session 8-muscle,contraction,structure,disease Flashcards

1
Q

which type(s) of muscle is voluntary and which is involuntary?

A

voluntary-skeletal

involuntary-cardiac and smooth

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2
Q

which muscle is striated/non striated?

A

striated=cardiac and skeletal

non striated=smooth

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3
Q

draw the ultrastructure of muscle, in terms of bands/zones and state which contains actin and myosin.

A

see notes on penultimate

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4
Q

draw the sliding filament model

A

see notes on penultimate

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5
Q

what are the names of the 3 types of muscle?

A

cardiac,skeletal and smooth

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6
Q

what is a satellite cell?

A

precursor to muscle cells

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7
Q

how does skeletal muscle repair itself?

A
  • tissue regenerates by mitotic activity of satellite cells, so that hyperplasia ( multiplication of cells) follows muscle injury
  • satellite cells can also fuse with existing muscle cells, increasing mass (skeletal muscle hypertrophy)
  • large damage repaired by connective tissue which leaves scar
  • decrease in nerve or blood supply causes muscle fibre degeneration and replaced by fibrous tissue
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8
Q

how does cardiac muscle repair itself?

A
  • cannot regenerate

- after damage, fibroblasts lay down scar tissue

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9
Q

how does smooth muscle repair itself?

A

-cells undergo mitosis and can form new smooth muscle cells

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10
Q

in cardiac muscle cells, what kind of position do the nuclei take up and how many nuclei are present in each cell?

A

central and 1 or 2 nuclei per cell

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11
Q

what kind of discs does the cardiac muscle contain?

A

intercalated

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12
Q

the T tubules in cardiac muscle are in line with which band(s)?

A

z bands

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13
Q

what band(s) are the t tubules in line with in skeletal muscle?

A

the A to i band junction

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14
Q

in smooth muscle cells, where are the nuclei located and how many nuclei are there per cell?

A

central and one per cell

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15
Q

what 3 features of large purkinje cell fibres make them suitable for their job of rapidly conducting action potentials, enabling the ventricles to contract in a synchronous manner?

A
  • abundant glycogen
  • sparse myofilaments
  • extensive gap junction sites
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16
Q

what happens to muscle fibres in disuse atrophy?

A

-shrink and weaken

17
Q

what natural process causes muscle atrophy and what is the medical term?

A

ageing

SARCOPENIA

18
Q

what is myasthenia gravis?

A

autoimmune destruction of end plate ACh receptors by antibodies
-loss of junctional folds at end plate (less SA for receptors)
-widening of synaptic cleft (slower diffusion rate of ACh)
PROBLEM: when affecting respiratory muscle

19
Q

Describe 3 symptoms of myasthenia gravis.

A
  • Fatigue and sudden falling
  • drooping eyelids (can be treated with ice-inhibits acetylcholinesterASE activity)
  • double vision
20
Q

how do you treat myasthenia gravis?

A

acetylcholinesterase inhibitors
Immune suppressants
Plasmapheresis-removal of harmful antibodies
Thymectomy

21
Q

how does botox disrupt neuromuscular transmission?

A

stops ACh release

22
Q

how does organophosphate affect neuromuscular transmission?

A

irreversibly inhibits acetylcholinesterase

  • ACh remains in receptors
  • muscle stays contracted
23
Q

Describe WHY muscular dystrophy occurs.

A
  • organ or tissue wastes away (can be through atrophy)
  • genetic fault causing absence of certain proteins that anchor actin filaments to sarcolemma
  • during contraction, muscle fibre tears apart
24
Q

In duchenne muscular dystrophy, what is the name of the protein that is completely absent and so cannot perform its role of binding actin to the sarcolemma?

A

dystrophin

25
Q

why do blood creatine kinase levels rise with DMD?

A

muscle cells open as they tear and so creatine kinase leaks into blood (blood test to diagnose DMD)

26
Q

what is pseudohypertrophy?

A

muscles become swollen with deposits of fat and fibrous tissue

27
Q

one symptom of DMD is gower’s sign:what is this?

A

using hands and knees to stand up from squat position-loss of proximal muscle strength

28
Q

what kind of disorder is malignant hyperthermia?

A

rare,autosomal dominant

29
Q

what sparks malignant hyperthermia?

A

general anaesthetic drugs

30
Q

what does succinylcholine do and does it act competitively or non competitively?

A

inhibits ACh activity by binding non competitively on receptors

31
Q

what is succinylcholine broken down with?(degraded slower than ACh)

A

butyrylcholinesterase

32
Q

what does malignant hyperthermia do in skeletal muscle?

A

uncontrolled increase in skeletal muscle oxidative metabolism-overwhelms bodies capacity to supply O2,remove CO2 and regulate
-leads to death

33
Q

what drug is used to treat malignant hyperthermia?

A

dantrolene=muscle relaxant by preventing calcium release

34
Q

What does the peri,Epi and endomysium contain?

A

Connective tissue, blood vessels and nerves

35
Q

What protein is a useful marker for cardiac ischaemia?

A

Troponin

36
Q

What is rigormortis?

A

Stiffening of joints and muscles in body, shortly after death

37
Q

What 2 things happen in DMD after muscle fibres tear?

A

Calcium enters and causes necrosis

Pseudohypertrophy-swelling before fat and connective tissue replace muscle fibres

38
Q

What type of inheritance is DMD?

A

X linked recessive