| Question |
Answer |
| 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 |
mr. charles11
