ToB - muscles

Question 1

describe the structure of skeletal muscle

Answer 1

multiple peripheral nuclei
connections via fascicle bundles and tendons
controlled via somatic (voluntary) and motor neurones
rapid and forceful
mesoderm derived
vary in colour

Question 2

which bands remain the same length and which bands narrow during contraction?

Answer 2

A band remains same

I and H band narrow during contraction

Question 3

describe how skeletal muscle develop (fusion)

Answer 3

myoblasts (muscle cells) from myogenic stem cells (through cell division)
fuse to form primary myotube (cytoplasms join, few nuclei present from few muscle cells fusing)
nuclei displaced (to peripheral) by newly synthesised actin and myosin
(in cardiac and smooth muscle there is no fusion)

Question 4

Describe red muscle fibres structure and contraction

Answer 4

small, rich in blood supply, myoglobin and mitochondria
weaker contraction, slower
rich in oxidative enzymes (not ATP)
less junctions
normally limb muscles, back

Question 5

describe white muscle fibres structure and contraction

Answer 5

large, low vascularisation, myoglobin and mitochondria
fast, strong contractions (rapid contractions)
rich in ATPase, poor in oxidative enzymes
more junctions
fingers, eyes

Question 6

what are myotendinous junctions?

Answer 6

skeletal muscle fibres connect (interdigitate) with tendon collagen bundles
the sarcolemma always lies between the collagen bundles and the muscle fibre’s myofilaments (actin + myosin)
(tendons made of collagen)

Question 7

Describe the repair of skeletal muscle

Answer 7

peripheral satellite cells can undergo mitosis and fuse with muscle cells to increase mass
muscle fibres cannot divide

Question 8

describe the initiation of contraction

Answer 8

1. nerve impulse travels down motor neuron
2. impulse releases ACh into synaptic cleft causing depolarisation of sarcolemma (through influx of Ca2+)
3. Na+ voltage gated channels open, Na+ enters cells (of post synaptic cleft)
4. depolarisation spreads from sarcolemma to T tubules
5. then down terminal cisternae
6. causing release of Ca2+ from terminal cisternae to sarcoplasm
7. the Ca2+ then bind to TnC causing interaction between myosin and actin

Question 9

describe the sliding filament theory

Answer 9

myosin head binds to actin with ATP (form cross bridge)
myosin head bends pulling actin filament towards M line (in hydrolysis of ATP) - working stroke
a new ATP molecule binds to the myosin head causing it to detach from actin, hydrolysis of the ATP causes the myosin head to cock back to original position for process to begin again

Question 10

describe cardiac muscle?

Answer 10

short branched cylinders
single central nucleus
connected via junctions - end to end
controlled via an intrinsic rhythm
cells are connected via intercalated disk which allow electrical and mechanical coupling
T tubules line with Z line not A-I junction

Question 11

describe Purkinje fibres

Answer 11

specialised myocytes
abundant glycogen
sparse myofilaments
extensive gap junction sites
rapid conduction

Question 12

describe the structure of smooth muscles

Answer 12

spindle shaped, tapering ends
single central nucleus
connected via gap and desmosome type junctions
involuntary control - local stimuli
slow sustained power, contraction requires less TP (ox/phos)
may remain contracted for hours or days
capable of being stretched
respond to nerve signals, hormones, drugs or blood gas conc

Question 13

what are the different types of atrophy?

Answer 13

disuse - bed rest, limb immobilisation, less fibres and cross bridges but same number of cells (fibre diameter decreases)
age - 30+ (muscle mass decrease)
denervation - motor neurones damage

Question 14

what is hypertrophy of muscle? structural changes?

Answer 14

increased fibre diameter and metabolic changes e.g. increased enzymes, mitochondria, glycogen and blood flow
replacement > destruction

Question 15

what happens in increasing frequency of stretching to muscle?

Answer 15

increase flexibility as increase sarcomeres (e.g. yoga)

Question 16

what happens in myasthenia gravis?

Answer 16

autoimmune destruction of ACh end plate receptors
end plate is less convolute
widening of synaptic cleft
this leads to fatigbility and sudden falling e.g. drooping eyelids and double vision
treated with AChesterase inhibitors

Question 17

What is botulism?

Answer 17

toxins block ACh release

can come from soil

Question 18

what is organophosphate poisoning

Answer 18

inhibit acetylcholinesterase so leads to constant depolarisation of sarcoplasm
death by asphyxiation commonly (abnormal breathing - body deprived of O2)

Question 19

what is DMD?

Answer 19

lack of dystrophin molecule to anchor muscle fibres to sarcolemma
muscles rip themselves apart during contraction
Ca2+ release into cell causing cell necrosis
produces pseudohypertrophy of muscle via fibrosis of the muscle (become fat & CT replace muscle fibres)
individuals wheelchair bound and respiratory failure common cause of death

Question 20

what are symptoms of DMD and treatment?

Answer 20

symptoms: gower’s sign (use hands and knees to support oneself upright), shortening and hardening of muscles
treatment: steroid therapy (slow down muscle damage)

Question 21

what is malignant hyperthermia?

Answer 21

susceptibility altered by an autosomal dominant gene
general anaesthetics e.g. succinylcholine can cause an overwhelming increase in skeletal muscle oxidative phosphorylation
depletes O2, increases CO2 production and increase temperature

Question 22

treatment for malignant hyperthermia?

Answer 22

treat with dantrolene (prevent skeletal muscle oxidative phosphorylation) & stop general anaesthetia

Question 23

how does general anesthetics make malignant hyperthermia worse?

Answer 23

inhibit ACh, causes buildup of Ca2+ in cells (influx of Ca2+ to release ACh)
for body to send Ca2+ to stores in SR requires ATP