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Hemodynamic Disorder

USCSOM: Pathology: Hemodynamic Disorders

QuestionAnswer
What is transudate? protein-poor edema that enters interstitial tissue
What are the 5 etiologies of edema? increased hydrostatic pressure; reduced plasma oncotic pressure; lymphatic obstruction; sodium retention; inflammation
What is the most likely cause of generalized increase in hydrostatic pressure? Congestive Heart Failure
What is the likely cause of reduced plasma oncotic pressure? loss or reduced synthesis of albumin
What is a likely cause of sodium and water retention? renal failure
What is hydrothorax? fliud in pleural space
What is ascites? fliud in peritoneal space
What is anasarca? severe generalized edema
What are the clinically important sites of edema? lung and brain
What are the clinical manefestations of pulmonary edema? dyspnea, cough, tachycardia, crackles, neck veins
What are the localized causes of brain edema? abscess, neoplasm, trauma
What are the generalized causes of brain edema? encephalitis, hypertensive crisis, trauma, obstruction of venous outflow
What is hyperemia? arteriolar dilation resulting in increased flow of blood to tissue
What results in chronic passive congestion? cellular degeneration or death; capillary rupture, small foci; hemosiderin laden macrophages
What is nutmeg liver? hepatocellular death and hemorrhage with hemosiderin laden macrophages
What are the three classifications of hemorrhage from smallest to largest? petachiae, purpura, ecchymosis
What is hemostasis? the balance of clotting and fluid state of blood
What are the three main general components to hemostasis? vascular wall, platelets, coagulation cascade
What is the first reaction to vascular injury? vasoconstriction
What are antithrombotic mechanisms of endothelium? barrier to subendothelium, prostacycling (PGI2) and NO, ADPase, heparin, thrombomodulin, tPA
What are prothrombotic mechanisms of the endothelium? vonWillebrand factor, makes tissue factor, tPA inhibitor
What two things do von Willebrand factor link? subendothelium to glycoprotein Ib receptors
What factors are secreted after platelet adherence? Calcium, ADP and thromboxane, Platelet factor 4
What does platelet factor 4 do? binds heparin inactivating it
What links platelets via GPIIb-IIIa? fibrinogen
What are the two main fxns of tissue factor? activate X and Xa, XI and XIa
What cements the platelets together into a clot? fibrin
What converts fibrinogen to fibrin? thrombin
What coagulation factors are clinically significant? V,VII,VIII,IX,X,XI, prothrombin, fibrinogen
What is prothrombin time? aka PT; extrinsic clotting cascade
What coagulation factors are involved in extrinsic clotting cascade? VII, X, V, II, fibrinogen; all require vit K
What is partial thromboplastin time? PTT; intrinsic clotting cascade
What factors are involved in the intrinsic clotting cascade? all except VII, XIII
What is Hageman factor? Factor XII in clotting cascade
What initiates the external clotting cascade? Tissue factor (thromboplastin)
What are the main anticoagulants? antithrombin, protein c, protein s, plasmin
What is the action of antithrombin? inactivates IXa, Xa, XIa, XIIa
What is the action of Protein C and Protein S? inactivate Va and VIIIa
What is the action of plasmin? breaks down fibrin
What substances can activate plasminogen? urokinase, tPA, streptokinase
What substances restric plasmin activity:? alpha-2 antiplasmin (free plasmin); plasmin activator inhibitor (PAI) inhibits tPA
What is DIC? disseminated Intravascular Coagulation
How is DIC measured? D-DIMER; plasmin-cleaved insoluble cross-linked fibrin
What is Virchow's Triad? factors favoring thrombosis; endothelial cell dmg, hypercoagulability, stasis
What is the most common genetic hypercoagulable state? factor V Leiden
What is Factor V Leiden? glut substitute for Arg; makes V resistant to degradation by protein C
What is coumarin Necrosis? a hypercoagulable state induced by giving coumarin to patients with low protein C
What is Heparin-induced Thrombocytopenia? giving heparin induces release of IV resulting in a prothrombotic state
Antiphospholipid antibody syndrome? serum Ab against anionic phospholipids; hypercoagulable state; recurrent thrombi, miscarriages
What is Bernard-Soulier Disease? defect of platelet adhesion; Glycoprotein Ib
What is Glanzmann's Thrombasthenia? defect of platelet aggregation; glycoprotein IIb/IIIa
What is thrombotic thrombocytopenic Purpura Abs for von Willebrand factor cleaving protease
What is Hemophilia A? factor VIII deficiency
What is Hemophilia B? Factor IX deficiency
What is the most common bleeding disorder? von Willebrand's disease
What are lines of Zahn:? alternating bands of mostly fibrin and mostly RBC
What are characteristics of arterial thrombi? usually occlusive; grey-white and friable
What are some risk factors for venous thrombosis? CHF, trauma, Sx, Pregnancy, cancer
What is an embolism? detached intravascular solid,liq,gas; originate from a dislodged thrombus
What is a mural thrombi? arterial thrombosis in cardiac chambers from MI, plaque, anuerysmal dilation
What is a paradoxical embolism? emobolous originating in veins passes to systemic circulation
What causes fat embolism? sever skeletal injury; burns, long bone fractures, soft tissue trauma
What are the bends and the chokes? decompression sickness; gas bubbles in tissue and gas emboli in lungs
What is amniotic fluid embolism? fetal amniotic fluid in maternal circulation; high mortality rate
Describe a Red Infarct. venous occlusions; dual circulation tissue; tissues with previously sluggish flow
Describe a white infarct. arterial occlusions in solid organs; limitation of blood flow; ischemic necrosis
What is the dominant histologic characteristic of post-infarction healing pattern? ischemic coagulative necrosis
What is a septic infarct? origin of embolus is infected tissue; usually from growth on heart valves
What are the five classifications of shock? cardiogenic, hypovolemic, septic, neurogenic, anaphylactic
What are the five unifying features of shock? high intracellular Ca, intracellular H+, cellular and interstial edema, catabolic metabolism, inflammation
What are the stages of shock? nonprogressive stage, progressive stage, irreversible stage
What happens in the nonprogressive stage of shock? maintain BP and CO; reflexes are making up for deficit
Describ ethe progessive stage of shock. widespread tissue hypoxia, lactic acidosis, decreased urinary output
Describe the irreversible stage of shock. lysosomal enzyme leakage, decreased contractility, renal failure
What is cardiogenic shock? decreased CO with adequate volume; loss of 40% myocardium
How do you approach cardiogenic shock? give fluids, ionotrope, manage infarct
Describe hemorrhagic shock. extreme hypotension due to loss of volume
What are rosen's empiric criteria for dx of shock? ill appearance; HR>100; RR>22; base deficit <-5; urine output <.5 mL/kg/hr; hypotension>20min
What are some treatments for hemmorhagic shock? colloids, controlled fluid resuscitation
What are the clincal manifestation of SIRS? elevated temp, elevated HR, elevated RR, elevated WBC
What is the clincical signs of neurogenic shock? hypotension and bradycardia
Created by: jlellerm