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Clinical Medicine II

What is multiple sclerosis autoimmune d/o affects the CNS, destruction of myelin
Does MS ↓ survival no but significantly impacts QOL
Where is MS more commonly seen Further away from the equator MC in females 2:1, Peak incidence ~40’s
What are the RF’s for MS Geography, Age, Environmental influences at young age, Genetics: vit D deficiency?
What are the proposed causes of MS Autoimmune: T-helpers are iniciators, Microbial: something starts the autoimmune response, Chronic Cerebrospinal Venous Insufficiency (CCSVI) theory,
What is the CCSVI theory obstructed drainage in veins of brain and spinal cord→reflux back up to brain, causes immune response
Where do MS lesions occur white matter in the CNS (brain/spinal cord)
What cells lead to destruction of myelin, how? CD4+ cells, cross BBB and produce cytokines→inflammation & damage
Where does the “sclerosis” part of MS come from Macrophages remove the degenerated areas→gliosis, shrunken areas of demylenation called a plaque or sclerotic area
Do the axons get damaged not from the dz process, but the scar that forms can damage under lying axon fibers
What is the clinical presentation of MS varies for every pt, depends on where the lesion is
What are primary sxs direct consequence of conduction produced by demyelination and axonal damage
What are secondary sxs complications from 1 sxs, Eg. Frequent UTI’s d/t urinary retention
What are tertiary sxs relate to the effect of dz on pt’s everyday life. Emotional, psychological and social effects eg. Self cath d/t urinary retention
What are common sxs of MS vision or parethesias often w/ pain. All are different!
Objects in the visual field appear to oscillate oscillopsia
Neck flexion causes an electric shock to spine Llhermitte’s sign
Though sxs may be very fluctuant, what is a sign for MS the neuro sxs worsen by heat, humidity or hot bath
What does the clinical course look like Unpredictability and varability, BUT characterized by exacerbations and remissions
What is the Relapsing/Remitting MS characteristics 85%, discrete attacks evolve days-wks, often completely recovery w/I weeks to months, slowly ↓ recovery, and sometimes doesn’t completely return to baseline
What are Secondary progressive MS (begins like RRMS) eventually experience steady deterioration of fxn unassociated w/ acute attacks
What are characteristics of primary progressive MS not experience attacks, but staed y functional decline, usually later in life but disability develops faster (40yo)
Characteristics of Progressive/Relapsing MS steady deterioration but with acute attacks
How do we distinguish b/w PRMS and PPMS indistinguishable
How do we diagnose MS >2 episodes, CNS white matter, Sxs >24 hrs, separated by at least 1m, present on nero exam, second sign intrathecal IgG synthesis or MRI
What is characteristic in 90% of pt’s w/ MS ↑igG in CSF protein is slightly elevated
What is a sign of an active lesion Gadolinium enhancement contrast
What are ways to dx MS MRI, Evoked potentials, CSF
Are size of lesions consistent w/ neuro deficit? no, depends on where lesion is for effects
What is seen in CSF w/ pt’s w/ MS mononuclear cell pleocytosis (↑lymphocytes), ↑IgG, protein ↑ slightly
DDx of MS Lupus, CNS vasculitis, Sarcoidosis, Syphilis, HIV, lyme dz, CVA/TIA, nutritional d/o eg. B12 deficiency
Tx of MS prevention o f relapses, tx sxs is key, tx acute attacks
If age of onset <40 yo whats the prognosis better than later in life
What are favorable prognosis <40, female, optic neuritis or sensory sxs as initial sxs, low attack frequency, type: relapsing/remitting
What measures neurological impairment of MS Kurtzke Expanded Disability Status Score
What are issues we need to address w/ pt and family with dx of MS life adjustments: grief, depression→suicide risk, financial and vocational, sexuality, family and pregnancy issues
Focus of rehab improving and optimizing fxn
What are 5 types of rehab PT, OT, Speech therapy, Cognitive rehab, vocational rehab
Created by: becker15
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