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Neurology - Sem 3 > Case 9 - Disorders of muscle > Flashcards

Case 9 - Disorders of muscle Flashcards

1
Q
  1. What are the 3 types of muscle?
  2. What are the 2 muscle types that are striated?
  3. Which 2 muscles are involuntary muscles?
  4. What is the function of skeletal muscle?
  5. How do muscle cells end up with just 1 neuron innervating them?
A
  1. Smooth muscle, skeletal muscle, cardiac muscle
  2. Cardiac & Skeletal muscle
  3. Cardiac & Smooth muscle
  4. Moving bones around joints
  5. Synaptic competition - so the most appropriate connection wins, others die as you train etc.
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2
Q
  1. What forms the tendons?
  2. What is a muscle cell called?
  3. Where do muscles form from in the embryo?
  4. What are the muscle cell precursor?
  5. How many axons innervate a single muscle fiber?
A
  1. Connective tissue sheath, which encloses the muscles
  2. Muscle fiber
  3. somites (33 of them)
  4. Myoblasts derived from the Mesoderm
  5. A single axon innervates a single muscle fiber
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3
Q

Define the following terms:

  1. Synergists
  2. Antagonist
  3. Hypertrophy
  4. Hyperplasia
  5. Atrophy
  6. Muscle tone
A
  1. Muscles that all work together, pulling in the same direction
  2. Muscles that have opposite actions, pulling in different directions
  3. Increase in the size of the cells, growth of muscle fibers
  4. Increase in the number of cells
  5. Degeneration of muscle fibers
  6. tautness when muscles are at rest, due to low rate of nerve impulses from spinal cord
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4
Q
  • What part of the spinal cord innervates somatic motor neurons?
  • Where are LMN found, What do they do?
  • What are the 2 types of LMN?
A
  • Ventral horn of the spinal cord
  • In the spinal cord, command muscle contraction
  • Alpha motor neuron & Gamma motor neurons
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5
Q

Identify:

  • Ventral horn
  • Ventral root
  • Mixed spinal nerve
A
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6
Q
  1. What is the function of an alpha motor neuron?
  2. What is a motor unit?
  3. What is a motor neuron pool?
  4. How is the contraction of muscle controlled? (x2)
  5. Why would you cycle through different motor units?
A
  1. Triggers the generation of force by muscle
  2. 1 AMN and the fibers it innervates
  3. Collection of AMN’s that innervate a single muscle
  4. Vary the firing rate of motor neurons OR recruit additional synergistic motor units
  5. Prevents fatigue of muscle fibers
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7
Q
  1. What NT is released by AMN at the neuromuscular junction?
  2. What does a single postynaptic AP cause in a muscle?
  3. What causes sustained contraction?
  4. What happens above 40Hz frequency of contraction?
  5. How many muscle fibers per motor unit do muscles for fine actions require compared to large muscles?
A
  1. Acetylcholine (ACh)
  2. Twitch - Rapid sequence of contraction & relaxation
  3. Continual AP’s
  4. Tetanic contraction - sustained muscle contraction
  5. Large muscles - have more muscle fibers per AMN, compared to smaller muscles.
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8
Q
  • What are the 3 sources of input into AMN’s?
  • What NT’s do the interneurons use?
A
  1. Muscle spindle
  2. Upper motor neurons - initiate and control voluntary movement
  3. Interneurons in the spinal cord - regulation of spinal motor programmes, can be excitatory or inhibitory
  • Excitatory signal - Glutamate
  • Inhibitory signal - GABA or Glycine
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9
Q

What are the 3 types of muscle fiber? What colour are they generally?

A
  1. Slow muscle - Red [Type I]
  2. Fast fiber - fatigable, White [Type IIb]
  3. Fast fiber - Fatigue resistant, White [Type IIa]
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10
Q

Which characteristics correspond to which type of fiber (Type I, Type IIb, Type IIa):

  • Type of metabolism
  • Mitochondria
  • Enzymes for oxidative metabolism
  • contraction speed
  • Length of contraction
  • Blood supply
  • Myoglobin content
  • Sarcoplasmic reticulum
  • Ca+ pump transport rate
  • Fatigue resistance
A
  • Slow fibers - Aerobic metabolism, Fast fibers - Anaerobic metabolism
  • Fast fibers - Less mitochondria, Slow fibers - large number of mitochondria
  • Slow fibers - large number of enzymes for oxidative metabolism
  • Slow fibers - slow contraction
  • Slow fibers - sustained contraction without fatigue
  • Slow fibers - Extensive blood vessels
  • Slow fibers - large stores of myoglobin, Fast fibers - deficit of myoglobin
  • Fast fibers - extensive SR for rapid release of Ca+
  • Fast fibers - high Ca+ pump transport rate
  • Type I & Type IIa - Resistant to fatigue, Type IIb - Non-resistant to fatigue
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11
Q
  1. Why would type I fibers need a smaller diameter?
  2. What is the sequence of recruitment for the muscle fibers?
A
  1. Requires O2 and so needs to have a short diffusion distance for the O2.
    1. Type IIb fibers have large diameter because they work anaerobically and so O2 diffusion is not important.
  2. Slow — FR — FF
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12
Q

Identify the fibers from the graph:

  • Fast fatigable
  • Fast-fatigue resistant
  • Slow
  1. Which fiber generates the strongest force?
A
  1. Fast fatigable fibers
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13
Q
  1. What is a slow motor unit?
  2. What is a fast fiber unit? How types are there?
  3. What is the difference in characteristics between them?
  • Motor neuron size, and conduction velocity
  • Types of muscle fibers
  • Activity (When are they activated)
A
  1. Contains only slow fibers (Red)
  2. Contains either FF or FR white fibers
  • slow motor unit - Small diameter, slow conduction, easy to excite.
    • Only a few muscle fibers
    • Mainly type I
    • First to be recruited, frequently active
  • Fast motor unit - large diameter, fast conduction, hard to excite.
    • Many muscle fibers
    • Type II
    • Recruited if strong contraction required
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14
Q

Resting membrane potential

  1. What is the ion pump responsible for setting the resting membrane potential (RMP)
  2. What does it do?
  3. K+ leaks out of the cell, but what keeps the inside negative?
A
  1. Na+/K+ pump
  2. Pumps 3K+ in for 2 Na+ out of the cell. Using ATP
  3. Proteins which are negative
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15
Q

Neuron stimulation

  1. What channels open?
  2. Which way does Na move?
  3. What happens to the inside of the cell?
  4. What happens to the Na+ channels during this time?
A
  1. Na+ channels open
  2. Na+ moves down concentration gradient INTO the cell
  3. Inside becomes more +ive
  4. Na+ channel inactivation gate, slowly closes
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16
Q

Repolarisation

  1. What happens here?
  2. What makes the cell negative again?
A
  1. Na+ channels inactivation gate shuts
    1. K+ channels open
  2. The K+ within the cell pours out, inside is more -ive.
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17
Q
  1. What is used to synthesise ACh?
  2. Where is it synthesised?
  3. What is ACh exchanged with to enter the vesicles?
  4. What is used to break down ACh?
A
  1. ATP supplied by mitochondria
  2. In the cytoplasm
  3. H+ (Proton)
  4. Acetylcholinesterase AChE
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18
Q

Identify the following & What is their function?

  • Dense bars
  • Axon
  • Vesicles
  • Ca+ Channels
  • Nicotinic Acetylcholine receptors
  • Voltage activated Na+ channels
  • Synaptic cleft
A
  • Holds the vesicles in place for release
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19
Q

ACh release

  1. What causes ACh vesicles to move to the membrane?
  2. Is Ca+ required for NT release?
  3. What are SNARE’s?
  4. What are the 2 types of SNARE?
A
  1. AP causes Ca+ ions to enter the cell
  2. No, vesicles release NT spontaneously - Ca+ increases the probability of vesicle fusion
  3. Thought to be involved in connecting the vesicle to the pre-synaptic membrane
  4. V SNARE - Vesicular snare, T SNARE - Target membrane snare
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20
Q

SNARE Hypothesis

  1. What is required to zip up the SNARE for fusion?
  2. What are the proteins required by the 2 SNARES?
A
  1. Ca+
  2. v-SNAREs - Synaptobrevin & Synaptotagmin t-SNAREs - Syntaxin & SNAP-25
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21
Q
  1. How many ACh molecules are required to activate the receptor?
  2. Where do they attach?
  3. What happens when ACh binds?
  4. What ions can pass through?
  5. In practice which ion is the only one which passes?
A
  1. 2
  2. a sub-unit
  3. Conformational change - opens channel to allow ions in
  4. Na+, K+, and Ca++
  5. Na+
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22
Q
  1. What does the passage of the Na+ ions do?
  2. What does the end plate potential do?
  3. What happens in the muscle fiber?
  4. What happens after contraction?
A
  1. Activate Nicotinic ACh receptors – Creates a local +ive potential change in the membrane (End plate potential)
  2. Initiates an AP in the muscle membrane - muscle contraction (EPSP)
  3. AP causes release of Ca+ from the Sarcoplasmic reticulum — Excitation contraction coupling.
  4. Reuptake of Ca+ into the SR, to stop contraction
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23
Q
  1. What happens to the tetrad during an AP?
  2. Where does most of the Ca+ flow through?
A
  1. AP causes conformational change in tetrad channels - opens Ca+ release channel in SR membrane
  2. Ca+ release channels
24
Q

Constituents of the muscle fiber:

  • Sarcoplasmic reticulum - What does this store?
  • Sarcolemma
  • Myofibrils - What are they responsible for?
  • Transverse (T) Tubule -
  • Nucleus
  • Mitochondria
A
  • Ca+
  • Myofibrils are responsible for contraction in response to an AP
25
Q
  1. What is the receptor that senses the AP in the T tubule?
  2. What are they linked to?
  3. What do these channels do?
A
  1. Dihydropyridine receptor
  2. Ryanodine channels (Ca+ release channels)
  3. Release Ca+ into the sarcoplasm
26
Q
  1. Which protein pumps the Ca+ back into the SR?
  2. Which protein aids in the storage of Ca+ in the SR?
A
  1. SERCA
  2. Calsequestrin
27
Q
  1. What is anchored to the Z lines?
  2. What is Myosin composed of?
  3. What does the myosin head function as?
A
  1. Actin filaments
  2. 2 heavy polpeptide chains, and 4 light chains
  3. ATPase
28
Q
  1. What is Actin made of? (4)
  2. What are the 3 types of troponin?
  3. What does Troponin I bind to?
  4. What does troponin T bind to?
  5. What does Troponin C bind to?
A
  1. F actin, G Actin, Tropomyosin, and Troponin
  2. Troponin I, C, T
  3. Actin
  4. Tropomyosin
  5. Calcium
29
Q

Identify:

  • I band
  • H band
  • A band
  • Z line
  • Titin
  • Sarcomere
  • M line
  • Thin filament
  • Thick filament
A
30
Q
  1. What causes rigor mortis?
A
  1. Muscles starved of ATP so myosin heads cannot detatch from actin
31
Q
  1. What happens to the sarcomere at rest?
A
  1. Myosin is free
    1. Troponin & Tropomyosin form a complex
32
Q
  1. What happens to the sarcomere during contraction?
  2. What happens on the Actin?
  3. What 2 things bind?
A
  1. Ca+ binds to Troponin C
  2. Tropomyosin shifts after conformational change, myosin binding site exposed
  3. Myosin binds to the exposed site on Actin
33
Q
  1. What causes the myosin head to disengage?
  2. What molecule is present on the myosin head before it binds?
A
  1. ATP binding, hydrolysed to ADP
  2. ADP
34
Q
  1. What are the 3 energy sources for muscle?
A
  1. Phosphocreatine, Glycolysis, and Oxidative metabolism
35
Q
  1. What is Isotonic contraction?
  2. What is isometric contraction?
  3. Which diagram shows which?
A
  1. When muscle shortens but tension on muscle is constant.
  2. When muscle doesnt shorten during contraction, load is so large that shortening is not possible. Tension but no shortening
36
Q
  1. What is a muscle spindle?
  2. Which sensory neurons detect their changes?
A
  1. Special skeletal muscle fibers contained in a fibrous capsule, which detect stretch of muscle
  2. Group I a snesory neurons
37
Q
  1. What happens to the firing rate of the axons when muscle is stretched?
  2. What happens to the firing rate of the axons when muscle is shortened?
  3. What kind of ion channels are opened when the muscle is stretched?
A
  1. Discharge rate goes up
  2. Discharge rate goes slack
  3. Mechanically sensitive ion channels
38
Q
  1. When the muscle is stretched what do the stretch receptors do?
  2. Give an example of this reflex?
A
  1. Cause the muscle to contract (Shorten it)
  2. Knee jerk reflex
39
Q
  1. What are intrafusal fibers? What are they innervated by?
  2. What are extrafusal fibers? What are they innervated by?
A
  1. fibers within the fibrous capsule, innervated by Gamma motor neurons
  2. Fibers outside of the muscle spindle, forming the bulk of muscle. Innervated by Alpha motor neurons
40
Q
  1. What are gamma motor neurons?
  2. What happens when they are activated?
  3. What is the effect of this?
A
  1. Innervate the intrafusal muscle fibers
  2. Leads to contraction of the 2 poles of the muscle spindle
  3. Increases the Ia activity
41
Q
  1. What are golgi tendon organs?
  2. Where are they found?
  3. What innervates them?
A
  1. Monitor muscle tension or force of contraction
  2. Junction between muscle and tendon
  3. Ib sensory axons - Smaller than Ia
42
Q
  1. What happens to golgi tendons when the muscle contracts?
  2. What do they synapse with?
  3. What is their function?
A
  1. Ib axons are squeezed, mechanosensitive ion channels are activated – AP triggered
  2. Spinal interneurons - inhibitory
  3. Protect muscle from being overloaded
43
Q
  1. What is muscle hypertrophy?
  2. What is another form of muscle hypertrophy?
A
  1. When the total mass of a muscle increases, increase in number of A & M filaments, so enlargement of muscle fibers
  2. When muscles are stretched to greater length, new sarcomeres are added to the ends
44
Q
  1. What is muscle atrophy?
  2. What pathway does this happen through?
  3. What are proteosomes?
A
  1. Decrease in the size of muscle fibers
  2. ATP-Dependent ubiquitin proteosome pathway
  3. Protein complexes which degrade damaged or uneeded proteins by proteolysis
45
Q
  1. What is ubiquitin?
    2.
A
  1. Regulatory protein which labels cells for proteasomal degradation
46
Q
  1. What is fiber hyperplasia?
  2. What are some of the triggers to decreasing the protein synthesis rate? (2)
  3. What are the triggers to Increasing the protein degredation rate? (4)
A
  1. Increase in number of fibers
  2. Akt, mTOR
  3. Glucocorticoids, myostatin, NF-kappaB, Reactive O2 species
47
Q
  1. Which hormone has an anabolic (Build) effect on muscle?
  2. What is the hormone that causes deposition of fat?
A
  1. Testosterone
  2. Estrogen
48
Q
  1. What are the metabolites used by muscle in exercise?
  2. Which cycle is used to produce glucose from lactate? Where does this happen?
  3. What is the last gasp source of energy for muscles? What enzyme does this?
A
  1. ATP, Phopho-creatine system, Glycogen-lactic acid system, Aerobic system
  2. Cori cycle using O2, Liver
  3. Regeneration of ATP using ADP, Myokinase
49
Q
  1. What is used to reconstitute ATP?
  2. What is used to reconstitute both PCS & ATP?
  3. What is used to reconsitute all other systems?
A
  1. Phospho-creatine system
  2. Glycogen-lactic acid system energy
  3. Oxidative metabolism (Aerobic)
50
Q
  1. What does the boutulinum toxin affect?
  2. What does Tetanus do?
A
  1. Cleaves synaptobrevin so disrupts SNARE complex formation - Paralysis
  2. Cleaves synaptobrevin in inhibitory neurons, so no inhibition of motor neurons - Tetany
    3.
51
Q
  1. What do curare, Bungarotoxin do?
  2. What does Sarin do?
A
  1. ACh receptor antagonists, so cause paralysis
  2. Desensitises receptor so they stop working, leads to paralysis
52
Q
  1. What is a compound fracture?
  2. What is a comminuted fracture?
A
  1. Bone communicates with the skin surface
  2. Bone is fragmented
53
Q
  1. What is a displaced fracture?
  2. What is a stress fracture?
  3. What is a greenstick fracture?
A
  1. Ends of the bone are not aligned
  2. Slowly developing fracture due to increased physical activity with repetitive loads
  3. Extends only partially through the bone, common in infants due to soft bones
54
Q
  1. What are the steps of bone repair?
  2. What are:
  • Osteoclasts
  • Osteoblasts
  • Osteocytes
A
  1. Haematoma — Soft callus — Hard callus — Lamellar bone
  • Cells which degrade bone
  • Cells which rebuild bone
  • Mature bone cells
55
Q
  1. What is an orthosis?
  2. What is an osteophyte?
A
  1. Surgical device which exerts external forces on part of the body to support joints or correct deformity
  2. Bony projection that occur at sites of cartilage degeneration or destruction
56
Q
  1. What are the 3 cmmon syndromes of the female athlete?
  2. What is the difference between primary and secondary amenorrhea?
A
  1. Eating disorders, menstrual dysfunction, decreased bone mineral density
  2. Primary is absence by age of 16, never had period. Secondary is absence of menstruation for 3 months for woman who has had period
57
Q
  1. What hormone is needed for menstruation?
A
  1. GnRH

Neurology - Sem 3 (15 decks)

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