Robbins Chapter 6 Morphology Flashcards
Principal morphologic manifestation of immune complex injury
acute vasculitis with necrosis of vessel wall and neutrophilic infiltration
Fibrinoid necrosis
necrotic tissue and deposits of immune complexes, complement, and plasma proteins
Fibrinoid necrosis morphology
smudgy eosinophilic area of tissue destruction
Immune complex morphology in the kidney
granular lumpy deposits of immunoglobulin and complement in immunofluorescence
electron-dense deposits along glomerular basement membrane in electron microscopy
Where are the most characteristic lesions from immune complexes deposited in SLE? (4)
blood vessels, kidney, skin, connective tissue
Blood vessel response in SLE
acute necrotizing vasculitis of capillaries, small arteries, and arterioles
What is arteritis characterized by in SLE
fibrinoid deposits in vessel walls
Blood vessels in chronic stages of SLE
fibrous thickening with luminal narrowing
Kidney response in SLE
glomerular lesions due to deposition of immune complex in basement membrane and glomerulus
6 patterns of glomerular disease in SLE
Class I glomerular disease in SLE
least common
minimal mesangial lupus nephritis
immune complex deposition in mesangium
Class II glomerular disease in SLE
Mesangial prolliferative lupus nephritis
characterized by mesangial proliferation
no involvement of glomerular capillaries
Class III glomerular disease in SLE
Focal lupus nephritis
involvement of fewer than 50% of all glomeruli
affected glomeruli exhibit swelling and proliferation with leukocyte accumulation
focal necrosis and crescent formation
red cell casts in urine
Class IV glomerular disease in SLE
Diffuse lupus nephritis - most common*
half or more of the glomeruli are affected
affected glomeruli show crescents that fill Bowman’s Space
thickening of capillary wall forming “wire loop”
proteinuria and hematuria
Class V glomerular disease in SLE
Membranous Lupus Nephritis
characterized by diffuse thickening of the capillary walls form deposition of subepithelial immune complexes
severe proteinuria or nephrotic syndrome
Class VI glomerular disease in SLE
Advanced sclerosing lupus nephritis
more than 90% of glomeruli are involved
Skin response in SLE
“butterfly” rash- erythema affects the face along the bridge of nose and cheeks
involved areas show vacuolar degeneration of basal layer or epidermis
deposition of Igs and complement along dermoepidermal junction
Joints response in SLE
nonerosive synovitis with little deformity
*makes it different from rheumatoid arthritis
Pericarditis and Serosal Cavity in SLE
inflammation of serosal lining
can be acute with fibrinous exudate
can be subacute with thickened and opaque
can be chronic fibrous tissue
Cardiovascular system response in SLE
valvular abnormalities of mitral or aortic valves
Libman-Sacks endocarditis and vegetations are large
Spleen response in SLE
splenomegaly, capsular thickening, follicular hyperplasia
“onion skin” lesions
Lungs response in SLE
pleuritis and pleural effusion
What can be tested in the bone marrow when diagnosing SLE?
LE bodies (hemotoxylin)
Morphology of Sjogren Syndrome
periductal and perivascular lymphocytic infiltration in salivary glands
ductal linings of epithelial cells show hyperplasia
can cause lymphoma
Results of lack of tears in Sjogren Syndrome
drying of corneal epithelium which becomes inflamed, eroded, and ulcerated
Results of lack of salvation in Sjogren Syndrome
oral mucosa may atrophy
inflammatory fissuring and ulceration
What is the main changing area in systemic sclerosis?
skin, alimentary tract, musculoskeletal system
Skin response in systemic sclerosis
diffuse, sclerotic atrophy
begins in fingers and then extends proximally to upper trunk and head/neck
atrophic changes in terminal phalanges
Histological skin in systemic sclerosis
edema and perivascular infiltrates containing CD4+
increased fibrosis
increased collagen
Alimentary tract response to systemic sclerosis
progressive atrophy and collagenous fibrosis replacement of the muscularis of esophagus and guy
Esophagus becomes like a “rubber-hose” inflexibility
Musculoskeletal response to systemic sclerosis
early stages- inflammation of synovium from hypertrophy and hyperplasia
later stages- fibrosis
Kidney response to systemic sclerosis
vascular lesions - interlobular arteries show thickening and deposits of collagen
proliferation of intimal cells
Lung response to systemic sclerosis
pulmonary vasospasm
pulmonary fibrosis
Heart response to systemic sclerosis
pericarditis with effusion, myocardial fibrosis and thickening of intramyocardial arterioles
3 classifications of rejection reactions
hyperacute, acute, and chronic rejection
Characteristics of hyperacute rejection
occurs within minutes or hours
cyanotic, mottles, flaccid
neutrophils accumulate
Characteristics of acute rejection
occurs within days of transplant
can be cellular mediated acute rejection
can be humoral mediated acute rejection
2 patterns of acute cellular (T cell mediated) rejection
tubulointerstitial patterns (type I)- tubulitis associated with tubular injury vascular patterns- endotheliitis- inflammation of vessels
Characteristics of acute antibody-mediated rejection
damage to glomeruli and small blood vessels
deposition of C4d
Characteristics of chronic rejection
4-6 months
dominated by vascular changes of intimal thickening, glomerulopathy, and peritubular capillaritis
