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BODY LOGISTICS > Muscle Tissue (Function and Dysfunction) > Flashcards

Muscle Tissue (Function and Dysfunction) Flashcards

1
Q

Cardiac vs smooth muscle

A

similarities
-central nuclei
-only one contractile cell type (no fast/slow twitch)
-wave like function, act as syncytium
-myocytes communicate through gap junctions(small molecules pass between adjacent cells

differences
-cardiac can be multinucleated
-cardiac is branched
-connexins in smooth muscle
-no sarcomeres in smooth muscle
-electrical conduction- specialised cells in cardiac muscle
-no troponin in smooth muscle as no sarcomere
-cardiomyocytes have intercalated discs

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2
Q

DHP

A

dihydropyridine

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3
Q

RyR

A

ryanodine receptor

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4
Q

neuromuscular junction

A

neuromuscular junction
point of contact between a motor neuron and a skeletal muscle cell

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5
Q

properties of neuromuscular junction

A

-small terminal swellings of the axon
-contains vesicles of acetylcholine

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6
Q

Innervation of skeletal muscle (neuromuscular junction)

A
  1. Initiation: nerve impulse along motor neuron axon arrives at neuromuscular junction
  2. Impulse prompts release of ACh into synaptic cleft causing local depolarisation of the sarcolemma
  3. Voltage gated Na+ channels open, Na+ ions enter cell
  4. General depolarisation spreads over sarcolemma into T tubules
  5. Voltage sensor proteins of T tubule membrane change their conformation
  6. Gated Ca2+ ion-release channels of adjacent terminal cisternas activated
  7. Ca2+ rapidly released into sarcoplasm
  8. Ca2+ binds to TnC subunit of troponin and contraction cycle initiated
  9. Ca2+ ions returned to terminal cisternas of sarcoplasmic reticulum
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7
Q

What’s a neuromuscular junction formed of?

A

Neurone and muscle

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8
Q

how does the average fibres per motor unit affect fine control and power?

A

Lower fibres per unit - more fine control
higher fibres per unit - more power

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9
Q

Kranocyte

A

a connective tissue cells that resides over the terminal Schwann cell - anchors nerve to muscle cell

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10
Q

T Tubes and sarcoplasmic reticulum of skeletal muscle structure

A

Look at lecture 12 pg 12

  • Sacrolemma
  • T
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11
Q

myasthenia gravis

A

*autoimmune disease
*antibodies block Ach receptor, and 30% reduction in receptor number is enough for symptoms
*endplate invaginations reduced and reduced synaptic transmission
-muscle weakness

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12
Q

Explain the histological appearance of myasthenia gravis

A

2 axons, round not crescent moon shape
More mitochondria for ATP
no invaginations for ACh receptor gene
Leads to non functioning muscle cell

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13
Q

Sliding filament theory

A
  1. Ca2+ binds to TnC of troponin, and conformational change moves tropomyosin away from actin’s binding sites
  2. Myosin cross bridge attached to actin myofilament
  3. Myosin head pivots and bends as it pulls on actin filament, sliding it towards the M line. ADP and Pi released
  4. As the new ATP attached to the myosin head, cross bridge detaches
  5. As ATP is hydrolysed into ADP and Pi by ATPase, cocking of myosin head occurs
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14
Q

myosin molecule

A

Tail: binds to other myosin molecules
Head: made of 2 globular protein subunits and reaches the nearest thin filament

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15
Q

what are the two protein components of actin?

A

F - actin fibres
G - actin globules

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16
Q

what part of the sarcomere is devoid of myosin heads?

A

the centre of the sarcomere (M line)

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17
Q

when does the myosin head cock?

A

when ATP that was bound to it is hydrolysed

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18
Q

When muscle contracts, do actin and myosin filaments shorten? Does sarcomere shorten?

A

No, Actin and myosin dont shorten
Yes, The sarcomere does shorten

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19
Q

What’s the points of origin?

A

Bone, typically proximal, greater mass and more stable during contraction than insertion point

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20
Q

What’s the point of insertion?

A

Structure the muscle attaches to
Tends to be moved by contraction
Tends to be distal (part that moves)
Could be bone, tendon, connective tissue
Usually tendon to bone
Greater motion than origin during contraction

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21
Q

what are the 5 different muscle roles in movement?

A

-agonists- prime movers
-antagonists - oppose prime movers
-synergists - assist prime movers (alone they can’t perform movement, but their angle of pull assists)
-neutralisers- prevent unwanted actions that an agonist can perform
-fixators- act to hold a body part immobile whilst another part is moving. Stabilise a joint

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22
Q

what are the three different levers in biomechanics?

A

-first class (see saw)
-second class (wheelbarrow)
-third class (fishing rod)

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23
Q

First class lever system

A

fulcrum between load and effort
E.g. extension/flexion of head

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24
Q

second class lever system

A

load between fulcrum and effort
E.g. plantar flexion of foot

25
Q

third class lever system

A

Effort applied between fulcrum and load
-most common
E.g. flexion of elbow
Mechanical disadvantage

26
Q

muscle compartments

A

groups of muscles with related functions surrounded by thick dense fascia
Can be anterior, posterior, lateral, medial

27
Q

compartment syndrome

A

involves the compression of nerves and blood vessels due to swelling within the enclosed space created by the fascia that separates groups of muscles

28
Q

Symptoms of compartment syndrome

A

-deep contestant poorly localised pain
-parasthesia (pins and needles)
-compartment may feel tense and firm
-swollen shiny skin, sometimes bruising
-prolonged capillary refill time

29
Q

fasciotomy

A

a surgical incision through the fascia to relieve tension or pressure

30
Q

what is the treatment for compartment syndrome?

A

fasciotomy

31
Q

what are the 4 regulators of muscle tone?

A

-motor neurone activity
-muscle elasticity
-use
-gravity

32
Q

muscle tone

A

the tension of a muscle when it is relaxed

33
Q

DONT mechanism of muscle hypertrophy

A

overstretching such that a bands and i bands no longer re-engage
new muscle fibrils are produced
new sarcomeres are added in the middle of existing sarcomeres
new muscle fibres arise from mesenchymal cells

34
Q

DONT what can lead to muscle atrophy?

A
  • disuse
    -surgery
    -disease
35
Q

how long does nerve regeneration take?

A

3 months

36
Q

Dúchenle muscular dystrophy

A

Most common form of muscular dystrophy
X linked recessive inheritance
Mutation of dystrophin gene
Dystrophin gene normally joins sarcolemma to actin microfibre

37
Q

what is the mechanism of what occurs during duchene muscular dystrophy?

A

absence of dystrophin allows:
-excess calcium enters muscle cell
-calcium taken up by mitochondria
-water taken with it
-mitochondria burst
-muscle cells burst
-CK and myoglobin levels extremely high in blood
-kidney can’t cope with myoglobin levels so kidney damage occurs
-muscle cells get replaced by adipose tissue

38
Q

Rhabdomyolysis

A

destruction of muscle to produce myoglobin

39
Q

what replaces muscle cells in duchene muscular dystrophy

A

adipose tissue

40
Q

Symptoms of muscular dystrophy

A

-shoulders and arms awkwardly held back when walking
-belly sticks out
-poor balance
-walking on toes due to tight heel cord
-thick lower leg muscles

41
Q

creatine kinase function

A

phosphorylate ATP as it leaves mitochondria

42
Q

What could cause increased plasma creatine kinase levels

A

-intramuscular injection
-vigorous physical exercise
-a fall
-rhabdomyolysis
-muscular dystrophy
-acute kidney injury (myoglobin not being cleared)

43
Q

within how many hours of a myocardial infarction should a troponin assay be conducted for absolute accuracy?

A

20

44
Q

How long after iscaemic damage is troponin released from cardiac muscle?

A

Within an hour

45
Q

Is the quantity of troponin released proportional to the degree of muscle damage?

A

No not necessarily

46
Q

What troponin is used to measure cardiac damage in the UK?

A

troponin I

47
Q

Why is troponin used as a marker for cardiac ischaemia?

A

The levels are elevated for much longer after a myocardial infarction, and it’s more specific

48
Q

what occurs when botulism toxin is given during botox?

A

Botulinum toxin (Botox) is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species. It prevents the release of the neurotransmitter acetylcholine from axon endings at the motor end plate of the neuromuscular junction, thus causing flaccid paralysis (non contractile state)

49
Q

what is botulism toxin used to treat clinically?

A

muscle spasms

50
Q

what is botulism toxin used for cosmetically?

A

to treat wrinkles

51
Q

Malignant hyperthermia

A

-severe reaction to anaesthetics
Succinylcholine binds to Ach receptor
Causes muscle rigidity and fasciculation due to increased ca2+ release, with excessive heat and metabolic acidosis
Increased muscle breakdown and hyperkalaemia
Affects males more than females

52
Q

What’s the mortality risk of malignant hyperthermia with and without treatment

A

With 5%
Without 75%

53
Q

organophosphate (used in pesticides) poisoning

A

-inhibits normal function of AchE so increased activity of Ach

54
Q

What are the muscarinic symptoms of cholinergic toxidrome (organophosphate poisoning

A

Salivation
Lacrimaition
Urination
Defecation
GI cramping
Emesis

Sludge

55
Q

What are the nicotinic symptoms of organophosphate poisoning?

A

Muscle cramps
Tachycardia
Weakness
Twitching
Fascilculations

Days of the week

56
Q

what are the muscarinic symptoms of organophosphate poisoning?

A

Salivation
Lacrimation
Urination
Defecation
GI cramping
Emesis

57
Q

what are the nicotinic symptoms of organophosphate poisoning?

A

Muscle cramps
Tachycardia
Weakness
Twitching
Fasciculations

58
Q

What is Fasciculations

A

Rapid movements of muscle

59
Q

What is emesis

A

emesis

BODY LOGISTICS (16 decks)

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