Musculoskeletal

Question 0

Sarcomere is from ____ to ____

Answer 0

Z disk to Z disk

Question 1

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

Answer 1

It can undergo hypertrophy only

It can increase number of nuclei when it gets bigger

Question 2

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

Answer 2

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

Question 3

Middle of A band is ____

Middle of I band is ____

Answer 3

Middle of A band is M line

Middle of I band is Z disk

Question 4

What are the steps that a neuromuscular junction gets activated

Answer 4

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.

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 6

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

Answer 6

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)

Question 7

Compare and contrast slow oxidative and fast glycolytic musle fiber types

Answer 7

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)

Question 8

Osteoclasts
Osteoblasts
Osteocytes

Answer 8

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

Question 9

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

Answer 9

Severe muscle wasting

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

Question 10

Duchenne muscular dystrophy: what is mutated?

Answer 10

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

Question 11

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

Answer 11

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)

Question 12

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

Answer 12

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

Question 13

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

Answer 13

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)

Question 14

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

Answer 14

Hematopoietic gives rise to osteoclast

Mesenchymal gives rise to osteoblasts

Question 15

Arthritis

Answer 15

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

Question 16

Gouty arthritis (gout)

Answer 16

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

Question 17

Bursitis

Answer 17

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

Question 18

Osteoarthritis vs. rheumatoid arthritis?

Answer 18

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

Question 19

Myeloma

Answer 19

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

Question 20

Osteomalacia

What is OM of growing bones called?

Answer 20

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

Question 21

Osteoporosis

Answer 21

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

Question 22

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

Answer 22

Sprain is injury to a joint

Strain is injury to a muscle or tendon at a joint

Question 23

Tennis elbow is inflammation of tissues around the _____

Answer 23

Lateral epicondyle of the humerus

Question 24

Lordosis seen in ___

Answer 24

Beer bellies and pregnant women

Predisposes them to back problems

Question 25

Osteoporosis has what specific changes in the bone?

Answer 25

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

Question 26

Why do old women get osteoporosis and not old men?

Answer 26

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

Question 27

Paget’s disease

Answer 27

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)

Question 29

Hyperparathyroidism

Answer 29

Too much PTH hormone, so PTH chews up bone

Leads to osteoporosis

Question 30

How does PTH keep calcium levels normal?

Answer 30

PTH activates vitamin D to take up calcium

Tells osteocytes to get Ca right now

Question 31

Osteomyelitis

Answer 31

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

Question 32

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

Answer 32

Metastasis to the bone from another cancer

Question 33

Osteoarthritis common sites?

Answer 33

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

Question 34

Rheumatoid arthritis common sites?

Answer 34

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

Question 35

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

Answer 35

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

Question 36

Talipes equinovarus

Answer 36

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

Question 37

Osteogenesis imperfecta

Answer 37

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

Question 38

Rickets

Answer 38

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