Lecture 15: Cardiovascular Disease II

Question 1

Types of hemodynamic disturbances

Answer 1

1. Edema
2. Hyperemia
3. Hemorrhage
4. Thrombosis
5. Embolism
6. Infarction
7. Shock

Question 2

Edema

Answer 2

Increased fluid in interstitial tissue spaces; effusion = fluid collection in body cavities

Question 3

Anasarca

Answer 3

Severe general edema w/ subQ tissue swelling

Question 4

Transudate vs exudate

Answer 4

Transudate = fluid leaving vessels due to pressure changes
Exudate = fluid leaving vessels due to inflam. processes (cell/protein content)

Question 5

Hyperemia

Answer 5

Active process secondary to arteriole dilation; red tissue color
- Increased inflow

Question 6

Congestion

Answer 6

Passive process due to slow moving blood; cyanosis
- Impaired outflow; chronic leads to chronic hypoxia, scarring

Question 7

Pulmonary congestion phases

Answer 7

1. Acute:
   - Cap. engorgement
   - Septal edema
   - Intra-alveolar hemorrhage
2. Chronic:
   - Alveolar septal fibrosis
   - Hemosiderin-laden mφ’s (heart failure cells)

Question 8

Hepatic congestion phases

Answer 8

1. Acute:
   - Central vein/sinusoid distension
   - Central hepatocyte dropout (necrosis)
2. Chronic:
   - Pressure atrophy
   - Centrilobular necrosis
   - Nutmeg liver
   - Fibrosis/cirrhosis

Question 9

Hemorrhage

Answer 9

Blood outside vessel;
- Hematoma: blood accumul. w/in tissue
- Bruises: skin, mucosal surfaces

Question 10

Effects of different types of hemorrhage

Answer 10

Acute: shock
Chronic: anemia
Loss w/in closed space: mass effects

Question 11

Types of bruises

Answer 11

1. Petechiae
2. Ecchymoses
3. Purpura

Question 12

Petechiae

Answer 12

Minute (1-2 mm) hemorrhages into skin, mucous membranes, serosal surfaces
Assoc. w/ local increased intravasc. P, thrombocytopenia, platelet defect., clotting factor defect.

Question 13

Ecchymoses

Answer 13

Larger (1-2 cm) subQ hematomas
Enzymatic conversion of RBCs to hemosiderin by mφ’s produces color changes

Question 14

Purpura

Answer 14

Slightly larger hemorrhages (3-5 mm); same disorders as petechiae + trauma, vasculitis, vascular fragility

Question 15

Normal vs pathologic hemostasis

Answer 15

Normal: Tight regulation maintains fluid, clot-free blood w/ rapid local plug formation at vascular injury sites
Path.: thrombosis

Question 16

Components of normal hemostasis

Answer 16

1. Vascular wall
2. Platelets
3. Clotting cascade

Question 17

Anti-thrombotic properties of endothelial cells

Answer 17

1. Anti-platelet (physical barrier, NO, prostacyclin)
2. Anti-coagulant (heparin-like, thrombomodulin, tissue factor pathway inhib.)
3. Fibrinolytic effects (tissue tPA)

Question 18

Events at site of vascular injury

Answer 18

1. Vasoconstriction
2. Primary hemostasis
3. Secondary hemostasis
4. Thrombosis (coag.)
5. Anti-thrombotic events (fibrinolysis)

Question 19

Formation of primary hemostatic plug

Answer 19

1. Platelet adhesion
2. Granule release
3. Platelet aggregation

Question 20

Pro-thrombotic clotting mediators

Answer 20

1. Thrombin (cleaves fibrinogen)
2. Plasminogen activator inhibitors
3. Tissue factor (clotting cascade activation)
4. von Willebrand’s factor (platelet adhesion)

Question 21

Fibrinolytic proteins

Answer 21

1. Plasmin (fibrinolysis)
2. Plasminogen
3. Plasminogen activators

Question 22

Virchow’s Triad of thrombosis

Answer 22

1. Endothelial injury
2. Hypercoagulability
3. Abnormal blood flow

Question 23

Pathogenesis of thrombus formation

Answer 23

1. Endothelial cell injury
2. Abnormal blood flow
3. Hypercoagulable state (primary genetic, secondary acquired)

Question 24

Primary (inherited) hypercoagulable states

Answer 24

• Factor V Leiden mutation
• Prothrombin mutation
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency

Question 25

Secondary (acquired) hypercoagulable states

Answer 25

- Immobility/bedrest - MI - A-Fib - Tissue damage (surgery, burns) - Cancer - Prosthetic valves etc.

Question 26

Arterial thrombi

Answer 26

Arise at site of injury, w/ Lines of Zahn - Pale - Retrograde propagation - Usually results in infarction - Coronary, cerebral, femoral arteries; atherosclerotic plaques

Question 27

Venous thrombi

Answer 27

Arise at sites of stasis (lower extremity veins), less firmly attached - Red/stasis - Almost always occlusive - Anterograde propagation

Question 28

Superficial venous thrombosis

Answer 28

- Local pain/swelling - Varicose veins, eczema, ulcers - Rarely embolize

Question 29

Deep vein thrombosis

Answer 29

- 50% asymptom. due to collateral vessels - Thromboembolism

Question 30

Fates of thrombi

Answer 30

- Propagate - Embolize - Dissolution - Organize + recanalize

Question 31

Embolism

Answer 31

Detached intravasc. solid/liquid/gas mass carried by blood to distant site (99% dislodged thrombi) - In systemic circ. typically result in end organ infarct