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BL Sem 1 > Lecture 11 & 12 - Muscles > Flashcards

Lecture 11 & 12 - Muscles Flashcards

1
Q

Desc. the diff. muscle types

A

Striated:

  • Skeletal: has myoglobin, voluntary control, direct nerve-muscle communication
  • Cardiac: has myoglobin, involuntary control, indirect nerve-muscle com.

Non-striated:
- Smooth: X myoglobin, involuntary, indirect

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2
Q

What is myoglobin? What is myoglobinuria an indication of? Causes what?

A
  • O2-storing mol. that provides O2 to working striated muscles (X bind to CO2, higher affinity at low pH)
    (single subunit of Hb)
  • When striated muscle undergoes necrosis/rhabdomyolysis –> myoglobin in bloodstream (myoglobinaemia) –> can cause renal dmg –> kidneys remove in urine –> tea-coloured
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3
Q

Define:

  1. Sarcolemma
  2. Sarcoplasm
  3. Sarcosome (X need use this term)
  4. Sarcomere
  5. Sarcoplasmic reticulum
A
  1. Plasma membrane of muscle cell
  2. Cytoplasm
  3. Mitochondria
  4. Func. unit of muscle (Z line to Z line)
  5. SER
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4
Q

Desc. skeletal muscle structure

A
  • Many myofibrils form fibre –> Endomysium surround muscle fibre –> many fibres form fascicle –> peri. wrap around fascicle –> epimysium surround muscle, contiguous with tendon
  • Peripheral nuclei (> 1) bordered by endomysium (contains capillaries & venules)
  • Dark longitudinal streaks (lines) = mitochondria, lie btw myofibrils
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5
Q

Desc. direction of movement

A
  • Movement always same direction as fascicle

- Tension created at origin, movement at insertion

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6
Q

Desc. the zones of striated muscle

e.g A band,…

A
  • A band: area of overlap btw actin and myosin
  • I band: thin fil, actin (tropomyosin)
  • H band: thick fil, myosin (in the middle w M line)
  • Z line: point of attachment for actin ( two Z line = sarcomere)
  • M line: middle, attachment for myosin

**Light microscopy only see I,A,Z line

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7
Q

There are three muscle contraction speeds: slow, fast, intermediate. Desc the color of it in microscope

A
  • Each fascicle at least one of each

- Slow = dark, fast= pale, intermediate = brown

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8
Q

Desc. the diff btw slow twitch and fast twitch muscle

A

Slow: (smaller diameter)

  • Type 1 (Slow oxidative fibres)
  • Rich capillary supply, aerobic res. (36 ATP)
  • High myoglobin = darker color
  • Many mitochondria/cytochromes
  • Fatigue resistant = endurance high
  • Standing/walking

Intermediate

  • Type 2A (Fast oxidative glycolytic)
  • Same as slow twitch
  • Moderate fatigue

Fast twitch: larger diameter

  • Type 2B (eye muscle)
  • Poor capillary supply = anaerobic (2 ATP)
  • Low myoglobin = white
  • Few mitochondria/cytochromes
  • Rapid fatigue
  • Strength/anaerobic activites
  • Sprinting/Jumping
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9
Q

Desc. structure of cardiac muscles

A
  • Striated
  • Centrally positioned nuclei
  • Intercalated disc: Has gap junctions (connexins) for conduction of electrical impulse or allow ions to pass
  • Branching
  • Surrounded by glycogen = high activity
    (increases w fasting)
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10
Q

Where and when is ANP and BNP released by?

A
  • ANP (atrial natriuretic peptide) from atria, BNP (brain-type natriuretic peptide) from ventricles
  • Released during heart failure (ANP)
  • Left ventricular hypertrophy/mitral valve disease (BNP)
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11
Q

What are the features of Purkinje fibres?

A
  • Abundant glycogen (white)
  • Sparse myofibrils (X striated)
  • Extensive gap junctions
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12
Q

Compare and contrast cardiac and skeletal muscles

A

Similarities:

  • Both striated
  • Both have sarcomeres (contraction mechanism similar)
  • but cardiac specific isoforms (Troponin I and T)

Differences:

  • Nuclei in cardiac is central
  • Sarcomere X well developed
  • No T-tubules
  • Cardiac communicate through gap junctions
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13
Q

Desc. structure of smooth muscle

A
  • Spindle-shaped (fusiform) with single large central nucleus
  • X striated/sarcomeres/T tubules
    -Few mitochondria
    (still actin-myosin)
  • Has numerous pinocytic cavolae: sampling of extracellular space –> contract yes or no
  • Gap junctions = nexus: small molecules (Ca2+) pass cell to cell
  • Varicosities release neurotransmitters
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14
Q

Function of smooth muscle. Where is it found? Disorders cause?

A
  • Slow, sustained contractions (less ATP)
  • contraction continues until [Ca2+] ⬇️
  • In GI tract, respiratory tract, arteries
  • Disorders can cause:
    i) high BP
    ii) painful menstruation (uterus is mostly smooth muscle, myometrium)

N.B contraction can lead to cell damage –> contracted smooth muscle shortens massively, lose most cytoplasm

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15
Q

Is mature muscle repair possible?

list for each category

A

Skeletal muscle:

  • Regenerate by mitotic activity of Satellite cells
  • Hyperplasia follows muscle injury OR S.C fuse w existing cell and increases mass (hypertrophy)

Cardiac muscle:

  • Incapable of regeneration
  • Scar tissue

Smooth muscle:

  • Retain mitotic activity –> good regenerative ability
  • Pregnant uterus myometrium becomes thicker (hypertrophy), hyperplasia to increase muscle mass
  • Asthma regenerate bronchi smooth muscle cell = leads to narrowing
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16
Q

What cell resides over terminal Schwann cell

A

Kranocyte

17
Q

What is the pathology behind myasthenia gravis? Symptoms?

A
  • Autoimmune diseaase
  • Antibodies block/destroy Ach receptors –> reduced synaptic transmission
  • Symptoms: Ptosis (dropping eyelids), blurred vision (diplopia), intermittent muscle weakness
18
Q

Desc. the sliding filament theory

  • also known as ratchet mechanism
  • the less contracted a muscle, the stronger the force
A
  1. Ca2+ channels open and Ca2+ binds to troponin (C) inducing conformational change –> dissociation of tropomyosin –> exposes actin binding site
  2. ATP attached to myosin head hydrolysed by myosin ATPase –> myosin binds –> myosin-actin cross bridges form
  3. Myosin head tilts towards centre of sarcomere (M line) –> two fil. slide over each other
    [Called a power stroke]
  4. ADP and Pi released –> sarcomere shorten –> muscle contraction
  5. ATP reattaches & hydrolyses –> myosin ready to bind again
  6. When nerve impulse stops, X Ca2+ ions –> troponin-tropomyosin re-cover actin binding site –> sarcomeres lengthen

**Actin and myosin X shorten, ONLY Z line

19
Q

What are the two components of actin? Desc. structure

A
  • F-actin fibres
  • G-actin globules: myosin binding site
  • Tropomyosin coil around actin –> reinforce it
  • Troponin complex attach to each tropomyosin
20
Q

What is myosin structure?

A
  • Myosin has two heads which protrude at opp. side of fil.

- In M line, myosin has NO MYOSIN HEADS!!

21
Q

What is the role of Ca+ in contraction?

A
  • Ca2+ binds to TnC of troponin –> conformational change –> tropomyosin moves away –> actin binding site exposed
  • Allows myosin head to bind
  • Tropomyosin heads sits in clef of G-actin spheres
22
Q

What causes compartment syndrome? Symptoms and treatment?

A
  • Limbs divided into compartments by fascia
  • Trauma in one compartment –> internal bleeding –> exerts pressure on blood vessels –> compartment syndrome
  • Symptoms: constant localised pain, paraesthesia (pins and needles), swollen & shiny skin, prolonged capillary refill time (press down turn red slow)
  • Treatment: fasciotomy (drain abcesses)
23
Q

What is the mechanism of muscle hypertrophy?

A
  • Overstretching: A & I bands X re-engage

- New muscle fibrils/sarcomeres formed

24
Q

What is the cause of muscle atrophy?

A
  • Disuse: bed rest, limb immobilisation, sedentary
  • Surgery: denervation of muscle (nerve regeneration takes 3 months)
  • Disease: Muscle dystrophy (loss of protein/fibre diameter/power)
25
Q

What is Duchene muscular dystrophy (most common)? Mode of inheritance? Caused by? Results in?

A
  • X-linked recessive
  • Due to mutation/absence of DYSTROPHIN gene –> excess Ca2+ enter cell –> taken up by mitochondria –> H2O follow –> mito. burst –> rhabdomyolysis –> creatine kinase & myoglobin plasma levels ⬆️
  • Results in muscle cells being replaced by adipose tissue

*Joins sarcolemma to actin microfibre (?)

26
Q

Symptoms of Duchene muscular dystrophy are…

A
  • Belly sticks out, shoulders and arms held back awkwardly when walking
  • Poor balance
  • Frequent falls
  • Waddling gait
  • Muscle pain and stiffness
27
Q

What can a rise of creatine kinase (enzyme) be an indication of?

A
  • Heart attacks, enzyme increase ∝ to infarct size
    (replaced w troponin I and T for diagnosis)
  • Vaccinations
  • Vigorous exercise
  • Rhabdomyolysis (due to e.g compartment syndrome)
  • Muscular dystrophy
  • Kidney injury
28
Q

Desc. measurement of troponin assays in myocardial damage

A
  • Troponin I and T marker for cardiac ischaemia (X O2) –> released within an hour
  • Measure within 20 hours
  • Smallest change can indicate, quantity X ∝ dmg
29
Q

Why X use myoglobin/CK/LDH to detect heart attacks?

A
  • Myoglobin: release fast, gone fast
  • CK: gone fast
  • LDH: low levels, misinterpret easily
30
Q

Desc. botulism toxin mechanism. Uses?

A
  • Toxin blocks neurotransmitter release at motor end plate –> flaccid paralysis
  • Treat muscle spasms (cervical dystonia), severe underarm sweating, uncontrollable blinking (blepharospasm), migraine, overactive bladder syndrome
  • Used cosmetically for wrinkles
31
Q

What is the most common form of botulism? Symptoms?

A
  • Infant botulism (risk factor eat honey first year of life)
  • Caused by bacterium in small intestine
  • Symptoms: (same for all types, X cause fever/affect consciousness)
    i) Weakness
    ii) Blurred vision
    iii) Vomiting
    iv) Tired/trouble speaking
32
Q

What is organophosphate poisoning? Causes? Symptoms?

A
  • Organophosphates are pesticides
  • Inhibits normal function of acetylcholinesterase (X breakdown Ach)
  • Muscarinic (relating to Ach receptor) symptoms:
    Salivation
    Lacrimation (tears formed)
    Urination
    Defecation
    GI cramping
    Emesis (vomiting)
  • Nicotinic symptoms
    Mon: Muscle cramps
    Tues: Tachycardia
    Weakness
    Twitching
    Fasciculations (twitch)
33
Q

What is malignant hyperthermia? Mode of inheritance? Results in?

A
  • Severe reaction to anaesthetics (succinylcholine: bind to Ach receptor)
  • Autosomal dominant (RyR1 gene)
  • Males > Females
  • Causes:
    i) massive contractile fasciculation (due to ⬆️Ca2+) –> excessive heat generation & metabolic acidosis (no O2, ⬆️lactate)
    ii) ⬆️muscle breakdown (overwork) and hyperkalaemia
34
Q

What are the symptoms of malignant hyperthermia? Morbidity risk?

A
  • Symptoms:
    i) Muscular rigidity
    ii) Rhabdomyolysis
    iii) Hyperkalemia
    iv) Hyperthermia
    v) Acidosis
    vi) Hypercapnia (CO2) and hypoxemia
  • Mortality risk: 5% w treatment, 75% w/o
35
Q

What are some risk factors of rhabdomyolysis?

A
  • Duchenne muscular dystrophy
  • McArdle’s disease: no glucose-6-phophatase in liver
  • LDH deficiency
  • Taking statins
36
Q

What is rigor mortis? Caused by? What increases it?

A
  • Stiffening of the joints and muscles a few hours after death
  • Due to diff. conc. of lactic acid and glycogen in muscle fibres
  • Increases in cold temp or if the dude did intense physical work before dying
37
Q

What is snake venom mechanism? Symptoms?

A
  • Principal polypeptide toxins bind to Ach receptors OR destroy Achesterase
  • Results in tetany (involuntary contractions) that can lead to death
38
Q

State function of:

  1. Tropomyosin
  2. TnP-I
  3. TnP-C
  4. TnP-T
    * If rhabdomyolysis 2-4 detected in blood
  5. T-tubules
A
  1. Tropomyosin: Blocks myosin binding site at low [Ca2+]
  2. TnP-I: prevents myosin from binding to actin in relaxed muscle
  3. TnP-C: When Ca2+ binds –> regulates movement of TnP-I –> expose site
  4. TnP-T: Forms TnP-tropomyosin complex –> position actin
  5. T-tubules: store Ca2+
39
Q

How is K+ ions related to smooth muscle contraction?

*if smooth muscle/rhabdomyolysis dmg –> K+ detected in blood

A
  • Cause influx of Ca2+ & activation of contractile machinery

BL Sem 1 (13 decks)

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