Muscle Tissue (Function and Dysfunction) Flashcards
Cardiac vs smooth muscle
similarities
-central nuclei
-only one contractile cell type (no fast/slow twitch)
-wave like function, act as syncytium
-myocytes communicate through gap junctions(small molecules pass between adjacent cells
differences
-cardiac can be multinucleated
-cardiac is branched
-connexins in smooth muscle
-no sarcomeres in smooth muscle
-electrical conduction- specialised cells in cardiac muscle
-no troponin in smooth muscle as no sarcomere
-cardiomyocytes have intercalated discs
DHP
dihydropyridine
RyR
ryanodine receptor
neuromuscular junction
neuromuscular junction
point of contact between a motor neuron and a skeletal muscle cell
properties of neuromuscular junction
-small terminal swellings of the axon
-contains vesicles of acetylcholine
Innervation of skeletal muscle (neuromuscular junction)
- Initiation: nerve impulse along motor neuron axon arrives at neuromuscular junction
- Impulse prompts release of ACh into synaptic cleft causing local depolarisation of the sarcolemma
- Voltage gated Na+ channels open, Na+ ions enter cell
- General depolarisation spreads over sarcolemma into T tubules
- Voltage sensor proteins of T tubule membrane change their conformation
- Gated Ca2+ ion-release channels of adjacent terminal cisternas activated
- Ca2+ rapidly released into sarcoplasm
- Ca2+ binds to TnC subunit of troponin and contraction cycle initiated
- Ca2+ ions returned to terminal cisternas of sarcoplasmic reticulum
What’s a neuromuscular junction formed of?
Neurone and muscle
how does the average fibres per motor unit affect fine control and power?
Lower fibres per unit - more fine control
higher fibres per unit - more power
Kranocyte
a connective tissue cells that resides over the terminal Schwann cell - anchors nerve to muscle cell
T Tubes and sarcoplasmic reticulum of skeletal muscle structure
Look at lecture 12 pg 12
- Sacrolemma
- T
myasthenia gravis
*autoimmune disease
*antibodies block Ach receptor, and 30% reduction in receptor number is enough for symptoms
*endplate invaginations reduced and reduced synaptic transmission
-muscle weakness
Explain the histological appearance of myasthenia gravis
2 axons, round not crescent moon shape
More mitochondria for ATP
no invaginations for ACh receptor gene
Leads to non functioning muscle cell
Sliding filament theory
- Ca2+ binds to TnC of troponin, and conformational change moves tropomyosin away from actin’s binding sites
- Myosin cross bridge attached to actin myofilament
- Myosin head pivots and bends as it pulls on actin filament, sliding it towards the M line. ADP and Pi released
- As the new ATP attached to the myosin head, cross bridge detaches
- As ATP is hydrolysed into ADP and Pi by ATPase, cocking of myosin head occurs
myosin molecule
Tail: binds to other myosin molecules
Head: made of 2 globular protein subunits and reaches the nearest thin filament
what are the two protein components of actin?
F - actin fibres
G - actin globules
what part of the sarcomere is devoid of myosin heads?
the centre of the sarcomere (M line)
when does the myosin head cock?
when ATP that was bound to it is hydrolysed
When muscle contracts, do actin and myosin filaments shorten? Does sarcomere shorten?
No, Actin and myosin dont shorten
Yes, The sarcomere does shorten
What’s the points of origin?
Bone, typically proximal, greater mass and more stable during contraction than insertion point
What’s the point of insertion?
Structure the muscle attaches to
Tends to be moved by contraction
Tends to be distal (part that moves)
Could be bone, tendon, connective tissue
Usually tendon to bone
Greater motion than origin during contraction
what are the 5 different muscle roles in movement?
-agonists- prime movers
-antagonists - oppose prime movers
-synergists - assist prime movers (alone they can’t perform movement, but their angle of pull assists)
-neutralisers- prevent unwanted actions that an agonist can perform
-fixators- act to hold a body part immobile whilst another part is moving. Stabilise a joint
what are the three different levers in biomechanics?
-first class (see saw)
-second class (wheelbarrow)
-third class (fishing rod)
First class lever system
fulcrum between load and effort
E.g. extension/flexion of head
second class lever system
load between fulcrum and effort
E.g. plantar flexion of foot
third class lever system
Effort applied between fulcrum and load
-most common
E.g. flexion of elbow
Mechanical disadvantage
muscle compartments
groups of muscles with related functions surrounded by thick dense fascia
Can be anterior, posterior, lateral, medial
compartment syndrome
involves the compression of nerves and blood vessels due to swelling within the enclosed space created by the fascia that separates groups of muscles
Symptoms of compartment syndrome
-deep contestant poorly localised pain
-parasthesia (pins and needles)
-compartment may feel tense and firm
-swollen shiny skin, sometimes bruising
-prolonged capillary refill time
fasciotomy
a surgical incision through the fascia to relieve tension or pressure
what is the treatment for compartment syndrome?
fasciotomy
what are the 4 regulators of muscle tone?
-motor neurone activity
-muscle elasticity
-use
-gravity
muscle tone
the tension of a muscle when it is relaxed
DONT mechanism of muscle hypertrophy
overstretching such that a bands and i bands 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
DONT what can lead to muscle atrophy?
- disuse
-surgery
-disease
how long does nerve regeneration take?
3 months
Dúchenle muscular dystrophy
Most common form of muscular dystrophy
X linked recessive inheritance
Mutation of dystrophin gene
Dystrophin gene normally joins sarcolemma to actin microfibre
what is the mechanism of what occurs during duchene muscular dystrophy?
absence of dystrophin allows:
-excess calcium enters muscle cell
-calcium taken up by mitochondria
-water taken with it
-mitochondria burst
-muscle cells burst
-CK and myoglobin levels extremely high in blood
-kidney can’t cope with myoglobin levels so kidney damage occurs
-muscle cells get replaced by adipose tissue
Rhabdomyolysis
destruction of muscle to produce myoglobin
what replaces muscle cells in duchene muscular dystrophy
adipose tissue
Symptoms of muscular dystrophy
-shoulders and arms awkwardly held back when walking
-belly sticks out
-poor balance
-walking on toes due to tight heel cord
-thick lower leg muscles
creatine kinase function
phosphorylate ATP as it leaves mitochondria
What could cause increased plasma creatine kinase levels
-intramuscular injection
-vigorous physical exercise
-a fall
-rhabdomyolysis
-muscular dystrophy
-acute kidney injury (myoglobin not being cleared)
within how many hours of a myocardial infarction should a troponin assay be conducted for absolute accuracy?
20
How long after iscaemic damage is troponin released from cardiac muscle?
Within an hour
Is the quantity of troponin released proportional to the degree of muscle damage?
No not necessarily
What troponin is used to measure cardiac damage in the UK?
troponin I
Why is troponin used as a marker for cardiac ischaemia?
The levels are elevated for much longer after a myocardial infarction, and it’s more specific
what occurs when botulism toxin is given during botox?
Botulinum toxin (Botox) is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species. It prevents the release of the neurotransmitter acetylcholine from axon endings at the motor end plate of the neuromuscular junction, thus causing flaccid paralysis (non contractile state)
what is botulism toxin used to treat clinically?
muscle spasms
what is botulism toxin used for cosmetically?
to treat wrinkles
Malignant hyperthermia
-severe reaction to anaesthetics
Succinylcholine binds to Ach receptor
Causes muscle rigidity and fasciculation due to increased ca2+ release, with excessive heat and metabolic acidosis
Increased muscle breakdown and hyperkalaemia
Affects males more than females
What’s the mortality risk of malignant hyperthermia with and without treatment
With 5%
Without 75%
organophosphate (used in pesticides) poisoning
-inhibits normal function of AchE so increased activity of Ach
What are the muscarinic symptoms of cholinergic toxidrome (organophosphate poisoning
Salivation
Lacrimaition
Urination
Defecation
GI cramping
Emesis
Sludge
What are the nicotinic symptoms of organophosphate poisoning?
Muscle cramps
Tachycardia
Weakness
Twitching
Fascilculations
Days of the week
what are the muscarinic symptoms of organophosphate poisoning?
Salivation
Lacrimation
Urination
Defecation
GI cramping
Emesis
what are the nicotinic symptoms of organophosphate poisoning?
Muscle cramps
Tachycardia
Weakness
Twitching
Fasciculations
What is Fasciculations
Rapid movements of muscle
What is emesis
emesis
