Muscle Flashcards
Which bands of a sarcomere contain actin myosin or both
Actin - a
Myosin - i,z
Both - a
Classify the 3 types of muscle
Smooth - involuntary
Striated - skeletal/voluntary
Striated - cardiac/involuntary
Outline the sliding filament theory
Actin, tropomyosin and troponin form filaments
Troponin covers binding sites on myosin
When ca2+ binds to Tnc of troponin, conformstional change exposes binding sites
Myosin heads can bind to actin -> contraction
Myosinhead tightly bound to actin
Atp binds to myosin causing it to uncouple from actin
Hydrolysis of atp causes uncoupled myosin head to bend and move 5mm
Myosin head binds weakly to actin filament causing release of inorganic phosphate and power stroke moving myosin head to original position
Myosin head binds tightly again and cycle repeats
Describe innervation of muscle and exitation contraction coupling
1) when ap arrives at presynaptic terminal, VG ca2+ channels open
2) influx of ca2+ causes release of ach from vesicles (exocytosis)
3) ach diffuses across synaptic cleft and binds to nicotanic ach receptors on motor end plate
4) post-synaptic receptors are ligand gated ion channels and ach causes them to open -> influx of na+ and eflux of k+ -> depolarsisation of sarcolemma
5) voltage sensoe proteins of t tubule membrane changes their conformation
6) gated ca2+ release channels of adjacent terminal cisternae activated by proteins change in conformation
7) ca2+ rapidly released from terminal cisternae into sarcoplasm
8) ca2+ binds to TnC subunit of troponin
9) contraction cycle is initiated and ca2+ is returned to terminal sarcoplasmic reticulum
Explain the mechanical continuity of muscle fibres, sheath, tendon and bone
Each muscle fibre is grouped with others in a fasicle, wrapped by perimysium. Fasicles wrapped in a connective tissue sheath (epimysium)
Muscle is attached to bone by tendons/aponeuroses
Muscles associated with layers of dense connective tissue - deep fascia which surrounds muscles and binds them to functionsl groups
Explain the heirachal composition of muscle
Myofibril Sarcoplasm Sarcolemma Endomysium Fasiculus Perimysium Epimysium Muscle Tendon
Describe repair in skeletal muscle
Cant divide but can regenerate by mitotic activity of satelite cells so that hyperplasia follows muscle injury. Satelite cells can also fuse with existing muscle cells to increase mass (hypertrophy)
Describe repair of cardiac muscle
Cant regenerate. Following damage fibroblasts invade, divide and lay down scar tissue
Describe repair of smooth muscle
Retain mitotic activity and can form new smooth muscle cells e.g. In pregnant uterus muscle wall becomes thicker by hypertrophy (swelling) and hyperplasia (mitosis) of individual cells
Describe the histology of cardiac muscle
Striated
1/2 centrally positioned nuclei per cell
Intercalated discs for electrical and mechanical coupling with adjacent cells
No distinct myofibrils, actin and myosin form continous masses
Mitochondira and sarcoplasmic reticulum penetrate cytoplasm through myofilaments
Describe the histology of smooth muscle
Spindle shape cells (fusiform) with a central nucleus
Not striated, no sarcomeres, no t tubules
Contraction slower and more sustained
Can be stretched
Responds to nerve, hormonal and drug signals
F - contractile wakks of passageways e.g. Respiratory tract
What are myoepithelial cells?
Stellate cells forming basketwork around the secretory units of exocrine glands -> assist secretion of sweat etc.
What are myofibroblasts?
At sites of wound healing produce collagenous matrix and contract (wound contraction and tooth erruption)
Outline the structure of the purkinje fibres
Large cells with abundant glycogen, sparse myofilaments and extensive gap junction sites
They are found in the inner ventricular walls of the heart
What is the function of the purkinje fibres?
Transmit action potentials from SAN -> atrioventricular node -> ventricles
To ensure spontaneous rythmic contraction
How is skeletal muscle remodelled?
Continous replacement of contractile proteins
About every two weeks
Describe atrophy (causes, symptoms, consequences)
Destruction>replacement
Disuse, aging, denervation
Weakness, flacidity, muscle atrophy
Muscle fibres are replaced with fibrous and fatty tissue, leads to contractures -> debilatating
Describe hypertrophy
Replacement>destruction
Increase in muscle mass from work, performed against load
More contractile proteins, increasing fibre diameter
Increase enzyme activity for glycolysis, mitochondria, stored glycogen
Describe myosenthia gravis
Autoimmune destruction of end plate Ach receptors
Loss of junctional folds at end plates
Widening of synaptic cleft
Symptoms: fatiguability, sudden falling (due to decreased ach) droopin eyelids (ptosis) double vision
Fluctuates due to general health, fatigue and emotions
What is botulism?
Toxins block ach release, no contractions
Treated with achesterase inhibitors
Describe organophosphate poisoning
Irreversibly inhibits ach, so ach remains in receptors -> stays contracted
Treated with atropine an antagonist of ach
Outline the patholhysiology of duchenne muscular disease
Recessive x linked form
Consequence of protein abnormality - muscle fibres tear apart upon contraction
Causing release of creatine phospho kinase into serum
Causes ca2+ to enter cell causing cell death
Pseudo hypertrophy before fat and connective tissue replace muscle fibres
Outline the pathophysiology of malignant hyperthermia
Rare autosomal dominant disorder
Causes life threatening reaction to drugs used for general anasthetic
E.g. Succinylcholine which inhibits ach by non-competitive inhibition on nicotinic receptors. It is degraded by butylcholinesterase more slowly than ach by acetylcholinesterase
In affected individuals drugs induce uncontrolled increase of skeletal muscle oxidative metabolism, quickly overwhelming the bodys capacity to supply O2, remove CO2 and regulate metabolism
What are the treatments for malignant hyperthermia?
Dantrolene a muscle relaxant that prevents release of Ca2+
This corrects hyperthemia, acidosis and organ disfunction
discontinue triggering agents
