANS

A

differences from skeletal muscle

50
Q

Interferes with the release of acetylcholine from LMN causing muscle paralysis and potential death. Treatment can include an anti-toxin.

A

botulism

51
Q

derived from mesoderm (and ectoderm), no striations, loacted in walls of hollow viscera, blood vessels, glands, dermis.

A

smooth muscle

52
Q

Skeletal Muscle regulation of contraction

A

By binding of Ca2+ to TnC, causes tropomyosin movement and exposes myosin-binding sites on actin filaments

53
Q

Cardiac muscle regulation of contraction

A

By binding of Ca2+ to TnC, causes tropomyosin movement and exposes myosin-binding sites on actin filaments

54
Q

Smooth muscle regulation of contraction

A

By phosphorylation of myosin light chain by myosin light chain kinase in the presence of Ca2+-calmodulin complex

55
Q

Muscle spindle function

A

monitors length and changes in length of muscle, and participates in stretch reflexes

56
Q

T-Tubule Structure and Function

A

deep invagination of the sarcolemma that allow depolarization of the membrane to quickly penetrate to the interior of the cell, signaling Ca2+ release from sarcolema.

57
Q

Transverse Portion of Intercalcated Disc

A

Adhering Junctions: Zonula Adherens and Macula Adherens (Desmosomes)

58
Q

Lateral Portion of Intercalcated Disc

A

Gap Junctions

59
Q

triad

A

A transverse tubule surrounded by two SR cisterna. Contact between these structures is located at the junction of the A and I bands.

60
Q

Terminal Cisternae

A

Enlarged areas of the SR surrounding the t-tubules that store calcium (increasing the capacity of the SR to release calcium) and release it when an action potential courses down the t-tubules, eliciting muscle contraction.

61
Q

Contraction mechanism of smooth muscle - detailed

A

Ca2+ binds to and activates calmodulin, which then binds to caldesmon. This binding causes the caldesmon protein to disengage from the actin filament, exposing the myosin-binding sites on the actin filament. Myosin motor heads are phosphorylated by myosin light-chain kinase, allowing the myosin head to interact with the actin filament and cause contraction.