Immunopathology LAB Flashcards
(11 cards)
Allergic rhinitis - nasal polyp: what can cause this? What changes are seen? (8)
Cause: type I hypersensitivity reaction, chronic -> tissue remodeling
Changes:
- -Virtually all infiltrating cell types found, spread apart over a significant area
- -Large masses of jelly-like hypocellular tissue (proteinaceous fluid - ECM proteins, no collagen)
- -Many glands
- -Hazy blue areas around glands = inflammatory cells
- —Red cells = eosinophils (NOT RBCs)
- —Plasma cells (have perinuclear hoff) -> IgE
- —Lymphocytes (round, dark nuclei; no visible cytoplasm)
- —Background = loose, watery, pinkish material (laid down by fibroblasts)
Rheumatic fever, heart: what can cause this? What changes are seen? (4)
Cause: type II hypersensitivity reaction -> damage to myocardium secondary to antibodies binding
Changes:
- -Lymphocytes, MOs, other inflammatory cells invading myocardium
- —MOs look very clear, lots of cytoplasm
- -Aschoff bodies: relatively indistinct; myocardial cells killed off and replaced by MOs -> giant cells
- -Nodular, hazy blue areas of inflammation
Atrophic gastritis, stomach: what can cause this? (2) What changes are seen? (4)
Cause: type II hypersensitivity -> autoimmune metaplastic atrophic gastritis - body creates Abs against products made by parietal cells -> kills parietal cells -> inflammation
–Also get molecular mimicry between H. pylori antigens and mucosa of stomach
Changes:
- -Very thin stomach wall! 2-3mm (like paper)
- -Intestinal metaplasia (looks like colon) - tons of mucous-secreting glands
- -No parietal cells or chief cells
- -Tons of inflammation in glands: lymphocytes, some neutrophils
Glomerulonephritis, crescentic, kidney: what can cause this? (2) What is a crescent? What changes are seen? (6)
Cause: usually caused by an immune reaction, either type II (anti-glomerular-basement-membrane antibody, Goodpasture’s disease) or type III (antigen-antibody complex deposition; many diseases)
Crescent = proliferation of epithelial cells lining Bowman’s space, push glomerulus out of the way and crush it
Changes:
- -Glomeruli have crescents growing into them
- —Proliferated epithelial cells with nuclei and white space around them
- —Glomeruli themselves tiny, hypereosinophilic, hypercellular
- -Protein, possibly red cells (from leakage of glomeruli) in tubules
- -Tubular cells have hypereosinophilia
- -Occasional neutrophils in interstitium
Chronic thyroiditis: what can cause this? What changes are seen? (3)
Cause: Hashimoto’s thyroiditis
Changes:
- -Lymphoid follicles seen in thyroid
- -Lymphocytes (lots, in germinal centers), plasma cells, macrophages -> chronic inflammation
- -Thyroid follicles infiltrated and destroyed by lymphocytes
Rheumatoid arthritis, synovium: what can cause this? What changes are seen? (3)
Cause: autoimmunity
Changes:
- -Synovium thickened, thrown up into villi (villous proliferation)
- -Scar tissue deposition
- -Lots of inflammatory cells beneath thin synovial layer (lymphocytes, plasma cells, highly activated fibroblasts)
Polyarteritis, liver and kidney: what can cause this? What changes are seen? (3)
Cause: type III hypersensitivity -> deposition of immune complexes in muscle layers of walls of medium to small sized muscular arteries -> complement damages tissue -> neutrophils infiltrate and cause lots of damage -> necrosis, thrombosis, scarring/obliteration of normal blood vessel
Changes:
- -Inflammatory infiltrate in media of vessels - smooth muscle layers being killed
- -Lumens occluded (or almost occluded) by thrombosis or other
- -Fibrin deposition (fibrinic necrosis)
- -Often -> major infarction -> necrosis
Transplanted kidney - acute rejection: what can cause this? What changes are seen? (6)
Cause: mediated by lymphocytes, takes weeks to a year
–Active ongoing damage to interstitium, tubules, and blood vessels -> scarring
Changes:
- -Inflammation everywhere (some aggregates, some not) - almost exclusively lymphocytic
- -Blood vessels can be specifically involved: walls attacked/damaged, lumen compressed
- —Lymphocytes in wall and in interstitium
- —Endothelium damaged or gone
- -Interstitium edematous, tubules far apart
- -Tubules infiltrated and targeted by lymphocytes -> scarring, destruction
Lupus erythematosus, heart: what can cause this? What changes are seen? (2)
Cause: systemic lupus erythematosus
Changes:
- -Small vessels destroyed -> microthrombi formation/fibrin deposition (pink spots, surrounded by purple inflammatory cells)
- -Larger vessels: light purple because of fibrinoid necrosis and inflammatory infiltration, lumen destroyed
Lupus erythematosus, kidney: what can cause this? What changes are seen? (3)
Cause: systemic lupus erythematosus -> immune complex deposition
Changes:
- -Diffuse thickening of basement membrane of glomeruli because of deposition of immune complexes
- —Glomeruli look a bit thicker than they should be (“wire loop”)
- —Best seen in glomeruli cut in cross section
Amyloidosis, kidney and liver: what can cause this? What changes are seen? (3)
Cause: varied, amyloid deposition
Changes:
- -All glomeruli extremely distorted, unrecognizable, from amyloid deposition in glomeruli
- -Tubules filled with proteinaceous material
- -Amyloid: waxy, homogeneous; compresses normal tissue elements
