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Term 3: Immunology/Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What are the 5 factors that can lead to Edema?

A
  1. Increased hydrostatic pressure
  2. Decreased oncotic pressure
  3. Lymphatic obstruction
  4. Sodium (water) retention
  5. Inflammation
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2
Q

How does heart failure lead to edema?

A

-Increased capillary hydrostatic pressure

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

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3
Q

What is lymphedema?

A

-obstruction of the lymphatics, leading to edema

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4
Q

What is hyperemia?

A
  • increased arterial blood flow to an area

- seen with edema

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5
Q

What is congestion?

A
  • decreased venous flow from an area

- seen with edema

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6
Q

What is a hematoma?

A

a mass-like collection of blood

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7
Q

What chemicals produced by normal vascular endothelium have antiplatelet effects?

A
  • PGI2

- NO

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8
Q

What chemicals produced by normal vascular endothelium have anticoagulant effects?

A

Heparin-like molecules

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9
Q

What chemicals produced by normal vascular endothelium have fibrinolytic effects?

A

Tissue-type plasminogen activator (t-PA)

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10
Q

What secretes tissue factor (III)?

A

Damaged vascular endothelium

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11
Q

What does Von Willebrand factor do?

A

aids in platelet adhesion to a wound

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12
Q

What does Tissue factor do?

A

Triggers the coagulation cascade

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13
Q

What do inhibitors of plasminogen activator do?

A

inhibit fibrinolysis

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14
Q

What factors prevent clotting/platelet aggregation?

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

**-t-PA (increases fibrinolysis)

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15
Q

What is contained within the alpha granules of platelets?

A
  • P-selectin
  • Fibrinogen
  • fibronectin
  • V & VIII
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16
Q

What is contained within delta granules of platelets?

A
  • ADP & ATP
  • Ca2+
  • 5-HT
  • Epinephrine
  • Histamine
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17
Q

What happens to platelets after a vascular injury?

A
  • Contact collagen and adhesive vWF
  • Adhesion and shape change
  • secretion from granules
  • Aggregation
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18
Q

What mediates platelet adhesion?

A

von Willebrand Factor (vWF)

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19
Q

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

A
  • 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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20
Q

What does thromboxane A2 do in clotting?

A
  • along with ADP, amplifies platelet aggregation = primary hemostatic plug
  • vasoconstriction
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21
Q

What factor initiates the extrinsic hemostatic pathway?

A

Intrinsic factor (III)

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22
Q

What factor initiates the intrinsic hemostatic pathway?

A

XII

23
Q

What happens when thrombin encounters normal endothelium?

A
  • has anticoagulant effects

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

24
Q

What does plasmin do?

A
  • breaks down fibrin

- interferes with fibrin’s polymerization

25
Q

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

A
  • Factor XII pathway catabolyzes plasminogen into plasmin

- plasmin is needed to break down clots

26
Q

What activates plasmin?

A
  • Factor XII

- tissue plasminogen activator (t-PA)

27
Q

What is thrombosis?

A

pathologic clotting of blood

28
Q

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

A
  • endothelial injury
  • abnormal flow (turbulence or stasis)
  • Hypercoagulability
29
Q

How does stasis and turbulence lead to thrombosis?

A
  • 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
30
Q

What is hypercoagulability?

A

-Loosely defined as any alteration of the coagulation pathways that predisposes to thrombosis

-Can be divided into:
Primary (genetic)
Secondary (acquired)

31
Q

What is the most common cause of primary hypercoagulability?

A

point mutations in factor V gene (Leiden mutation)

-leads to inactivation of protein C and loss of an important antithrombotic pathway

32
Q

What is Heparin-induced Thrombocytopenia Syndrome?

A
  • 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
33
Q

How do we prevent heparin-induced thrombocytopenia?

A

use low molecular weight heparin

34
Q

What is Antiphospholipid Antibody syndrome?

A
  • 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

35
Q

What is embolization?

A

-when a thrombus breaks off and goes elsewhere

36
Q

How does liver failure lead to edema?

A
  • lower amount of albumin produced
  • decreased venous oncotic pressure
  • less fluid reabsorbed into veins from interstitium
37
Q

What is Anasarca?

A

Generalized whole body edema

38
Q

What results in Nutmeg liver?

A

-Chronic congestion of the liver

39
Q

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

A
  • Petechiae
  • Purpura
  • Ecchymosis
40
Q

At what point does platelet aggregation become irreversible?

A

When fibrinogen is laid down and converted to fibrin

41
Q

What is a Leiden mutation?

A
  • Mutation in factor V

- Inactivation of protein C, thus loss of an important antithrombotic pathway

42
Q

What is thrombocytopenia?

A

Decreased platelet count

43
Q

What is a saddle embolus?

A
  • an embolus that straddles the bifurcation of the main pulmonary artery
  • cause of sudden death
44
Q

What is a paradoxical embolus?

A

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

45
Q

What is a Fat embolus?

A
  • A fat globule travels to the lungs

- usually from a bone fracture

46
Q

What is an infarction?

A

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

47
Q

What is a red infarct?

A
  • hemorrhagic
  • caused by venous obstruction and occur in organs with double blood flow
  • look at notes to understand this
48
Q

What is a white/pale infarct?

A

-an infarct caused by arterial occlusion

49
Q

What causes septic shock?

A

-vasodilation due to endotoxins

50
Q

What are the clinical stages of shock?

A
  1. Primary = compensated
  2. Progressive = lactic acidosis, renal failure
  3. Irreversible = severe organ damage
51
Q

What is contraction band necrosis?

A
  • occurs in heart coagulative necrosis
  • flat, spindle shaped nuclei
  • cells have contracted down
52
Q

What is acute tubular necrosis of the kidneys?

A
  • coagulative necrosis of proximal tubules

- PT cells have lost nuclei

53
Q

What is diffuse alveolar damage?

A
  • fibrin seals off alveoli after bleeding into lung

- occurs in settings of shock or breathing smoke in a fire

Term 3: Immunology/Pathology (17 decks)

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