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PATHO I > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

C&C post-mortem versus ante-mortem thrombi

A
  • 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
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2
Q

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

A
  • Arterial: platelet > fibrin
  • Venous: fibrin > platelet
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3
Q

What ruptures to typically elicit an aterial thrombosis?

A

atherosclerotic plaque

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4
Q

What are major risk factors for an arterial thrombosis?

A
  • Atherosclerosis
  • HTN
  • Smoking
  • Diabetes
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5
Q

What locations are popular for arterial thrombi?

A

Places of turbulent blood flow such as arterial bifurcations

LA/LV; cerebral arteries; aorta

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6
Q

What are the diseases of arterial thrombosis?

A
  • Acute coronary syndrome
  • Ischemic stroke
  • Limb claudication and ischemia
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7
Q

What is the composition of arterial thrombi?

A

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

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8
Q

What is the main Tx of arterial thrombi?

A

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

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9
Q

What are the risk factors for venous thrombi?

A
  • Virchow’s Triad
  • Hyercoagulability
  • Oral contraceptives & HRT
  • Pregnancy
  • Post-partum
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10
Q

What are the main locations of venous thrombi?

A
  • Veins of muscles
  • Valves in veins
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11
Q

What are the consequences (diseases) of venous thrombi?

A
  • DVT
  • PE
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12
Q

What is the composition of venous thrombi?

A
  • Mainly fibrin
  • Sluggish venous circulation leads to trapped RBCs –> red, stasis, thrombi
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13
Q

What is the Tx for venous thrombi?

A

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

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14
Q

What are lines of Zahn?

A

Alternating layers of Pale plts & fibrin with dark RBCs layer

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15
Q

How does smoking lead to increased coagulability?

A

Endothelial damage

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16
Q

How does obesity lead to increased coagulability?

A

Systemic inflammation

17
Q

How does nephrotic syndrome lead to increase coagulability?

A

Loss of plasma anti-thrombin in urine

18
Q

How does HRT/OCP lead to increased coagulability?

A
  • Increased synthesis of coagulation factors (prothrombin & fibrin)
  • Decreased synthesis of anti-thrombin III
19
Q

How does pregnancy lead to increased coagulability?

A
  • Increased clotting factors
  • Protein C & S decrease
  • Venous stasis in uterus enlarges
20
Q

How does cancer increase coagulability?

A

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

21
Q

What is the mechanism of HIT?

A
  • 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
22
Q

What is paradoxical about antiphospholipid antibody syndrome?

A
  • Increased risk of thrombosis in vivo (body)
  • Anticoagulant affects in vitro (lab studies)
23
Q

AAS can occur simultaneously with what autoimmune disease?

A

SLE; 40% of cases are secondary to SLE

24
Q

AAS is defined as:

A
  • 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)
25
Q

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

A
  • Hypercoagulability
  • Halt of blood flow (stasis)
  • Hurt of endothelium (endothelial dysfunction/damage)
26
Q

How does endothelial injury lead to increased coagulability?

A
  • 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
27
Q

How does CHF lead to an increase in edema?

A
  • 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
28
Q

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

A
  • Loss of albumin
  • Diminished plasma oncotic pressure
29
Q

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

A

Lymphedema

30
Q

C&C pitting edema versus non-pitting edema

A

** 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)

31
Q

Why do ecchymoses change colors?

A
  • First, RBC –> red/blue
  • Bilirubin –> blue-green
  • Hemosiderin –> golden brown

PATHO I (8 decks)

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