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
why do blood creatine kinase levels rise with DMD?
muscle cells open as they tear and so creatine kinase leaks into blood (blood test to diagnose DMD)
26
what is pseudohypertrophy?
muscles become swollen with deposits of fat and fibrous tissue
27
one symptom of DMD is gower's sign:what is this?
using hands and knees to stand up from squat position-loss of proximal muscle strength
28
what kind of disorder is malignant hyperthermia?
rare,autosomal dominant
29
what sparks malignant hyperthermia?
general anaesthetic drugs
30
what does succinylcholine do and does it act competitively or non competitively?
inhibits ACh activity by binding non competitively on receptors
31
what is succinylcholine broken down with?(degraded slower than ACh)
butyrylcholinesterase
32
what does malignant hyperthermia do in skeletal muscle?
uncontrolled increase in skeletal muscle oxidative metabolism-overwhelms bodies capacity to supply O2,remove CO2 and regulate -leads to death
33
what drug is used to treat malignant hyperthermia?
dantrolene=muscle relaxant by preventing calcium release
34
What does the peri,Epi and endomysium contain?
Connective tissue, blood vessels and nerves
35
What protein is a useful marker for cardiac ischaemia?
Troponin
36
What is rigormortis?
Stiffening of joints and muscles in body, shortly after death
37
What 2 things happen in DMD after muscle fibres tear?
Calcium enters and causes necrosis | Pseudohypertrophy-swelling before fat and connective tissue replace muscle fibres
38
What type of inheritance is DMD?
X linked recessive