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HEMODYNAMIC DISORDER I. EDEMA -accumulation of fluids within the cells, interstitial tissues and body cavities -Transudate: caused by increased hydrostatic pressure or reduced plasma protein -Exudate: caused by increased vascular permeability NASAL POLYP -Non-neoplastic; inflammatory edema due to frequent irritation
Microsopically: Pseudostratified columnar epithelium with loose stroma infiltrated by inflammatory cells (eosinophils); edematous mucosa Gross: Fingerlike, Grayish, Polypoid, With fluid
II. HYPEREMIA AND CONGESTION HYPEREMIA- an active process in which arteriolar dilation leads to increased blood flow CONGESTION- a passive process resulting from reduced outflow of blood from a tissue ACUTE SUPPURATIVE APPENDICITIS (hyperemia)
SY 2011-2012
1
NUTMEG APPEARANCE
Microscopically: neutrophilic infiltration within muscularis DILATED CENTRAL VEINS, CENTRAL HEMORRHAGIC NECROSIS CHRONIC PASSIVE CONGESTION, LUNGS CARDIAC SCLEROSIS
Microscopically: Thickened alveolar walls (due to dilation of capillaries). - dilated blood vessels containing abundant RBCs. presence of protein rich edematous fluid.
PRESENCE OF FIBROSIS BREACHING BETWEEN THE CENTRAL ZONAL REGIONS II. HEMORRHAGE -extravasation of blood into the extravascular space ASPERGILLOSIS (with intra-alveolar hemorrhages)
HEMOSIDERIN-LADEN MACROPHAGES
IV. THROMBOSIS -pathologic coagulation of blood resulting in the formation of solid mass with a chamber of the heart or with the blood vessels -Virchows triad: endothelial injury, alterations in normal blood flow (turbulence, stasis), hypercoagulability MURAL THROMBUS
V. INFARCTION -an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage -Anemic (white) infarct: in arterial occlusion; in solid tissues; end arteries -Hemorrhagic (red) infarct: venous occlusion,in loose tissues, tissues with rich anastomosis RENAL INFARCTION
Histo: Focal necrosis; Necrosis of glomerulus Acidophilic tombstone HEMORRHAGIC INFARCTION, LUNGS
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