Pathophysiology of Skeletal Muscle Flashcards

Question

_Aspirin and Musculoskeletal Pain - Mechanism_ * Inhibits COX * Reduces synthesis of prostaglandins * Part of arachidonic acid pathway * Arachidonic acid and prostaglandins have many effects * Gastro-intestinal adverse effects of chronic aspirin * ... bleeding * U..

Answer 1

* Inhibits COX * Reduces synthesis of prostaglandins * Part of arachidonic acid pathway * Arachidonic acid and prostaglandins have many effects * Gastro-intestinal adverse effects of chronic aspirin * **Stomach bleeding** * **Ulcers**

Answer 2

* Anabolic effects of testosterone: * **Increases** protein synthesis * **Decreases** catabolism (by opposing cortisol & glucocorticoids) * **Reduces** fat: increase BMR, increase differentiation to muscle (rather than fat cells) * Anabolic steroid abuse * Used to increase muscle size and strength * Large doses required – leads to damaging side effects (kidney, liver, heart, mood changes) * male – testes atrophy, sterility, baldness * female – breast/uterus atrophy, menstrual changes, facial hair, deepening of voice

Answer 3

* Anabolic effects of testosterone: * Increases protein synthesis * Decreases **catabolism** (by opposing cortisol & glucocorticoids) * Reduces **fat**: increase **BMR**, increase differentiation to muscle (rather than **fat** cells) * Anabolic steroid **abuse** * Used to increase muscle size and strength * Large doses required – leads to damaging side effects (kidney, liver, heart, mood changes) * male – testes atrophy, sterility, baldness * female – breast/uterus atrophy, menstrual changes, facial hair, deepening of voice

Answer 4

* Used to increase muscle size and strength * Large doses required – leads to damaging side effects (**kidney**, liver, heart, **mood** changes) * Male – testes **atrophy**, sterility, baldness * Female – breast/uterus atrophy, menstrual changes, facial hair, deepening of voice

Answer 5

* Used to increase **muscle** size and strength * Large doses required – leads to damaging side effects (kidney, liver, heart, mood changes) * Male – testes atrophy, sterility, baldness * Female – breast/uterus atrophy, **menstrual** changes, **facial** hair, **deepening** of voice

Answer 6

* Used to increase muscle size and strength * Large doses required – leads to damaging side effects (kidney, liver, heart, mood changes) * Male – **testes** atrophy, sterility, baldness * Female – **breast/uterus** atrophy, menstrual changes, facial hair, deepening of voice

Answer 7

* Used to increase muscle size and strength * **Large doses** required – leads to damaging side effects (kidney, liver, heart, mood changes) * Male – testes atrophy, **sterility, baldness** * Female – breast/uterus atrophy, menstrual changes, facial hair, deepening of voice

Answer 8

* Exposed to **zero gravity** (long-term exposure) * **Decrease** in weight bearing in bones and muscles, over time, transition of Type 1 (slow) fibres to Type IIA/IIX fibres (Faster fibres) * Lose slow fibres, gain fast fibres * Decrease in relative muscle mass - all muscles undergo some atrophy, but predominantly weight bearing muscles

Answer 9

* Exposed to zero gravity (long-term exposure) * Decrease in weight bearing in bones and muscles, over time, transition of Type **1** (slow) fibres to **Type IIA/IIX fibres** (Faster fibres) * Lose slow fibres, gain fast fibres * Decrease in relative muscle mass - all muscles undergo some atrophy, but predominantly weight bearing muscles

Answer 10

* Exposed to zero gravity (long-term exposure) * Decrease in weight bearing in bones and muscles, over time, transition of Type 1 (**slow**) fibres to Type IIA/IIX fibres (**Faster** fibres) * Lose **slow** fibres, gain **fast** fibres * Decrease in relative muscle mass - all muscles undergo some atrophy, but predominantly weight bearing muscles

Answer 11

* Exposed to zero gravity (long-term exposure) * Decrease in weight bearing in bones and muscles, over time, transition of Type 1 (slow) fibres to Type IIA/IIX fibres (Faster fibres) * Lose slow fibres, gain fast fibres * Decrease in **relative muscle** mass - all muscles undergo some **atrophy**, but predominantly **weight** bearing muscles

Answer 12

* Muscles of posture are not being consistently used * Transition of type **I** fibres to type **IIA** * Weight-bearing muscle **atrophy** * Decrease muscle protein synthesis * Myofibrillar breakdown * Decreased strength (due to ¯ size) * Loss of type I fibres * Treat by resuming minor activity early, Add physiotherapy to prevent contractures.

Answer 13

* Muscles of posture are not being consistently used * Transition of type I fibres to type IIA * Weight-bearing muscle atrophy * Decrease muscle protein **synthesis** * Myofibrillar breakdown * Decreased **strength** (due to ¯ size) * Loss of type **I** fibres * Treat by resuming minor activity early, Add physiotherapy to prevent contractures.

Answer 14

* Muscles of posture are not being consistently used * Transition of type I fibres to type IIA * Weight-bearing muscle atrophy * Decrease muscle protein synthesis * Myofibrillar breakdown * Decreased strength (due to ¯ size) * Loss of type I fibres * Treat by resuming **minor activity** early, Add **physiotherapy** to prevent **contractures**.

Answer 15

Dont need to memorise

Answer 16

* If limb immobilised for long periods: * Process of growth is **reversed** * **Sarcomeres** are removed in series from myofibrils * Resulting in **shortening** of muscle called a contracture * Patients with paralysed limbs must have physical therapy to prevent contractures occurring

Answer 17

* If limb immobilised for long periods: * Process of growth is reversed * Sarcomeres are removed in series from myofibrils * Resulting in shortening of muscle called a contracture * Patients with **paralysed** limbs must have **physical** **therapy** to prevent contractures occurring

Answer 18

* They develop as **myoblasts** * Which are mononucleate * Then the **myoblasts** fuse * The **nuclei** are peripheral * The multinucleate cells do not divide * Mitosis with multiple nuclei usually impossible * Skeletal muscles are enlarged by: * Fibre enlargement * Increased vascularisation

Answer 19

* They develop as myoblasts * Which are mononucleate * Then the myoblasts fuse * The nuclei are peripheral * The **multinucleate** cells do not divide * **Mitosis** with multiple nuclei usually impossible * Skeletal muscles are enlarged by: * Fibre enlargement * Increased vascularisation

Answer 20

* They develop as myoblasts * Which are mononucleate * Then the myoblasts fuse * The nuclei are peripheral * The multinucleate cells do not divide * Mitosis with multiple nuclei usually impossible * Skeletal muscles are enlarged by: * **Fibre** enlargement * Increased **vascularisation**

Answer 21

* They develop as myoblasts * Which are mononucleate * Then the myoblasts fuse * The nuclei are **peripheral** * The multinucleate cells do not divide * Mitosis with **multiple** nuclei usually impossible * Skeletal muscles are enlarged by: * Fibre enlargement * **Increased** vascularisation

Answer 22

* During **inflammation** and **degeneration** of damaged muscle tissue * previous quiescent myogenic cells, called satellite cells, are activated * These proliferate, differentiate and fuse onto extant fibres * They contribute to forming multinucleate myofibers

Answer 23

* During inflammation and degeneration of damaged muscle tissue * previous **quiescent** myogenic cells, called **satellite** cells, are activated * These proliferate, differentiate and fuse onto extant fibres * They contribute to forming multinucleate myofibers

Answer 24

* During inflammation and degeneration of damaged muscle tissue * previous quiescent myogenic cells, called **satellite** cells, are activated * These proliferate, differentiate and fuse onto **extant** fibres * They contribute to forming **multinucleate** myofibers

Answer 25

* **Progenitor** cells in muscle * Also called “satellite cells” * NOT related glial satellite cells * Essential for **regeneration** & **growth** * Most are quiescent * Activated by mechanical strain * Activation —\> proliferation & differentiation

Answer 26

* Progenitor cells in muscle * Also called “satellite cells” * NOT related glial satellite cells * Essential for regeneration & growth * Most are **quiescent** * Activated by mechanical **strain** * Activation —\> **proliferation** & **differentiation**

Answer 27

**Quiescent** = opposite of active. Not dividing, low metabolism, little or no observable activity.

Answer 28

* **Muscle** pain * Causes of myalgia: * Injury, overuse, infections, auto-immune * Can by associated with **Rhabdomyolysis**

Answer 29

* Muscle pain * Causes of myalgia: * **Injury, overuse, infections, auto-immune** * Can by associated with Rhabdomyolysis

Answer 30

pain in a muscle or group of muscles.

Answer 31

Muscular weakness due to muscular muscle fibre dysfunction

Answer 32

* Muscular **weakness** due to muscular muscle fibre **dysfunction** * Cf. neuropathy & neurogenic disorders * Failure to contract cause possibly muscle or nerve * Systemic vs. familial * Dystrophies: familial, progressive * Stuck in degeneration-regeneration cycle * Eventually regenerative ability is lost

Answer 33

* Muscular weakness due to muscular muscle fibre dysfunction * Cf. neuropathy & neurogenic disorders * Failure to contract cause possibly muscle or nerve * **Systemic** vs. **familial** * Dystrophies: familial, progressive * Stuck in degeneration-regeneration cycle * Eventually regenerative ability is lost

Answer 34

* Muscular weakness due to muscular muscle fibre dysfunction * Cf. neuropathy & neurogenic disorders * Failure to contract cause possibly muscle or nerve * Systemic vs. familial * **Dystrophies**: familial, progressive * Stuck in degeneration-regeneration cycle * Eventually **regenerative** ability is lost

Answer 35

* Muscular **weakness** due to muscular muscle fibre dysfunction * Cf. neuropathy & neurogenic disorders * Failure to **contract** cause possibly muscle or nerve * Systemic vs. familial * Dystrophies: familial, progressive * Stuck in degeneration-regeneration cycle * Eventually regenerative ability is lost

Answer 36

* weakness of voluntary movement, or * partial loss of voluntary movement or * impaired movement

Answer 37

* weakness of **voluntary** movement, or partial loss of **voluntary** movement or **impaired** movement * Usually referring to a limb - From Greek “to let fall”

Answer 38

* **fasciculations** : involuntary visible twitches in single motor units (neurogenic), which commonly occur in lower motor neuron diseases such as damage to anterior horn cell bodies characteristic of ALS or polio * clinically appear as brief ripples under the skin * **fibrillations** : involuntary spontaneous contractions of individual muscle fibres (myogenic) invisible to the eye but identified by electromyography

Answer 39

* fasciculations : involuntary **visible** twitches in single motor units (neurogenic), which commonly occur in **lower** motor neuron diseases such as damage to anterior horn cell bodies characteristic of ALS or polio * clinically appear as brief ripples under the skin * fibrillations : involuntary spontaneous contractions of individual muscle fibres (myogenic) **invisible** to the eye but identified by **electromyography**

Answer 40

* fasciculations : involuntary visible twitches in single motor units (neurogenic), which commonly occur in lower motor neuron diseases such as damage to anterior horn cell bodies characteristic of ALS or polio * clinically appear as brief ripples under the skin * fibrillations : involuntary spontaneous contractions of individual muscle fibres (myogenic) invisible to the eye but identified by electromyography

Answer 41

no - require electromyography

Answer 42

* Rapid **breakdown** of skeletal muscle * Not **cardiac** muscle, not **myocardial infarct** * Risk of kidney failure * Cellular proteins (esp myoglobin) released into blood can “clog” renal glomeruli * Urine is “tea coloured”, no urine produced 12 hours after injury * Leads to electrolyte changes: hyperkalaemia * Treatment: * Intravenous fluids (to treat shock) * possibly haemodialysis, etc

Answer 43

* Rapid breakdown of skeletal muscle * Not cardiac muscle, not myocardial infarct * Risk of **kidney** **failure** * Cellular proteins (esp myoglobin) released into blood can “clog” renal glomeruli * Urine is “**tea** coloured”, no urine produced 12 hours after injury * Leads to **electrolyte** changes: hyperkalaemia * Treatment: * Intravenous fluids (to treat shock) * possibly haemodialysis, etc

Answer 44

* Rapid breakdown of skeletal muscle * Not cardiac muscle, not myocardial infarct * Risk of kidney failure * Cellular proteins (esp myoglobin) released into blood can “clog” renal glomeruli * Urine is “tea coloured”, no urine produced 12 hours after injury * Leads to electrolyte changes: **hyperkalaemia** * Treatment: * **Intravenous** fluids (to treat **shock**) * possibly **haemodialysis**, etc

Answer 45

**Rhabdomyolysis** = Rhabdomyolysis is a condition in which damaged skeletal muscle (Ancient Greek: rhabdomyo-) tissue breaks down rapidly (Greek -lysis).

Answer 46

* Creatine Phosphokinase * CK or CPK abbreviations used interchangeably * The **enzyme**, not creatine phosphate * distinct forms of CPK found in different tissues * skeletal muscle CPK isoform is CK-**MM** * cardiac muscle CPK isoform is CK-**MB** * when tissue damaged and cells lyse there is a release of tissue specific CK from cells into blood * Elevations in CK-MM occur after skeletal muscle trauma or necrosis * muscular dystrophies, polymyositis and rhabdomyolysis * Test = “Total CK” (CK-MM is not a clinical test)

Answer 47

* Creatine Phosphokinase * CK or CPK abbreviations used interchangeably * The enzyme, not creatine phosphate * distinct forms of CPK found in different tissues * **skeletal** muscle CPK isoform is CK-MM * **cardiac** muscle CPK isoform is CK-MB * when tissue **damaged** and cells **lyse** there is a release of tissue specific CK from cells into blood * Elevations in CK-MM occur after skeletal muscle trauma or necrosis * muscular dystrophies, polymyositis and rhabdomyolysis * Test = “Total CK” (CK-MM is not a clinical test)

Answer 48

* Creatine Phosphokinase * CK or CPK abbreviations used interchangeably * The enzyme, not creatine phosphate * distinct forms of CPK found in different tissues * skeletal muscle CPK isoform is CK-MM * cardiac muscle CPK isoform is CK-MB * when tissue damaged and cells lyse there is a release of tissue specific CK from cells into blood * Elevations in CK-**MM** occur after skeletal muscle **trauma** or **necrosis** * muscular dystrophies, polymyositis and rhabdomyolysis * Test = “Total CK” (CK-MM is not a clinical test)

Answer 49

* Creatine Phosphokinase * CK or CPK abbreviations used interchangeably * The enzyme, not creatine phosphate * distinct forms of CPK found in different tissues * skeletal muscle CPK isoform is CK-MM * cardiac muscle CPK isoform is CK-MB * when tissue damaged and cells lyse there is a release of tissue specific CK from cells into blood * Elevations in CK-MM occur after skeletal muscle trauma or necrosis * muscular dystrophies, polymyositis and rhabdomyolysis * Test = “**Total CK”** (CK-MM is not a clinical test)

Answer 50

* distinct forms of CPK found in different tissues * **skeletal** muscle CPK isoform is CK-MM * **cardiac** muscle CPK isoform is CK-MB

Answer 51

* Myoglobin " **Buffers** O2” * Protein + Haem group * “**tea** coloured” * In plasma indicates **rhabdomyolysis** or MI * Can lead to renal failure * Urine tested for myoglobin * Diagnostic: Hyperkalaemia * When muscle cells lyse * They release K+ * This increases serum K+ * Nb: ò serum K = cause of rhabdo, * Increased K = result of rhabdo

Answer 52

* Myoglobin " Buffers O2” * Protein + Haem group * “tea coloured” * In plasma indicates rhabdomyolysis or MI * Can lead to **renal** failure * **Urine** tested for myoglobin * Diagnostic: Hyperkalaemia * When muscle cells lyse * They release K+ * This increases serum K+ * Nb: ò serum K = cause of rhabdo, * Increased K = result of rhabdo

Answer 53

* Myoglobin " Buffers O2” * Protein + Haem group * “tea coloured” * In plasma indicates rhabdomyolysis or MI * Can lead to renal failure * Urine tested for myoglobin * Diagnostic: **Hyperkalaemia** * When muscle cells lyse * They release K+ * This increases serum K+ * Nb: ò serum K = cause of rhabdo, * Increased K = result of rhabdo

Answer 54

* Myoglobin " Buffers O2” * Protein + Haem group * “tea coloured” * In plasma indicates rhabdomyolysis or MI * Can lead to renal failure * Urine tested for myoglobin * Diagnostic: Hyperkalaemia * When muscle cells lyse * They release K+ * This increases serum K+ * Nb: decreasd serum K = **cause** of rhabdo, * Increased K = **result** of rhabdo

Answer 55

* Rhabdomyolysis

Answer 56

* ATP **depleted** after death * Muscle cell does not **resequester** Ca2+ into SR * Increases **Cytosolic** Ca2+ * Ca2+ allows crossbridge cycle contraction * Until ATP & creatine-P run out * W/o ATP à myosin stops just after **power** stroke * With myosin still bound to actin * Rigor mortis ends when muscle tissue degrades after **3** days

Answer 57

* **Progressive** muscle weakness and fatigability * Often starts with **eye** muscles * Caused by depletion of nAChR * Arises as the immune system inappropriately produces auto-antibodies against nAChR

Answer 58

* Progressive muscle **weakness** and **fatigability** * Often starts with eye muscles * Caused by depletion of **nAChR** * Arises as the immune system inappropriately produces auto-antibodies against nAChR

Answer 59

* Progressive muscle weakness and fatigability * Often starts with eye muscles * Caused by depletion of **nAChR** * Arises as the immune system inappropriately produces **auto-antibodies against nAChR**

Answer 60

auto-antibodies against nAChR

Answer 61

* **less** depolarisation of muscle fibres * many fibres do not reach **threshold** * repeated stimulation -\> neuromuscular **fatigue** * symptoms include ptosis, diplopia, * with weakness in eyelid and extraocular muscles * proximal muscle weakness

Answer 62

* less depolarisation of muscle fibres * many fibres do not reach threshold * repeated stimulation -\> neuromuscular fatigue * symptoms include **ptosis, diplopia**, * with **weakness** in eyelid and extraocular muscles * proximal muscle **weakness**

Answer 63

* **AChE** inhibitors * Pyridostigmine * Increase **ACh** activity at NMJ. ACh released from nerve terminals into synapse not rapidly catabolised but can bind to the remaining **AChRs** for longer time * Edrophonium (a/k/a tensilon): short-lived **AChE** inhibitor for diagnosis, temporarily improves symptoms eg ptosis * Other category of treatment is directed at immune system * Thymectomy – reduces symptoms in 70% of patients. Exact mechanism unknown. Rebalance immune system? * Use of immunosuppressive drugs e.g. corticosteroids * Plasmapheresis = removal of anti AChR antibodies from blood stream

Answer 64

* AChE inhibitors * Pyridostigmine * Increase ACh activity at NMJ. ACh released from nerve terminals into synapse not rapidly catabolised but can bind to the remaining AChRs for longer time * **Edrophonium** (a/k/a tensilon): short-lived AChE inhibitor for diagnosis, temporarily improves symptoms eg ptosis * Other category of treatment is directed at immune system * Thymectomy – reduces symptoms in **70**% of patients. Exact mechanism unknown. Rebalance immune system? * Use of immunosuppressive drugs e.g. corticosteroids * Plasmapheresis = removal of anti AChR antibodies from blood stream

Answer 65

* AChE inhibitors * **Pyridostigmine** * Increase ACh activity at NMJ. ACh released from nerve terminals into synapse not rapidly catabolised but can bind to the remaining AChRs for longer time * Edrophonium (a/k/a tensilon): **short**-lived AChE inhibitor for diagnosis, temporarily improves symptoms eg **ptosis** * Other category of treatment is directed at immune system * Thymectomy – reduces symptoms in 70% of patients. Exact mechanism unknown. Rebalance immune system? * Use of **immunosuppressive** drugs e.g. corticosteroids * Plasmapheresis = removal of anti AChR antibodies from blood stream

Answer 66

* AChE inhibitors * Pyridostigmine * Increase ACh activity at NMJ. ACh released from nerve terminals into synapse not rapidly catabolised but can bind to the remaining AChRs for longer time * Edrophonium (a/k/a tensilon): short-lived AChE inhibitor for diagnosis, temporarily improves symptoms eg ptosis * Other category of treatment is directed at immune system * Thymectomy – reduces symptoms in 70% of patients. Exact mechanism unknown. Rebalance immune system? * Use of immunosuppressive drugs e.g. **corticosteroids** * **Plasmapheresis** = removal of anti AChR antibodies from blood stream

Answer 67

* a/k/a **Floppy Baby** Syndrome * One of most common genetic causes of **infant** death * Severity and time of onset can **vary** greatly * Death of lower motor neurons in anterior horn of spine * Muscle atrophy —\> hypotonia & muscle weakness * Via apoptosis * Fibre type grouping * Sensory system is spared (b/c not in anterior horn) * Caused by genetic defect * SMN1 gene * Required for survival of anterior horn neurons * Autosomal recessive * Other genes cause similar syndromes

Answer 68

* a/k/a Floppy Baby Syndrome * One of most common genetic causes of infant death * Severity and time of onset can vary greatly * Death of **lower** motor neurons in anterior horn of spine * Muscle **atrophy** —\> hypotonia & muscle weakness * Via **apoptosis** * Fibre type grouping * Sensory system is spared (b/c not in anterior horn) * Caused by genetic defect * SMN1 gene * Required for survival of anterior horn neurons * Autosomal recessive * Other genes cause similar syndromes

Answer 69

* a/k/a Floppy Baby Syndrome * One of most common genetic causes of infant death * Severity and time of onset can vary greatly * Death of lower motor neurons in anterior horn of spine * Muscle atrophy —\> **hypotonia** & muscle **weakness** * Via apoptosis * **Fibre** **type** grouping * Sensory system is spared (b/c not in anterior horn) * Caused by genetic defect * SMN1 gene * Required for survival of anterior horn neurons * Autosomal recessive * Other genes cause similar syndromes

Answer 70

* a/k/a Floppy Baby Syndrome * One of most common genetic causes of infant death * Severity and time of onset can vary greatly * Death of lower motor neurons in anterior horn of spine * Muscle atrophy —\> hypotonia & muscle weakness * Via apoptosis * Fibre type grouping * **Sensory** system is spared (b/c not in anterior horn) * Caused by **genetic** defect * SMN1 gene * Required for survival of anterior horn neurons * Autosomal **recessive** * Other genes cause similar syndromes

Answer 71

* Death of **lower** motor neurons in anterior horn of spine * Muscle atrophy —\> hypotonia & muscle weakness * Via **apoptosis** * **Fibre** type grouping * **Sensory** system is spared (b/c not in anterior horn) * Caused by genetic defect * Autosomal **recessive**

Answer 72

* During **spinal muscular** atrophy * Cycles of **denervation** are followed by collateral **reinnervation** * Surviving axons innervate surrounding fibres * Resulting in fibre type grouping * In healthy muscles (Figure A), motor units are intermingled. During reinnervation, nearby surviving neurons re-innervate the denervated fibres, resulting in clusters (Figure B)

Answer 73

* During spinal muscular **atrophy** * **Cycles** of denervation are followed by collateral reinnervation * Surviving axons **innervate** surrounding fibres * Resulting in fibre type grouping * In healthy muscles (Figure A), motor units are intermingled. During reinnervation, nearby surviving neurons re-innervate the denervated fibres, resulting in clusters (Figure B)

Answer 74

* During spinal muscular atrophy * Cycles of denervation are followed by collateral reinnervation * Surviving axons innervate surrounding fibres * Resulting in fibre type grouping * In healthy muscles (Figure A), motor units are **intermingled**. During reinnervation, nearby surviving neurons re-innervate the denervated fibres, resulting in **clusters** (Figure B)

Answer 75

* During **spinal** muscular atrophy * Cycles of denervation are followed by collateral reinnervation * Surviving axons innervate surrounding fibres * Resulting in fibre type grouping * In healthy muscles (Figure A), motor units are intermingled. During reinnervation, nearby surviving neurons **re-innervate the denervated** fibres, resulting in clusters (Figure B)

Answer 76

* Genetic (**rare**) susceptibility to gas **anaesthetics** * Eg sevoflurane * Mutation in RyR means gas **anaesthetic** -\> Ca2+ release * Autosomal Dominant * Channel is susceptible if any of subunits are * Result: SERCA works too hard (to pump Ca back into SR) * Increased O2 consumption, Increased CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), hyperkalaemia, muscles become rigid

Answer 77

* Genetic (rare) susceptibility to gas anaesthetics * Eg sevoflurane * **Mutation** in **RyR** means gas anaesthetic à Ca2+ release * Autosomal **Dominant** * Channel is susceptible if **any** of subunits are * Result: SERCA works too hard (to pump Ca back into SR) * Increased O2 consumption, Increased CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), hyperkalaemia, muscles become rigid

Answer 78

* Genetic (rare) susceptibility to gas anaesthetics * Eg sevoflurane * Mutation in RyR means gas anaesthetic à Ca2+ release * Autosomal Dominant * Channel is susceptible if any of subunits are * Result: **SERCA** works too hard (to pump Ca back into SR) * Increased O2 consumption, Increased CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), hyperkalaemia, muscles become rigid

Answer 79

* Genetic (rare) susceptibility to gas anaesthetics * Eg sevoflurane * Mutation in RyR means gas anaesthetic à Ca2+ release * Autosomal Dominant * Channel is susceptible if any of subunits are * Result: SERCA works too hard (to **pump** **Ca** **back** into SR) * Increased O2 consumption, Increased CO2, acidosis, tachypnea, muscles overheat, the body **overheats**, muscles are damaged (**rhabdomyolysis**), hyperkalaemia, muscles become **rigid**

Answer 80

* Genetic (rare) susceptibility to gas **anaesthetics** * Eg sevoflurane * Mutation in RyR means gas **anaesthetic** -\> Ca2+ release * Autosomal Dominant * Channel is susceptible if any of subunits are * Result: SERCA works too hard (to pump Ca back into SR) * Increased O2 **consumption**, Increased **CO2**, **acidosis**, **tachypnea**, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), **hyperkalaemia**, muscles become rigid

Answer 81

* If anaesthetic received - and nothing is done... * Muscle cells **open** and **leak** their contents * Plasma CK-**MM** increases * Kidney failure possible: urine red from myoglobin * Dantrolene sodium can stop the abnormal calcium release * Inhibits ryanodine receptor

Answer 82

* If anaesthetic received - and nothing is done... * Muscle cells open and leak their contents * Plasma CK-MM increases * **Kidney** failure possible: **urine** red from myoglobin * Dantrolene sodium can stop the **abnormal** calcium release * Inhibits ryanodine receptor

Answer 83

In malignant hyperthermia - **dantrolene sodium** can stop the abnormal calcium release (Inhibits ryanodine receptor)

Answer 84

In malignant hyperthermia - dantrolene sodium can stop the abnormal calcium release (Inhibits **ryanodine** receptor)

Answer 85

In **malignant hyperthermia** - dantrolene sodium can stop the abnormal calcium release (Inhibits ryanodine receptor)

Answer 86

In malignant hyperthermia - dantrolene sodium can stop the abnormal **calcium** release (Inhibits ryanodine receptor)

Answer 87

* Group of **inherited** disorders * Severe and progressive **wasting** of muscle * Muscle weakness * Due to myopathy, not neuropathy * Waddling gate * Contractures * Cardiorespiratory muscle involvement

Answer 88

* Group of inherited disorders * Severe and progressive wasting of muscle * Muscle **weakness** * Due to **myopathy**, not **neuropathy** * Waddling gate * Contractures * Cardiorespiratory muscle involvement

Answer 89

* Group of inherited disorders * Severe and progressive wasting of muscle * Muscle weakness * Due to myopathy, not neuropathy * **Waddling** gate * **Contractures** * **Cardiorespiratory** muscle involvement

Answer 90

* Group of inherited disorders * **Severe** and **progressive** wasting of muscle * Muscle weakness * Due to **myopathy**, not neuropathy * Waddling gate * Contractures * Cardiorespiratory muscle involvement

Answer 91

* **x**-linked disease * affects 1:3500 live **male** births * one third of cases arise spontaneously * progressive loss of muscle tissue * replaced by fibrofatty connective tissue * Mutation: gene for dystrophin protein

Answer 92

* x-linked disease * affects 1:**3500** live male births * one third of cases arise spontaneously * **progressive** loss of muscle tissue * replaced by fibrofatty connective tissue * Mutation: gene for dystrophin protein

Answer 93

* x-linked disease * affects 1:3500 live male births * one third of cases arise spontaneously * progressive loss of muscle tissue * replaced by **fibrofatty** connective tissue * Mutation: gene for **dystrophin** protein

Answer 94

* x-linked disease * affects 1:3500 live male births * •one **third** of cases arise spontaneously * progressive loss of muscle tissue * replaced by fibrofatty **connective** tissue * Mutation: gene for dystrophin protein

Answer 95

**Gowers**' sign is a medical sign that indicates weakness of hip and thigh muscles associated with muscular dystrophy. The patient that has to use his hands and arms to "walk" up his own body from a squatting position.

Answer 96

**Gowers**' sign is a medical sign that indicates weakness of hip and thigh muscles associated with **muscular dystrophy**. The patient that has to use his hands and arms to "walk" up his own body from a squatting position.

Answer 97

* Lack of muscle use can lead to **contractures** or atrophy * Duchenne muscular dystrophy – dystrophin (**X**-linked) * Exercise training —\> **hypertrophy** * Rhabdomyolysis * Crush injury * Diagnostic Tests * Oxygen carrier in urine: myoglobin * Energy for contraction: creatine phosphokinase * Biopsy to show regeneration: fibre type grouping * EC coupling: rigor mortis & malignant hyperthermia * Pharmacology: AChE Inhibitors (MG - myasthenia gravis), Dantrolene (MH - malignant hyperthermia) * Insufficient neural signalling: myasthenia gravis & SMA (spinal muscular atrophy)

Answer 98

* Lack of muscle use can lead to contractures or atrophy * Duchenne muscular dystrophy – dystrophin (X-linked) * Exercise training —\> hypertrophy * **Rhabdomyolysis** * Crush injury * Diagnostic Tests * Oxygen carrier in urine: **myoglobin** * Energy for **contraction**: creatine phosphokinase * Biopsy to show **regeneration**: fibre type grouping * EC coupling: **rigor** mortis & malignant **hyperthermia** * Pharmacology: AChE Inhibitors (MG - myasthenia gravis), Dantrolene (MH - malignant hyperthermia) * Insufficient neural signalling: myasthenia gravis & SMA (spinal muscular atrophy)

Answer 99

* Lack of muscle use can lead to contractures or atrophy * Duchenne muscular dystrophy – dystrophin (X-linked) * Exercise training —\> hypertrophy * Rhabdomyolysis * Crush injury * Diagnostic Tests * Oxygen carrier in urine: myoglobin * Energy for contraction: creatine **phosphokinase** * Biopsy to show regeneration: **fibre type** grouping * **EC** coupling: rigor mortis & malignant hyperthermia * Pharmacology: **AChE** Inhibitors (MG - myasthenia gravis), Dantrolene (MH - malignant hyperthermia) * Insufficient neural signalling: myasthenia gravis & SMA (spinal muscular atrophy)

Answer 100

* Lack of muscle use can lead to contractures or atrophy * Duchenne muscular dystrophy – dystrophin (X-linked) * Exercise training —\> hypertrophy * Rhabdomyolysis * Crush injury * Diagnostic Tests * Oxygen carrier in urine: myoglobin * Energy for contraction: creatine phosphokinase * Biopsy to show regeneration: fibre type grouping * EC coupling: rigor mortis & malignant hyperthermia * Pharmacology: AChE Inhibitors (MG - myasthenia gravis), **Dantrolene** (MH - malignant hyperthermia) * Insufficient **neural** signalling: myasthenia gravis & SMA (spinal muscular atrophy)

Answer 101

* Lack of muscle use can lead to contractures or **atrophy** * **Duchenne** muscular dystrophy – dystrophin (X-linked) * Exercise training —\> hypertrophy * Rhabdomyolysis * **Crush** injury * Diagnostic Tests * Oxygen carrier in urine: myoglobin * Energy for contraction: creatine phosphokinase * Biopsy to show regeneration: fibre type grouping * EC coupling: rigor mortis & malignant hyperthermia * Pharmacology: AChE Inhibitors (**MG - myasthenia gravis**), Dantrolene (MH - malignant hyperthermia) * Insufficient neural signalling: myasthenia gravis & **SMA (spinal muscular atrophy)**

Pathophysiology of Skeletal Muscle Flashcards

(126 cards)