Cardiac Physiology: Clotting and Resolution Flashcards

1
Q

What is the #1 cause of death?

A

Cardiovascular Disease

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2
Q

What is the major underlying cause of CVD?

A

Ischemia due to: - Atherosclerosis (plaque buildup) Artery Spasm

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3
Q

High blood cholesterol is linked to what physiological process?

A

Atherogenesis

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4
Q

Inflammatory mechanisms couple dyslipidemia with the formation of what?

A

Atheroma formation

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5
Q

Early Atherogenesis is characterized by?

A

Leukocyte recruitment and expression of pro-inflammatory cytokines

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6
Q

What system modulates inflammation?

A

Nervous System

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7
Q

Thrombosis is promoted by what physiological pathway and is responsible for MI and most strokes?

A

Inflammatory pathways

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8
Q

Prevention of blood loss

A

Hemostasis

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9
Q

What are the mechanisms of hemostasis? (4)

A

Vascular spasm, formation of a platelet plug, blood coagulation, and fibrous tissue growth

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10
Q

What happens during vascular constriction associated with trauma? (3)

A

-Neural reflexes (SNS induced constriction from pain) -Local myogenic spasm (responsible for most constriction) -Local humoral factors (thromboxane A2 from platelets and is especially important in smaller vessels)

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11
Q

The degree of spasm is directly proportional to what?

A

Severity of the trauma

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12
Q

T/F? Platelets function as whole cells but cannot divide.

A

True

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13
Q

Platelets contain:

A

Contractile proteins, enzymes, Calcium, ADP/ATP, Thromboxane A2, serotonin, growth factors

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14
Q

What does the platelet cell membrane contain?

A

Glycoproteins and phospholipids

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15
Q

T/F? Glycoproteins avoid normal epithelium but adhere to damaged area?

A

True

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16
Q

What platelet factor do phospholipids contain?

A

Platelet factor 3 (AKA thromboplastin which initiates clotting)

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17
Q

Describe the steps of platelet activation.

A
  1. Swell 2. Irregular form w/ radiating processes protruding from surface 3. contractile proteins activated causing granule release 4. Secrete ADP, Thromboxane A2 and serotonin
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18
Q

Thromboxane A2

A

Vasoconstrictor; potentiates the release of granule contents

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19
Q

Platelets have a half life of ___ and are eliminated by ___?

A

8-12 days; macrophage

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20
Q

What is the role of endothelium?

A

-Prevents platelet aggregation, produces PGI2 (prostacyclin), and produces factor VIII (clotting)

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21
Q

Describe Prostaglandin synthesis

A

-Insert picture

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22
Q

Describe Thromboxane synthesis

A

-Insert picture

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23
Q

Why take aspirin to prevent heart attacks?

A

Low dose aspirin inhibits primarily COX1 associated with the platelet which inhibits production of thromboxane A2

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24
Q

Aspirin and ibuprofen block thromboxane A2 and prostacyclin. What is the mechanism?

A

Blocks fatty acid COX which converts arachidonic acid to PGG2 and PGH2

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25
Q

Inhibition of COX 1 has its primary affect on which synthesis pathway?

A

Platelets and the formation of Thromboxane A2

26
Q

Inhibition of COX 2 has its primary affect on which synthesis pathway?

A

Endothelial pathway and formation of PGI2

27
Q

What is the function of anticoagulants?

A

Prevents clots from forming

28
Q

What is the function of chelators?

A

Tie up calcium

29
Q

Complexes with anti-thrombin III?

A

Heparin

30
Q

What inhibits Vitamin K dependent factors?

A

Dicumarol

31
Q

What factors are synthesized by hepatocytes?

A

Factors II, VII, IX, X

32
Q

What is the difference between anticoagulants and lysis of clots?

A

Anticoagulants PREVENT clots from forming while lysis dissolves clots that have already formed.

33
Q

Endogenous activators of plasminogen are found where?

A

Tissues, plasma and urine

34
Q

Exogenous activators of plasminogen?

A

Streptokinase and tissue plasminogen activator (tPA)

35
Q

Most tissue damage associated with infarction occurs upon reperfusion. Why?

A

There is formation of highly reactive oxygen species (free radicals)

36
Q

The ability to open up alternate routes of blood flow to compensate for a blocked vessel

A

Collateralization – requires angiogenesis and vasodilation

37
Q

What system may impede collateralization via vasoconstriction?

A

SNS

38
Q

the extrinsic mechanism of blood coagulation is initiated by?

A

Chemical factors released by damaged tissues

39
Q

The intrinsic mechanism of blood coagulation is initiated by?

A

Components found in blood or from damaged vessels upon exposure to collagen or foreign substances

40
Q

What is hepatocyte’s (liver’s) role in clotting?

A

The liver synthesis 5 clotting factors: I: fibrinogen II: prothrombin VII: SPCA IX: AHF B X: Stuart factor

41
Q

Coumarin (warfarin or Coumadin) depresses liver formation of II, VII, IX, X by blocking what?

A

Vitamin K

42
Q

Describe hemophilia

A

Sex linked (X chromosome) therefore occurs almost exclusively in males. 85% of cases have a defect in factor VIII and 15% have defect in factor IX; varying degree in severity

43
Q

What is the key step in clotting?

A

Conversion of fibrinogen to fibrin which requires thrombin

44
Q

Describe the intrinsic pathway of clotting

A

~~~~Insert picture~~~

45
Q

Describe the extrinsic pathway of clotting

A

~~~Insert picture~~~

46
Q

Describe anti-phospholipid antibody syndrome

A

Autoimmune disorder where body makes antibodies against phospholipids in cell membranes; causes abnormal clots to form

47
Q

What are risk factors in heart disease

A

Increasing age, males, hereditary, tobacco smoke, high blood cholesterol, high BP, physical inactivity, obesity, diabetes mellitus and high blood homocysteine

48
Q

Amino acid in the blood that may irritate blood vessels promoting atherosclerosis

A

Homocysteine; can also cause cholesterol to change into oxidized LDL

49
Q

high levels of Homocysteine in the blood can reduced by supplementing what?

A

Folic acid, B6 and B12

50
Q

Which two antigen sets are likely to cause blood transfusion reactions if mismatched?

A

ABO and Rh

51
Q

Which antibodies cause lysis of RBCs by activating the compliment system?

A

Primarily IgM; lysis releases proteolytic enzymes rupturing cell membrane

52
Q

Which blood type is the universal donor?

A

O negative

53
Q

Which blood type is the universal recipient?

A

AB positive

54
Q

Hemolysis due to mismatched transfusions tend to be immediate or delayed? What is the most lethal effect?

A

Delayed (hemolysis to donor’s RBCs not recipient); Kidney failure

55
Q

What is the mechanism of kidney failure?

A

Toxic substances are released from lysed RBCs, circulatory shock, and hemoglobin from lysed RBC precipitate and blocks renal tubules

56
Q

What is the most common and most antigenic Rh blood type?

A

D Antigen (Rh + 85%)

57
Q

What is another name for Erthroblastosis Fetalis?

A

Hemolytic disease of the newborn

58
Q

Describe hemolytic disease of the newborn.

A

Characterized by agglutination and hemolysis of the fetus’ RBC by the mother’s anti Rh agglutinins

59
Q

How can erythroblastosis fetalis present and what is the mechanism?

A

Jaundice; Agglutination of fetal blood release Hgb which is converted by macrophages to bilirubin

60
Q

If a neonate (1-2 months) presents with anemia, enlarged liver and spleen, and has precipitation of bilirubin in neurons of the brain, what is a possible cause?

A

Erythroblastosis fetalis; mother’s anti agglutins from can circulate for 1-2 months causing RBCs to be destroyed and anemia results.

61
Q

What is the prevention and treatment of Erythroblastosis Fetralis?

A

Treatment: replace neonate’s blood with Rh - blood

Prevention: administration of RhoGAM to mother at 28-30 weeks