Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
23 Cards in this Set
- Front
- Back
|
Define the following terms sarcolemma, sarcoplasma, sarcosome, sarcoplasmic reticulum.
|
All relate specifically to muscle. Sarcolemma – plasma membrane, Sarcoplasm – cytoplasm, Sarcosome- mitochondria, Sarcoplasmic reticulum- Endoplasmic reticulum.
|
|
|
Classify the 3 forms of muscle:
|
Muscle is mesodermaly derived tissue which has much mitochondria as highly active cells and microfilaments: actin & myosin for contractibility and thus movement.
Striated: Cardiac (non voluntary) and skeletal muscle (voluntary) Non-striated: Smooth muscle (non voluntary) Length: Skeletal – 1mm -20cm long, Cardiac- 50-100micrometres, Smooth – 20-200 micrometres (5mm in uterus) Diameter: Skeletal- 10-100micrometers, Cardiac-10-20micometers, Smooth-5-10micrometers Morphology( form &structure): Skeletal – long cylinders, multinucleated peripheral nuclei, striations, Cardiac – Short branched cylinders, single nucleus centrally positioned,striations, Smooth- fusiform, central nucleus, no striations. |
|
|
Describe the macroscopic (seen with eye) and ultrastructural appearance of skeletal muscle.
|
Skeletal muscle is pink due to myoglobin pigment and being highly vascularised. There are 3 forms of skeletal muscle: red- small, slow, lot of myoglobin, White-large, fast, easily fatigued, Intermediate-size & speed.
Skeletal muscle is surrounded by epimysium and contains many fascicles, surrounded by perimysium, which house bundles of muscle fibres, each surrounded by endomysium. Each muscle fibre is composed of columns of myofibrils which are made up of myofilaments – actin & myosin, forming adjacent sarcomeres. Muscle fibres are long cylindrical shaped with multiple, peripheral nuclei, and arranged parallel to each contraction axis- seen in longitudinal sections. The epimysium is dense connective tissue which penetrates the muscle and separates muscle fibres into fascicles. The perimysium is a looser connective tissue and the endomysium is made up of reticular fibres –type 3 collagen. These connective tissue layers contain vascular and neuro supplies for the muscle cells. |
|
|
Describe banding in muscle fibres.
|
Muscle fibres are long parallel, cylindrical shaped with multiple, peripheral nuclei. Sarcosomes are ordered in rows next to fibres. Lipid droplets and glycogen provide energy.
In longitudinal sections, perpendicular dark and light cross banding can be seen which is why it is a striated muscle. Cross banding is caused by the arrangement of myofilaments, actin - thin and myosin - thick, in sarcomere- contractile unit. MHAZI – m line is in H which is in A next to Z which is in I. Myosin – many myosin molecules, which each have a head, linked together Actin - globular protein, 2 actin filaments twist around each other - tropomyosin and troponin bind at regular intervals along actin chain. A band – dark – both actin and myosin with heads I Band – light – only actin H zone – lies in A, paler – only myosin, no heads M line – middle of H, dark – where myosin tails meet Z line - thin, dark - where actin chains are anchored |
|
|
Describe the development of skeletal muscle.
|
Mesodermal cells differentiate into myoblasts which combine to form multinucleated (syncitium) myotubules surrounded by sarcolemma. The synthesis of actin & myosin filaments push nuclei to periphery. Muscle cells are terminally differentiated.
|
|
|
Explain how power output from muscles increases.
|
Power is determined by the number of myofilaments within each muscle fibre. Therefore hypertrophy(enlargement) increases number of proteins in the muscle fibre and this can be done by doing exercise. Division of muscle cells can’t happen as they are terminally differentiated.
|
|
|
Outline the mechanisms of the sliding filament model of muscle contraction.
|
Actin: 2 twisted strands of actin, tropomyosin coils around actin helix, reinforcing it. Troponin complex attaches to tropomyosin.
Myosin: has 2 heads, heads aren’t present in H band. During muscle contraction width of A bands stay the same, as Z lines move towards the M line. H band and I band become much thinner. 1. Ca2+ are released from sarcoplasmic reticulum into sarcoplasm 2. Ca2+ bind to troponin complex, causing change in conformation which moves tropomyosin away from actin, exposing myosin binding site 3. Myosin head binds to myosin binding site on actin and ADP+Pi are released. - The release of Pi stabilises the bond between head and actin and allows power stroke to happen. 4. Head bends and pulls the actin in the direction of the M line – the power stroke causing movement. 5. ATP binds to myosin head, releasing head from actin. - In death the lack of ATP causes the rigor conformation to remain – rigor mortis 6. Actin returns to resting position and H & I bands re-thicken. 7. Hydrolysis of ATP changes head to normal position. |
|
|
Describe the sarcotubular system ultrastructure in skeletal muscle and cardiac muscle.
|
In skeletal muscle the T(transverse) tubule is in line with the AI junction. It extends down from the sarcolemma and associated with 2 terminal cisternae of sarcoplasmic reticulum on either side forming a triad. From the terminal cisternae, sarcotubules extend and fuse above H band.
In cardiac muscle the T tubules are in line with the Z lines and form a diad instead of a triad. |
|
|
Describe the mechanism of innervation of muscle and excitation contraction coupling.
|
1. Nerve impulse from motor neurone reaches neuromuscular junction.
2. Acetylcholine diffuses across the synaptic cleft to receptors on the sarcolemma of the muscle fibre. 3. The binding of Ach and receptors opens the voltage gated sodium channels in the sarcolemma causing depolarisation of the sarcolemma and generating an action potential. 4. The action potential is carried along the sarcolemma and down the t tubules, which triggers the release of Ca2+ from adjacent terminal cisternae SR, into sarcoplasm. 5. Ca2+ ions bind to troponin complex molecules and stimulate contraction of sarcomere. 6. Contraction occurs in many sarcomeres synchronously 7. After contraction initiation, calcium ions return to sarcoplasm reticulum. |
|
|
How does the structure of cardiac muscle differ to skeletal muscle.
|
Cardiac muscle cells are striated like skeletal however have a single central nucleus. The myofilaments in cardiac muscle cells form continuous masses in the sarcoplasm, unlike skeletal with their distinct myofibrils. They also have intercalated discs which act as Z lines and intercellular junctions( desmosomes and gap junctions). They allow communication between adjacent cells, electrical and mechanical coupling of cells. Also the T tubules are in line with the Z line instead of AI junction as in skeletal muscle cells and form a diad instead of a triad.
|
|
|
Explain how the heart contracts.
|
Cardiac muscle cells have an inherent rhythm.
Sino atrial node ( LHS top atrial wall) – collection of specialised cardiac muscle cells that control rate of involuntary contraction. 1. To increase rate of contraction: receives input from sympathetic nervous system 2. To decrease rate of contraction: receives input from parasympathetic nervous system. 3. Spreads impulse to atrial muscles initiating contraction. Atrioventricular node ( AV node – in septum) Receives impulse from SA node, holds it up for a few milliseconds, and then spreads the impulse along the bundle of his which then travels to the purkinje fibres, initiating contraction. |
|
|
Why are tropinin assays a useful diagnostic tool.
|
The smallest change in cardiac specific tropinin blood levels eg troponin I and T is indicative of cardiac damage. Tropinin is released from ishaemic cardiac cells within an hour. It is the assay of choice by emergency units ( more so than heart muscle enzyme assays – creatine kinase) although does not indicate level of damage. Troponin levels remain high for a week unlike creatine kinase which only lasts for 2 days.
|
|
|
Explain the mechanical continuity of muscle fibres, muscle sheath, tendon & bone.
|
Skeletal muscle fibres interdigitate with tendon collagen bundles. Sarcolemma lies between muscle fibres myofilaments and collagen bundles. This is called the myotendious junction. Tendon connects muscle to bone.
Extrinsic skeletal muscle in tongue is attached to bone. Intrinsic Skeletal muscle of tongue, is not attached to bone allowing tongue to move in shape not position. It terminates by interdigitation with collagen fibres and extracellular matrix of nearby connective tissue. |
|
|
Explain the hierarchical composition of a typical skeletal muscle outlining the principal components at molecular, organellar, cellular, histological and regional anatomical levels.
|
Molecular: microfilaments of actin and myosin make up myofibrils. Myofibrils arranged in columns in muscle fibre.
Organellar: Multiple, Peripheral nuclei deep to the sarcolemma of muscle fibre. Sarcosomes- Mitochondria in rows by microfibrils. Glycogen stores and lipid droplets provide energy. Sarcoplasmic reticulum surrounds each microfibrils Cellular: muscle cells i.e muscle fibres arranged in bundles called fascicles surrounded by a loose connective tissue called perimysium- vascular, neuro supply. Satellite cells – stem cells- differentiate into muscle fibres. Histological : striated, connective tissue layers: epimysium, perimysium, endomysium – vascular and neuro supply ( junction folds at neuromuscular junction) |
|
|
Discuss the limited nature of repair possible in mature muscle.
|
Skeletal:
Muscle cells have terminally differentiated however satellite cells can divide to increase number of cells, replacing those lost ( hyperplasia). Satellite cells can also fuse with muscle cells to increase size (hypertrophy). Scar tissue may develop. Cardiac: More resistant to injury than other types of muscle but when injured cannot regenerate so scar tissue develops. Smooth muscle: Cells retain mitotic ability and so can form new smooth muscle cells |
|
|
Describe the histology of heart and smooth muscle, relating structure to function.
|
Smooth
Structure: fusiform cells with central nucleus ( corkscrew when contracted), actin and myosin filaments less ordered arrangement attach to dense bodies scattered in the sarcoplasm and occasionally attach to sarcolemma , forms sheets, bundles and layers, associated with connective tissue Function: walls and cavities remain contracting for long periods, vasodilation and vasoconstriction, GI & respiratory tract – peristalysis. Heart: Structure: striated, central nucleus, intercalated disc (mechanical and electrical coupling of adjacent cells), branched, rich capillary supply. Function: contraction of heart. |
|
|
Outline the structures and function of the purkinje fibres of the heart.
|
Structure: large specialised myocardial cells with fewer microfilaments, fibrils and intercalated discs, abundant glycogen and extensive gap junctions.
Position: lie beneath the endocardium on the inner surface of the heart along the interventricular septum. Function: ensures rapid spread of impulse across the whole heart. Receives impulses from bundle of his |
|
|
.
What are the functions of skeletal muscle: |
Movement, heat generation, posture, stability of joints.
|
|
|
Describe the process of skeletal muscle remodelling and its relevance to atrophy and hypertrophy
|
Actin and myosin filaments are continuously renewing – proteins every 2 weeks. Muscles remodel so they can carry out the actions required of them.
Power output by muscles is dependent on number of muscle fibres. Atrophy is the degradation of cells causing wasting away of tissue or organ Hypertrophy is the enlargement of cells causing increase in tissue or organ size. Atrophy is caused by: Disuse: bed ridden/ elderly/immobilisation of limbs. Loss of protein and power, reduction of cells. Age: gradually from 30 yrs old. Results in hypothermia, can’t generate heat – shivering. Denervation: sign of motor neuron damage, reinnervation within 3 months or muscle fibres will shrink to a quarter of their original size. Hypertrophy: due to exercise. Increases power output by muscles – increased muscle fibre diameter, increased protein, increased enzymes & sarcosomes(mitochondria) and increased blood flow. |
|
|
Outline the physiology of the neuromuscular junction and describe the pathogenesis and clinical features of myasthenia gravis.
|
Neuromuscular junction: motor end plate of nerve terminal forms junctional folds in sarcolemma of muscle fibre. Neurotransmitters – acetylcholine are released in synaptic cleft and bind to nicotinic receptors on sarcolemma and initiate action potential.
Myasthenia gravis: Pathogenesis: autoimmune disease, destruction of Ach receptors by antibodies. Widening of the synaptic cleft, loss of junctional folds and end plate(interdigitation). Symptoms – depend greatly on general health and emotional well being - ach released in burst -> large release but as levels decrease there is not enough to stimulate available receptors less resistant to competitive inhibition - Loose ability to walk as muscles can’t support body and causes sudden falling - Fatigue - Drooping eyelids- ptosis ( the most active muscles are the first to be affected eg face, tongue, eyes) - Double vision ( diplopia) - Failure of respiratory muscles eventually leads to death – respiratory insufficiency or respiratory infections. Treatment: - Acetylcholinesterase inhibiters – acetylcholine has a long half life in the synaptic cleft so more chance of colliding with receptor |
|
|
State how neuromuscular transmission is disrupted in botulism and organophosphate poisoning
|
Botulism: Toxins from botulism organisms cause paralysis by inhibiting release of Ach from presynaptic neuron.
Organophosphate poisoning: organophosphates from pesticides inhibit acetylcholinesterase. Therefore acetylcholine accumulates and causes asphyxiation –suffocation. |
|
|
Describe the pathophysiology of duchenne muscular dystrophy
|
Pathophysiology:
- Sex linked recessive defect on X chromosome - Faulty production of dystrophin which is present in sarcoplasm and anchors actin to sarcolemma - Therefore cell pulls itself apart on contraction - Creatine kinase released into cells - Calcium floods into cells and causes necrosis – cell death - Fats and connective tissue enter cells replacing muscle fibre and causing pseudohypertrophy – increase in muscle mass not due to increase in contractile proteins. Signs and symptoms - Can be misdiagnoses and dyspraxia – clumsiness - Gower’s signs – uses hands and arms to move up body from squatting position due to lack of hip and thigh muscle strength - Contractures – imbalance between agonist and antagonist muscles - Fall over a lot – slow to start walking - In wheel chair 7-12 yrs old Treatment - Steroids - Ribosomal interaction to synthesise dystrophin - Death early 20’s -30 |
|
|
Describe the pathophysiology of malignant hyperthermia
|
Chanalopathie – abnormal function/ absence of ion channels in muscles or nerves
- Caused by anaesthetics - Calcium ions don’t move back in sarcoplasmic reticulum after muscle contraction initiation. - Muscles stay contracted and cause hypermetabolism: increased glycolysis, acidosis, tachycardia , temperature –hyperthermia - Overwhelms body’s ability to supply oxygen, remove CO2 , regulate temperature and so circulatory collapse. |
