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Body Logistics > Lecture 10-Muscle Tissue (Function And Disease) > Flashcards

Lecture 10-Muscle Tissue (Function And Disease) Flashcards

1
Q

Compare and Contrast Cardiac and Smooth muscle

A

Differences

  • smooth muscle does not contain sarcomeres
  • electrical conduction requires specialised cells in cardiac muscle (SAN and AVN)
  • no troponin in smooth muscle

In common
-Nuuclei are central not peripheral
-Only one contractile cell type
-acts as a syncytium (wave-like function). One muscle cell linked to another
-Myocytes communicative through gap junctions
(Cardiomyocytes-intercalated disks)

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2
Q

Cardiac innervation can occur two ways . What are they and what do they do?

A

Parasympathetic - slows down intrinsic heart rate by acting on the SAN in the atria

Sympathetic- increases the heart rate by action on the ventricles

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3
Q

How does the sympathetic pathway increase heart rate /contraction?

A
  • neurotransmitter (adrenaline) released from sympathetic nerve and acts on the sarcolemma (plasma membrane )
  • induces electrical signal which depolarises the sarcolemma . Depolarisation spreads down t tubules into sarcoplasmic reticulum .
  • channels in SR undergo conformational changes in which its shape changes to allow calcium to pass through
  • calcium released into sarcoplasm and binds to troponin calcium (c) on actin
  • actin-myosin binding site is exposed for myosin head to bind
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4
Q

Innervation of skeletal muscle

A
  • nerve impulse releases acetylcholine (only nt involved in skeletal)
  • binds to receptor on the sarcolemma
  • initiates an action potential along the muscle

Each fibre has its own nerve point

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5
Q

The events leading up to contraction of skeletal muscle

A
  • initiation: nerve impulse along motor neurone axon arrives at neuromuscular junction
  • impulse causes release of acetylcholine into synaptic cleft causing depolarisation of sarcolemma
  • sodium channels open and enter the skeletal muscle cell
  • depolarisation spreads over sarcolemma and into t tubules
  • voltages sensor proteins of t tumble membrane change their conformation
  • gated calcium ion release channels of adjacent terminal cistern are are activated by the step above
  • calcium ions are rapidly released into the sarcoplasm
  • calcium binds to TnC subunit of troponin and contraction cycle is initiated
  • calcium ions are returned to the terminal cisternae of sarcoplasmic reticulum
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6
Q

What is the pathophysiology of myasthenia gravis?

A

An autoimmune disease in which antibodies block the acetylcholine receptor on the end plates of a muscle cell

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7
Q

Clinical features of myasthenia gravis

A

Reduced synaptic transmission

Intermittent muscle weakness

End plate invaginations in synaptic clefts reduced

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8
Q

Symptoms of myasthenia gravis

A

Drooping eyelids -Ptosis

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9
Q

Structure of a myosin molecule

A

Rod like structure from which 2 heads protruding

  • thick filaments consists of many myosin molecules whose heads protrude at opposite ends of filaments
  • 2 twists of myosin complex
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10
Q

Structure of actin molecule

A

Two protein components that includes F acting fibres and G actin globules

A tropomyosin-troponin complex sits over binding sites

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11
Q

Features of the functional contraction unit

A
  • tropomyosin molecules coil around the actin helix reinforcing it
  • a troponin compels is attached to each topomyosin molecule
  • in the centre of the sacromere, there are no myosin heads ion the thick filaments
  • myosin heads extend towards rage actin filaments in regions of potential overlap
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12
Q

Role of ionic calcium in the contraction mechanism

A
  • binding of Calcium to TnC of troponin causing a conformational change which moves tropomyosin from actin’s binding site
  • this allows myosin heads to bind to actin and contraction begins
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13
Q

The mechanism of the sliding filament theory

A
  • ATP bings to myosin head and causes it change shape
  • atpase hydrolysis atp and stays attached to the myosin head which causes a conformational change
  • as adp and inorganic phosphate leaves myosin head, another conformational change in which the working stroke occurs
  • once atp and inorganic phosphate has left atp binding site is revealed

Always continues in the presence of calcium ions and atp

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14
Q

What happens to the actin and myosin lengths during contraction?

A

The lengths stay the same

Only the sarcomeres shorten
Z Lines come together

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15
Q

Skeletal muscles work as levers in synergy and this are in compartments

Features of this compartments

A

-they are muscles with similar action grouped together
-surrounded by thick dense fascia
-based on location
Anterior
Posterior
Lateral medial

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16
Q

Why does compartment syndrome occur ?

How is treated ?

A
  • limbs are divided into compartments delineated by fascia (band of sheet of connective tissue )
  • trauma in one compartment could cause internal bleeding which exerts pressure on blood vessels and nerves

Treated by fasciotomy-covered by skin graft

17
Q

What does compartment syndrome result in?

A
  • deep constant poorly localised pain aggravated by passive stretch of muscle group
  • paresthesia(pins and needles)
  • compartments may feel tense and firm cause of swelling
  • swollen shiny skin with sometimes obvious bruising
  • prolonged capillary refill time
18
Q

Definition of muscle tone

A

Muscle tone is defined as the tension in a muscle at rest

19
Q

Definition of muscle strength

A

The muscle ability to contract and create force in response to resistance

20
Q

What is muscle tone regulated by?

A
  • motor neurone activity
  • muscle elasticity
  • use
  • gravity
21
Q

When destruction of muscle is greater than replacement , what occurs?

A

Atrophy -wasting of muscle tissues

22
Q

When replacements of muscles is greater than destruction , what occurs ?

A

Hypertrophy - bigger muscles

23
Q

How long does it take to replace contractile proteins ?

A

2 weeks

24
Q

Whats the mechanism for muscle Hypertrophy?

A
  • over-stretching of muscles such that A and I bands can 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
25
Q

What’s the mechanism is muscle atrophy ?

A

Disuse-bed rest, limb immobilisation, age

Surgery - denervation of muscle (nerve regeneration takes 3 months)

Disease -Muscular dystrophies

Loss of proteins , reduced fibre diameter , loss of muscle power

26
Q

Key features of Duchene muscular dystrophy

A
  • most common type of dystrophy
  • diagnosis is based on results of muscle biopsy, increased levels of creating kinase in the blood, electromyography and genetic testing
  • generally affects only boys as its inherited through x-linked recessive pattern
  • mutation of dystrophin gene
  • muscle cells replaced by adipose tissue
27
Q

Duchene Muscular Dystrophy

What does the absence of Dystrophin allow ?

A
  • Excess calcium to enter muscle cell
  • calcium taken up by mitochondria
  • water taken with it
  • mitochondria burst
  • muscle cell burst (rhabdomyolysis)
  • creative kinase and myoglobin levels extremely high in blood
28
Q

What is creative kinase and what can it be used to measure ?

A

An enzyme in metabolically active tissues e.g muscle

Used to measure to diagnose heart attacks

Released into the blood by damaged skeletal muscle and brain tissue

29
Q

What can a rise is creatine kinase result from ?

A
  • intramuscular injections (vaccinations)
  • vigorous physical exercise
  • a fall (elderly)
  • rhabdomyolysis(severe muscle break down )
  • muscular dystrophy (weakening and breakdown of skeletal muscles overtime)
  • acute kidney injury (myoglobin not being cleared )
30
Q

Key features of botulism toxin and Botox

A
  • toxin produced by bacterium
  • prevents the release of acetylcholine
  • causes non contractile state of skeletal muscle : flaccid paralysis
  • clinically used to treat muscle spasms (cervical dystonia)
  • use cosmetically to treat wrinkles ( Botox)
31
Q

Key features of Organophosphate poisoning (pesticides)

A
  • inhibits the function of acetylycholinesterase by binding to it
  • ach activity at junction is potentiated
32
Q 
Cholinergic Toxidrome (organophosphate poisoning )
-Too much acetylcholine in neuromuscular junction

What are the Muscarinic symptoms? (muscles )

A 
S-salivation 
L-Lacrimation 
U-Urination 
D-Defecation 
G-GI cramping 
E-Emesis (vomiting )
33
Q 
Cholinergic Toxidrome (organophosphate poisoning )
-Too much acetylcholine in synaptic  junction

What are the Nicotinic symptoms? (Nerves )

A 
M-Muscle cramps 
T-Tachycardia 
W-Weakness
T-Twitching 
F-Fasciculations (spontaneous contractions of muscle fibres)

Body Logistics (6 decks)

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