Musles- Small Details Flashcards

1
Q

What would cause tea coloured urine?

A

Myoglobinurea

Death of striated muscle releases myoglobin into blood- if above renal threshold it is seen in the urine

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2
Q

What muscle type would you not find myoglobin in?

A

Smooth muscle

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3
Q

Which striated muscle type is glycolytic?

A

Fast twitch fibres (Type 2B)

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4
Q

What is the difference between hypertrophy and hyperplasia?

A

Hypertrophy- enlargement in size

Hyperplasia- increase in cell number

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5
Q

Give 3 features of Purkinje Fibres

A

Abundant glycogen

Sparse myofibrils

Extensive Gap junctions

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6
Q

What are caveolae (found in smooth muscle)

A

Cave like invagination that can sample the external environment

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7
Q

Describe muscle repair in the 3 muscle type

A

Smooth muscle- can undergo mitosis

Skeletal muscle- can’t undergo mitosis but can regenerate using satellite cells or fuse together existing muscle cells to increase mass (hypertrophy)

Cardiac muscle- incapable of repair. Fibroblasts lay down scar disuse in damaged muscle

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8
Q

Describe how contraction is initiated at cardiac muscle?

A
  1. Action potential arrives at sarcolemma
  2. Depolarisation interacts with voltage sensitive DHAP receptor- calcium enters the myocyte from the myocyte. Known as calcium spark
  3. Calcium spark causes CICR from the RyR of the sarcoplasmic reticulum
  4. Calcium binds to troponin-C on actin filament causing movement away from actin allowing myosin to bind and contraction can occur
  5. SERCA takes calcium back into the SER once contraction is complete
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9
Q

Explain how smooth muscle contraction occurs from vericosisities

A

Calcium release from mitochondrion causes neurotransmitter release from vericosities

Causes sarcolemma to depolarise and VOCC to open- calcium enters the cell

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10
Q

Explain how smooth muscle contraction occurs from hormone receptor binding

A
  1. Hormone binds to GPCR- IP3 production as secondary messenger binds to SER causing calcium release
  2. Calcium binds to calmodulin. 4 calcium must bind to active it
  3. Active calmodulin binds to MLCK which phosphorylase seems circular myosin II. Phosphorylation causes myosin to linearise
  4. Linear actin is able to bind to actin- forms dense bodies (2 myosin and 1 actin)
  5. Contraction continues until calcium levels decrease or phosphates dephosphorlyates myosin II
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11
Q

Describe the events leading to skeletal muscle contraction

A
  1. Nerve impulse arrives at NMJ causing ACh release
  2. ACh binds to nACh receptor - allows sodium ions to enter cell
  3. Depolarisation spreads over sarcolemma into T tubules- picked up by voltage sensor proteins e.g ryanadine
  4. Ryanadine causes Calicum release from SR
  5. Calcium binds to troponin C- contraction occurs
  6. Calcium returns to the SR once calcium complete
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12
Q

How does muscle hypertrophy occur?

A

Over stretching of muscle- A and I binds can’t re-engage
New muscle fibres are produced from mesenchymal stem cells
New sarcomeres are added to existing sarcomeres to lengthen the muscle

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13
Q

How does atrophy occur?

A

Disuse, surgery or disease

Loss of protein, reduced fibre diameter = loss of muscle power

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14
Q

How is Duchene Muscular Dystrophy caused?

A

X linked recessive mutation of the dystrophin gene

Excess calcium taking across muscle memebrane and taken up by the mitochondria. Water follows causing mitochondria to burst
Known as rhabdomyolysis

Creating kinase and myoglobin seen in blood

Damaged muscle cells get replaced by adipose tissue

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15
Q

What are the symptoms of Duchene muscular Dystrophy?

A
Belly sticks out
Sway back
Poor balance
Shoulders and arms held back
Tight heel cord causes walking on toes 
Weak muscles causes foot drop
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16
Q

How does botulism toxin work?

A

Blocks neurotransmitter release at motor end plate
Causes loss of muscle tone

Used clinically to treat muscle spasm or cosmetically

17
Q

How to organophosphates work?

A

Inhibit acetylcholinesterase = continual stimulation of the muscles