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97 Cards in this Set
- Front
- Back
What is Anasarca?
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Severe and generalized edema.
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What happens with lymphatic obstruction?
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Edema due to impaired fluid drainage.
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What happens in renal disease, with sodium retention?
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So much water! Edema.
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What causes LOCAL increases of hydrostatic pressure?
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Impaired venous outflow (like deep venous thrombosis).
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What causes GENERALIZED increases in venous pressure?
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CHF (usually right-sided).
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What is secondary aldosteronism?
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Renal hypoperfusion causes activation of Renin-angiotensin blah blah.
Can happen d/t CHF (will result in increased load on an already failing heart) or hypoproteinemia. Either way, will only make edema worse. |
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What causes reductions in oncotic pressure?
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* Nephrotic syndrome.
* Liver pathology- reduced synthesis. * Protein malnutrition. |
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What causes orange-peel skin in breast cancer?
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Edema of overlying skin- accentuates depression at site of hair follicles.
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What does salt and water retention cause, in regards to venous pressure?
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Increased hydrostatic pressure.
Decreased oncotic pressure. |
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What is the prominent feature of CHF?
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Edema of the dependent parts (eg legs when standing).
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What causes edema of all parts of the body equally?
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Renal dysfunction/nephrotic syndrome.
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What causes pulmonary edema?
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Left ventricular failure.
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What happens when you have edema in alveolar spaces?
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Creates favorable environment for bacterial infection.
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What is Hyperemia?
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Active hyperemia- active process!
Augmented tissue inflow because of arteriolar dilation. Tissue appears red. (blushing) |
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What is congestion (=passive hyperemia)?
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Impaired outflow from a tissue.
Tissue appears blue-red. Can be generalized (heart failure). Can be local (venous obstruction, portal hypertension). |
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What can chronic passive congestion cause?
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Chronic hypoxia.
d/t stasis of poorly oxygenated blood. |
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What do hyperemia and congestion refer to?
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Local increased volume of blood in a particular tissue.
Hyperemia- active (arterial dilation). Congestion- passive (no outflow). |
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What are "heart failure cells"?
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Hemosiderin-lader macrophages in alveolar spaces, in chronic pulmonary congestion.
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What do you see in Acute pulmonary congestion?
Chronic? |
Acute: alveolar capillaries engorged with blood.
Chronic: Thickened and fibrotic septa, HLM. |
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What causes localized edema?
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* Inflammatory reaction- blisters.
* Elephantiasis- d/t blockage of lymphatic drainage. |
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What is a major cause of increased hydrostatic pressure?
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Portal hypertension.
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What happens to the liver in acute hepatic congestion?
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Periportal hepatocytes- fatty changes.
Central hepatocytes- degeneration. |
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What happens to the liver in chronic hepatic congestion?
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Central regions are red-brown and depressed d/t loss of cells.
NUTMEG LIVER, can lead to "cardiac cirrhosis". Can see HLM. |
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What is a Hematoma?
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Accumulation of blood within tissue.
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What is a petechiae?
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1-2mm hemorrhage into skin/mucous/serosal surface.
Can be caused by locally increased hydrostatic pressure, thrombocytopenia.. Rocky Mountain Spotted Fever. |
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What is purpura?
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3mm-1cm hemorrhage.
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What is ecchymoses?
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over 1-2 cm subcutaneous hematomas.
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what is primary hemostasis?
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Aggregate of platelets that form a hemostatic plug, minutes after endothelial injury.
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How is TF synthesized?
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By endothelium, exposed at site of injury.
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What is secondary hemostasis?
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The sequence of activating the coagulation cascade and activating of thrombin (causes fibrin deposition and further platelet recruitment and granule release).
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What does Thrombin do?
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* Fibrin deposition.
* Further platelet recruitment and granule release |
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What mechanisms do endothelial cells use to maintain liquid blood flow?
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1. Antiplatelet effects: PGI2 and NO, vasodilators, inhibit their adherence.
2. Anticoagulant effect: Heparin-like molecules on membranes (cofactors with antithrombin), THROMBOMODULIN. 3. Fibrinolytic effect: tPA. |
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What does Protein C do?
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Inhibits clotting by cleaving Va and VIIIa.
Requires Protein S. |
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What are the PROthrombotic properties of endothelium?
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1. Production of vWF (product of normal endothelium!).
2. Production of TF. 3. Inhibition of plasminogen activators by PAIs. |
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What happens after vascular injury?
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1. ECM constituents exposed.
2. Platelets adhere (using vWF-glycoprotein Ib). 3. Secretion of both granules from platelets and their activation. 4. Platelet aggregation (enhanced by TxA2, ADP, Thrombin). |
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What does vWF do?
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Bind glycoprotein Ib on platelets- the only association strong enough to overcome the high shear forces of flowing blood.
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What does platelet activation do?
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Expression of phospholipid complexes, required for the intrinsic clotting pathway.
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What does Fibrin do with platelets?
Fibrinogen? |
Fibrin: Cements the platelet plug in place.
fibrinogen: connects multiple platelets together to form large aggregates. |
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What is PGI2?
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Vasodilator- inhibits platelet aggregation.
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What is TxA2?
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Vasoconstrictor- activates platelet aggregation.
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How does aspirin affect clotting?
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Inhibits COX (that synthesizes TxA2).
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What is the coagulation cascade assembled on? What is required?
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Phospholipid complexes (like on activated platelets), requires Ca.
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What activates the intrinsic pathway?
Extrinsic? |
Intrinsic: Hageman (12).
Extrinsic: TF. |
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What are some natural anticoagulants?
(3) |
1. Antithrombin- activated by binding to heparin-like molecules on endothelial cells.
2. Protein C and Protein S, both dependent on Vitamin K. Activate Thrombomodulin. 3. Tissue Factor Pathway Inhibitor (TFPI)- inactivates factors 10a, 7a. |
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What does plasmin do?
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Breaks down fibrin to FSP and interferes with its polymerization.
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What do Fibrin-Split Products (FSP) function as?
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Weak anti-coagulants.
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What do elevated levels of FSP (Fibrin Split Product) indicate?
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Abnormal thrombotic state- like DIC.
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What is the Virchow traid?
(factors that predispose to thrombus formation) |
1. Endothelial injury (not just physical- any perturbation in pro/anticoagulant balance).
2. Stasis/turbulance. 3. Blood hypercoagulability. |
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How do alteration in normal blood flow (stasis and turbulance) affect thrombi creation?
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1. Disrupt laminar flow- bring platelets into contact with the endo.
2. Prevent dilution of activated clotting factors. 3. Retard inflow of clotting factor inhibitors. 4. Promote endo cell activation. |
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What are some causes for stasis?
(2) |
1. Sickle-cell anemia (cause vascular occlusions).
2. Dilated atrium + Atrial fibrillation. |
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What is primary hypercoagulability?
Secondary? |
Primary: genetic.
Secondary: Acquired. |
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What is the Leiden mutation?
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Mutation in factor V- makes it resistant to cleavage by protein C.
Patient are prone to recurrent deep venous thrombi. |
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What do elevated levels of homocysteine cause?
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A&V thrombi, d/t inhibition of anticoagulants.
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Caused for acquired hypercoagulability?
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1. Increased hepatic synthesis of coagulation factors (BCP, pregnancy).
2. Release of procoagulant tumor products. 3. Smoking. 4. Obesity. |
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What is anti-phospholipid antibody syndrome?
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AB that induce hypercogulable state- by direct platelet activation, inhibition of production of PGI2, or interference with Protein C.
Patients are prone to recurrent thrombi and miscarriages. |
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Where do arterial thrombi begin?
Venous? |
Arterial: areas of endothelial injury/turbulence.
Venous: Areas of stasis. |
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What do lines of Zahn imply?
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Thrombosis at a site of blood flow (not too small vessels, live patient).
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What is unique about post-mortem clots?
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Yellow chicken fat supernatant.
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What is the color of arterial thrombi?
Venous? |
Arterial: white.
Venous: red (contain more enmeshed RBC). |
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What does the fibrinolytic pathway do?
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Rapid shrinkage and total lysis of RECENT thrombi (before extensive fibrin polymerization).
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What happens to older thrombi?
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They become organized- ingrowth of endo cells, SMC and fibroblasts into the fibrin-rich thrombus.
Capillay channels are formed- RECANALIZATION. |
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What can happen in large thrombi?
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Instead of organizing, the center undergoes enzymatic digestion.
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Which venous thrombus embolizes more from legs- superficial or deep?
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Deep.
(extra dangerous because there are no symptoms of thrombus- collateral bypass channels..) |
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What can cause venous thrombi?
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1. Stasis (eg d/t cardiac failure- heart can't push blood out, new blood can't get in).
2. Advanced age. 3. Reduced physical activity (also, no milking action from muscles in legs). 4. Hypercoagulability (pregnancy!). |
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Causes for arterial thrombi?
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1. Atherosclerosis.
2. MI. |
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Who is affected the most by arterial thrombi?
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1. Legs (75%).
2. Brain > kidney > liver. |
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What causes DIC?
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It's a potential complication of any conditoin associated with widespread activation of Thrombin.
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What happens in DIC?
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Suddent onset of widespread fibrin thrombi in MICROcirculation, that cause rapid consumption of platelets (and coagulation proteins) WHILE activating fibrinolytic mechanisms- leads to infernal bleeding.
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Where do most pulmonary embolisms originate?
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Deep leg veins.
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What is a paradoxical emboli?
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From one circulatior to another (like venous -> arterial through defect in heart).
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What can pulmonary thrombi lead to?
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Pulmonary hypertension and right heart failure.
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Where do most arterial thrombi originate?
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Mural thromby.
(2/3: because of left ventricle wall infarct). |
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What causes fat embolism?
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Fracture of long bones (fatty marrow).
RARELY: soft tissue trauma and burns. |
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What causes air embolism?
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Sudden changes in atmospheric pressure (decompression sickness).
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What us Caisson disease?
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Persistence of gas embolism in skeletal system- causes multiple foci of ischemic necrosis.
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What happens in amniotic fluid embolism?
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Shock, coma, DIC.
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Why is DIC caused by amniotic embolism?
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Because there are thrombogenic substances in the amniotic fluid.
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What is an infract?
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Area of ischemic necrosis, caused by occlusion of either arterial supply/venous drainage.
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What causes most infarcts (99%)?
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Thrombotic/embolic events- mostly arterial.
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What causes red infarcts?
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1. Venous occlusions.
2. Loose tissues (lungs)- blood collects.. 3. Tissues with dual circulation. 4. Flow re-established to site of previous arterial occlusion and necrosis. |
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What causes white infarcts?
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Arterial occlusion in end-arterial circulation.
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What kind of necrosis do you see in an infarct?
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Ischemic coagulative.
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What happens in septic infarctions?
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The infarct is converted into an abscess.
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Slowly developing occlusions are...
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less likely to cause infarction, because they provide time for deveopment of alternative perfusion pathways.
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Which tissue is most vulnerable to hypoxia?
Least? |
Most: Neurons (3-4 min), myocytes (20-30 min).
Least: Fibroblasts (hours). |
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What is cardiogenic shock?
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Myocardial pump failure.
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What is Neurogenic shock?
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Due to loss of vascular tone- after spinal cord injury or anesthetic accidents.
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Which infections are usually involved in septic shock?
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Gram-negative.
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What can septic shock lead to?
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* Acute respiratory distress syndrome.
* DIC. |
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What are the 3 phases of shock?
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1. Nonprogressive- compensatoy sympathetic mechanisms are activated.
2. Progressive- hypoperfusion and acidoses (d/t glycolysis). 3. Irreversible. |
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What happens in septic shock?
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1. TLR4 bind LPS (usually).
2. Endothelial cells, with TLR4, stop producing anticoagulants. 3. Macrophages produce cytokines. |
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What do you see in the first phase of shock?
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* Tachycardia.
* Peripheral vasoconstriction (cold skin- except for septic shock!). * Renal conservation of fluid. |
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What happens to the lungs in pure hypovolemic shock?
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Not much- resistant to hypoxic injury.
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What happens to the liver in shock?
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Fatty liver!
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What typesof shcok are included in distributive shock?
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* Septic shock
* Anaphylactic shock. * Neurogenic Shock. |
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What happens in distributive shock?
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Blood volume and CO are normal, but blood is maldistributed to the tissues because of alterations in BV.
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What is the most likely location for a hemorrhagic stroke?
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Hemorrhage into the basal ganglia.
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