Path Hemodynamic Disorders (6)

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mse263
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258453
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Path Hemodynamic Disorders (6)
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2014-01-26 14:09:06
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Pathology
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MBS Pathology
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Exam 1
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  1. What are the components of normal blood circulation?
    • 1. intact blood vessels
    • 2. normal blood pressure (normotensive)
    • 3. normal osmolarity
    • 4. normal blood flow (not slowed/blocked)
  2. Starling’s Law of the Capillaries
    • fluids leave or enter the capillaries depending on how the pressures in the capillary & interstitial spaces relate to each other
    • the net effect of the opposing pressures determining the direction and the rate of fluid flow
  3. Edema
    • increased fluid in interstitial tissue spaces caused by altered vascular homeostasis
    • can occur in body cavities (hydrothorax, hydropericardium, hydroperitoneum) & is called ascites
  4. Anasarca
    • severe systemic edema
    • significant edema can impair wound healing or clearance of an infection
  5. Where is edema immediately life-threatening?
    • the brain
    • edema in subcutaneous tissue may signal potential underlying cardiac or renal diseases
  6. Common Causes of Edema
    • ↑ hydrostatic pressure

    • decreased colloid osmotic pressure

    • lymphatic obstruction (lymphedema): interstitial fluid can't be drained

    • primary renal Na+ retention w/ associated water retention (eg. in renal failure)

    • increased vascular permeability (eg. during inflammation)
  7. How does an increase in hydrostatic pressure cause edema?
    • it forces fluid out of the vessels
    • an example of a generalized increase: congestive heart failure (CHF)
    • an example of a regional increase: deep vein thrombosis
  8. How might a decrease in colloid osmotic pressure cause edema?
    • it reduces the need for fluid to move into vessels out of the interstitium
    • can happen when there's a reduced plasma albumin concentration as a result of liver disease or malnutrition [Kwashikor/PEM]
    • can also result from increased protein loss w/ protein-losing glomerulopathies or nephrotic syndrome
  9. Hyperemia
    • an active increased inflow of blood to a tissue that results from vasodilation of pre-capillary arterioles
    • manifests as redness (erythema)
    • capillary beds become engorged with OXYGENATED blood
  10. Congestion
    • a passive decreased outflow of blood
    • manifests as cyanosis & can lead to ischemia
    • capillary beds become engorged with DEOXYGENATED venous blood
  11. Cyanosis
    blue or purple coloration of the skin due to the tissues near the skin surface having low oxygen saturation
  12. Nutmeg Liver (Congestive Hepatopathy)
    • chronic passive congestion of the liver that causes dysfunction due to venous congestion
    • usually due more superficially to cardiac dysfunction (i.e. congestive heart failure)
    • liver can be seen to have dark spots where congested hepatic venules are
  13. Heart Failure Cells
    • hemosiderin-containing macrophages
    • in left heart failure the left ventricle can not keep pace with incoming blood from the pulmonary veins
    • the resulting backup causes increased pressure on the alveolar capillaries & RBCs leak out
    • alveolar macrophages (dust cells) ingest the red blood cells & become engorged with brownish hemosiderin, a byproduct of RBC degredation
  14. Hemorrhage
    • loss of blood escaping from the circulatory system into the extravascular space

    • can happen in the capillaries as a result of chronic congestion or changes in vessel permeability

    • can be due to bleeding diathesis, an unusual susceptibility to bleeding (hemorrhage) mostly due to hypOcoagulability

    • can be the result of rupture of larger vessels due to trauma or aneurism
  15. Hematoma
    • localized collection of blood outside the blood vessels
    • is usually in liquid form relatively or completely confined within an organ, tissue, or space
    • simple: ecchymosis
    • life-threatening: subdural hematoma
  16. Petechia
    • a small red/purple spot on the body, caused by a minor Hemorrhage resulting from broken capillary blood vessels
    • potential causes include locally increased
    • intravascular pressure, low platelet counts (thrombocytopenia - no clotting), defective platelet function (as in uremia), or a loss in vascular wall support (Vit C deficiency)
  17. Purpura
    • red or purple discolorations on the skin caused by Hemorrhage underneath the skin usually secondary to Secondary trauma, Vasculitis, Allergic reaction, or Increased vascular fragility (as in amyloidosis)
    • similar but larger than Petechia
  18. Ecchymosis
    • larger subcutaneous hematoma/purpura
    • NOT caused by trauma
  19. Hemothorax
    • a condition that results from blood accumulating in the pleural cavity
    • shows up cloudy/opaque on an X-ray
  20. Hemostasis
    • results from tightly controlled processes that maintain blood in a fluid, clot-free state in normal vessels
    • process which causes bleeding to STOP, keeping blood within a damaged blood vessel
    • the opposite of hemostasis is hemorrhage
  21. Blood Clot (Thrombus)
    • the final product of the blood coagulation step in hemostasis
    • it's achieved by platelets aggregating to form a platelet plug & the activation of the humoral coagulation system (i.e. clotting factors)
    • a blood clot/thrombus is NORMAL in response to injury, but pathologic in instances of thrombosis (= an unprovoked clot)
  22. Thrombosis
    • formation of a blood clot within an INTACT vessel
    • pathologic counterpart of hemostasis
    • not the same thing as a blood clot; is like a pathologic, unprovoked blood clot
  23. What are the 3 components of hemostasis?
    • 1. endothelium (vascular wall)
    • 2. platelets
    • 3. coagulation cascade
  24. Primary Hemostasis
    • 1. Transient vasoconstriction
    • 2. Endothelial injury exposes highly thrombogenic substances (eg. vWF & those from the ECM)
    • 3. Platelet activation, adherence, & aggregation
    • RESULT: formation of a PRIMARY hemostatic plug
  25. Secondary Hemostasis
    • 1. Release of tissue factor (factor III/thromboplastin in endothelial cells) & phospholipids (platelets)
    • 2. Coagulation cascade generates thrombin
    • 3. Thrombin cleaves fibrinogen into fibrin
    • 4. Fibrin meshwork consolidates the primary platelet plug
    • 5. A secondary, more stable, hemostatic plug forms from polymerized fibrin, platelets, RBCs, & WBCs
    • 6. Hemostatic plug limited to the site of injury by counter-regulatory mechanisms
  26. von Willebrand factor (vWF)
    • facilitates platelet adhesion to wound sites
    • functions as an adhesion bridge between subendothelial collagen & the glycoprotein lb (Gplb) platelet receptor
  27. Once a layer of platelets adhere to a wound, how is platelet aggregation accomplished?
    • fibrinogen bridges GpIIb-IIIa receptors on different platelets, attaching them to each other
  28. Glanzmann Thombasthenia
    • GpIIb-IIIa deficiency
    • a receptor found on the surface of platelets that allows them to bind to fibrinogen & clot together
  29. von Willebrand Disease
    von Willebrand factor deficiency - without it platelets can't initially bind to the site of a wound
  30. Bernard-Soulier Syndrome
    GpIb deficiency - a receptor found on the surface of platelets that allows them to bind to vWF & coagulate over a wound
  31. Thrombin
    • abundant conversion enzyme in the blood coagulation cascade
    • promotes platelet aggregation & release of TXA2, neutrophil adhesion, + monocyte, leukocyte, & endothelial activation
    • endothelial cells go on to produce NO, PGI2, & tPA (function to down-regulate blood clots later)
  32. Thromboxane A2 (TXA2)
    • induces platelet aggregation
    • made in platelets & released by them when thrombin stimulates them to aggregate
    • AA → PGG2 → PGH2 → TXA2 → TXB2
  33. PGI2
    • prostacyclin is an eicosanoid that INHIBITS platelet activation
    • (is also an effective vasodilator)
  34. tPA
    protein involved in the breakdown of blood clots
  35. Heparin
    an anti-coagulant drug that promotes the high-affinity binding of antithrombin to thrombin, thereby reducing blood clotting
  36. What happens to plasminogen after it has been activated?
    it becomes Plasmin, an important enzyme present in blood that degrades many blood plasma proteins, including fibrin clots (degradation of fibrin = fibrinolysis)
  37. *Virchow's Triad
    • describes the 3 broad factors that contribute to thrombosis (pathologic blood clot)
    • Hypercoagulability
    • Hemodynamic changes (stasis, turbulence)
    • Endothelial injury/dysfunction
  38. Endothelial injury
    • endothelium integrity is the most important factor in the formation of thrombosis, especially in the heart & arteries
    • any disruption in the balance of pro-thrombotic & anti-thrombotic activities of the endothelium can influence local clotting
    • dysfunction can be caused by hypertension, turbulent blood flow, bacterial products, radiation injury, metabolic abnormalities, cigarette smoke etc.
  39. Abnormal Blood Flow (Hemodynamic Changes)
    • promotes endothelial activation, enhancing procoagulant activity, leukocyte adhesions, etc., partly through flow-induced changes in endothelial cell gene expression
    • disruption of laminar flow brings platelets into contact with the endothelium
    • eg. Turbulence (arterial/cardiac thrombosis) or Stasis (venous thrombi)
  40. Hypercoagulability
    • Primary: genetic defects that predispose a person to thrombosis (eg. prothrombin mutations, homocystinuria)
    • Secondary: anything not genetic that predisposes a person to coagulation (prolonged bedrest or immobilization, myocardial infarct, cancer, atrial fibrillation, tissue injury, heparin-induced thrombocytopenia, antiphospholipid antibody syndrome)
  41. *Factor V
    • a protein of the coagulation system that cleaves prothrombin to prethrombin
    • prothrombin → prethrombin → thrombin (↑ CLOTS)
  42. *Factor V Leiden
    • an inherited disorder of blood clotting in which a variant of human factor V causes a HYPERcoagulability disorder
    • in this disorder, the Leiden variant of factor V cannot be inactivated by activated protein C (which is antithrombic)
  43. Natural Anticoagulants
    • protein C (when activated it INactivates Factor V)
    • protein S (cofactor to protein C)
    • AT-III (Antithrombin, inhibits coagulation cascade)
    • fibrinolytic factors (t-PA)
    • platelet aggregation inhibitors (PGI2, NO, adenosine diphosphatase)
  44. *Which way do arterial & venous thrombi (coagulations) tend to grow?
    • Arterial thrombi tend to grow retrograde/against the flow of blood
    • Venous thrombi extend IN the direction of blood flow
    • aka both types of thrombi tend to propagate TOWARD the heart
  45. Lines of Zahn
    • a characteristic of thrombi that appear particularly when formed in the heart or aorta

    • they have visible & microscopic alternating layers (laminations) of platelets mixed w/ fibrin, which appear lighter, as well as darker layers of RBCs

    • their presence implies thrombosis at a site of rapid blood flow that happened before death

    • they are less apparent in veins or smaller arteries where flow is not as constant

  46. Mural Thrombi
    • a thrombus in the heart chambers or aortic lumen
    • can be seen on the surface/wall of the heart or vessel
    • may develop in the part of a wall that doesn't contract to the same degree as others, like an area where there was once an infarct
    • differences in contraction rate can lead to mural thrombus
  47. Arterial Thrombi
    • frequently occlusive, meaning blood flow may be completely cut-off
    • are produced by platelet & coagulation activation, formed as a friable meshwork of platelets, fibrin, RBC, & degenerating leukocytes
    • (friable = the ability of a solid substance to be reduced to smaller pieces with little effort; implies the clot could break into smaller pieces & possibly occlude smaller vessels)
  48. Phlebothrombosis
    • a venous thrombosis
    • these are almost always occlusive
    • can create a long cast in the lumen
    • are produced largely by activation of the coagulation cascade
    • are frequently caused by venous stasis (slow blood flow in the veins)
  49. Postmortem Clots
    • gelatinous, w/ a dark red dependent portion (RBC) & a yellow ‘chicken fat’ supernatant
    • are usually not attached to an underlying wall
  50. *Thrombus Outcomes
    • • Propagation: thrombi accumulate additional platelets & fibrin; can get large & long
    • • Embolization: thrombi dislodge & travel to other sites in the vasculature; in an area w/ a diameter smaller than the clot → stuck (embolism)
    • • Dissolution: fibrinolysis, rapid shrinkage, & total disappearance of clot
    • • Organization & Recanalization
  51. Thrombus Recanalization
    • when around a thrombus there's ingrowth of endothelial cells, smooth muscle cells, & fibroblasts in an effort to restore blood flow through that vessel (almost as if the clot just becomes part of/is sucked onto the vessel wall)
    • capillary channels form & re-establish blood flow continuity through the lumen
    • resulting lumen is much smaller; there's variable size reduction depending on the clot size & amount of recanalization
    • as a result blood flow through such a vessel is reduced compared to the original amount of flow
  52. What's the difference between a thrombus and an embolism?
    • a thrombus is a pathological blood clot that causes a blockage at its site of origin
    • an embolism is the lodging of an embolus that causes a blockage which may affect a site away from the actual embolism
  53. *Embolism
    • • a detached intravascular solid, liquid, or gaseous mass carried by blood to a site distant from its point of origin where it lodges & causes a blockage
    • • emboli lodge in vessels too small to allow further passage, causing partial or complete vascular occlusion
    • • such a blockage may affect a part of the body away from the actual site of the embolism (downstream of it)
  54. What substances are often responsible for embolisms?
    • • almost all emboli represent some part of a dislodged thrombus (thromboembolism)
    • • other examples of embolus's include fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or foreign bodies
  55. What is a major consequence of embolism?
    ischemic necrosis (infarction) of tissue downstream of a blockage
  56. Infarction
    • an area of ischemic necrosis (tissue death) caused by a lack of oxygen due to an obstruction of the tissue's blood supply
    • obstruction/occlusion can be of either the arterial supply or the venous drainage
  57. *What are the 2 types of infarctions?
    • 1. Red → liver, lung
    • 2. White → heart [MI], spleen
    • are divided according to the amount of blood present
  58. Red (Hemorrhagic) Infarct
    • generally affects loose organs the occlusion consists more RBCs & fibrin strands
    • can be seen in brain, lungs, liver, GI tract (small intestines), testis, ovary
  59. Causes/Components of Red Infarct
    • 1. Venous Occlusions
    • 2. Loose tissues that allow blood to collect in the infarct zone
    • 3. Tissues w/ Dual Circulation: permit the flow of blood from an unobstructed parallel supply to rescue the ischemic tissue (lung/intestines)
    • 4. Tissues previously congested because of sluggish venous blood outflow
    • 5. Reperfusion of previously ischemic tissue: flow is re-established to a site of previous arterial occlusion & necrosis
  60. White (Anemic) Infarct
    • occurs w/ arterial occlusions or in solid organs (heart, spleen, kidney) w/ end arterial circulations
    • the solidity of the tissue limits the amount of amount of nutrients (blood/oxygen/glucose/fuel) that can flow into an area of ischemic necrosis from adjoining capillary beds
    • is usually wedged-shaped
  61. *Shock
    systemic hypotension is due either to reduced cardiac output or to reduced effective circulating blood volume → impaired tissue perfusion & cellular hypoxia
  62. Cardiogenic Shock
    low cardiac output from pump failure
  63. Hypovolemic Shock
    low cardiac output from LOSS of blood or plasma volume
  64. Septic Shock
    • caused by the host's innate immune response to bacterial or fungal cell molecules (ENDOTOXIN) w/ systemic production of cytokines that over-activate endothelial, inflammatory, & immune cells
    • host cells cause excessive vasodilation, hypotension, peripheral pooling of blood, DIC, & overall metabolic disturbances
    • the eventual result is multiple organ dysfunction
  65. Disseminated Intravascular Coagulation (DIC)
    • a serious disorder in which the proteins that control blood clotting become over active
    • aka microvascular thrombosis
  66. Stages of Shock
    • shock of any form causes pathology by inducing prolonged tissue hypoxic injury
    • 1. Initial nonprogressive phase: reflex compensatory mechanisms are activated & perfusion of vital organs is maintained
    • 2. A progressive stage characterized by tissue hypoperfusion & onset of worsening circulatory & metabolic imbalance (eg. acidosis)
    • 3. An irreversible stage that sets in after the body has incurred cellular & tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible

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