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MSK > Phys > Flashcards

Phys Flashcards

1
Q

Describe the action and effect of botulinus toxin

A

Action: Blocks presynaptic ACh release

Effect: Total blockage can cause paralysis of respiratory muscles, eventual death (flaccid paralysis)

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2
Q

Describe the action and effect of curare

A

Action: Competitive AChR antagonist

Effect: Decreases the size of the end-plate potential; can relax and paralyze muscles (flaccid paralysis)

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3
Q

Describe the action and effect of neostigmine

A

Action: AChE inhibitor

Effect: Prolongs and enhances action of ACh at motor end-plate. Used to tx myasthenia gravis or reverse NMJ blockade

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4
Q

Describe the action and effect of hemicholinium

A

Action: Blocks reuptake of choline into presynaptic terminal

Effect: Depletes ACh stores from presynaptic terminal, leading to weakness

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5
Q

Describe the action and effect of tetrodotoxin

A

Action: Blocks neuronal Na+ channels

Effect: No Na+ channels = no AP = no ACh release = flaccid paralysis

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6
Q

Describe the pathophys and effect of myasthenia gravis

A

Pathophys: Autoimmune attack on nicotinic ACh receptors

Effect: Weakening of skeletal muscles; usually first observed in the small facial/eye muscles. Treat with AChE inhibitors such as neostigmine

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7
Q

Describe calcium-induced calcium release

A

An AP traveling down the sarcolemma causes DHPRs in the T-tubules to open, allowing Ca++ to enter. This Ca++ opens RyRs, allowing Ca++ release from the SR.

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8
Q

When pCa is plotted against muscle force, what does the curve look like and why?

A

Sigmoidal curve due to cooperative binding

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9
Q

What causes malignant hyperthermia and how is it treated?

A

Genetic mutations of RyRs result in pathologic opening in response to certain “-ane” anesthetics and depolarizing agents such as succinylchoine.

The pathologic opening allows Ca++ leak, drives muscle contraction, and causes the SERCA pump to work overtime to remove Ca++.

The metabolic ramp up that is required to fuel the SERCA pump with ATP causes malignant hyperthermia.

MH is treated with dantrolene.

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10
Q

What holds the sarcomere together?

A

Costameres connect the sarcomere of the muscle to the sarcolemma

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11
Q

Describe the pathophys of muscular dystrophy

A

Lacking or mutated dystrophin results in poor connections in muscle tissue, making it susceptible to damage from eccentric forces. Can see interstitial muscle fibrosis, dislocated nuclei, and patches of necrotic fibers due to this damage.

If/when membrane ruptures, Ca++ floods in from ECF, causing contractures.

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12
Q

What causes the dissociation of the actin-myosin complex?

A

ATP binding

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13
Q

What allows myosin heads to return to their resting conformation?

A

ATP hydrolysis

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14
Q

How is the actin-myosin weak cross-bridge state strengthened?

A

Release of Pi

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15
Q

Which bands change during contraction?

A

I band
H band

(A does not change)

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16
Q

Stretching a muscle has what effect on passive and active tension?

A

Increases passive tension

Decreases active tension

17
Q

Contracting a muscle has what effect on muscle movement and tension?

A

Limits movement

Reduces tension development

18
Q

How can muscle force be modulated?

A
  1. ) Recruit more motor units
  2. ) Increase the frequency of stimulation of those unit
  3. ) Improve synchronization of stimulation
19
Q

What impact does training have on muscle recruitment and force?

A

Lowers motor unit thresholds
Provides more myelin (helps increase the frequency of stimulation)
Improves synchronization (highly trained athletes tend to recruit high threshold units FIRST, giving more power or dexterity)

^^ All of these things help increase force

20
Q

At what points of load and velocity of shortening do muscles have the most power?

A

High velocity * medium load

21
Q

Describe Type 1 muscle fibers in terms of twitch speed, size of motor neuron, power, endurance, mitochondria, capillary density, and fuel:

A 
Type I:
Slow twitch
Small motor neuron
Low power
High endurance
Lots of mitochondria
High capillary density
Fuel = triglycerides

(aerobic)

22
Q

Describe Type IIa muscle fibers in terms of twitch speed, size of motor neuron, power, endurance, mitochondria, capillary density, and fuel:

A 
Type IIa:
Fast twitch
Large motor neuron
High power
Moderate endurance
Lots of mitochondria
Intermediate capillary density
Fuel = CP/Glycogen

(aerobic)

23
Q

Describe Type IIb muscle fibers in terms of twitch speed, size of motor neuron, power, endurance, mitochondria, capillary density, and fuel:

A 
Very fast twitch
Very large motor neuron
Very high power
Low endurance
Few mitochondria
Low capillary density
Fuel = GP/Glycogen

(anaerobic)

24
Q

What are the 4 functions of bone?

A

Scaffolding/protection
Storage (Ca++ and Pi)
Hematopoiesis/leukopoiesis
Endocrine fxn

25
Q

What is the function of OPG?

A

OPG acts as a decoy receptor for RANKL.

Inhibits differentiation of precursor cells into osteoclasts; this encourages bone maintenance.

26
Q

What is the function of RANKL?

A

When not outnumbered by OPG, RANKL binds RANK and activates precursor cells to differentiate into osteoclasts. This encourages bone loss (to replenish Ca+).

27
Q

Describe the process of osteoclast maturation

A

PTH and vitamin D stimulate osteoblasts to release RANKL and M-CSF

M-CSF binds to stem cells, causing differentiation into pre-osteoclast precursors

RANKL binds RANK: precursors become pre-osteoclasts

OPG release is inhibited, so pre-osteoclasts are now able to mature

Mature osteoclasts begin resportion of bone

28
Q

Describe the process of osteolysis

A

Osteoclasts bind to bone via integrins and vitronectins

RANKL is bound to the osteoclast and promotes release of lysosomes and HCl into the lacuna

29
Q

What inhibits the process of osteolysis?

A

Calcitonin

The process can be prevented by OPG acting as a decoy for RANKL, also

30
Q

What occurs when plasma Ca++ levels fall?

A

Calcitriol and PTH levels rise

RANKL expression is increased

Encourages osteolysis to increase serum [Ca++] and [Pi].

31
Q

In a healthy person, how long is the bone turnover cycle?

A

Activation - reversal: ~3 weeks
Reversal to Quiescence: ~3 months

(About 112 days total)

32
Q

How does estrogen support bone maintenance?

A

By:
Encouraging apoptosis of osteoclasts
Decreasing RANKL-induced differentiation of precursors into pre-osteoclasts
(Decreasing bone absorption)

33
Q

How does vitamin D regulate bone mass in adults, and where does it come from?

A

From the kidneys

Encourages Ca++ and Pi absorption by activating osteoclasts and inhibiting osteoblasts

(this occurs if vitamin D is very high or if Ca++ is very low)

34
Q

How does GH/IGF-1 regulate bone mass in adults, and where does it come from?

A

From the pituitary gland/liver

Activates osteoblasts and stimulates chondrocyte proliferation

35
Q

How does testosterone/estrogen regulate bone mass in adults, and where does it come from?

A

From aromatase precursors/testes/ovaries

Activates osteoblasts
Stimulates chondrocyte proliferation

36
Q

How does PTH regulate bone mass in adults, and where does it come from?

A

From the parathyroid gland

Continuously activates osteoclasts

Pulsatile PTH activates osteoBLASTS.

When [Ca++ and Pi] are low, PTH is released to encourage osteolysis, increases Ca++ and Pi serum levels.

37
Q

How does calcitonin regulate bone mass in adults, and where does it come from?

A

From thyroid T cells

Inhibits osteoclasts: promotes Ca++ excretion in order to lower plasma [Ca++].

38
Q

Why are women at a heightened risk for osteoporosis post-menopause?

A

Dropping levels of estrogen (which is normally anabolic to bone)

MSK (4 decks)

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