Skeletal Muscle Contraction

Question 1

Testosterone

Answer 1

Decreases catabolism
Increases protein synthesis
Reduces dat

Question 2

Effects of bed rest

Answer 2

Transition of type 1 fibres to type 2 fibres
Less muscle protein synthesis
Fewer thin and thick fibres
Loss of size and strength
Add physiother apy to prevent contractures where sarcomeres are shortened making it impossible to straighten joints

Question 3

Contracture

Answer 3

When limbs become immobilised for long periods

Process of growth is reversed

Shortening of muscles

sarcomeres are removed in series from myofibrils

Question 4

Myalgia

Answer 4

Muscle pain

Causes: injury, causes, infection, autoimmune

Can be associated with Rhabdomyolysis

Question 5

Myopathy

Answer 5

Muscle disease

Muscular weakness due to muscular muscle fibre dysfunction

Can be systemic(inflammation more generally) or familial

Question 6

Paresis

Answer 6

Weakness/partial loss of voluntary movement

Or impaired movement

Question 7

Involuntary twitches

-fasciculations

Answer 7

Involuntary visible twitches

Question 8

Involuntary twitches

-fibrillations

Answer 8

Involuntary spontaneous contractions

Only visible by electromyography

Question 9

Rhambdomyolysis

Answer 9

Rapid breakdown of skeletal muscle

Risk of kidney failure due to loss of electrolytes within the muscle

Cause- crash injuries, drugs, hyperthermia, ischaemia to the skeletal muscle

Treatment: IV fluids (to treat shock)
Haemodialysis (to get rid of the myoglobin)

Symptoms&signs: muscles pains, vomiting, confusion, dark urine

Question 10

Creatinine phosphokinase/ CPK/CK

Answer 10

Release of CK when cells lyse after necrosis of muscle trauma

Question 11

What does myoglobin in plasma suggest?

Answer 11

Indicates rhab or MI

Question 12

Rigor Mortis

Answer 12

Depletion of ATP after death
Myosin bound to actin
Ends after 3 days

Question 13

Myasthenia gravies

Answer 13

Progressive muscle weakness
Often starts with eye weakness
depletion of nicotinic AChR
Immune system inappropriately produces auto-antibodies against nAChR

Symptoms- ptosis, Diplopia, fatigue

Question 14

MG Treatment

Answer 14

AChE inhibitors
-Neostigmine
Increase in ACh activity

Edrophonium- short lived AChE inhibitor- only temporary loss of symptoms- this can be diagnostic

Thymectomy
Plasmapheresis

Question 15

SMA

Answer 15

Aka floppy baby syndrome

Death of LMN

Deinnervation leads to muscle atrophy via apoptosis

Caused by genetic defect

Question 16

Fibre Type grouping

Answer 16

Biopsy to show regeneration: fibre type grouping

Clustering of same type of fibres

Collateral reinnervation

Question 17

Malignant hyperthermia

-inc treatment

Answer 17

Autosomal dominant Genetic (Rare) susceptibility to gas anaesthetics e.g sevoflurane

Mutation in RyR means gas anasthetic leads to uncontrolled Ca2+ release

SERCA activated leading to increase o2 consumption, increased co2 leading to acidosis, hyperthermia which can lead to rhabdomyolisis- skeletal muscle become rigid

Treatment- dantrolene sodium to stop abnormal ca2+ release

Question 18

Muscular dystrophy

Answer 18

Severe and progressive wasting of muscles

Question 19

Duchenne muscular dystrophy

-what is the hallmark feature??

Answer 19

X linked disease

Progressive loss of muscle tissue which is replaced by fibrofatty connective tissue

mutation- dystrophin gene- largest gene so susceptible to mutations

Gower sign

Question 20

Is the patellar reflex a stretch or tension reflex

Answer 20

stretch reflex

this reflex is also monosynaptic

Question 21

What innervates spindle fibres?

Answer 21

gamma motor neurones adjust sensitivity of spindle fibres

Question 22

Is the Golgi-tendon reflex mono or disynaptic reflex?

Answer 22

Disynaptic as there is a synapse with inhibitory neurone AND motor neurone.