Pathology Robbins Chapter 4 Hemodynamic disorders, Thromboembolic Disease, Shock
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| DIC | Disseminated Intravascular Coagulation. widespread fibrin microthrombi in microcirculation.
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| DIC causes paradoxical ______ | DIC can cause uncontrollable bleeding via "consumption coagulopathy". Consumption of platelets and coagulation factors
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| embolism | any intravascular solid, liquid, or gas
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| paradoxic embolism | emboli passes through heart wall defect to go to circulation (rather than lungs)
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| Percent of pulmonary embolisms that are clinically silent? | 60-80%
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| 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
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| 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
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| second most common cause of embolism? | fat embolism
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| Most common cause of fat embolism | occur in 90% of severe skeletal injuries.
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| 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.
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| Thrombocytopenia | any disorder in which there is an abnormally low amount of platelets
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| caisson disease | persistent gas emboli in poorly vascularized portions of the skeleton (heads of femurs, tibia, humeri) lead to ischemic necrosis
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| red infarcts occur in: | If there is collateral circulation or congestion:
-venous occlusions
-loose tissues
-tissues with dual circulation (lung, sm intestine)
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| White infarcts occur when: | blood cannot get to infarcted area:
-in solid organs with end-arterial circulation (eg: heart, kidney, spleen)
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| Shock | systemic hypoperfusion
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| shock caused by? (list the three classes) | -cardiogenic
-hypovolemic
-septic
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| most common cause of septic shock | 70% are caused by gram-negative (LPS) bacilli expressing endotoxin (endotoxic shock).
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| end stage of shock? | multiorgan system failure
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| Patients surviving initial complications shock are at risk for? | Renal insufficiency w/ electrolyte imbalances
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| anasarca | severe systemic edema
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| most common cause of systemic edema? | congestive heart failure
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| 5 main causes of edema | -increased hydrostatic pressure
-reduced plasma osmotic pressure
-lymphatic obstruction
-sodium retention
-inflammation
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| dependent edema. What is it? What disease is most likely cause? | edema that is influenced by gravity. Typical of CHF (swollen ankles)
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| First sign of hypoproteinemia? | periorbital/eyelid edema. Hypoproteinemia causes more systemic edema, but first seen in loose connective tissue.
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| What do slices of lungs effected by pulmonary edema look like? | "frothy, blood-tinged mixture of air, edema fluid and erythrocytes?"
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| locally increased blood volume. | hyperemia (active) and congestion (passive)
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| hyperemia | active process in which arteriolar dilation leads to increased blood flow (eg at sites of inflammation or skeletal muscle during exercise)
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| congestion | a passive process resulting from reduced outflow of blood from a tissue. (can be systemic: cardiac failure, or local: isolated venous obstruction
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| nutmeg liver | chronic passive congestion of the liver
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| chronic congestion can lead to has what tell-tale sign? | hemosiderin-laden macrophages. Chronic congestion causes small hemorrhagic foci; catabolism of extravasated red cells
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| 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.
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| heart failure cells | hemosiderin laden macrophages. Caused by chronic congestion (which is often caused by congestive heart failure)
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| 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
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| 1-2 mm hemorrhage | petechiae
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| >= 3 mm hemorrhage | purpura
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| > 1-2 cm hemorrhage | ecchymoses
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| 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)
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| how much blood loss is "ok" | Rapid loss of up to 20%, or slow losses of even larger amounts, may have little impact.
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| accumulation of blood in joints | hemarthrosis
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| First response to vascular injury (with cause)? | arteriolar vasoconstriction mediated by reflex neurogenic mechanisms and local secretion of endothelin
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| endothelin | proteins that constrict blood vessels and raise blood pressure. released by endothelium
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| platelet's "stick" to extra-cellular matrix via | vWF: von Willibrand Factor
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| What is the receptor on platelets that bind with vWF | GPIb. Glycoprotein Ib.
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| vWF disease | Bleeding disorder. Qualitative or quantitative deficiency of von Willebrand factor (vWF). Most common hereditary coagulation abnormality.
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| 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.
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| alpha granule | one of two granule types released by platelets. alpha granules contain:
- P-selectin
- factors V and VIII
- TGF-beta
- fibrinogen
- fibronectin
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| dense or delta granules contain | - ADP
- ATP
- ionized calcium
- histamine
- seratonin
- epinephrine
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| ADP amplifies | ADP amplifies ADP release (amplification)
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| ADP activates: | "ADP is a potent activator of platelet aggregation"
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| Thromboxane A2 properties? | - vasoconstrictor
- activates new platelets (which makes more Thromboxane A2)
- increases platelet adhesion
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| 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
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| clopidogrel | aka Plavix. The drug works by irreversibly inhibiting ADP receptors on platelets (thereby blocking platelet aggregation)
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| primary hemostatic plug | platelet aggregation
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| secondary hemostatic plug | irreversibly fused mass of platelets (bound by fibrin)
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| action of t-PA | activates plasminogen to plasmin which degrades fibrin
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| source of t-PA | thrombin induces endothelial t-PA release
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| PAI | plasminogen activator inhibitors. prevent t-PA from breaking up fibrin
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| plasmin function | degrades fibrin clots.
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| activates plasminogen to plasmin (2 things) | t-PA
urokinase
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| ______ inhibits thromin, IXa, Xa, XIa, and XIIa | antithrombin complexed with heparin-like-molecules
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| PGI2 | prostacyclin. decreases platelet aggregation/adherence. also is a vasodilator
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| what deactivates factors Va and VIIIa? | activated protein C
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| 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.
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| TFPI | tissue factor pathway inhibitor. a cell surface protein that directly inhibits tissue facor - factor VIIa and factor Xa activities.
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| nitric oxide effect on platelets? | stops platelet adhesion. also a vasodilator
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| Factor V Leiden | a variant of human factor V that causes a hypercoagulability disorder. Leiden factor V cannot be inactivated by activated protein C.
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| Polycythemia | increase in hematocrit. can result in small vessel stasis & thrombosis
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| antiphospholipid antibody syndrome | occurs in patients with antibodies against anionic phospholipids (platelets) that can activate platelets. May cause hypercoagulation
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| which direction to arterial thrombi grow? in veins? | all thrombi grow toward the heart. Arterial thrombi grow toward the heart (retrograde).
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| 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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