-
- Extracellular hyaline
- - homogenous glassy, pink appearance (H & E)
- - old scars may appear hyalinized
- - walls of arterioles may become hyalinized- deposition of BM material
-
- Hyaline accumulation
- - staining with PAS and diatase digestion(hydrolyzing glycogen)
- - hyaline droplets are distinguishable as little pink droplets
-
- Excessive IC deposits of glycogen
- - abnormality in glucose or glycogen metabolism
- - Best carmine stains for glycogen (rose to violet color)
- - clear vacuoles within cytoplasm
- - fixed with absolute alcohol
-
- Glycogen in renal tubules seen in DM (H & E stain)
- - with DM glycogen found in renal tubular epithelial cells, liver, heart muscle and beta cells of pancreas
-
glycogen storage disease stained with PAS
-
pigment (carbon) deposition from anthrocosis or air pollution
-
- Lipofuscin deposition (yellow-brown granule)
- - endogenous, insoluble wear and tear pigment
- - telltale sign of free radical damage
- - not injurious to cell or function
- - liver and heart of aging patients
- - also seen in severe malnutrition and cancer cachexia
-
- Hemosiderosis
- -IC Fe accumulation
- - Seen in increase Fe intake, hemolytic anemia, repeated blood transfusions (beta- Thal patient)
-
Prussian blue stain of hemosiderosis
-
- Psammona bodies
- - dystrophic calcification that may form in papillary cancers
- - IC, EC or both locations
-
- Heterotopic bone
- - dystrophic calcification
- - IC, EC or both
- - basophilic, amorphous, granular, sometimes clumper appearance
-
- Metastatic calcification of the lung
- 4 principal causes of hypercalcemia
- - increased PTH - destruction of bone tissue
- - vit D related issue - renal failure
-
Major components of acute inflammation
- - vasodilation(histamine & NO)=>increased blood flow
- - leakage from microvasculature (exudate= plasma+proteins)
- - leukocyte immigration (mostly n0)
-
endothelial injury
- - occurs in arterioles, capillaries and venules
- - caused by burns and some microbial toxins
- - rapid and may be long lived (hours to days)
-
leukocyte-mediated vascular injury
- - in venules and pulmonary capillaries
- - associated with late stages of inflammation
- - long lived
-
increased transcytosis
- occurs iin venules
- induced by VEGF
-
- Lymphangitis
- inflammation of lymphatics
- red streaks seen clinically near skin wound
-
- Lymphadenitis
- painful inflammation and enlargement of draining lymph nodes
- hyperplasia of lymphoid follicles
- increased lymphocytes and macrophages
-
-
n0 migration thru blood vessels
- 1- rolling= P-selectin, E-selectin, (enodthelial expressed) 2- integrin activation by chemokines= proteoglycan
- 3- stable adhesion- integren:ICAM-1
- 4- diapedisis- PECAM-1(CD31)
-
- L- n0 inflammatory infiltrate seen early in inflammation
- M- mononuclear(lymphocytes and monocytes) seen later
-
bactericidal/permeability increasing protein
- binds bacterial endotoxin
- important in defense against some G- bacteria
-
alternatively activated macrophages
- important in tissue repain (arginase, proline, polyaminases and TGF-beta
- important in resolution of inflammation (IL-10, TGF-beta)
-
abscess
- always neutrophils
-
prostacyclin (PGl2)
- causes vasodilation
- inhibits platelet aggregation
cell derived mediator
-
Thromboxane A2 (TXA2)
- causes vasoconstriction
- promotes platelet aggregation
cell derived mediator
-
PGD2 and PGE2
- vasodilation
- increased vascular permeability
cell derived mediator
-
Lipoxin- LXA4 and LXB4
inhibits neutrophil adhesion and chemotaxis
-
-
Leukotriene B4 (LTB4)
- vasoconstriction
- bronchospasm
- increased vascular permeability
-
NO
cell derived
- inhibits cellular component of inflammatory response
- microbicidal
- inhibits leukocyte recruitment
- inhibits many features of mast cell-induced inflammation
- causes vasodilation
- reduced platelet aggregation and adhesion
-
PAF
cell derived
- vasoconstriction and bronchoconstriction
- vasodilation and increased vascular permeability at low concentrations
- increased WBC adhesion to endothelium
- chemotaxis, degranulation and oxidative burst
- boosts eicosanoid synthesis
-
LAP stain
- leukocyte ALP staining
- differentiates between leukomoid and leukemia
- LAP+= leukomoid
- leukemia cells are in arrested development
-
chronic inflammation characteristics
- infiltration with mononuclear cells (m0, lymphocytes, plasma cells)
- tissue destruction (induced by offending agent and inflammatory cells)
- healing by connective tissue replacement of damaged tissue (angiogenesis and scarring)
-
- Plasma cell
- Russel bodies present (RER and proteins
-
- Eosinophil
- IgE mediated immune reaction
- helmith/parasitic infections
- granules contain major basic protein
- causes lysis of mammalian epithelial cells
- contribute to tissue destruction in allergies
-
- serous inflammation
- blister from burn or viral infection
-
- caseous granulomaclassic TB granuloma with central caseous necrosis surrounded by mutliple Langerhan cells, epitheloid cells and lymphocytes
- - seen in TB, syphillis and cat-scratch disease
-
- non caseous granuloma
- - leprosy, sarcoidosis and Chrons
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