Hemodynamics Flashcards
C&C post-mortem versus ante-mortem thrombi
- 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
What is the main difference between an arterial clot and a venous clot?
- Arterial: platelet > fibrin
- Venous: fibrin > platelet
What ruptures to typically elicit an aterial thrombosis?
atherosclerotic plaque
What are major risk factors for an arterial thrombosis?
- Atherosclerosis
- HTN
- Smoking
- Diabetes
What locations are popular for arterial thrombi?
Places of turbulent blood flow such as arterial bifurcations
LA/LV; cerebral arteries; aorta
What are the diseases of arterial thrombosis?
- Acute coronary syndrome
- Ischemic stroke
- Limb claudication and ischemia
What is the composition of arterial thrombi?
White thrombi (mainly plts – endothelial injury –> plt activation)
What is the main Tx of arterial thrombi?
Anti-plt agents (e.g., ASA & Plavix)
What are the risk factors for venous thrombi?
- Virchow’s Triad
- Hyercoagulability
- Oral contraceptives & HRT
- Pregnancy
- Post-partum
What are the main locations of venous thrombi?
- Veins of muscles
- Valves in veins
What are the consequences (diseases) of venous thrombi?
- DVT
- PE
What is the composition of venous thrombi?
- Mainly fibrin
- Sluggish venous circulation leads to trapped RBCs –> red, stasis, thrombi
What is the Tx for venous thrombi?
Anti-coagulant agents (e.g., heparin, warfarin)
What are lines of Zahn?
Alternating layers of Pale plts & fibrin with dark RBCs layer
How does smoking lead to increased coagulability?
Endothelial damage
How does obesity lead to increased coagulability?
Systemic inflammation
How does nephrotic syndrome lead to increase coagulability?
Loss of plasma anti-thrombin in urine
How does HRT/OCP lead to increased coagulability?
- Increased synthesis of coagulation factors (prothrombin & fibrin)
- Decreased synthesis of anti-thrombin III
How does pregnancy lead to increased coagulability?
- Increased clotting factors
- Protein C & S decrease
- Venous stasis in uterus enlarges
How does cancer increase coagulability?
Increase of procoagulant factors (e.g., tissue factor)
What is the mechanism of HIT?
- 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
What is paradoxical about antiphospholipid antibody syndrome?
- Increased risk of thrombosis in vivo (body)
- Anticoagulant affects in vitro (lab studies)
AAS can occur simultaneously with what autoimmune disease?
SLE; 40% of cases are secondary to SLE
AAS is defined as:
- 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)
What are the (3) Hs of Virchow’s Triad?
- Hypercoagulability
- Halt of blood flow (stasis)
- Hurt of endothelium (endothelial dysfunction/damage)
How does endothelial injury lead to increased coagulability?
- 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
How does CHF lead to an increase in edema?
- 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
What pressure is altered in nephrotic syndrome or liver disease to result in edema? Why?
- Loss of albumin
- Diminished plasma oncotic pressure
What type of edema is lipid, protein rich that is within the interstitial space and maintains a high viscosity?
Lymphedema
C&C pitting edema versus non-pitting edema
** 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)
Why do ecchymoses change colors?
- First, RBC –> red/blue
- Bilirubin –> blue-green
- Hemosiderin –> golden brown
