Musculoskeletal Flashcards
1
Q
What musculoskeletal diseases are caused by autoimmune?
A
- Sclerodema
- Lupus
- Myasthenia gravis
- myasthenic syndrome
- rhumatoid arthritis
- anklylosing spondylitis
2
Q
What are genetic musculoskeletal disease?
A
- Muscular dystophy
- marfan’s syndrome
- achondroplasia
3
Q
What is scleroderma
A
- autoimmune disease
- numerous antibodies (ANA, anticentromere, scl 70 …)
- unknown trigger
- occurs primarilyin middle-aged (35-50) women (>4:1)
- all autoimmune diseases tend to afflict women more than men because autoimmune diseases begin during hormonal changes
- initially damages small blood vessels which leads to tissue ischemia and fibrosis
- BIG problem is blood vessel effects
- Excessive produciton of collagen (fibrosis) that affects
- skin
- GI tract
- lungs
- kidneys
4
Q
What are scleroderma symptoms on the hands?
A
- Calcium deposits
- tissue dies and attracts calcium from blood
- looks like chalk
- tissue dies and attracts calcium from blood
- puffy fingers
- raynauds
- same physiology as cold day, but happens at much higher tempa nd shuts off blood completely
- digital ulcers and scars (from raynaud’s and cut off of circulation)
5
Q
What is CREST?
A
“limited scleroderma”
- Calcinosis
- Raynaud’s phenomenon
- esophageal dysfunction- acid reflux and decrease in motility of esophagus
- sclerodactyly- thickening and thighteningof skin on the fingers and hands
- telangiectasia- dilation of capillaries causing red marks on skin surface
6
Q
What is diffuse scleroderma?
How does it affect heart, lung, kidney, GI tract, joints?
A
- LUng fibrosis- leading cause of death from scleroderma
- decrease in diffusion
- decrease in compliance
- pulmonary arterial hypertension- PAH (very common)
- RV failure
- Heart
- cor pulmonale–> right heart failure
- fibrosis–> left heart failure
- pericarditis
- Kidney<– few will die from kidney failure d/t HD
- basement memebrane fibrosis–> decreased GFR, proteinuria (slow)
- Scleroderma renal crisis–> rapid onset renovascular disease (rapid)
- GI tract
- hypomotility, malabsorption
- Large joint contractures
- loss of joint mobility (including mouth/jaw)
- pain and fatigue
7
Q
What is systemic lupus erythematosus?
A
- Autoimmune disease- type III hypersensitivity
- ANA (anti-nuclear antibodies)- also found in other autoimmune diseases
- unknown trigger
- Occurs primarily in young (15-30) women (>5:1), black and hispanics more than whites
- immune complexes damage blood vessels leading to vasculitis
- blood vessel damage can affect any organ- symptoms vary widely from patient to patient
- kidney is generally the most affected organ
- however, with HD, not likely to die from it
- CV disease is now the biggest problem and cause of death
- kidney is generally the most affected organ
8
Q
Are lungs highly affected in lupus?
A
NO, generally cv disease is leading cause of death
9
Q
What is Duchenne muscular dystrophy?
A
- x-linked genetic disorder that affects dystrophin, dystrobrevin or dystroglycans
- dystrophin links actin in muscle to sarcolemma to the basal lamina and evens tension through entire muscle fiber
- without dystrophin, we cannot evenly distribute tension throughout entire muscle fiber and when muscle contracts, it tears.
10
Q
What tends to be around muscle cells of someone with muscular dystrophy?
A
- neutrophils because the muscle cell is damaged and your body sees need for repair
- muscles will not adapt and get stronger like normal because there is still no dystrophin
- also have variation in fiber size, degerating and regernerating fibers, immune cell infiltrationa nd increased fibrosis
11
Q
What is myasthenia gravis?
A
- Antibodies bind to acetylcholine receptors and prevent them from working (IgG mediated)
- the more muscles are used throughout the day, the weaker the muscle gets because less and less acetylcholine vesicles are available
- now, less acetylcholine released and very few ach receptors are available, so more weakness occurs throughout the day
12
Q
What is myasthenic syndrome?
A
- IgG antibodies attacking presynaptic VG calcium channel
- Therefore, acetylcholine is never triggered to be released into cleft
- no change in muscle strength throughout the day
- acetylcholinesterase inhibitor does not have any effect on patient.
- Receptor plentiful but not enough Ach in cleft (not even released to begin with)
13
Q
Review of process for activation of neuromuscular junction (NMJ)
A
- Pre-synaptic voltage gated calcium channel allows Ca to come into presynpatic terminal
- signals acetylcholine vesicles to be released into cleft
- Acetylcholine diffuses, binds to acetycholine-gated cation channel
- cell depolarizes and voltage gated Na channel opens, allowing Na to enter cell, further depolarizing cell
- then voltage gated Ca channel opens, simultaneously opening gated Ca release channel on sarcoplasmic reicticulum
- Ca released into cell, causing actin/myosin formation and cell contraction
14
Q
What is effect of myastehnia gravis on NMJ?
A
Blocked ACh receptors
15
Q
What is effect curare at NMJ?
A
Drug that blocks ACh receptors temporarily and paralyzes muscle
18
Q
What do undifferentiated mesenchymal cells differentiate into?
A
- Fibroblasts
- Cohrodroblast
- Osteoblasts
- Also (not covered)
- smooth muscle cells
- endothelial cells
- mesothelial cells
- adipocyte
