Musculoskeletal Flashcards

0
Q

Sarcomere is from ____ to ____

A

Z disk to Z disk

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1
Q

Can a skeletal muscle undergo hyperplasia or hypertrophy? Can it increase number of nuclei?

A

It can undergo hypertrophy only

It can increase number of nuclei when it gets bigger

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2
Q

Are A band and I bands dark or light? Which gets shorter with contraction?

A

A is dArk (myosin and overlapping actin)
I is light (actin only)
I band gets shorter with contraction, A stays the same

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3
Q

Middle of A band is ____

Middle of I band is ____

A

Middle of A band is M line

Middle of I band is Z disk

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4
Q

What are the steps that a neuromuscular junction gets activated

A

Action potential comes down axon, when depolarization gets to axon terminus, voltage gated ca channel opens and ca moves into the axon
Axon terminus releases Ach into cleft and binds Ach-ligand gated Na channel on muscle cell, Na moves into the cell and cell depolarizes, as cell potential goes up, voltage-gated Na channel opens and more Na comes in
More depolarization opens voltage-gated ca channel, ca moves into the cell from outside via T-tubules, which opens ca-gated ca channel and ca comes into cell from SR too causing contraction.

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5
Q

List the 4 steps of the sliding filament model. Bind. Flick. Release. Reposition.

A
  1. ATP binds to myosin head, causing dissociation from actin
  2. As ATP is hydrolyzed, a conformation change occurs. ADP and Pi remain associated with the myosin head
  3. Myosin head attaches to actin filament, causing release of Pi
  4. Pi release triggers a ‘power stroke’, a conformation change in the myosin head that moves actin and myosin filaments relative to each other. ADP is released
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6
Q

Talk about troponin, tropomyosin, actin, and myosin, how does the binding occur?

A

Calcium binds to TnC on the troponin, which exposes the myosin binding site on actin. Tropomyosin was blocking the binding site originally.

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6
Q

Myosin releases, repositions, binds, and ficks until _____ (3 reasons)

A

1 Run out of actin and can’t contract any further
2 Ca is removed from SR (muscle is relaxed)
3 Cell runs out of ATP, myosin can’t release and muscle can’t relax bc myosin attached (rigor mortis)
Note: ATP has to bind in order for myosin to release, when repositioned, ATP is broken down to ADP (ATP not used to bind or flick)

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7
Q

Compare and contrast slow oxidative and fast glycolytic musle fiber types

A

Slow: low ATPase, slow speed of contraction, resists fatigue, high oxidative capacity, low anaerobic enzyme content, lots of mitochondria and capillaries, high myoglobin content, red, low glycogen, small fiber diameter, ex. tongue (can talk for a long time)
Fast: high ATPase, fast contractions, fatigues quickly, low oxidative, high anaeorbic content, not much mitochondria or capillaries, low myoglobin content, white, high glycogen content, large fiber diameter, ex. Lats (can’t do a lot of pull-ups)

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8
Q

Osteoclasts
Osteoblasts
Osteocytes

A

Osteoclasts: macrophage syncytium that breaks down bone
Osteoblasts: build bone
Osteocytes: mature osteoblasts

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9
Q

Duchenne muscular dystrophy: would an old person leak CK after vigorous activity?

A

Severe muscle wasting

No, he doesn’t have muscle left to leak CK

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10
Q

Duchenne muscular dystrophy: what is mutated?

A

Dystrophin, a protein that anchors the sarcomere. When defected, actin attached to membrane along cell isn’t anchored properly, it rips plasma membrane every time a person exercises, micro-tears in the sarcolemma allows CK to leak out (if there is any). Normally, the tear repairs, but is DMD, it doesn’t repair.
Most common is X-linked, almost always affects males

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11
Q

Myasthenic syndrome: what happens on a cellular level to lead to weakness? Does an Acetylcholinesterase-Inhibitor help?

A

Progressive autoimmune disease
Antibodies bind to Ca channel, calcium can’t come in, no Ach is released, paralysis, they are weak all day
Note: an Ach inhibitor WOULDN’T help (there’s no Ach)

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12
Q

Myasthenia Gravis: what happens on a cellular level to lead to weakness? Does an Ach-inhibitor help?

A

Progressive autoimmune disease
Antibodies against Ach receptors, Ca comes in, vesicles fuse, Ach is released but CAN’T bind, cell can’t depolarize, paralysis
They can do things in the morning, but weakness gets worse during the day, with use (starts with droopy eyelids)
Acetylcholinesterase inhibitor DOES help so that Ach has time to read with receptors

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13
Q

MG blocks ___
Curare blocks _____
Clostridium botulinum blocks ____
Clostrididum tetani works by ___

A

MG blocks Ach receptors
Curare blocks neuromuscular blockade (on post-synaptic membrane)
Botulinum blocks the neurotransmitter from being released (blocks vesicle fusing with membrane)
Tetani releases an excessive amount of neurotransmitters (overstimulation of muscle membrane leads to lock jaw)

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14
Q

Hematopoetic stem cells give rise to ____
Mesenchymal cells give rise to _____
(Osteoblast vs. osteoclast)

A

Hematopoietic gives rise to osteoclast

Mesenchymal gives rise to osteoblasts

15
Q

Arthritis

A

Inflammation of a joint, usually accompanied by pain, swelling, and changes in structure

16
Q

Gouty arthritis (gout)

A

Metabolic disorder, occurs when sharp uric acid crystals deposit in a joint

17
Q

Bursitis

A

Inflammation of bursa, causing pain, swelling, and restriction of movement
Commonly in shoulder, elbow, knee

18
Q

Osteoarthritis vs. rheumatoid arthritis?

A

OA: from wear and tear, degeneration of articular cartilage
RA: inflammation of synovial membrane and is the most debilitating of the chronic forms, auto-immune disorder attacking the joints, inflammation is the CAUSE not the EFFECT

19
Q

Myeloma

A

Most common form of bone cancer, in which malignant tumors in the bone marrow interfere with RBC production and cause destruction of bone

20
Q

Osteomalacia

What is OM of growing bones called?

A

Disease characterized by softening of the bones due to demineralization (loss of calcium and phosphorus)
Caused by vitamin D deficiency
Bone softening results in skeletal deformities
OM of growing bones is called rickets

21
Q

Osteoporosis

A

Loss of bone mass/density that makes the bones so porous that they crumble under ordinary stress
Loss of estrogen, deficiency of calcium and vitamin D, low levels of exercise

22
Q

Sprain is injury to a ____, strain is injury to a ____

A

Sprain is injury to a joint

Strain is injury to a muscle or tendon at a joint

23
Q

Tennis elbow is inflammation of tissues around the _____

A

Lateral epicondyle of the humerus

24
Q

Lordosis seen in ___

A

Beer bellies and pregnant women

Predisposes them to back problems

25
Q

Osteoporosis has what specific changes in the bone?

A

Trabeculi (spongy bone) narrows, gets more spongy, loses strength
Cortical (compact bone) thins (this is weight-bearing bone)
Crush fractures are common

26
Q

Why do old women get osteoporosis and not old men?

A

Men start with bigger bones
Men lose bone material at a slower rate
Men die younger

27
Q

Paget’s disease

A

Increased metabolic activity in bone characterized by rapid break down and rebuilding of bone, increased osteoclast activity. All this remodeling enlarges and softens the bone.
Treat with bisphosphonates (slows rate of bone breakdown)

29
Q

Hyperparathyroidism

A

Too much PTH hormone, so PTH chews up bone

Leads to osteoporosis

30
Q

How does PTH keep calcium levels normal?

A

PTH activates vitamin D to take up calcium

Tells osteocytes to get Ca right now

31
Q

Osteomyelitis

A

Inflammation of the core of the bone
As the abcess grows, sequestrum (dead bone) gets surrounded by new bone
Treat by injecting ABX

32
Q

What is more common, primary bone cancer or mets to the bone from another cancer?

A

Metastasis to the bone from another cancer

33
Q

Osteoarthritis common sites?

A

Hips
Knees
Lower lumbar/ cervical vertebrae
Interphalangeal and tarsometatarsal joints
Eroded cartilage in these areas causes bone on bone, painful movements

34
Q

Rheumatoid arthritis common sites?

A
Not necessarily weight-bearing joints, hands and feet are common sites
Ulnar deviation (fingers bend toward ulna) due to erosion of the bone
35
Q

How does someone find out they have gout?How did it happen?

A

They wake up and their toe hurts, get an x-ray and its not broken
Uric acid crystals form (white top) from diet (rich in nucleotides/meat)
Macrophages don’t have the enzymes to break down the crystals creating an inflammatory response

36
Q

Talipes equinovarus

A

Common birth defect caused by oligohydramnios, baby gets cramped in the uterus (face looks smushed, legs turn in)
Baby needs some physical therapy, maybe braces

37
Q

Osteogenesis imperfecta

A

Brittle bone disease due to collagen I deficiency (collagen makes the bone strong under tension), bones break easily, collagen defect causes blue eyes
Treat with metal rods

38
Q

Rickets

A

Due to a lack of vitamin D or calcium, the bone bends easily (doesn’t break), causes bow-legged in children
Note: Adults will get Osteomalacia instead of rickets if they have calcium/vitamin D deficiency