Muscle Flashcards

1
Q

state what is in each band of skeletal muscle - MHAZI

A
m line is in the h-band 
within the h- band is myosin 
within the a band is actin and myosin 
in the i band there is the z line 
the i band is made up of actin only
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2
Q

give the structure of actin

A

the actin molecule is helixal
it contain tropomysoin coiled around it to reinforce the helix
troponin complexes are bound to the tropomyosin.

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3
Q

describe the structure of myosin

A

rod like structure from which two heads protrude

many myosin molecules together make a filament and heads protrude at opposite ends of filament

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4
Q

describe the role of calcium in contraction

A

calcium ions bind to the TnC of troponin causing a confomational changes that moves the tropomyosin away from actin’s binding sites
allows myosin heads to bind to actin and contraction begins

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5
Q

describe the sliding filament model

A

calcium binds to troponin causing tropomyosin to pull away from binding sites on actin
myosin head attaches to actin - cross bridge
head of myosin changes angle moving actin filament along and ADP released
*ATP molecule binds to myosin head and cross bridge breaks
myosin head bends back as ATP hydrolysis occurs
head of myosin reattaches to actin
and pivots and bends pulling actin towards the m line

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6
Q

describe the events leading to a contraction

A
  1. nerve impulse along motor neurone arrives at neuromuscular junction.
  2. the impulse causes the release fo acetyl choline into the synaptic cleft and there si a localised depolarisation of the sarcolemma
  3. voltage gated sodium channels open and sodium enters the cell
  4. this causes a general depolarisation which spreads over the sarcolemma and down the t tubules
  5. the action potential triggers calcium release from terminal cisternae of sarcoplasmic reticulum.
  6. calcium binds to troponin TnC
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7
Q

Describe the continuity of muscle with tendon

A

the muscle fibres interdigitate with the collagen bundles of the tendon

the sarcolemma is always present between myofibrils of the muscle fibres and the collagen bundles

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8
Q

Give some features of cardiac muscle

and ultra structure

A
striated 
centrally positioned nuclei 
intercalated discs 
branches 
The endomysium is rich in capillaries - white spaces between pink fibrils 

myofibrils are continuous masses in the cytoplasm
mit and er are between the myofibrils
gap junctions are dark black squiggly lines

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9
Q

give the t tubule position in the skeletal and cardiac muscle

A

Skeletal - t tubules are in line with the A-I band junction
forms triad

Cardiac - t tubules are inline with the z lines
form diads

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10
Q

give the structure and function of the purkinje fibres

A

specialised myocardial cells of which distal conducting cells carry impulses to ventricular muscle from the AVN (down bundle of His, branches into purkinje fibres) allows the wave of contraction to occur from the apex causing ventricular systole
allows ventricles to contract in synchronous manor. ( areas close to AVN = thin PF and regions far from AVN = thick fibres

large cells with abundant glycogen, sparse myofilaments and extensive gap junctions

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11
Q

describe histology of smooth muscle

A

fusiform
central nuclei
no striations, sarcomeres or t tubules

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12
Q

describe smooth muscle contractions

A

slow and sustained
requires less ATP
can be stretched
can be contracted for days/ hours

responds to nerve impulses, hormones, local blood gas concentrations and drugs

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13
Q

give examples of modified smooth msucle cells

A

myoepithelial cells - in secretory units of exocrine glands

myofibroblasts - at sites of wound healing producing a cartilaginous matrix and contract

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14
Q

which nervous system innovates smooth muscles and from where?

A

the autonomic nervous system

neurotransmitters from varicosities

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15
Q

which muscle cells can divide?

A

skeletal muscle cells cannot divide

cardiac muscle cannot regenerate

smooth muscle cells retain their mitotic activity

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16
Q

what can change in muscle to adapt it?

A
SR swells 
increase in actin and myosin proteins 
increase in z band width 
increase in ATPase 
increase volume of mit 
increase density of t tubule system 
little hyperplasia
17
Q

give the changes to muscles in endurance and high resistance exercise

A

high resistance
increase in actin and myosin, fatter muscle fibres and muscle mass and strength
may lead to hypertrophy

endurance
stimulates syntehsis of mit proteins, vascular changes to allow fro greater oxygen utilization - shift to oxidative metabolism

18
Q

what can cause atrophy

A

sedentary life style - bed rest

loss of protein = reduced fibre diabeter = loss of power

Age

denervation -

19
Q

describe events of impulse transmition from motor neurone to muscle

A

opening of voltage gated calcium channels on presynaptic membrane causes vesicles containing acetyl choline to be released into the synaptic cleft
ach binds to recpeotrs on the motor end plate
ach opens sodium channels
sodium entry depolarises the muscle sarcolemma causing calcium release from the sacroplasmic reticulum hence muscle contraction

20
Q

describe myasthenia gravis and give symptoms

A

autoimmune destruction of the end plate ACh receptors
loss of junctional folds at end-plate
widening of synaptic cleft

fatigability and sudden falling
drooping upper eyelids and double vision
fatigue, emotions, symptoms change

21
Q

give treatments for myasthenia gravis

A

acetylcholinesterase inhibitors
immune suppressants
thymectomy
plasmapheresis - removal of harmful antibodies from serum

22
Q

describe Duchennes muscular dystrophy

A

lack of dystrophin

sarcolemma and actin and myosin filaments are not connected anymore

23
Q

describe the damage to muscle fibres in Duchenne

A

muscle fibres tear on contraction
creatine phosphokinase is released into blood
calcium ions enter cells causing necrosis
pseudohypertrophy - swelling before fat and CT replace muscle fibres

24
Q

describe presentation and treatments of Duchenne muscular dystrophy

A

early onset gowers signs
contractures

steriod therapy
genetic research into gene threapy and stem cells

25
Q

descirbe maligant hyperthermia

A

a channelopathy

a side effect from anaethetics

affects ion channels in sarcoplasmic reticulum and all the calcium is released together
increases intracellular calcium ions

causes prolonged contraction
heat generated can be fatal