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MBBS > 204 MSK - Physiology > Flashcards

204 MSK - Physiology Flashcards

1
Q

Steps in excitation-contraction coupling

A
  1. Electrical activity (action potential) enters, opens voltage-gated Ca2+ channels.
  2. Ca2+ enters cell & increase intracellular Ca2+
  3. Ca2+ binds to troponin C → tropomyosin on actin that covers myosin-binding sites (usually 7) move away, exposing the binding site
  4. Myosin head bind to actin causing the muscle to bend - power stroke (aka. Contraction)
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2
Q

The sliding filament theory of skeletal muscle contraction.

A
  1. Myosin binding sites on actin exposed.
  2. Myosin binds to actin *only at a high energy state (upright position)
  3. Power stroke - myosin head tilts backward; thin filament pulled inward toward the center of the sarcomere
  4. Cross-bridge disconnected & re-energized
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3
Q

Malignant hyperthermia

A

Autosomal dominant disease

Calcium release with inhaled anesthesia – halothane; succinylcholine can be a cause

Increase in [Ca2+] → muscle fibers to contract → generates excessive heat

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4
Q

Symptoms of malignant hyperthermia

A

Muscle rigidity
Hyperthermia
Tachypnea, tachycardia, ↑ metabolic rate
Dramatic swings in BP

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5
Q

Treatment of malignant hyperthermia

A

Dantrolene

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6
Q

Management of malignant hyperthermia

A

Cooling of body, ventilation
Hydration with IV fluids
Diuretics

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7
Q

Skeletal muscle is ______ muscle

A

striated

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8
Q

Contraction & relaxation of muscle requires?

A

ATP

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9
Q

Muscular dystrophy

A

Inherited disease

Muscle weakness & degeneration due to absence or deficiency of dystrophin

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10
Q

Excitation-contraction coupling - how does Ca2+ enter?

A
  1. Muscle action potential enters T tubule from the plasma membrane
  2. Dihydropyridine receptors (DHPR) activated as it is voltage-gated - DHPR & ryanodine receptors (RYR) are physically connected on SR
  3. Depolarization of T tubule activates DHPR & opens RYR (uncoupling) → Ca2+ flow exits SR & binds to troponin C → contraction
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11
Q

Excitation-contraction coupling - how is Ca2+ removed?

A
  1. Ca2+ pumped back into SR by sarcoendoplasmic reticulum Ca2+ ATPase (SERCA)
  2. It Is a slower process so the muscle can remain contracted even after action potential terminated → longer relaxation phase
  3. Ca2+ entering SR binds with calsequestrin & stored
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12
Q

Dystrophin

A

Connects actin w extracellular matrix

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13
Q

Neuromuscular junction

A

The junction between axon terminal & motor endplate

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14
Q

What type of neuron innervate skeletal muscle fibers?

A

Alpha motor - fast, no delay

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15
Q

Motor unit

A

All the muscle fibers supplied by a single motor neuron

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16
Q

Neuromuscular transmission (9)

A
  1. Action potential reaches axon terminal → Opens voltage-gated Ca2+ channels
  2. Ca2+ enters the axon terminal
  3. Causes exocytosis of ACh containing vesicles
  4. 2 molecules of ACh binds to nicotinic ACh receptors
  5. Na+ enter the endplate
  6. Generation of endplate potential (EPP) (threshold -40mV)
  7. Opens voltage-gated Na+ channels in muscle
  8. Muscle action potential is generated - propagates in both directions
  9. ACh degradation
17
Q

Termination of neuromuscular transmission

A
  1. ACh is broken down by acetylcholinesterase (AChE)
  2. Choline is taken back by axon terminal for the synthesis of ACh
  3. Ion channels close → muscle membrane repolarizes
18
Q

Complications of malignant hyperthermia

A

Increased muscle metabolism & ATP consumption causes lactic acidosis → hypoxia & hypercarbia (excess CO2)

The rigidity of respiratory muscles → respiratory acidosis & hypoxia

19
Q

Drugs Affecting Neuromuscular Transmission

A

Curare - binds to nicotinic ACh receptors
Succinylcholine - acts like ACh
Organophosphate pesticides (malathion) & nerve gases (sarin) - inhibits AChE

20
Q

DUMBELS (organophosphate pesticides affecting neuromuscular transmission)

A 
Diarrhea
Urination
Miosis
Bradycardia
Emesis
Lachrymation
Salivation
21
Q

Anecdote of organophosphate pesticides

A

Pralidoxime - reactivates AChE

22
Q

Myasthenia gravis

A

Autoimmune disease

Antibodies against nicotinic ACh receptors (post-synaptic)

23
Q

Lambert-Eaton syndrome

A

Antibodies against voltage-gated Ca2+ channels in the axon terminal (pre-synaptic)

24
Q

Why does weakness improve w repeated activity in Lambert-Eaton syndrome?

A

Presynaptic Ca2+ channels are affected

  • increase stimulation means more a.p. → increases intracellular Ca2+
  • Causes exocytosis of more ACh
25
Q

Neurotransmitter at NMJ is?

A

ACh

26
Q

Myasthenia gravis is treated w?

A

Cholinesterase inhibitor - edrophonium

MBBS (28 decks)

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