Muscle Function And Disease Flashcards
How and where is the skeletal muscle innervated?
At the neuromuscular junction
Nervous impulses release acetylcholine from the vesicles
They bind to receptors on the sarcolemma which initiates and action potential along the muscle
How does ratio of fibres per motor unit relate to control/strength?
The fewer units the more control a muscle has.
The more units the more power a muscle has.
What is a kranocyte cell?
Resided over the terminal Schwann cell of a nerve.
It anchors the nerve to the muscle cell and forms a dome to stop neurotransmitters travelling to and activating other muscles.
What events lead to the contraction of a skeletal muscle?
1) nerve impulse along motor neurone arrives at neuromuscular junction
2) release of Ach into synaptic cleft, causes local depolarisation of sarcolemma
3) voltage-gated Na+ channels open and Na+ enters cell
4) depolarisation spreads over sarcolemma and into T tubules
5) voltage sensor proteins of T tubule change conformation
6) gated Ca2+ ion-release channels of adjacent terminal cisternea activated by 5
7) ca2+ rapidly released into sarcoplasm
8) Ca2+ binds to TnC subunit of troponin and contraction cycle initiated
9) Ca2+ ions returned to terminal cisternae of sarcoplasmic reticulum
Describe the pathology of Myasthenia Gravis.
An autoimmune disease
Antibodies against Ach receptor (block them)
30% reduction in receptor number is enough for symptoms
End plate invagination in synaptic clefts are reduced
Reduced synaptic transmission
Intermittent muscle weakness (ie Ptosis-droopy eyelid)
Name the two protein components of ACtin.
Actin fibres
Actin globules
What covers actin’s hiding sites?
Tropomysosin-troponin complex’s
Where does Ca2+ bind to on the troponin complex?
It binds to TnC
What is the role of ionic calcium in the contraction mechanism?
As Ca2+ binds to the TnC of troponin, a confromation change moves tropomyosin away from actin’s binding sites.
This allows myosin heads to bind to actin and contraction begins.
The tropomysosin sits in the cleft of actin-globulin spheres
Describe how contraction works in terms of actin-myosin bridges etc.
1) myosin crops bridge attaches to actin myofilament
2) working stroke-the myosin head pivots and pulls on the actin filament, ATP is used and ADP is released
3) a new ATP joins the myosin head detaching the cross bridge
4) as ATP is split to ADP the myosin head cocks
What is a muscle origin?
Usually bone, typically proximal. Has greater mass and is more stable in contraction than the insertion point.
What is a muscle insertion?
Tends to be moved in contraction. Tends to be distal. Bone tendon or connective tissue. Greater motion than origin in contraction.
What is an agonist (in muscle terms)?
The prime mover (a main muscle responsible for a particular movement ie raising arm)
What is an antagonist (in muscl terms)?
They oppose prime movers stopping them moving to far (throwing hand back past head instead of a controlled raise)
What is a synergist (In muscle terms)?
They assist prime movers (acting alone they cannot perform movement but their angle of pull assists an agonist)
What is a neutraliser (in muscle terms)?
Prevent unwanted action that an agonist could perform, (prevent unwanted MUSCLE action)
What is a fixation )in muscle terms)?
They act to hold a body part immobile whilst another part is moving. (Hold a joint stable)
Describe the motion of a first class lever.
Like a see saw
Effort at one end, load at other
Few examples -extension of head
Describe the motion of a second class lever.
Wheelbarrow
Effort at one end fulcrum at other
Plantar flexion of foot
Describe the motion of a third class lever
Fishing rod Effort between load and fulcrum Mechanical disadvantage Most common in body Raising forearm by bending elbow
In reference to muscles, what are compartments?
Muscles with similar actions are grouped into compartments
They are surrounded by thick dense fascia to hold them together
The compartments are based on location (anterior, posterior, lateral or medial)
What is compartment syndrome?
Trauma in a compartment may cause internal bleeding, this exerts pressure on blood vessels and nerves.
This is called compartment syndrome
What are the signs/symptoms of compartment syndrome?
A deep, constant poorly localised pain
Aggravated by passive stretch f the muscle group (sitting)
Parenthesis (altered sensation ie pins & needles)
Compartment feels tense and firm
Swollen shiny skin
Bruising
Prolonged capillary refill time
What I the treatment for compartment syndrome?
Cut open the compartment to let the fluid out and reduce the pressure. This is called a fasciotomy.
‘Tis is then covered by a skin graft
What regulates muscle tone?
Motor neurone activity
Muscle elasticity
Use
Gravity_ astronauts loose it
What is muscle tone?
Muscles never fully relax
They retain an amount of tension and stiffness (muscle tone)
It ensures muscles are ready to react and it improves with exercise
How long does it take to replace contractile protiens in muscle remodelling?
2 weeks (its a continual process)
What is th mechanism for muscle hypertrophy?
Overstretch so that A and I bands can no longer engage
New fibrils are produced
New sarcomers added in middle of existing sarcomeres
New fibres form mesenchymal cells
(Over stretching features in some muscle pathologies such as enlarged ventricles)
What is the mechanism for muscle atrophy?
Disuse
Surgery
Disease
Loss of protein, causes reduced fibre diameter which means a loss of muscle power.
List some signs/symptoms of Duchene muscular dystrophy.
Shoulders and arms held back awkwardly walking Swayed back Weak butt muscles Bent knees to take weight Thick lower leg muscles (adipose mainly not strong) Tight heel cord-walk on toes Stomach sticks out due t weak muscles Poor balance, clumsy walking Foot drop sue to weak front leg muscles
How is duchene’s inherited?
Most common form of muscular dystrophy
X-linked recessive
Mutation of DYstrophin gene
Muscle cells replaced by adipose tissue
How does duchene’s replace muscle with fat?
The absence of dystrophin allows= Excess calcium to enter muscle cell Calcium is taken up by mitochondria Water is taken with it Mitochondria burst Muscle cells burst (rhabdomyolysis)
What is prescient in large amounts in the bloodstream of someone with duchene’s?
Creatin kinase and myoglobin
What is creatine kinase?
An important enzyme in metabolically active tissues *muscle
Can be used to diagnose MI but supersede by troponin 1
What can cause a rise in Creatine KInase (CK) in the blood?
Intramuscular injections Vigorous physical exercise A fall (esp in elderly) Rhabdomyolysis (severe muscle breakdown) Muscular dystrophy Acute kidney injury
What are troponin asseys used for and when should it be measured?
Used as marker for cardiac ishcemia
Released within an hour of MI
Measure within 20 hours for accuracy
Not necessarily proportional to amount of damage
What is botu;ism toxin and what’s its use?
A toxin produced by Clostridium botulinum
Blocks neurotransmitter release at motor end plate
Causes non-contractile state of skeletal muscle
Clinically treats muscle spasms
Cosmetically treats wrinkles
How does organophosphate poisoning work?
A type of pesticide
Inhibits normal function of ACH esterase
Ach activity at neuromuscular junction potentiated
Effects on somatic and autonomic signalling
Causes cholinergic toxindrome
Why can organophosphate poisoning cause either muscarinic symptoms or nicotine causes symptoms?
Depends wethe the ACH is sat on a muscle or nicotine cycle receptor
What are the muscurinic symptoms of CHolinergic toxidrome?
Salivation Lacrimation (crying) Urination Defecation GI Cramps Emesis (vomiting)
What are the nicotine symptoms of cholinergic toxidrome?
Muscle Cramps Tachycardia Weakness Twitching Fasciculations (muscle twiches)
