Pathology Robbins Chapter 4 Hemodynamic disorders, Thromboembolic Disease, Shock
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| DIC | show 🗑
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| DIC causes paradoxical ______ | show 🗑
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| show | any intravascular solid, liquid, or gas
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| show | 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? | show 🗑
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| show | 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 | show 🗑
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| second most common cause of embolism? | show 🗑
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| Most common cause of fat embolism | show 🗑
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| show | 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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| show | any disorder in which there is an abnormally low amount of platelets
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| caisson disease | show 🗑
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| show | If there is collateral circulation or congestion:
-venous occlusions
-loose tissues
-tissues with dual circulation (lung, sm intestine)
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| show | blood cannot get to infarcted area:
-in solid organs with end-arterial circulation (eg: heart, kidney, spleen)
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| show | systemic hypoperfusion
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| shock caused by? (list the three classes) | show 🗑
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| show | 70% are caused by gram-negative (LPS) bacilli expressing endotoxin (endotoxic shock).
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| end stage of shock? | show 🗑
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| show | Renal insufficiency w/ electrolyte imbalances
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| anasarca | show 🗑
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| show | congestive heart failure
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| show | -increased hydrostatic pressure
-reduced plasma osmotic pressure
-lymphatic obstruction
-sodium retention
-inflammation
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| show | edema that is influenced by gravity. Typical of CHF (swollen ankles)
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| show | 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? | show 🗑
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| locally increased blood volume. | show 🗑
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| show | 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 | show 🗑
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| nutmeg liver | show 🗑
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| chronic congestion can lead to has what tell-tale sign? | show 🗑
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| show | 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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| show | hemosiderin laden macrophages. Caused by chronic congestion (which is often caused by congestive heart failure)
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| show | - acute congestion will cause capillary dilation w/edema
- chronic congestion will cause areas of hemorrhage with hemosiderin laden macrophages
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| show | petechiae
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| >= 3 mm hemorrhage | show 🗑
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| show | ecchymoses
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| show | - hemoglobin (red/blue) to bilirubin (yellow) to biliverdin (greenish/blue) to hemosiderin (golden brown)
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| show | 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 | show 🗑
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| show | arteriolar vasoconstriction mediated by reflex neurogenic mechanisms and local secretion of endothelin
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| show | proteins that constrict blood vessels and raise blood pressure. released by endothelium
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| show | vWF: von Willibrand Factor
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| What is the receptor on platelets that bind with vWF | show 🗑
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| show | Bleeding disorder. Qualitative or quantitative deficiency of von Willebrand factor (vWF). Most common hereditary coagulation abnormality.
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| show | 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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| show | 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 | show 🗑
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| ADP amplifies | show 🗑
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| ADP activates: | show 🗑
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| Thromboxane A2 properties? | show 🗑
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| show | activated platelets leads to appearance of NEGATIVELY charged PHOSPHOLIPIDS. These bind Ca2+ and act as sites for coagulation cascade
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| show | aka Plavix. The drug works by irreversibly inhibiting ADP receptors on platelets (thereby blocking platelet aggregation)
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| primary hemostatic plug | show 🗑
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| secondary hemostatic plug | show 🗑
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| action of t-PA | show 🗑
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| show | thrombin induces endothelial t-PA release
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| show | plasminogen activator inhibitors. prevent t-PA from breaking up fibrin
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| show | degrades fibrin clots.
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| show | t-PA
urokinase
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| ______ inhibits thromin, IXa, Xa, XIa, and XIIa | show 🗑
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| show | prostacyclin. decreases platelet aggregation/adherence. also is a vasodilator
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| show | activated protein C
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| How does protein C get activated? | show 🗑
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| TFPI | show 🗑
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| nitric oxide effect on platelets? | show 🗑
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| Factor V Leiden | show 🗑
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| Polycythemia | show 🗑
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| antiphospholipid antibody syndrome | show 🗑
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| which direction to arterial thrombi grow? in veins? | show 🗑
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| show | 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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