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Robbins Path CH4
Pathology Robbins Chapter 4 Hemodynamic disorders, Thromboembolic Disease, Shock
| Question | Answer |
|---|---|
| DIC | Disseminated Intravascular Coagulation. widespread fibrin microthrombi in microcirculation. |
| DIC causes paradoxical ______ | DIC can cause uncontrollable bleeding via "consumption coagulopathy". Consumption of platelets and coagulation factors |
| embolism | any intravascular solid, liquid, or gas |
| paradoxic embolism | emboli passes through heart wall defect to go to circulation (rather than lungs) |
| Percent of pulmonary embolisms that are clinically silent? | 60-80% |
| What is effect of pulmonary embolism on large/medium/small pulmonary arteries? | Large: If >60% of blood to lungs blocked: death. Medium artery PE: pulmonary hemorrhage (not infarct b/c of collateral blood) Small artery: get incorporated into wall or leave a fibrous web. Small end-arteriole block may infarct |
| vegetation | abnormal growth. often associated with endocarditis. can be made of fibrin/platelets. often labeled infective or non-infective. can be root cause of thrombi |
| second most common cause of embolism? | fat embolism |
| Most common cause of fat embolism | occur in 90% of severe skeletal injuries. |
| Signs of fat embolism | Usually 1-3 days post injury, sudden tachypnea, dyspnea, tachycardia. 20%-50% of patients have diffuse petechial rash and may have neurological symptoms. |
| Thrombocytopenia | any disorder in which there is an abnormally low amount of platelets |
| caisson disease | persistent gas emboli in poorly vascularized portions of the skeleton (heads of femurs, tibia, humeri) lead to ischemic necrosis |
| red infarcts occur in: | If there is collateral circulation or congestion: -venous occlusions -loose tissues -tissues with dual circulation (lung, sm intestine) |
| White infarcts occur when: | blood cannot get to infarcted area: -in solid organs with end-arterial circulation (eg: heart, kidney, spleen) |
| Shock | systemic hypoperfusion |
| shock caused by? (list the three classes) | -cardiogenic -hypovolemic -septic |
| most common cause of septic shock | 70% are caused by gram-negative (LPS) bacilli expressing endotoxin (endotoxic shock). |
| end stage of shock? | multiorgan system failure |
| Patients surviving initial complications shock are at risk for? | Renal insufficiency w/ electrolyte imbalances |
| anasarca | severe systemic edema |
| most common cause of systemic edema? | congestive heart failure |
| 5 main causes of edema | -increased hydrostatic pressure -reduced plasma osmotic pressure -lymphatic obstruction -sodium retention -inflammation |
| dependent edema. What is it? What disease is most likely cause? | edema that is influenced by gravity. Typical of CHF (swollen ankles) |
| First sign of hypoproteinemia? | periorbital/eyelid edema. Hypoproteinemia causes more systemic edema, but first seen in loose connective tissue. |
| What do slices of lungs effected by pulmonary edema look like? | "frothy, blood-tinged mixture of air, edema fluid and erythrocytes?" |
| locally increased blood volume. | hyperemia (active) and congestion (passive) |
| hyperemia | active process in which arteriolar dilation leads to increased blood flow (eg at sites of inflammation or skeletal muscle during exercise) |
| congestion | a passive process resulting from reduced outflow of blood from a tissue. (can be systemic: cardiac failure, or local: isolated venous obstruction |
| nutmeg liver | chronic passive congestion of the liver |
| chronic congestion can lead to has what tell-tale sign? | hemosiderin-laden macrophages. Chronic congestion causes small hemorrhagic foci; catabolism of extravasated red cells |
| Hemosiderin | Hemosiderin is most commonly found in macrophages and is especially abundant in situations following hemorrhage, suggesting that its formation may be related to phagocytosis of red blood cells and hemoglobin. |
| heart failure cells | hemosiderin laden macrophages. Caused by chronic congestion (which is often caused by congestive heart failure) |
| signs of acute vs chronic congestion? | - acute congestion will cause capillary dilation w/edema - chronic congestion will cause areas of hemorrhage with hemosiderin laden macrophages |
| 1-2 mm hemorrhage | petechiae |
| >= 3 mm hemorrhage | purpura |
| > 1-2 cm hemorrhage | ecchymoses |
| Progression of color changes of a bruise (also name the chemical's that impart the colors) | - hemoglobin (red/blue) to bilirubin (yellow) to biliverdin (greenish/blue) to hemosiderin (golden brown) |
| how much blood loss is "ok" | Rapid loss of up to 20%, or slow losses of even larger amounts, may have little impact. |
| accumulation of blood in joints | hemarthrosis |
| First response to vascular injury (with cause)? | arteriolar vasoconstriction mediated by reflex neurogenic mechanisms and local secretion of endothelin |
| endothelin | proteins that constrict blood vessels and raise blood pressure. released by endothelium |
| platelet's "stick" to extra-cellular matrix via | vWF: von Willibrand Factor |
| What is the receptor on platelets that bind with vWF | GPIb. Glycoprotein Ib. |
| vWF disease | Bleeding disorder. Qualitative or quantitative deficiency of von Willebrand factor (vWF). Most common hereditary coagulation abnormality. |
| Bernard-Soulier syndrome | rare autosomal recessive coagulopathy (bleeding disorder) that causes a deficiency of glycoprotein Ib (GpIb), the receptor for von Willebrand factor, which is important in clot formation. |
| alpha granule | one of two granule types released by platelets. alpha granules contain: - P-selectin - factors V and VIII - TGF-beta - fibrinogen - fibronectin |
| dense or delta granules contain | - ADP - ATP - ionized calcium - histamine - seratonin - epinephrine |
| ADP amplifies | ADP amplifies ADP release (amplification) |
| ADP activates: | "ADP is a potent activator of platelet aggregation" |
| Thromboxane A2 properties? | - vasoconstrictor - activates new platelets (which makes more Thromboxane A2) - increases platelet adhesion - |
| activated platelets leads to appearance of ______ charged ______ on platelet surface. Why are these important? | activated platelets leads to appearance of NEGATIVELY charged PHOSPHOLIPIDS. These bind Ca2+ and act as sites for coagulation cascade |
| clopidogrel | aka Plavix. The drug works by irreversibly inhibiting ADP receptors on platelets (thereby blocking platelet aggregation) |
| primary hemostatic plug | platelet aggregation |
| secondary hemostatic plug | irreversibly fused mass of platelets (bound by fibrin) |
| action of t-PA | activates plasminogen to plasmin which degrades fibrin |
| source of t-PA | thrombin induces endothelial t-PA release |
| PAI | plasminogen activator inhibitors. prevent t-PA from breaking up fibrin |
| plasmin function | degrades fibrin clots. |
| activates plasminogen to plasmin (2 things) | t-PA urokinase |
| ______ inhibits thromin, IXa, Xa, XIa, and XIIa | antithrombin complexed with heparin-like-molecules |
| PGI2 | prostacyclin. decreases platelet aggregation/adherence. also is a vasodilator |
| what deactivates factors Va and VIIIa? | activated protein C |
| How does protein C get activated? | thrombomodulin modifies thrombin so that it can cleave proteins C and S. activated protein C deactives factors Va and VIIIa. |
| TFPI | tissue factor pathway inhibitor. a cell surface protein that directly inhibits tissue facor - factor VIIa and factor Xa activities. |
| nitric oxide effect on platelets? | stops platelet adhesion. also a vasodilator |
| Factor V Leiden | a variant of human factor V that causes a hypercoagulability disorder. Leiden factor V cannot be inactivated by activated protein C. |
| Polycythemia | increase in hematocrit. can result in small vessel stasis & thrombosis |
| antiphospholipid antibody syndrome | occurs in patients with antibodies against anionic phospholipids (platelets) that can activate platelets. May cause hypercoagulation |
| which direction to arterial thrombi grow? in veins? | all thrombi grow toward the heart. Arterial thrombi grow toward the heart (retrograde). |
| HIT | heparin-induced thrombocytopenia. exogenous unfractionated heparin causes immune system to target heparin & platelet factor 4. Platelets get activated. Creates prothrombic state (paradoxical to heparin injection) and lowered platelet count. |
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lbgator
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