- increased arterial blood flow to an area - seen with edema

- decreased venous flow from an area - seen with edema

Hemodynamics Flashcards by Walker Short

What are the 5 factors that can lead to Edema?

Increased hydrostatic pressure
Decreased oncotic pressure
Lymphatic obstruction
Sodium (water) retention
Inflammation

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How does heart failure lead to edema?

-Increased capillary hydrostatic pressure

-Decreased renal blood flow triggers RAAAs
=retention of Na+ and water, increasing blood volume

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What is lymphedema?

-obstruction of the lymphatics, leading to edema

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What is hyperemia?

increased arterial blood flow to an area

- seen with edema

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What is congestion?

decreased venous flow from an area

- seen with edema

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What is a hematoma?

a mass-like collection of blood

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What chemicals produced by normal vascular endothelium have antiplatelet effects?

PGI2

- NO

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What chemicals produced by normal vascular endothelium have anticoagulant effects?

Heparin-like molecules

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What chemicals produced by normal vascular endothelium have fibrinolytic effects?

Tissue-type plasminogen activator (t-PA)

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What secretes tissue factor (III)?

Damaged vascular endothelium

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What does Von Willebrand factor do?

aids in platelet adhesion to a wound

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What does Tissue factor do?

Triggers the coagulation cascade

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What do inhibitors of plasminogen activator do?

inhibit fibrinolysis

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What factors prevent clotting/platelet aggregation?

Prostacyclin (PGI2)
NO
ADPase
Heparin-like molecules
thrombomodulin
Proteins C & S

**-t-PA (increases fibrinolysis)

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What is contained within the alpha granules of platelets?

P-selectin
Fibrinogen
fibronectin
V & VIII

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What is contained within delta granules of platelets?

ADP & ATP
Ca2+
5-HT
Epinephrine
Histamine

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What happens to platelets after a vascular injury?

Contact collagen and adhesive vWF
Adhesion and shape change
secretion from granules
Aggregation

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What mediates platelet adhesion?

von Willebrand Factor (vWF)

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What happens and what is the purpose of platelet shape change?

platelets rapidly change from smooth discs to spikey things
Alterations in glycoprotein increase affinity for fibrinogen
Platelet surface increases negatively charged phospholipids which bind calcium and enhances coagulation

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What does thromboxane A2 do in clotting?

along with ADP, amplifies platelet aggregation = primary hemostatic plug
vasoconstriction

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What factor initiates the extrinsic hemostatic pathway?

Intrinsic factor (III)

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What factor initiates the intrinsic hemostatic pathway?

XII

What happens when thrombin encounters normal endothelium?

has anticoagulant effects

- changes from procoagulant to anticoagulant to prevent clotting from extending beyond site of vascular injury

What does plasmin do?

breaks down fibrin

- interferes with fibrin’s polymerization

Why does a Factor XII deficiency lead to problems with overclotting?

- Factor XII pathway catabolyzes plasminogen into plasmin | - plasmin is needed to break down clots

What activates plasmin?

- Factor XII | - tissue plasminogen activator (t-PA)

What is thrombosis?

pathologic clotting of blood

What are factors that lead to thrombosis (Virchow's Triad)?

- endothelial injury - abnormal flow (turbulence or stasis) - Hypercoagulability

How does stasis and turbulence lead to thrombosis?

- Promote endothelial activation and enhance procoagulant activity and leukocyte adhesion - Disrupt laminar flow and bring platelets into contact with the endothelium - Prevent washout and dilution of activated clotting factors

What is hypercoagulability?

-Loosely defined as any alteration of the coagulation pathways that predisposes to thrombosis -Can be divided into: Primary (genetic) Secondary (acquired)

What is the most common cause of primary hypercoagulability?

point mutations in factor V gene (Leiden mutation) -leads to inactivation of protein C and loss of an important antithrombotic pathway

What is Heparin-induced Thrombocytopenia Syndrome?

- HIT occurs following the administration of unfractionated heparin - Can induce the appearance of antibodies that recognize the complexes of heparin and platelet activating factor 4 on the surface of platelets - Binding of these antibodies to platelets results in their activation, aggregation, and consumption (hence the term thrombocytopenia) - These changes can lead to a prothrombotic state

How do we prevent heparin-induced thrombocytopenia?

use low molecular weight heparin

What is Antiphospholipid Antibody syndrome?

- mechanism is unclear, but think about necessity of negative phospholipid membrane in platelets - Clinically includes recurrent thromboses, repeated miscarriages, cardiac valve vegetations, and thrombocytopenia **Antibodies in this disease can give a false positive serologic test for syphilis

What is embolization?

-when a thrombus breaks off and goes elsewhere

How does liver failure lead to edema?

- lower amount of albumin produced - decreased venous oncotic pressure - less fluid reabsorbed into veins from interstitium

What is Anasarca?

Generalized whole body edema

What results in Nutmeg liver?

-Chronic congestion of the liver

What are the three types of blood in the skin, from smallest to largest?

- Petechiae - Purpura - Ecchymosis

At what point does platelet aggregation become irreversible?

When fibrinogen is laid down and converted to fibrin

What is a Leiden mutation?

- Mutation in factor V | - Inactivation of protein C, thus loss of an important antithrombotic pathway

What is thrombocytopenia?

Decreased platelet count

What is a saddle embolus?

- an embolus that straddles the bifurcation of the main pulmonary artery - cause of sudden death

What is a paradoxical embolus?

-a clot from venous circulation ends up in arterial circulation through a shunt in the heart

What is a Fat embolus?

- A fat globule travels to the lungs | - usually from a bone fracture

What is an infarction?

An area of coagulative necrosis as a result of ischemia from decreased blood flow

What is a red infarct?

- hemorrhagic - caused by venous obstruction and occur in organs with double blood flow * look at notes to understand this

What is a white/pale infarct?

-an infarct caused by arterial occlusion

What causes septic shock?

-vasodilation due to endotoxins

What are the clinical stages of shock?

1. Primary = compensated 2. Progressive = lactic acidosis, renal failure 3. Irreversible = severe organ damage

What is contraction band necrosis?

- occurs in heart coagulative necrosis - flat, spindle shaped nuclei - cells have contracted down

What is acute tubular necrosis of the kidneys?

- coagulative necrosis of proximal tubules | - PT cells have lost nuclei

What is diffuse alveolar damage?

- fibrin seals off alveoli after bleeding into lung | - occurs in settings of shock or breathing smoke in a fire