Etiology Clinical Manifestations Pathophysiology Systemic Lupus Erythematosus

Etiology clinical manifestations pathophysiology

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Etiology Clinical Manifestations Pathophysiology Systemic Lupus Erythematosus Chronic multisystem inflammatory disease; Primarily women 20-40; African american Butterfly rash, photosensitivity, nonerosive arthritis peripheral joints, serositis, arthralgia, pul hemorrhage, proteinuria, sz, anemia, leukopenia, thrombocytopenia Antibodies formed against nucleic acid, RBCs, coag protein, phospholipids, lymphocytes, plts, results in activation of complement and tissue damage occur Rheumatoid Arthritis -systemic autoimmune dx Chronic inflammation in connective tissue; more common women; HLA-DRBI gene increased risk, over 60, nulliparity, smoking, obesity Breast feeding lowers risk Symmetrical joint swelling, erythemic joints-warm, loss of fx in joints, morning stiffness better w/movement, weight loss, weakness, anorexia, nodules- elbows/fingers(invasive); fingers/feet/wrist/elbows / Ankles/knees IgM autoantibodies form against IgG and form antigen antibody complex, deposited into synovial membranes, rx occurs, tissue damage; progressive dx, irreversible, deformity, disability f. Analyze the pathophysiology of solid organ transplant rejection. g. Examine the role of the human leukocyte antigen (HLA) in solid organ rejection. Infection 7. Analyze the concepts of infectious disease.
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h. Examine the process of infection: Colonization, invasion, multiplication and spread Concept Process Description Colonization Invasion Multiplication Spread i. Analyze the following infectious disease terms: Fulminant presentation-little or no prodromal stage, subclinical infection-no CM or acute infection evolve to chronic Concept Definition Incubation period Pathogen begins active replication, no CM dependent on microorganism ex: salmonella 6-8 hours, hepatits b 50-180 days Prodromal stage Initial appearance of CM, normally mild Invasion period Rapid multiplication of organism, activation of immune/inflammatory responses, organism specific CM and CM of inflammation Convalescence Containment of infection, resolution CM Communicability Immunogenicity Infectivity Pathogenicity Portal of entry Toxigenicity Virulence Endemic Epidemic Pandemic j. Differentiate between the structure, pathogenic properties and mechanisms by which bacteria, viruses and fungi cause disease. Organism Structure Pathogenic Properties Normal Provide line of defense against Abnormal gut microbiome-
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flora- bacteria Skin, oropharynx, colon, vagina pathogens, assist digestion, help rid toxins, help mature immune system, produce vitamin K, parkinsons, alzheimers, CAD, obesity, liver cx, lymphoma, colorectal cx, anx/dep Breast feed-positively influence gut flora Abx- kill normal flora ex: yeast infection common when women on abx Bacteria Capsule-protect against phagocytosis Plasmids-extra chromosomal DNA, carry genes for abx resistance/toxin production Pili-hair, help bacteria attach to cell surface ie: N. gonorrhoeae Glycocalyx-slime assist with adherence to skin, heart valve, catheter ie: streptococcus mutans- plaque on teeth Virus-small No organized cell structure, virus can infect virus, protein coat (capsid) surrounds core, protect nucleic acid(DNA or RNA) and attach to host cell Lipo protein envelop- derived from host cell plasma membrane ie: HIV
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  • Fall '15
  • david,mary

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