week 2 neuro summary.pdf

2.1 intro and clinical presentation autoimmune disease MS autoimmune disease autoimmunity classifications 1. systemic :entire body is affected ex: lupus, RA, dematomyositis 2. organ specific : organ targeted by immune system based on receptor sensitivity ex: thyroid- hashimoto or graves type 1 diabe...

2.1 intro and clinical presentation autoimmune disease MS autoimmune disease autoimmunity classifications 1. systemic :entire body is affected ex: lupus, RA, dematomyositis 2. organ specific : organ targeted by immune system based on receptor sensitivity ex: thyroid- hashimoto or graves type 1 diabetes-pancreas neuromuscular- myasthenia gravis myelin- MS and BS are target tissues pathophysiological differences GBS- PNS MS-CNS- brain and sc autoimmune pathophysiology autoimmunity: immune-mediated response of self antigens immune system begins to attack body by generation of auto antibodies normal circumstances: body has a natural autoimmunity and auto antibodies that exist as a way for the body to develop effective immune-related responses to pathogens. exaggeration of autoimmune response occurs if pt becomes susceptible. etiology (combo) genetics lifestyle environment diet stress normal aging microbiome: influencer of local and systemic inflammatory responses -according to rosenbaum and colleagues genetic allele: shown to provide the predisposition regardless of trigger -according to atassie and kosali molecular mimicry once external stresses are added to a normal system, body's immune system responds by releasing inflammatory cytokines to mediate problem=causes activation of selfreactive lymphocytes= destruction of the target tissues. immune system mistakes body for pathogenic molecules MS target tissue: myelin, oligodendrocytes and nerve cells of CNS *all autoimmune diseased originate from maladaptive factors in body but target tissue is diff -ppl w autoimmune disease are more prone to others if they dont mitigate prob why the fek do this gotta be so long clinical presentation myelin: meant to serve as insulator to nerves & aid in transmission of APs (bc of nodes of ranvier) forms a coating around nerve creating a tunnel so APs can flow w no slowdown symptoms: begin w visual disturbances ex: diplopia and nystagmus presentations extensions of plaques paresthesias bradykinesia fatigue abnormal tone tremors ataxia pain dysarthria generalized weakness forming damsons fingers around corpus callosum bc of break down of myelin and nervous tissue white plaques shown in T2-weighted MRI to diagnose MS -could be a distinguishing factor to rule in/out 4 phenotypes of MS 1. clinically isolated syndrome (CIS) isolated event of inflammatory demyelination that could progress to other forms if left unchecked no other clinical features shown only MRI can show can progress to 2. relapsing remitting (most common) discrete attacks followed by near baseline recovery 3. 4. secondary progressive worsening symptoms after relapse attack primary progressive continuous worsening of symptoms from 1st onset occurs w/out earlier relapses pts may have relapses attacks thru progression relapsing remitting for a little and then convert to secondary and get worse Summary Multiple Sclerosis manifests as an organ-specific autoimmune disease 4 Multiple Sclerosis Phenotypes 1. Clinically Isolated Syndrome 2. Relapsing Remitting 3. Secondary Progressive 4. Primary Progressive different presentations bc different lesions show up in new spots