Musculoskeletal Flashcards
1
Q
What is scleroderma?
who does it affect most
A
- An initial damage is caused to small blood vessels (unknown what causes this) which leads to tissue ischemia and fibrosis
- fluid leaks out of the vessels, causing an inflammatory response, laying collagen which causes fibrosis
- This can happen to blood vessels anywhere in the body
- Because it is autoimmune, it requires a genetic component AND an environmental trigger
- women 35-45 years old (4:1; women:men)
2
Q
What is an early sign of scleroderma and what can this turn into later?
A
- Raynaud’s is an early sign
- If the perfusion is so poor to the fingers, they will get scars or become necrotic
- eventually can form calcium deposits.
3
Q
What is “limited” Scleroderma?
A
- CREST
- C- Calcinosis
- calcium deposits on skin
- R- Raynaud’s Phenomenon
- spasm of blood vessels in response to cold or stress
- E- Esophageal dysfunction (too stiff to allow food to pass)
- acid reflux and decrease in motility of esophagus
- S- Sclerodactyly
- Thickening and tighetening of the skin on the fingers and hands
- T- Telangiectasia
- Dilation of capillaries causing red marks on the skin surface
- Small, dilated capillaries (if in mouth, can bleed with DVL)
4
Q
What is “diffuse” scleroderma?
A
- Lung fibrosis (leading cause of death in scleroderma
- decrease in diffusion, decrease in compliance
- pulmonary arterial hypertension
- Right heart failure (cor pulmonale); common
- Left heart failure (fibrosis); non common
- pericarditis
- Kidney- baseent membrane fibrosis- decreased GFR & proteinuria (slow)
- scleroderma renal crisis- (rapid)
- Gi tract- hypomotility, malabsorption
- Joint contractures- loss of mobility
5
Q
Systemin Lupus Erythematosus (SLE)
What type of sensitivity?
Who does it affect?
A
- Type III sensitivity
- primarily affects young women (15-30); blacks and hispanics more than whites
6
Q
Systemic Lupus Erythematosus (SLE)
How does this disease work?
A
- Pt has anti-nuclear antibodies
- damaged cells do not go through apoptosis correctly, allowing for release of DNA which the antibodies bind to, leading to further destruction?
- Immune complexes damage blood vessels
- this can happen to any organ
7
Q
How does Systemic lupus erythematosus affect the different systems?
A
- Cardiovascular disease is now the leading cause of lupus now that there is dialysis
8
Q
What are the different parts of muscle fibers?
A
- One cell runs entire length of muscle
- myofibril is made up of A-band, I-band, and z-disk
- A-band and I-band slide together, overlapping, when muscle is contracted.
9
Q
A
- Nerve impulse comes through axon and depolarized calcium channel at end of axon. Calcium causes release of acetylcholine
- Acetylcholine causes ligand dependent Na channel to open and Na moves into sarcoplasm, depolarizing cell.
- Depolarized sarcoplasm opens Na voltage gated channel and further depolarizes.
- Voltage gated Ca channel in sarcoplasm opens which opens calcium channel (dihydropyridine, DHP) in Sarcoplasmic reticulum. (this is where T-tubule is depolarized)
- Calcium moves from SR into sarcoplasm which contracts cell.
10
Q
What is Duchenne muscular dystrophy?
A
- There is not enough Dystrophin, which is a protein that connects the muscle fiber to the endomysium
- Without it, everytime the person uses their muscles, it rips the plasma membrane
- a normal person would recover to be stronger
- person with MD just gets weaker
- High levels of CK from these cellular injuries
- until they no longer have any muscles left to injure
11
Q
Who is most often affected by Duchenne’s?
A
- Young boys
- usually wheelchair bound by 8
12
Q
How does Myesthenia gravis work?
What type of hypersensitivity is it?
A
- Type II hypersensitivity
- Antibodies that react with acetylcholine receptors either prevent the receptors from working or destroy them
- Requires much more ACh to get the same response as a normal person because the ACh has to find the few functioning receptors
- They are strongest in the am when they have higher stores of ACh
- Weakness is improved with acetylcholinesterase inhibitors
13
Q
What is myesthenic syndrome?
A
- Ca++ channel at the end of neuron is blocked by antibody
- Acetylcholine cant get out
- They are weak all day, do not start stronger and get weaker
- weakness is not improved with acetylcholinesterase inhibitors
14
Q
How does curare work?
botulinum toxin?
tetani toxin?
A
- Curare: works by competetively blocking the acetylcholine receptor
- Botulinum: ACh vessicles cant fuse with membrane and cant be released
- very long lasting
- Tetani: uncontrolled fusion of ACh vessicles to the membrane
- causing overstimulation
15
Q
What are osteoclasts?
osteoblasts?
osteocytes?
A
- Osteoclasts- macrophage that breaks down bone
- Osteoblasts: cells that lay down bone
- Osteocytes: mature osteoblasts
- Know the difference between spongy/trebeculae and compact/cortico
21
Q
What parts of the bone are affected in osteoporosis?
A
- cortical- gets new holes
- trabecular bone- gets thinner
23
Q
What sites are most commonly affected by osteoarthritis?
A
