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Robbins Path CH4

Pathology Robbins Chapter 4 Hemodynamic disorders, Thromboembolic Disease, Shock

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.
Created by: lbgator



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