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Path 4 Hemo


severe and generalized edema w/ widespread subcutaneous tissue swelling Anasarca
protein POOR fluid from increased hydrostatic pressure or reduced plasma protein. Due to Heart/Kidney/Liver Fails and some malnutritions Transudate
protein RICH from inflamm edema from increased vascular permeability Exudate
active process in which arteriolar dilation leads to increased blood flow. Red erythema Hyperemia
passive process resulting from reduced outflow of blood from tissue. Dusky reddish blue cyanosis. Hemosiderin-laden macrophages (heart failure cells in alveoli). Nutmeg liver. Congestion
extravasation of blood into the extravascular space. Hematoma, petechiae (^ intravasc press, thrombocytopenia, defective platelets), purpura, ecchymoses (hemoglobin [red-blue] to bilirubin [blue-green] to hemosiderin [gold-brown]) Hemorrhage
GpIIb-IIIa receptors form bridges between platelets: deficiency = Glanzmann thrombasthenia
endothel injury, stasis (venous) or turbulent (can cause endothel injury) blood flow, and hypercoag of blood (point mutations in factor V and prothrombin genes are most common inherited causes Virchow’s triad
unfractionated heparin induces antibods that recognize complexes of heparin and platelet factor 4 -> platelet activation, aggregation and consumption -> prothrombotic state even w/ heparin admin and low platelet counts. LMW is better Heparin Induced Thrombocytopenia (HIT)
thromboses, repeated miscarriages, cardiac valve vegetations, thrombocytopenia. Hypercoag state d/t antibody binding. both a. and v. thrombi grow toward heart. lines of Zahn (distinguish antemortem thrombosis from clots that are post) Antiphospholipid Antibody Syndrome
thrombi in heart chambers or aortic lumen Mural thrombi
thrombi on heart valves Vegetations
Most common arterial thrombi occlusion sites coronary, cerebral, and femoral arteries
tumor inflamm and coag and procag factor release -> thromboembolism Trousseau Synd
sudden onset of widespread fibrin thrombi in microcirculation -> consumption coagulopathy Disseminated Intravascular Coagulation (DIC)
detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin -> ischemic necrosis (infarct) of downstream tissue. Embolism
Most PEs originate from ... leg DVTs. - Saddle embolus. Sudden death, R heart fail (cor pulmonale), cardiovasc collapse occur when 60% or more of pulm circ obstructed.
Most Systemic Thromboembolisms arise from ... intracardiac mural thrombi. - Major sites of embolization are LEs and brain.
occurs in 90% of severe skeletal injuries (mostly asymp). Fat embolism
from decompression sickness (sudden decrease in atmospheric press, the bends) Air embolism
venous occlusions, loose tissues where blood can collect, dual circulations, previously congested sluggish venous outflow, flow re-established to site of previous arterial occlusion and necrosis. Red infarcts
arterial occlusions in solid end organs (heart, spleen, kidneys) Infarcts are wedge shaped, occluded vessel at apex and periphery of organ forms base. White infarcts
characterized by systemic hypotension due to reduced cardiac output or reduced effective circulating blood vol. -> impaired tissue perfusion and cell hypoxia. Shock Cardiogenic– from low cardiac output dt myocardial pump fail Hypovolemic– from low cardiac output dt loss of blood or plasma vol Septic– dt vasodilation and peripheral pooling of blood as part of a systemic immune rxn to bacterial or fungal infec
most causes of death in intensive care units. Most frequently triggered by gram-pos bacteria. Septic Shock
reflex compensatory mechs maintain organ perfusion (sympathetic stimulation causes: tachycardia, periph vasoconstrict, renal conservation of fluid) Nonprogressive stage of Shock
tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances (excessive lactic acid lowers tissue pH) Progressive stage of Shock
cell and tissue injury too severe to survive even w/ hemodynamic correction Irreversible stage of Shock
Created by: Jakphooey