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Physiology III Exam 1 > Cardiac Physiology: Clotting and Resolution > Flashcards

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
Inhibition of COX 1 has its primary affect on which synthesis pathway?
Platelets and the formation of Thromboxane A2
26
Inhibition of COX 2 has its primary affect on which synthesis pathway?
Endothelial pathway and formation of PGI2
27
What is the function of anticoagulants?
Prevents clots from forming
28
What is the function of chelators?
Tie up calcium
29
Complexes with anti-thrombin III?
Heparin
30
What inhibits Vitamin K dependent factors?
Dicumarol
31
What factors are synthesized by hepatocytes?
Factors II, VII, IX, X
32
What is the difference between anticoagulants and lysis of clots?
Anticoagulants PREVENT clots from forming while lysis dissolves clots that have already formed.
33
Endogenous activators of plasminogen are found where?
Tissues, plasma and urine
34
Exogenous activators of plasminogen?
Streptokinase and tissue plasminogen activator (tPA)
35
Most tissue damage associated with infarction occurs upon reperfusion. Why?
There is formation of highly reactive oxygen species (free radicals)
36
The ability to open up alternate routes of blood flow to compensate for a blocked vessel
Collateralization -- requires angiogenesis and vasodilation
37
What system may impede collateralization via vasoconstriction?
SNS
38
the extrinsic mechanism of blood coagulation is initiated by?
Chemical factors released by damaged tissues
39
The intrinsic mechanism of blood coagulation is initiated by?
Components found in blood or from damaged vessels upon exposure to collagen or foreign substances
40
What is hepatocyte's (liver's) role in clotting?
The liver synthesis 5 clotting factors: I: fibrinogen II: prothrombin VII: SPCA IX: AHF B X: Stuart factor
41
Coumarin (warfarin or Coumadin) depresses liver formation of II, VII, IX, X by blocking what?
Vitamin K
42
Describe hemophilia
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
What is the key step in clotting?
Conversion of fibrinogen to fibrin which requires thrombin
44
Describe the intrinsic pathway of clotting
~~~~Insert picture~~~
45
Describe the extrinsic pathway of clotting
~~~Insert picture~~~
46
Describe anti-phospholipid antibody syndrome
Autoimmune disorder where body makes antibodies against phospholipids in cell membranes; causes abnormal clots to form
47
What are risk factors in heart disease
Increasing age, males, hereditary, tobacco smoke, high blood cholesterol, high BP, physical inactivity, obesity, diabetes mellitus and high blood homocysteine
48
Amino acid in the blood that may irritate blood vessels promoting atherosclerosis
Homocysteine; can also cause cholesterol to change into oxidized LDL
49
high levels of Homocysteine in the blood can reduced by supplementing what?
Folic acid, B6 and B12
50
Which two antigen sets are likely to cause blood transfusion reactions if mismatched?
ABO and Rh
51
Which antibodies cause lysis of RBCs by activating the compliment system?
Primarily IgM; lysis releases proteolytic enzymes rupturing cell membrane
52
Which blood type is the universal donor?
O negative
53
Which blood type is the universal recipient?
AB positive
54
Hemolysis due to mismatched transfusions tend to be immediate or delayed? What is the most lethal effect?
Delayed (hemolysis to donor's RBCs not recipient); Kidney failure
55
What is the mechanism of kidney failure?
Toxic substances are released from lysed RBCs, circulatory shock, and hemoglobin from lysed RBC precipitate and blocks renal tubules
56
What is the most common and most antigenic Rh blood type?
D Antigen (Rh + 85%)
57
What is another name for Erthroblastosis Fetalis?
Hemolytic disease of the newborn
58
Describe hemolytic disease of the newborn.
Characterized by agglutination and hemolysis of the fetus' RBC by the mother's anti Rh agglutinins
59
How can erythroblastosis fetalis present and what is the mechanism?
Jaundice; Agglutination of fetal blood release Hgb which is converted by macrophages to bilirubin
60
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?
Erythroblastosis fetalis; mother's anti agglutins from can circulate for 1-2 months causing RBCs to be destroyed and anemia results.
61
What is the prevention and treatment of Erythroblastosis Fetralis?
Treatment: replace neonate's blood with Rh - blood Prevention: administration of RhoGAM to mother at 28-30 weeks

Physiology III Exam 1 (3 decks)

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