LECOM Path Ch 6 Immunology
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| Type I hypersensitivity Immune mechanism | Production of IgE-> crosslink on mast cell FcR-> releases histamine, enzymes, heparin
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| Type I hypersensitivity causes | edema, SM contraction, vasodilation, increased mucus; later recruits inflammatory cells
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| Prototypical Type 1 hypersensitivity reaction Disorder | Anaphylaxis; atopic bronchiole asthma
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| Lipid mediators released in Type I HSR | PAF, PGD2, LTB4, C4, D4
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| Mast cell degranulation can be activated by | IgE, C5a, C3a, IL-8, temperature, adenosine, codeine/morphine
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| Type I HSR late phase consists of | eos, neuts, basos, monos, CD4+ T-cell infiltrates
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| This IL helps differentiate T-cell into TH2 cell | IL-4
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| TH2 cells release these 3 IL’s, and their actions | IL-4: Induce B-cell IgE switch, and TH2 cell growth; IL-5: develop and activate eosinophils; IL-13: enhances IgE and mucus production
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| These are the two most potent vasoactive and spasmogenic agents known | LTC4 and LTD4
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| This is the most abundant mmediator produced by mast cells | PGD2
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| LTB4 does what? | chemotactic for neuts, eos, and monos
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| Most potent eosinophil activating cytokine known | IL-5
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| Atopic individuals have increased what compared to normal people? | increased serum IgE levels and increased levels of IL-4 producing TH2 cells
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| Loci associated with atopic individuals | 5q31; IL-3,4,5,9,13, and GM-CSF
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| Type II HSR Immune Mechanism | Produce IgG or IgM-> bind cell surface Ag or tissue->target cell destruction by compliment or FcR
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| 5 Type II HSR Prototypical Disorders | Autoimmune hemolytic anemia, Goodpasture’s Syndrome, Acute Rheumatic Fever, Myasthenia gravis, Graves Disease
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| Type II HSR activates the compliments system by what pathway and produces what 2 byproducts, and what do they do? | Classic; C3b/C4b; deposit on cell surface, opsonizing the cell
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| IgG Ab on a cell causes and leads to what? | opsonization; phagocytosis
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| What is ADCC? | antibody dependent cellular cytotoxicity
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| Inflammation in Ab and Ab-complex HSR (II/III) is due to ____ and _____ | complement and Fc receptor dependent reactions
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| Type III HSR has a propensity to attack | vessel walls
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| 3 steps of Type III HSR are | formation of complex in circulation; deposition in tissue; inflammatory reaction
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| Formation of Ab-Ag complex usually takes | 1 week
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| The most pathogenic complexes are: what size? Formed with excess Ab or Ag? | medium sized and formed in slight Ag excess
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| Clinical Sxs of Type III HSR usually present how long after injection? And what are they? | 10 days; fever, urticarial, joint pain, lymphadenopathy, proteinuria
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| What can be measured to monitor the activity of Type III HSR diseases? | C3 levels; get used up during episodes
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| Morphology of Type III HSR: | acute necrotizing vasculitis; many neuts; “fibrinoid necrosis”; IF stain shows lumpy granular deposits of Ig and compliment
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| Localized area of necrosis on skin, immune complexes seen in vascular beds. Name of reaction? | Arthrus Reaction
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| Type IV HSR is mediated by which cells and after what? | CD4+ T-cells: environmental and self-antigens; CD8+ T-Cells: post viral infection
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| CD4+ T-cell HSR are also called what ? | DTH- Delayed Type Hypersensitivity
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| TH1 cells mediated disease is dominated by what cells? | Macrophages
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| TH17 cell mediated disease is dominated by what cells? | neutrophils
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| Upon recognizing Ag on APC’s CD4+ cells secrete what? And it does what? | IL-2: autocrine growth factor
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| What must APCs produce to induce TH1 cell differentiation? What also promotes TH1 cell growth? | IL-12; IFN-γ
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| What must APCs produce to induce TH17 cell differentiation? What also promotes TH17 cell growth? | IL-1, IL-6, IL-23; w/ TGF-β
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| TH1 cells mainly secrete what? | IFN-γ
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| What cell does IFN-γ affect in Type IV HSR? What does it do? | macrophages; altered to express more MHC-II
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| What do altered, activated macrophages in TH1 cell meditated Type IV HSR secrete? | TNF, IL-1, IL-12
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| TH17 cells secrete mainly what? | IL-17, IL-21, IL-22
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| What does IL-17 and IL-22 do in TH17 cell mediated Type IV HSR? | attract neutrophils and monocytes
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| What type of HSR is contact dermatitis? | Type IV
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| Morphologically, what is characteristically seen in DTH-SR? What type of cells, and where? | mononuclear (CD4+) and macrophages, perivascular cuffing; venules with endothelial hypertrophy
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| With chronic disease, what is seen after 2-3 weeks? What is the predominant cell? | granuloma; epitheliod cell , which is a transformed macrophage
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| Two preformed mediators involved in CD8+ cell mediated killing? | perforins and grannzymes
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| Mechanism of CD8+ mediated cell killing: | CTls recognize infected cell w/ class I MHC-> release perforin and granzymes which are endocytosed-> perforin releases granzymes-> granzymes cleave caspases->caspases induce apoptosis
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| Developing T cells are found where? | thymus
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| Developing B cells are found where? | bone marrow
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| What is responsible for developing peripheral self-tissue antigens for thymic APCs to show T cells? | AIRE autoimmune regulator protein
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| If a T-cell has a high affinity for self-antigens what 2 things can happen? (ideally) | negative selection or if it is CD4+ can become a Treg Cell
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| If a B-cell strongly recognizes a self-antigen, ideally, what 2 things can happen? | induce receptor editing or apoptosis
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| Example of T-cell Second Signal and 2 costimulators | CD28; B7-1 and B7-2
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| 2 inhibitory receptors involved in T-cell anergy | CTLA-4 and PD-1
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| Peripheral Tolerance:? Name 3 ways and which cells are involved. | Anergy: T-and B cells; Suppression byT-regulatory cells; activation induced cell death of CD4+ T-cells and B cells
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| T-regs have what 3 things | CD25, IL-2 receptor, Foxp3
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| Name of severe autoimmune disease that results from Foxp3 mutations | IPEX
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| Polymorphiisms in CD25 are linked to what disease | Multiple Sclerosis
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| What is CD95 | Fas
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| What cells display Fas ? | many cells
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| What cells display Fas-L? | Activated T-cells
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| Human disease caused by Fas mutation? | autoimmune lymphoproliferative syndrome
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| 3 “immune privileged” sites | Testes; brain; eye
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| Genes most contributory to autoimmune predisposition | HLA
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| Polymorphisms in this gene are associated with RA, DM type 1, and others. Most frequently implicated mutations | PTPN-22
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| Polymorphisms in NOD-2 contributes to what disease | Crohn disease
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| Mutations in these two genes are associated with MS and others | IL-2 receptor(CD25); IL-7 receptor α-chain
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| Name associated with new Ag from inside tissues not normally scanned by the immune system having lymphs that now recognize and attack these self-Ag | epitope spreading
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| Predominant damage caused by macrophages results from mediation by these cells | TH1 cells
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| Predominant damage caused by neutrophils and monocytes results from mediation by these cells | TH17 cells
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| Population SLE is most common in: sex? Age? Race? | black and Hispanic women age 20-30
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| Most common Ab in SLE | Generic ANA
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| 2 Most diagnostic SLE Ab? | Anti-dsDNA and Smith Ag
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| Some SLE Pt’s will have a false positive in serology testing for what disease? What is the Ab causing it? | Syphilis; anti-phospholipid-β2-glycoprotein complex
Pt has hypercoagable state, multiple spontaneous miscarriages; focal cerebral ischemia w/ anti-dsDNA Ab Dx? w/o anti-ds DNA Ab or ANA Dx?
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| Pt has Scl-70 and Anticentromere Ab. Dx? | Diffuse Systemic Sclerosis aka Scleroderma
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| Anticentromere Ab is specific for what Dx? | CREST
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| SS-A (Ro) and SS-B(La) Ab are specific for what Dx? | Sjogren Syndrome
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| Antihistone Ab is very specific for what Dx? | drug induced Lupus
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| Ab toward for histidyl-tRNA synthase; Jo-1 Ab is specific for what Dx? | Inflammatory myopathies
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| 5 classes of SLE nephritis in order | Minimal Mesangial; Mesangial Proliferative; Focal Proliferative; Diffuse Proliferative; Membranous
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| Distinguish Class III vs IV | III <50% glomeruli are involved; IV is the most severe
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| Specific morphology of Type IV SLE nephritis | >50% glomeruli; crescents fill Bowman’s Space; hematuria, proteinuria, HTN, Renal insufficiency
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| Pt with SLE and diffuse thickening of renal capillary walls has “Wire Loop”. What does this tell you? | Usually Type III or IV and ACTIVE DISEASE
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| If you expect SLE and Pt has other Sxs. What would the malar skin look like? | vacuolar degeneration of basal epidermal layer, complexes at dermalepidermal junction
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| Autopsy: vegetations on heart valve leaflets. SLE vs RA | SLE vegetations are larger, and on all surface of the leaflet vs on closing line in RA
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| Spleen in SLE Pt | Splenomagaly, capsular thickening, onion skin arteries
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| MCC of death in SLE | renal failure with intercurrent infection
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| 23yo BF Pt with skin plaques with raised erythematous boarders on face and head. No systemic involvement. ANA positive, anti-dsDNA negative, anti-histone negative. Dx? | Chronic Discoid Lupes Erythematosus
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| 23yo BF Pt with widespread erythematous skin rash, hematuria, pain in fingers and feet with no deformity, anti-SS-A positive, anti-histone negative. Dx? HLA genotype? | Subacute Cutaneous Lupus Erythematosus; HLA-DR3
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| 23yo BF Pt has bilateral feet and hand pain with no deformities, fever. Normal neuro and renal. Pt is a missionary returning from Africa. Anti-dsDNA Negative. Dx? Serology? HLA type? | Drug Induced Lupus Erythematosus 2ndary to isoniazid; anti-histone positive; HLA-DR4
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| 2 most common Sxs of Sjogrens | xerostomia, keratoconjuctivitis sicca (dry eyes)
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| Suspect Sjogren’s Pt’s also have? | RA
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| Sjogren’s: Decrease in tears and saliva are from | lymphocytic infiltrate and fibrosis of the lacrimal and salivary glands
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| 4 Ab in Sjogren’s | ANA; SS-A; SS-B; Rheumatoid factor (anti-self IgG)
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| Most important Ab in Sjogren’s, high levels predispose to earlier onset, longer duration, extraglandular involvement | anti SS-A
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| 2 viruses possibly associated w/ Sjogren’s. 1 that can mimic Sjogren’s. | EBV, HCV; HTLV-1 can clinically and pathologically mimic
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| Earliest morphologic change in Sjogren’s | periductal/perivascular lymphocytic infiltration
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| Mechanism: Progression of Damage in Sjogren’s | lymph infiltrate becomes extensive->follicles w/ germinal cells in large salivary glands-> ductal epithelial hyperplasia->acini atrophy->fibrosis-> atrophy->steatotic change
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| Sjogren’s presents most commonly in? | 50-60yo women
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| Renal Changes in Sjogren’s vs SLE | no glomerular lesions in Sjogren; tubulointerstitial nephritis w/ renal tubular acidosis
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| Who is more likely to experience extraglandular Sxs? What are they? | High SS-A titer; diffuse pulmonary fibrosis, peripheral neuropathy, tubulostitial nephritis
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| Even with SS-A and SS-B, and ANA, what is done to confirm dx? | lip biopsy
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| Difference in Diffuse vs Limited Scleroderma | Diffuse: Widespread skin involvement, early visceral involvement, rapid progression
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| What can Pt’s with Limited Scleroderma develop and what is a marker for it? | CREST syndrome; anti-centromere Ab
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| Ab associated with Diffuse Scleroderma | everyone has ANA; anti Scl-70 (DNA topoisomerase)
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| What is associated with limited scleroderma and anti-centromere Ab? Sxs? | CREST syndrome; Calcinosis, Reynaud’s phenomenon, Esophageal dismotility, sclerodactyly, Telangiectasia
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| Early morphological hallmark of Scleroderma | microvascular disease; intimal proliferation of digital arteries; capillary dilation and leaking
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| 2 measurable levels pointing to endothelial and platelet activation in scleroderma | increased vWf; increased circulating platelet aggregates
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| In addition to vascular injury, what else adds to the pathogenesis of scleroderma | fibroblast activation
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| Change seen in vascular smooth muscle in Scleroderma | increased adrenergic receptors
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| 4 prominent areas of change in systemic scleroderma | Skin, alimentary tract, MS system, kidney
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| Skin changes in systemic scleroderma | strophy starts distally moves proximally from fingers; perivascular CD4+ infiltrates; fibrosis of the dermis with “drawn mask face”, cutaneous ulceration, autoamputation of fingers
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| Most prominent changes in Ailimentary tract in systemic scleroderma | lower 2/3 of esophagus develops “ruber hose inflexibility; LES dysfunction, GERD; loss of micro/villi in small bowel=malabsorption
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| Fibrosis of joints occur in Scleroderma but what differentiates it from RA? | Joint destruction is rare
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| Kidney changes in scleroderma resemble what other process? What differentiates them | malignant HTN; Scleroderma changes (mucin/collagen-ous intimal thickening only of 150-500um vessels
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| Pulmonary changes in Scleroderma is indistinguishable from this process? | Idiopathic Pulmonary Fibrosis
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| MC Systemic Scleroderma presents in? distinguishing feature | 50-60yo BF; cutaneous change
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| This is the first sign of Systemic Scleroderma in 70% of people. | Reynaud’s Phenomenon
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| Rapid deterioration of Pt with Systemic Scleroderma, resulting in death. MCC? | Malignant HTN with fatal renal failure
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| Pt was told she had symptoms of SLE. Had mild renal involvement that resolved when you gave her corticosteroids. High titer of Ab to ribonucleoprotein particle (RNP)- containing U1 ribonucleoprotein. Dx? And 2 serious complications | Mixed Connective Tissue disease; pulmonary HTN, Renal disease like systemic sclerosis
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| APC involved is the Pt’s: Direct or Indirect Pathway of Tissue Rejection? | Indirect
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| APC involved is in the graft: Direct or Indirect Pathway of Tissue Rejection? | Direct
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| Activated CD8+ cells that can directly injure graft tissue can only be activated in the Direct or Indirect Pathway of Tissue Rejection? | Direct
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| Which is the major pathway of acute cellular rejection, Direct or Indirect Pathway of Tissue Rejection? | Direct
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| Which pathway is the major pathway involved in chronic rejection, Direct or Indirect Pathway of Tissue Rejection? | indirect
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| Rejection of graft that happens in minutes or hours after transplant? What is the causative agent? What branch of immunity is involved? | Hyper acute rejection; pre-formed antidonor Ab; humoral immunity
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| Acute humoral rejection targets what, predominantly for injury in the graft | graft vasculature
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| Upon removal of a rejected kidney there is Ig and Compliment in vessel walls, endothelial damage, neutrophils, and platelet + thrombin thrombi. Dx? | Hyperaccute rejection
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| Rejection of kidney in first month. Interstitial and glomerular and peritubular mononuclear cells, CD4 and CD8+; focal tubular necrosis and vascular endothelial cell injury. Dx? | Acute Cellular Rejection
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| Reason recognizing Acute Cellular Rejection with no Humoral Rejection is important. | Treatment with immunosuppression is very well tolerated and has good response
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| Rejection of kidney in first month. Thickened vascular intima with fibroblasts, myocytes, and foamy macrophages; small areas of renal cortical infarction and atrophy. Neutrophillic infiltrates. Dx? | Acute humoral rejection
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| What can you find that is a strong correlation to Humoral rejection, that will be deposited in allografts? How is it formed? What can you treat with if this is found? | CD4d; classical pathway activation of the compliment system; treat with B-cell depleting agents
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| Rejected kidney. Obliterative intimal fibrosis in cortical arteries, renal ischemia, shrunken parenchyma, duplication of glomerular basement. Interstitial plasma cells and eosinophils Dx? | Chronic Rejection
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| Mainstay in immunosuppressive drugs | cyclosporine
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| MOA of cyclosporine | blocks NFAT; prevents cytokine production namely IL-2
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| 3 locations of common Acute GVH attacks and Sxs | skin epithelia, desquamating rash; liver, small bile duct destruction w/ jaundice; ulceration of the intestine, bloody diarrhea
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| 4 locations of common Chronic GVH attacks and Sxs | skin, destruction of skin appendages and fibrosis; esophageal strictures, liver, cholestatic jaundice; lymphnodes, depletion of lymphocytes
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| Step taken to mediate GVH? Adverse effects of this step? | deplete Donor T-cell population prior to transplant; EBV related B-cell lymphoma and graft rejection increases
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