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
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
3
Q
Define:
- Sarcolemma
- Sarcoplasm
- Sarcosome (X need use this term)
- Sarcomere
- Sarcoplasmic reticulum
A
- Plasma membrane of muscle cell
- Cytoplasm
- Mitochondria
- Func. unit of muscle (Z line to Z line)
- SER
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
5
Q
Desc. direction of movement
A
- Movement always same direction as fascicle
- Tension created at origin, movement at insertion
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
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
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
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)
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)
11
Q
What are the features of Purkinje fibres?
A
- Abundant glycogen (white)
- Sparse myofibrils (X striated)
- Extensive gap junctions
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
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
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
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
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
- Ca2+ channels open and Ca2+ binds to troponin (C) inducing conformational change –> dissociation of tropomyosin –> exposes actin binding site
- ATP attached to myosin head hydrolysed by myosin ATPase –> myosin binds –> myosin-actin cross bridges form
- Myosin head tilts towards centre of sarcomere (M line) –> two fil. slide over each other
[Called a power stroke] - ADP and Pi released –> sarcomere shorten –> muscle contraction
- ATP reattaches & hydrolyses –> myosin ready to bind again
- 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
What is Duchene muscular dystrophy (most common)? Mode of inheritance? Caused by? Results in?
- 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
Symptoms of Duchene muscular dystrophy are...
- Belly sticks out, shoulders and arms held back awkwardly when walking
- Poor balance
- Frequent falls
- Waddling gait
- Muscle pain and stiffness
27
What can a rise of creatine kinase (enzyme) be an indication of?
- 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
Desc. measurement of troponin assays in myocardial damage
- 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
Why X use myoglobin/CK/LDH to detect heart attacks?
- Myoglobin: release fast, gone fast
- CK: gone fast
- LDH: low levels, misinterpret easily
30
Desc. botulism toxin mechanism. Uses?
- 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
What is the most common form of botulism? Symptoms?
- 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
What is organophosphate poisoning? Causes? Symptoms?
- 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
What is malignant hyperthermia? Mode of inheritance? Results in?
- 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
What are the symptoms of malignant hyperthermia? Morbidity risk?
- 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
What are some risk factors of rhabdomyolysis?
- Duchenne muscular dystrophy
- McArdle's disease: no glucose-6-phophatase in liver
- LDH deficiency
- Taking statins
36
What is rigor mortis? Caused by? What increases it?
- 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
What is snake venom mechanism? Symptoms?
- Principal polypeptide toxins bind to Ach receptors OR destroy Achesterase
- Results in tetany (involuntary contractions) that can lead to death
38
State function of:
1. Tropomyosin
2. TnP-I
3. TnP-C
4. TnP-T
* If rhabdomyolysis 2-4 detected in blood
5. T-tubules
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
How is K+ ions related to smooth muscle contraction?
| *if smooth muscle/rhabdomyolysis dmg --> K+ detected in blood
- Cause influx of Ca2+ & activation of contractile machinery
