Quiz 8.20.21 Flashcards

1
Q

How do statins lead to myopathy?

A

Generally, HMG-CoA reductase converts HMG-CoA to mevalonic acid, which in turn produces Q10 (ubiquinone). Statin prevents production to mevalonic acid, leading to decreased Q10, decreased functioning of mito, decreased ATP availability.
Deregulation of mito may also cause calcium leak out of mito, uptake and overload by SR, then reexit by ryanadine.
Statins may also reduce cholesterol in muscles, making them less effective.
Statin may prevent functioning of GTP binding proteins, contributing to apoptotic signalling.

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2
Q

How do quinolones cause myopathy

A

unknown.
Possible metalloproteins interfere w/ cell membranes.
Other theory = altered metabolism of tendon cells, leading to decreased collagen.

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3
Q

Aims of Choosing Wisely

A

Decrease harm, reduce duplicate procedures, choose evidence based care, decide on necessary tests/procedures, promote communication between providers/pt

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4
Q

Impact of Choosing Wisely.

A

May help providers and patients find sweet spot wrt care, costs, outcomes.

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5
Q

4 steps to implement Choosing Wisely

A
  1. Engage team (start conversations, identify barriers to starting, educate entire team)
  2. Engage patients (talk about purpose of tests, risks, benefits, costs, provide accessible education materials)
  3. Est. concrete, standardized plan.
  4. Collect data that measures effectiveness of intervention.
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6
Q

Recommended exercises for those w/ muscular diseases

A

Walking running (not downhill), resistance training (low load), balance, flexibility.

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7
Q

Symptoms of FSHD

A

Muscle weakness in face, scapula fixators, humeral muscles, food flexors. May have difficulty manipulating mouth.

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8
Q

Duchenne symptoms

A

Proximal muscle weakness, esp. at upper legs. 2-3 y/o @ onset. Often enlarged calves, death by 20 yo.

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9
Q

Becker symptoms

A

Milder Duchene, onset in teens,

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10
Q

Limb Girdle

A

Can start at any age, muscle weakness @ hips/ shoulders.

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11
Q

Most common muscular dystrophies

A
Duchenne/Becker
Myotonic
FSHD
Limb Girdle
(all <15/100,000)
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12
Q

Cell junctions of smooth, skeletal, and cardiac cells

A

Skeletal: None
Smooth: Gap junctions to coordinate function, but cells anchored in ECM.
Cardiac: Intercalated disks w/ electrical and ionic coupling. (Use desmosomes)

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13
Q

What happens after Ach binding

A

Opening of sodium channels on sarcolemma causing an EPP, which downstream acts on DHRP, etc etc.

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14
Q

Trigeminal Nerves (CN V1 - CN V3)

A

V1 - forehead, nose
V2 - upper jaw
V3 - lower jaw, ear

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15
Q

Nerves to back of head-neck

A

C2-C4

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16
Q

Nerves to arms

A

C5-T1

17
Q

Nerves to chest/abs

A

T2-L2

18
Q

Nerves to legs

A

L3-S1

19
Q

Nerves to groin

A

S1-S4

20
Q

Muscle Spindles mechanism of action

A

Sense overstretch, uses type 1a, and II, which contract the muscle and relax the antagonist to shorten muscle.

21
Q

Golgi tendon mechanism of action

A

Uses type 1b neurons, detects stretching of tendons which indicates overcontracting of muscle, causes muscle to relax and antagonist to contract.

22
Q

Inheritance patterns of Duschene, Limb-Girdle, FSHD, Becker’s and pathology.

A

FSHD: Autosomal dominant (shortened D4Z4), leads to rounding of muscle fibers, internal nuclei, scarring.
Beck, Duchenne: X-linked recessive. (exon deletion and frameshift mutation, respectively). Shortage/depletion of dystrophins.
Myotonic: Autosomal Dominant, repeat mutation @ DMPK gene. Clumping of RNA in muscle nuclei.

23
Q

Normal creatine Kinase

A

22-400, but up to 700 normal if African American.