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Flashcards in Muscle Deck (45)
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Classify the 3 types of muscle

Smooth - involuntary
Striated - skeletal/voluntary
Striated - cardiac/involuntary

1

Which bands of a sarcomere contain actin myosin or both

Actin - a
Myosin - i,z
Both - a

2

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

3

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

4

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

5

Explain the heirachal composition of muscle

Myofibril
Sarcoplasm
Sarcolemma
Endomysium
Fasiculus
Perimysium
Epimysium
Muscle
Tendon

6

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)

7

Describe repair of cardiac muscle

Cant regenerate. Following damage fibroblasts invade, divide and lay down scar tissue

8

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

9

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

10

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

11

What are myoepithelial cells?

Stellate cells forming basketwork around the secretory units of exocrine glands -> assist secretion of sweat etc.

12

What are myofibroblasts?

At sites of wound healing produce collagenous matrix and contract (wound contraction and tooth erruption)

13

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

14

What is the function of the purkinje fibres?

Transmit action potentials from SAN -> atrioventricular node -> ventricles
To ensure spontaneous rythmic contraction

15

How is skeletal muscle remodelled?

Continous replacement of contractile proteins
About every two weeks

16

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

17

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

18

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

19

What is botulism?

Toxins block ach release, no contractions
Treated with achesterase inhibitors

20

Describe organophosphate poisoning

Irreversibly inhibits ach, so ach remains in receptors -> stays contracted
Treated with atropine an antagonist of ach

21

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

22

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

23

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

24

Describe the structure of a peripheral nerve

Outside the CNS nerve fibres bound together in bundles by connective tissue to form peripheral nerves

Axon surrounded by endoneurium, many axons in a fasicle surrounded by a perineurium, many fasicles with blood vessels within epineurium

25

What are the differences between myelinated and non-myelinated neurones?

Grey matter - myelinated
Faster transmission as schwan cells insulate pns, oligodendrocytes cns
Somatic is all myelinated
Myelin provides track for regrowth of damaged
White - non-myelinated

26

How does demyleination affect conduction speed?

Slower as impulse has further to travel as salutatory conduction is inhibited
E.g. Multiple sclerosis is destructively removed, replaced by scar tissuewhich prevents conduction. Oligodendrocytes a d axons are also damaged leading to slow velocity

27

Describe the structure of a nerve cell and nerve cell body (perikaryon)

Nucleolus, nucleus, nissil substance(granular substance full of rer), dendrite(projections that amplify nerve signals)

28

Explain the function of schwann cells

Wrap around nerve fibres to insulate axon, lipid content so dont conduct

29

Explain function of nodes of ranvier

Gap to allow depolaraisation -> salutartory propagation (faster)