Hemodynamics

Question 1

C&C post-mortem versus ante-mortem thrombi

Answer 1

• Post-mortem are gelatinous & jelly-like w/o Lines of Zahn; more fragile; weakly attached; fragmented erythrocytes; chicken fat
• Ante-mortem display Lines of Zahn; fibrin meshwork & platelet aggregates; adherent to vessel walls (not fragile); gray strands of deposited fibrin

Question 2

What is the main difference between an arterial clot and a venous clot?

Answer 2

• Arterial: platelet > fibrin
• Venous: fibrin > platelet

Question 3

What ruptures to typically elicit an aterial thrombosis?

Answer 3

atherosclerotic plaque

Question 4

What are major risk factors for an arterial thrombosis?

Answer 4

• Atherosclerosis
• HTN
• Smoking
• Diabetes

Question 5

What locations are popular for arterial thrombi?

Answer 5

Places of turbulent blood flow such as arterial bifurcations

LA/LV; cerebral arteries; aorta

Question 6

What are the diseases of arterial thrombosis?

Answer 6

• Acute coronary syndrome
• Ischemic stroke
• Limb claudication and ischemia

Question 7

What is the composition of arterial thrombi?

Answer 7

White thrombi (mainly plts – endothelial injury –> plt activation)

Question 8

What is the main Tx of arterial thrombi?

Answer 8

Anti-plt agents (e.g., ASA & Plavix)

Question 9

What are the risk factors for venous thrombi?

Answer 9

• Virchow’s Triad
• Hyercoagulability
• Oral contraceptives & HRT
• Pregnancy
• Post-partum

Question 10

What are the main locations of venous thrombi?

Answer 10

• Veins of muscles
• Valves in veins

Question 11

What are the consequences (diseases) of venous thrombi?

Answer 11

• DVT
• PE

Question 12

What is the composition of venous thrombi?

Answer 12

• Mainly fibrin
• Sluggish venous circulation leads to trapped RBCs –> red, stasis, thrombi

Question 13

What is the Tx for venous thrombi?

Answer 13

Anti-coagulant agents (e.g., heparin, warfarin)

Question 14

What are lines of Zahn?

Answer 14

Alternating layers of Pale plts & fibrin with dark RBCs layer

Question 15

How does smoking lead to increased coagulability?

Answer 15

Endothelial damage

Question 16

How does obesity lead to increased coagulability?

Answer 16

Systemic inflammation

Question 17

How does nephrotic syndrome lead to increase coagulability?

Answer 17

Loss of plasma anti-thrombin in urine

Question 18

How does HRT/OCP lead to increased coagulability?

Answer 18

• Increased synthesis of coagulation factors (prothrombin & fibrin)
• Decreased synthesis of anti-thrombin III

Question 19

How does pregnancy lead to increased coagulability?

Answer 19

• Increased clotting factors
• Protein C & S decrease
• Venous stasis in uterus enlarges

Question 20

How does cancer increase coagulability?

Answer 20

Increase of procoagulant factors (e.g., tissue factor)

Question 21

What is the mechanism of HIT?

Answer 21

• Platelet factor 4 (PF4) is released by activated plts and binds to heparin
• A complex is formed, leading to IgG Abs against it
• The IgG + complex bind to cell surface of Plt leading to Plt activation & aggregation
• This ultimately leads to thrombosis (arterial/venous)
• Macrophages phagocytize Plts in thrombosis
• prothrombotic state

Question 22

What is paradoxical about antiphospholipid antibody syndrome?

Answer 22

• Increased risk of thrombosis in vivo (body)
• Anticoagulant affects in vitro (lab studies)

Question 23

AAS can occur simultaneously with what autoimmune disease?

Answer 23

SLE; 40% of cases are secondary to SLE

Question 24

AAS is defined as:

Answer 24

• Anti-phospholipid antibodies (Anti-cardiolipin Ab; Anti-β-2-glycoprotein-I Ab)
  PLUS one of the following
• Venous thromboembolism (DVT, PE)
• Arterial thromboembolism (Stroke, TIA)
• Frequent fetal loss (miscarriages)

Question 25

What are the (3) Hs of Virchow's Triad?

Answer 25

* Hypercoagulability * Halt of blood flow (stasis) * Hurt of endothelium (endothelial dysfunction/damage)

Question 26

How does endothelial injury lead to increased coagulability?

Answer 26

* Down-regulate thrombomodulin leading to sustained activation of thrombin * Secretion of plasminogen activator inhibitors (PAI) which limits fibrinolysis and down-regulates expression of t-PA

Question 27

How does **CHF** lead to an increase in **edema**?

Answer 27

* Reduced CO --> venous congestion --> increased capillary hydrostatic pressure * Reduced CO --> hypoperfusion of kidney --> JG cell activation --> Na + H2O retention * Cannot increase CO in response to blood volume leading to increase fluid retention, venous pressure, and edema

Question 28

What pressure is altered in nephrotic syndrome or liver disease to result in edema? Why?

Answer 28

* Loss of **albumin** * Diminished plasma **oncotic pressure**

Question 29

What type of edema is **lipid, protein rich** that is within the **interstitial space** and maintains a **high viscosity**?

Answer 29

Lymphedema

Question 30

C&C **pitting edema** versus **non-pitting edema**

Answer 30

** Pitting edema** * residual indentation after pressure * Hydrostatic fluid **retention** * Hydrostatic **protein deficiency** **Non-pitting edema** * no residual indentation * Lymphedema (lymph obstruction) * Myxedema (hypothyroidism) * Hyperthryoidism (pretibial)

Question 31

Why do **ecchymoses** change colors?

Answer 31

* First, RBC --> red/blue * Bilirubin --> blue-green * Hemosiderin --> golden brown