Lecture 14: Muscle Tissue Function & Dysfunction Flashcards
How does the structure of striated muscle contribute to muscle contraction?
Sliding filament theory
How does the structure of cardiac muscle cells relate to their function?
- Striated, relatively short and branched
- Can contract spontaneously and rhythmically
- Involuntary, supplied by the autonomic nervous system
How does the structure of smooth muscle cells relate to their function?
- Elongated fibres, spindle-shaped cells
- Fibres arranged in bundles or sheets
- Provides power to propel the contents through the lumen
What is the structure of the Purkinje Fibres?
Large cells with
- abundant glycogen
- sparse myofibrils
- extensive gap junction sites
What is the function of the Purkinje Fibres?
- Conduct action potentials rapidly to enable ventricles to contract in a synchronous manner
What is the process of skeletal muscle remodeling?
Continual process of replacement of contractile proteins
What is muscle hypertrophy?
Replacement of contractile proteins is more than the destruction, new sarcomeres added in the middle of existing sarcomeres, new muscle fibers arise from mesenchymal cells
Happens during muscle overstretching
What is muscle atrophy?
Destruction of contractile proteins are more than replacement, loss of proteins, reduced fibre diameter, loss of muscle power
Happens when there is disuse, surgery or disease
What is the mechanism of innervation of muscle and excitation contraction coupling?
- Acetylcholine released by axon of motor neuron crosses cleft and binds to receptors on motor end plate
- Action potential generated is propagated across surface membrane and down T tubules of muscle cell
- Action potential triggers Ca2+ release from sarcoplasmic reticulum
- Ca2+ released binds to troponin on actin filaments, tropomyosin physically moved aside to uncover cross-bridge binding sites on actin
- Myosin cross bridges attach to actin and bend, pulling actin filaments toward centre of sarcomeres using ATP
- Ca2+ taken up by sarcoplasmic reticulum when there’s no more action potential
- When Ca2+ not bound to troponin, tropomyosin goes back to block binding sites on actin, contraction ends and actin slides back
What is the physiology of the neuromuscular junction?
- Small terminal swellings of axon containing vesicles of acetylcholine
- Nerve impulse releases acetylcholine, which binds receptors on the sarcolemma, which initiates an action potential propagated along the muscle
What is the pathogenesis of myasthenia graves?
- Caused by error in transmission of nerve impulses to muscles
- Antibodies block, alter or destroy acetylcholine receptors at neuromuscular junction
- Muscles cannot contract
What are the clinical features of myasthenia gravis?
- Ptosis: drooping of one or both eyelids
- Diplopia: blurred or double vision due to weak muscles that control eye movement
- Change in facial expression
- Difficulty swallowing
- Shortness of breath
- Impaired speech
- Weakness in limbs
What are the mechanisms of the sliding filament model of muscle contraction?
- Myosin cross bridge attaches to actin filament
- Myosin head pivots and bends as it pulls on the actin filament, sliding it toward the M line, using ATP and releasing ADP in the process
- As new ATP attaches to myosin head, cross bridge detaches
- As ATP is converted into ADP, cocking of myosin head occurs
How is neuromuscular transmission disrupted in botulism?
- Infection with bacterium Clostridium botulinum
- toxin prevents release of acetylcholine from ends of axons into neuromuscular junction
- causes flaccid paralysis
How is neuromuscular transmission disrupted in organophosphate poisoning?
- Inhibits the action of acetylcholinesterase in neuromuscular junctions
- Leads to excess of acetylcholine that stays in the receptor
- Causes tetany (involuntary muscle contraction)
- Can be absorbed by all routes (inhalation, ingestion, dermal absorption)
