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97 Cards in this Set

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