Gen Path 4

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Anonymous
ID:
28773
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Gen Path 4
Updated:
2010-08-03 10:00:37
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Robbins general pathology
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Description:
Hemodynamic disorders, thromboembolic disease and shock
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  1. Describe the pathogenesis of edema in ht failure.
    • 1) Decr cardiac output
    • 2) Decr. effective bld vol --- incr. ADH --- incr. renal H2O retention
    • 3) Incr. renin
    • 4) Incr. aldosterone
    • 5) Renal Na retention
    • 6) Incr plasma volume
    • 7) Transudation
  2. Describe pathogenesis of renal failure causing edema.
    • 1) Incr. renal Na and water retention
    • 2) Incr. plasma volume
    • 3) Transudation
  3. Name the pro-thrombotic properties of endothelium.
    • 1) Anti-platelet: intact endothelium, NO, PGI2 (vasodil, inh plt ag), ADPase
    • 2) Anti-coag: hep sulfate (binds AT - inactivates T, IXa, Xa, XIa, XIIa), thrombomodulin (binds T then activates prot C which attachs to prot S and cleaves Va and VIIIa), TFPI (complexes with TF-Va and Xa)
    • 3) Fibrinolytic effects - tPA
  4. Name the pro-thrombotic effects of endothelium.
    • 1) Plt effects: plts adhere to subend collagen via vWF (in WP bodies of endo)
    • 2) Procoag effects: TF prod (induced by IL6, TNF), bind IXa and Xa
    • 3) Anti-fibrinolytic: plasminogen activator inhibitors
  5. Describe the steps in normal hemostasis.
    • 1) Vascular injury leads to transient vasoconstriction.
    • 2) Plts adhere to exposed ECM via vWF --- plt activation -- shape change -- granule release -- ADP and TxA2--- plt ag --- plt plug
    • 3) Activation of coag cascade d/t TF exposure --- x-linked fibrin
    • 4) Fibrinolysis via tPA, thrombomodulin
  6. List contents of alpha granules.
    • P-selectin
    • fibrinogen
    • fibronectin
    • factors V and VIII
    • plt factor 4
    • PDGF
    • TGF-b
  7. List the contents of the dense granules.
    • ADP
    • ATP
    • Ca
    • Hist
    • Serotonin
    • Epinephrine
  8. What three things happen when plts contact ECM.
    • 1) Adhesion and shape change - vWF bridge with GP1b on plt
    • 2) Secretion - after adhesion granule contents secreted
    • 3) Aggregation - d/t ADP and TxA2, reversible until T generated, fibrinogen bridges plts via GPIIbIIIa
    • PGI2 - vasodil and inh aggregation, TxA2 vasocontr and cause plt aggregation - ASA block syn of TxA2
  9. Summarize the effects of thrombin.
    • Plt aggregation and granule release
    • Induces endoth to produce:
    • - adhesion molecules
    • - tPA
    • - NO, PGI2
    • - PDGF
    • Activate inflam cells
  10. List the steps of the intrinsic pathway.
    • XII -- XIIa via HMWK, and Prekallikrein -- Kallikrein
    • XIIa - activates XI -- XIa
    • XIa activates IX to IXa
    • IXa, VIIIa, Ca and PL comprise the tenase complex and activates X to Xa
  11. List the steps of the extrinsic pathway.
    • TF-VII -- activates IX to IXa
    • IXa along with VIIIa, Ca and PL --- tenase complex activates X to Xa
  12. List the steps of the common pathway.
    • Xa, Va, Ca, PL make up the prothrombinase complex
    • Activates II -- IIa (prothrombin to thrombin)
    • Thrombin then cleaves fibrinogen to fibrin
    • Fibrin is crosslinked by VIII
  13. Name the three endogenous anticoagulants:
    • 1) AT - inh T, IXa, Xa, XIa and XIIa - activated by hep
    • 2) Protein C and S - vit K dep, inh Va and VIIIa (in prothrombinase and tenase), activated by T-thrombomodulin
    • 3) TFPI - binds factor Xa and TF-VIIa and inactivates
  14. Describe the process of fibrinolysis.
    • Plasminogen --- cleaved to plasmin by:
    • 1) tPA or uPA - tPA most NB, most active when bound to fibrin
    • 2) Factor XII dep - XIIa conververts prekal to kal, kal then converts plasminogen to plasmin
    • INHIBITED by: free plasmin binds to a2-antiplasmin, endoth can produce PAIs (increased by T and other cytokines - to favor coag)
  15. What three factors predispose to thrombosis (Virchow's triad).
    • 1) endothelial injury
    • 2) altered bld flow - laminar bld flow keeps plts in center, away from endoth
    • 3) hypercoag - AT loss in PLN or PLE; liver dz; cushings (d/t incr in procoag by liver)
  16. State differences between arterial and venous thrombi.
    • arterial:
    • - site of turbulence or endoth injury
    • - toward ht against blood flow
    • - usually occlusive, grey/white, friable
    • venous:
    • - site of stasis
    • - toward ht with bld flow
    • - always occlusive - red or stasis thrombi
  17. List types of embolisms.
    • 1) Pulmonary
    • 2) Systemic
    • 3) Fat
    • 4) Air
    • 5) Amniotic fluid
  18. Where do red (venous) infarcts occur vs while (arterial) infarcts?
    • Red: lung, SI, with dual bld supply
    • White: solid organs with end-arterial circulation - ht, spleen, kidney
  19. Describe the pathogenesis of endotoxic shock.
    • 1) Free LPS binds to LPS binding protein
    • 2) Complex binds to cell surface CD14
    • 3) LPS then binds to TLR4 - directly activate endoth cells, WBCs or initiate cytokine production
    • - binding of TLR4 on endo cells decr. TFPI and thrombomodulin --- hypercoag
    • - binding of TLR4 on monos - activation, release of IL1 and TNF
    • 4) LPS can also directly activate complement
    • 5) Monos react to LPS by prod IL1, IL6, TNF and IL8
    • 6) IL1 and TNF - stim exp of adhesion mol by endoth cells - enhance inflammation and clear infection
  20. What happens with low doses of LPS?
    • 1) WBC activation - produce TNF, IL1, IL6, IL8
    • 2) Complement activation
    • 3) TNF and IL1 activatae endothelial cells to produce adhesion mol - local inflammation and clear infection
  21. What happens with moderate doses of LPS?
    • 1) more cytokines produced
    • 2) see systemic effects of IL1 and TNF (fever, APP)
    • 3) decr endoth prod of TFPI and thrombomod -- tip coag toward thrombosiss
  22. What happens with high doses of LPS?
    • Septic shock d/t high concentrations of cytokines and 2ry effectors
    • systemic vasodilation, decreased myocardial contractility, widespread endoth injury and activation leading to leukocyte adhesion and pulmonary alveolar damage (ARDS) -- activation of coag --- DIC
    • NOTE: mice without CD14 or TLR4 do not react to LPS
  23. What is the progression of cytokine production during septic shock?
    TNF, then IL1, then IL6/IL8
  24. What are the stages of shock?
    • 1) Nonprogressive stage
    • - compensatory mech activated and vital organs protected
    • - baroreceptor reflexes, catechol release, activation of renin-angiotensin, ADH, sympathetic stim
    • - see tachycardia, peripheral vasocontriction, renal fluid conservation
    • 2) Progressive stage
    • - tissue hypoperfusion, hypoxia and lactic acidosis - pH blunts arteriole response and get pooling of bld
    • - worsening of cardiac output, endoth damage d/t hypoxia --- DIC
    • - organ failure, urine output fails
    • 3) Irreversible stage
    • - widespread cell injury, organ shut-down
    • - in adrenal get cortical cell lipid depletion - conversion of inactive cells to active cells to produce steroids

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