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  1. What is hemostatsis?
    Damage to the wall is repaired by hemostasis,
  2. Hemostasis involves the formation of?
    a thrombus (clot) at the site of vessel injury
  3. Hemostasis stages?
    primary and secondary.
  4. Primary hemostasis?
    forms a weak platelet plug
  5. Primary hemostasis is mediated by?
    interaction between platelets and the vessel wall
  6. Secondary hemostasis?
    stabilizes the platelet plug
  7. Secondary hemostasis is mediated by?
    the coagulation cascade.
  8. What is Step 1 in secondary hemostasis?
    Transient vasoconstriction of damaged vessel
  9. How is Step 1 in secondary hemostasis mediated?
    by reflex neural stimulation and endothelin release from endothelial cells
  10. What is Step 2 in secondary hemostasis?
    Platelet adhesion to the surface of disrupted vessel
  11. In step 2 of secondary hemostasis, how does platelet adhesion occur?
    Von Willebrand factor (vWF) binds exposed subendothelial collagen,
  12. How do platelets bind to vWF?
    via the GPIb receptor
  13. vWF is derived from?
    the Weibel-Palade bodies of endothelial cells and a-granules of platelets.
  14. What is Step 3 in secondary hemostasis?
    Platelet degranulation
  15. In step 3 of secondary hemostasis what does Adhesion induce?
    shape change in platelets and degranulation with release of multiple mediators
  16. What are the mediators released in step 3 of secondary hemostasis?
    ADP and TXA
  17. What is the role of ADP in step 3 of secondary hemostasis?
    it is released from platelet dense granules; promotes exposure of GPIIb/IIIa receptor on platelets.
  18. What is the role of TXA in step 3 of secondary hemostasis?
    it is synthesized by platelet cyclooxygenase (COX) and released; promotes platelet aggregation
  19. What is step 4 in secondary hemostasis?
    Step 4—Platelet aggregation
  20. Where and how do Platelets aggregate in step 4 of secondary hemostasis?
    at the site of injury via GPIIb/IIIa using fibrinogen (from plasma) as a linking molecule;
  21. What does platelet aggregation result in?
    formation of platelet plug
  22. Platelet plug?
    It is weak; coagulation cascade (secondary hemostasis) stabilizes it.
  23. What are disorders of primary hemostasis usually due to?
    Usually due to abnormalities in platelets;
  24. Disorders of primary hemostasis are divided into?
    quantitative or qualitative disorders
  25. What are some Clinical features for disorders of primary hemostasis?
    mucosal and skin bleeding.
  26. What is the most common overall symptom in mucosal bleeding?
  27. What are symptoms of mucosal bleeding?
    epistaxis, hemoptysis, GI bleeding, hematuria, and menorrhagia. Intracranial bleeding occurs with severe thrombocytopenia.
  28. What are the symptoms of skin bleeding?
    include petechiae (1-2 mm), ecchymoses (> 3 mm), purpura (> 1 cm), and easy bruising;
  29. Petechiae are a sign of what?
    thrombocytopenia and are not usually seen with qualitative disorders.
  30. What are some useful laboratory studies for disorders of primary hemostasis?
    platelet count, bleeding time, blood smear, bone marrow biopsy
  31. Platelet count
    normal 150-400 K/pL; < 50 K/pL leads to symptoms,
  32. Bleeding time
    normal 2-7 minutes; prolonged with quantitative and qualitative platelet disorders
  33. Blood smear
    used to assess number and size of platelets
  34. Bone marrow biopsy
    used to assess megakaryocytes, which produce platelets
  35. What is immune thrombocytopenic purpura?
    (ITP) is an autoimmune production of IgG against platelet antigens (GPIIb/IIIa)
  36. What is the most common cause of thrombocytopenia in children and adults?
    immune thrombocytopenic purpura
  37. In ITP where are the autoantibodies produced?
  38. In ITP what results in thrombocytopenia?
    Antibody-bound platelets are consumed by splenic macrophages
  39. ITP is divided into?
    acute and chronic forms
  40. Acute form of ITP?
    arises in children weeks after a viral infection or immunization;selflimited, usually resolving within weeks of presentation
  41. Chronic form of ITP?
    arises in adults, usually women of chilbearing age. May be primary or secondary (e.g SLE).
  42. What is the risk involved in chronic ITP?
    May cause short-lived thrombocytopenia in offspring since antiplatelet IgG can cross the placenta.
  43. laboratory findings for ITP include
    decreased platelet count, often < 50 K/pL, Normal PT/FTT, Coagulation factors are not affected. increased megakaryocytes on bone marrow biopsy
  44. What is the Initial treatment for ITP?
  45. How will children and adults respond to the initial treatment for ITP?
    Children respond well; adults may show early response, but often relapse.
  46. In addition to corticosteroids what else is used in the treatment of ITP?
    IVIG is used to raise the platelet count in symptomatic bleeding, but its effect is short-lived,
  47. What is a permenant solution for patients with ITP?
    Splenectomy eliminates the primary source of antibody and the site of platelet destruction (performed in refractory cases).
  48. What is microangiopathic hemolytic anemia?
    Pathologic formation of plateletmicrothrombin small vessels
  49. How are plateletmicrothrombin formed and what is the result?
    Platelets are consumed in the formation of microthrombi sheering the RBCs as they cross microthrombi, resulting in hemolytic anemiawith schistocytes
  50. What is microangiopathic hemolytic anemia seen in?
    thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)
  51. What is TTP due to?
    decreased ADAMTS13 which is an enzyme that normally cleaves vWF multimers into smaller monomers for eventual degradation.
  52. How does TTP lead to microangiopathic hemolytic anemia?
    1. Large, uncleaved multimers lead to abnormal platelet adhesion, resulting in microthrombi.
  53. Decreased ADAMTS13 is usually due what?
    an acquired autoantibody;
  54. TTP is most commonly seen in?
    adult females
  55. HUS is due to?
    Hemolytic uremic syndrome is due to endothelial damage by drugs or infection.
  56. HUS is classically seen in?
    children with E coli G157;H7 dysentery, which results from exposure to undercooked beef
  57. How is E Coli related to microangiopathic hemolytic anemia?
    E coli verotoxin damages endothelial cells resulting in platelet microthrombi
  58. The clinical findings for HUS and TTP include
    Skin and mucosal bleeding, Microangiopathic hemolytic anemia, Fever, Renal insufficiency, CNS abnormalities
  59. Renal insufficiency is more common in HUS or TTP?
    HUS — thrombi involve vessels of the kidney
  60. CNS abnormalities are more common in HUS or TTP?
    TTP — Thrombi involve vessels of the CNS
  61. Laboratory findings for microangiopathic hemolytic anemia include?
    Thrombocytopenia with increased bleeding time Normal PT/PTT (coagulation cascade is not activated), anemia with schistocytes, increased megakaryocytes on bone marrow biopsy
  62. Treatment for microangiopathic hemolytic anemia?
    involves plasmapheresis and corticosteroids, particularly in TTP.
  63. What are the qualitative platelet disorders?
    bernard-soulier, Glanzmann thrombasthenia, asprin, uremia
  64. Bernard-Soulier syndrome
    is due to a genetic GPIb deficiency; platelet adhesion is impaired.
  65. In Bernard-Soulier what lab test are you interested in?
    Blood smear which shows mild thrombocytopenia with enlarged platelets.
  66. Glanzmann thrombasthenia is due to?
    a genetic GPIIb/IIIa deficiency; platelet aggregation is impaired.
  67. Aspirin and microangiopathic hemolytic anemia?
    it irreversibly inactivates cyclooxygenase; lack of TXA, impairs aggregation.
  68. Uremia and microangiopathic hemolytic anemia
    disrupts platelet function; both adhesion and aggregation are impaired.
  69. What does secondary hemostasis do?
    Stabilizes the weak platelet plug via the coagulation cascade
  70. In secondary hemostasis the coagulation cascade generates?
    thrombin, which converts fibrinogen in the platelet plug to fibrin.
  71. In secondary hemostasis what happens to fibrin?
    It is cross-linked, yielding a stable platelet-fibrin thrombus.
  72. Where are the factors of the coagulation cascade produced?
    In the liver in an inactive state.
  73. What does activation of the factors of the coagulation cascade require?
    exposure to an activating substance, Phospholipid surface of platelets, calcium
  74. What are the activating substances involved in the activation of the factors of the coagulation cascade?
    Tissue thromboplastin activates factor VII (extrinsic pathway). Subendothelial collagen activates factor XII (intrinsic pathway).
  75. Where does the Calcium involved in the activation of the factors of the coagulation cascade come from?
    derived from platelet dense granules
  76. Disorders of secondary hemostasis are usually due to?
    factor abnormalities
  77. What are the clinical features of disorders of secondary hemostasis?
    they include deep tissue bleeding into muscles and joints (hemarthrosis) and rebleeding after surgical procedures (e.g circumcision and wisdom tooth extraction).
  78. Laboratory studies for Disorders of secondary hemostasis include?
    PT (prothrombin time) and PTT (partial thromboplastin time)
  79. Prothrombin time (PT)
    measures extrinsic (factor VII) and common (factors II, V, X, and fibrinogen) pathways of the coagulation cascade
  80. Extrinsic pathway of the coagulation cascade
    factor VII
  81. Common pathway of the coagulation cascade
    factors II, V, X, and fibrinogen
  82. Partial thromboplastin time (PTT) measures
    intrinsic (factors XII, XI, IX, VIII) and common (factors II, V, X, and fibrinogen) pathways of the coagulation cascade
  83. What is involved in Hemophilia A?
    Genetic factor VIII (FVIII) deficiency, X-linked recessive (predominantly affects males)
  84. Does Hemophilia A require a family history of it?
    Can arise from a new mutation (de novo) without any family history
  85. Hemphilia A presents with?
    deep tissue, joint, and postsurgical bleeding
  86. Clinical severity of hemophilia A depends on?
    the degree of deficiency
  87. Laboratory findings of hemophilia A include
    1. increased PTT; normal PT 2. decreased FVIII 3. Normal platelet count and bleeding time
  88. What does treatment of hemophilia A involve?
    recombinant FVIII.
  89. What is christmas disease?
    Hemophilia B - Genetic factor IX deficiency, Resembles hemophilia A, except FIX levels are decreased instead of FVIII
  90. What is coagulation factor inhibitor?
    Acquired antibody against a coagulation factor resulting in impaired factor function; anti-FVIII is most common,
  91. Clinical and lab findings for hemophilia B?
    its similar to hemophilia A, PTT does not correct upon mixing normal plasma with patient's plasma (mixing study) due to inhibitor; PTT does correct in hemophilia A.
  92. How can you tell the difference between hemophilia A and B?
    mixing study
  93. von Willebrand Disease
    Genetic vWF deficiency
  94. What is the most common inherited coagulation disorder?
    von Willebrand disease
  95. Does von Willebrand Disease result in qualitative or quantitative disorders?
    Multiple subtypes exist, causing quantitative and qualitative defects;
  96. What is the most common type of von Willebrand Disease?
    is autosomal dominant with decreased vWF levels
  97. von Willebrand Disease presents with?
    mild mucosal and skin bleeding; low vWF impairs platelet adhesion.
  98. Laboratory findings for von Willebrand Disease include
    1. increased bleeding time 2. increased PTT: normal PT — Decreased FVIII half-life (vWF normally stabilizes FVIII); 3. Abnormal ristocetin test
  99. What is usually not seen with von Willebrand Disease that is unusual
    deep tissue, joint, and postsurgical bleeding are usually not seen.
  100. Why is there an Abnormal ristocetin test in von Willebrand disease
    Ristocetin induces platelet aggregation by causing vWF to bind platelet GPIb; lack ofvWF —> impaired aggregation —> abnormal test.
  101. What is the treatment for von willebrand disease?
    desmopressin (ADH analog), which increases vWF release from Weibel-Palade bodies of endothelial cells
  102. How does vitamin K deficiency relate to hemostasis?
    Disrupts function of multiple coagulation factors
  103. What is involved in Vitamin K activation?
    Vitamin K is activated by epoxide reductase in the liver
  104. What does Activated vitamin K do?
    it gamma carboxvlates factors II, VII, IX, X, and proteins C and S; gamma carboxylation is necessary for factor function.
  105. Vitamin K deficiency occurs in?
    1. Newborns 2. Long-term antibiotic therapy 3. Malabsorption
  106. Why is there vitamin K deficiency in newborns?
    its due to lack of GI colonization by bacteria that normally synthesize vitamin K; vitamin K injection is given prophylactic ally to all newborns at birth to prevent hemorrhagic disease of the newborn
  107. How does Long-term antibiotic therapy elad to Vitamin K deficiency?
    disrupts vitamin K-producing bacteria in the GI tract
  108. How does Malabsorption lead to Vitamin K deficincy?
    leads to deficiency of fat-soluble vitamins, including vitamin K
  109. What are some other causes of secondary hemostasis?
    liver failure, large volume transfusion,
  110. How does liver failure lead to secondary hemostasis?
    decreased production of coagulation factors and decreased activation of vitamin K by epoxide reductase;
  111. How is the effect of liver failure on coagulation followed?
    followed using PT.
  112. How does Large-volume transfusion lead to secondary hemostasis?
    it dilutes coagulation factors, resulting in a relative deficiency
  113. What is Heparin induced thrombocytopenia?
    Platelet destruction that arises secondary to heparin therapy
  114. How does Heparin induced thrombocytopenia lead to thrombosis?
    Fragments of destroyed platelets may activate remaining platelets, leading to thrombosis
  115. What is disseminated intravascular coagulation?
    Pathologic activation of the coagulation cascade
  116. What does disseminated intravascular coagulation result in?
    1. Widespread microthrombi result in ischemia and infarction, 2. Consumption of platelets and factors results in bleeding, especially from IV sites and mucosal surfaces (bleeding from body orifices).
  117. Is disseminated intravascular coagulation usually primary or secondary?
    Almost always secondary to another disease process
  118. What are some situations that may result in disseminated intravascular coagulation?
    Obstetric complications, sepsis, adenocarcinoma, Acute promyelocytic leukemia, Rattlesnake bite
  119. Obstetric complications and disseminated intravascular coagulation
    Tissue thromboplastin in the amniotic fluid activates coagulation
  120. Sepsis and disseminated intravascular coagulation
    (especially with E. coli or Neisseria meningitidis) — Endotoxins from the bacterial wall and cytokines (e.g TNF and IL-1) induce endothelial cells to make tissue factor.
  121. Adenocarcinoma and disseminated intravascular coagulation
    Mucin activates coagulation.
  122. Acute promyelocytic leukemia and disseminated intravascular coagulation
    Primary granules activate coagulation.
  123. Rattlesnake bite and and disseminated intravascular coagulation
    Venom activates coagulation
  124. Laboratory findings for disseminated intravascular coagulation include?
    decreased platelet count, increased PT/PTT, decreased fibrinogen, Microangiopathic hemolytic anemia, Elevated fibrin split products, particularly D-dimer
  125. What is the best screening test for DIC?
    Elevated D-dimer
  126. D dimer is derived from?
    splitting of cross-linked fibrin; D-dimer is not produced from splitting of fibrinogen.
  127. Treatment of DIC involves?
    addressing the underlying cause and transfusing blood products and cryoprecipitate (comains coagulation factors), as necessary.
  128. What does normal fibrinolysis do?
    Normal fibrinolysis removes thrombus after damaged vessel heals
  129. Tissue plasminogen activator (tPA)
    converts plasminogen to plasmin
  130. Plasmin
    cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation.
  131. a2-antiplasmin
    inactivates plasmin.
  132. What are the disorders of fibrinolysis due to? What does this result in?
    plasmin overactivity resulting in excessive cleavage of serum fibrinogen.
  133. What are some examples of disorders of fibrinolysis?
    radical prostatectomy, cirrohsis of the liver
  134. How does radical prostatectomy lead to a disorder of fibrinolysis?
    Release of urokinase activates plasmin
  135. How does cirrhosis of the liver lead to a disorder of fibrinolysis?
    reduced production of a2-antiplasmin
  136. How does disorders of fibrinolysis present?
    with increased bleeding (resembles DIC)
  137. Laboratory findings for disorders of fibrinolysis include
    Increased PT/PTT, increased bleeding time with normal platelet count, Increased fibrinogen split products without D-dimers
  138. Why is there increased fibrinogen split products without D-dimers in disorders of fibrinolysis?
    Serum fibrinogen is lysed; however, D-dimers are not formed because fibrin thrombi are absent
  139. Why is there increased bleeding time with disorders of fibrinolysis?
    Plasmin blocks platelet aggregation
  140. Why is there increased PT/PTT with disorders of fibrinolysis?
    Plasmin destroys coagulation factors.
  141. What is the treatment for disorders of fibrinolysis?
    it is aminocaproic acid, which blocks activation of plasminogen.
  142. What is thrombosis?
    Pathologic formation of an intravascular blood clot (thrombus), Can occur in an artery or vein,
  143. What is the most common location for thrombosis?
    it is the deep veins (DVT) of the leg below the knee
  144. What is thrombosis characterized by?
    lines of Zahn and attachment to vessel wall
  145. What are the lines of Zahn?
    alternating layers of platelets/fibrin and RBCs
  146. What distinguishes thrombus from a postmortem clot?
    lines of Zahn and attachment to vessel wall
  147. What are three major risk factors for thrombosis?
    disruption in blood flow, endothelial cell damage, and hypercoagulable state (Virchow triad)
  148. What is normal blood flow?
    blood flow is normally continuous and laminar; keeps platelets and factors dispersed and inactivated
  149. What happens to blood flow that causes an increase in the risk for thrombosis?
    Stasis and turbulence of blood flow increases risk for thrombosis
  150. What are some examples of disruption of normal blood flow?
    Immobilization—increased risk for deep venous thrombosis 2. Cardiac wall dysfunction (e.g arrhythmia or myocardial infarction) 3. Aneurysm
  151. How does endothelial cell damage increase the risk for thrombosis?
    Endothelial damage disrupts the protective function of endothelial cells, increasing the risk for thrombosis
  152. How do endothelial cells prevent thrombosis?
    1. Block exposure to subendothelial collagen and underlying tissue factor 2. Produce prostacyclin (PGI2) and NO, 3. Secrete heparin-like molecules, 4. Secrete tissue plasminogen activator (tPA) 5. Secrete thrombomodulin
  153. How does endothelial cells use the secretion of tPA to prevent thrombosis?
    converts plasminogen to plasmin, which (1) cleaves fibrin and serum fibrinogen, (2) destroys coagulation factors, and (3) blocks platelet aggregation
  154. How does the secretion of thrombomodulin from endothelial cells prevent thrombosis?
    redirects thrombin to activate protein C, which inactivates factors V and VIII
  155. How do endothelial cells use the secretion of heparin-like molecules to prevent thrombosis?
    augment antithrombin III (ATIII) which inactivates thrombin and coagulation factors
  156. How does endothelial cells use the production of prostacyclin (PGI2) and NO to prevent thrombosis?
    vasodilation and inhibition of platelet aggregation
  157. What are the causes of endothelial cell damage?
    atherosclerosis, vasculitis, and high levels of homocysteine
  158. Vitamin B12 and folate deficiency result in?
    mildly elevated homocysteine levels, increasing the risk for thrombosis.
  159. What does folic acid circulate as?
    methyl-THF (tetrahydrofolate, THF) in the serum,
  160. How does THF participate in the synthesis of DNA precursors?
    Methyl is transferred to cobalamin (vitamin B12) which transfers methyl to homocysteine resulting in methionine
  161. What does a lack of vitamin B12 or folate lead to?
    decreased conversion of homocysteine to methionine resulting in buildup of homocysteine
  162. Cystathionine beta synthase (CBS) deficiency results in what?
    high homocysteine levels with homocystinuria,
  163. What does CBS do?
    CBS converts homocysteine to cystathionine
  164. CBS deficiency leads to?
    homocysteine buildup
  165. CBS deficiency is characterized by?
    vessel thrombosis, mental retardation, lens dislocation, and long slender fingers
  166. what is a hypercoagulabe state due to?
    excessive procoagulant proteins or defective anticoagulant proteins; may be inherited or acquired
  167. What is the classic presentation for a hypercoagulable state?
    recurrent DVTs or DVT at a young age, usually occurs in the deep veins of the leg; other sites include hepatic and cerebral veins
  168. What are some causes of a hypercoagulable state?
    protein C and S deficiency, factor V Liden deficiency, prothrombin 20210A, ATIII deficiency, oral contraceptives
  169. protein C or S deficiency
    (autosomal dominant) decreases negative feedback on the coagulation cascade (hypercoagulable state)
  170. Proteins C and S normally do what?
    inactivate factors V and VIII
  171. Protein C and S deficiency increases the risk for what?
    warfarin skin necrosis
  172. What does the initial stage of warfarin therapy result in?
    a temporary deficiency of proteins C and S (due to shorter half-life) relative to factors II, VII, IX, and X
  173. In preexisting C or S deficiency, what danger does the initial stage of warfarin therapy present?
    a severe deficiency is seen at the onset of warfarin therapy increasing the risk for thrombosis, especially in the skin
  174. What is Factor V Leiden?
    a mutated form of factor V that lacks the cleavage site for deactivation by proteins C and S
  175. What is the most common inherited cause of hypercoagulable state?
    Factor V Leiden
  176. What is Prothrombin 20210A?
    it is an inherited point mutation in prothrombin that results in increased gene expression,
  177. Increased prothrombin (prothrombin 20210A) results in what?
    increased thrombin, promoting thrombus formation.
  178. What does ATIII deficiency result in?
    decreases the protective effect of heparin-like molecules produced by the endothelium, increasing the risk for thrombus
  179. What do heparin-like molecules normally do?
    activate ATIII, which inactivates thrombin and coagulation factors
  180. What happens in ATIII deficiency?
    PTT does not rise with standard heparin dosing.
  181. Pharmacologic heparin works by doing what?
    binding and activating ATIII
  182. High doses of heparin in someone with ATIII deficiency results in what?
    activate limited ATIII; Coumadin is then given to maintain an anticoagulated state.
  183. How are oral contraceptives associated with a hypercoagulable state?
    Estrogen induces increased production of coagulation factors, thereby increasing the risk for thrombosis
  184. What is an embolism?
    Intravascular mass that travels and occludes downstream vessels; symptoms depend on the vessel involved
  185. What is a thromboembolus due to?
    a thrombus that dislodges;
  186. What is the most common type of embolus?
    thromboembolus (>95%)
  187. Atherosclerotic embolus is due what?
    to an atherosclerotic plaque that dislodges.
  188. Atherosclerotic embolus is characterized by what?
    the presence of cholesterol clefts in the embolus
  189. Fat embolus is associated with what?
    bone fractures, particularly long bones, and soft tissue trauma
  190. When does a fat embolus develop?
    while fracture is still present or shortly after repair
  191. What is fat embolus characterized by?
    dyspnea (fat, often with bone marrow elements, is seen in pulmonary vessels and petechiae on the skin overlying the chest
  192. Gas embolus is classically seen in what?
    decompression sickness.
  193. Decompression sickness
    Nitrogen gas precipitates out of blood due to rapid ascent by a diver (gas embolus)
  194. What does gas embolus presents with?
    joint and muscle pain (bends) and respiratory symptoms (chokes)
  195. Caisson disease
    Chronic form of gas embolus that is characterized by multifocal ischemic necrosis of bone
  196. Gas embolus and laproscopic surgery?
    may also occur during laparoscopic surgery (air is pumped into the abdomen)
  197. Amniotic fluid embolus
    enters maternal circulation during labor or delivery
  198. How does amniotic fluid embolus present?
    with shortness of breath, neurologic symptoms, and DIC (due to the thrombogenic nature of amniotic fluid)
  199. How is amniotic fluid embolus characterized?
    by squamous cells and keratin debris, from fetal skin, in the embolus
  200. pulmonary embolism is usually due to?
  201. What is the most common source of thromboembolus?
    deep venous thrombus (DVT) of the lower extremity usually involving the femoral, iliac, or popliteal veins
  202. Pulmonary embolism is most often clinically silent because?
    the lung has a dual blood supply via pulmonary and bronchial arteries and the embolus is usually small (self-resolves)
  203. When does pulmonary infarction occur?
    if a large- or medium-sized artery is obstructed in patients with pre-existing cardiopulmonary compromise; only 10% of PEs cause infarction
  204. How does pulmonary infarction present?
    with shortness of breath, hemoptysis, pleuritic chest pain, and pleural effusion
  205. In pulmonary infarction what does the V/Q lung scan show?
    a mismatch; perfusion is abnormal.
  206. In pulmonary infarction what does the spiral CT show?
    a vascular filling defect in the lung
  207. What is useful in determining DVT?
    lower extremity Doppler ultrasound is useful to detect DVT
  208. In pulmonary infarction what happens the the D-dimer
    it is elevated
  209. In pulmonary infarction what does gross examination reveal?
    a hemorrhagic, wedge-shaped infarct
  210. In pulmonary infarction sudden death occurs with?
    a large saddle embolus that blocks both left and right pulmonary arteries or with significant occlusion of a large pulmonary artery
  211. In pulmonary infarction sudden death with a large saddle embolus, death is due to?
    electromechanical dissociation
  212. Pulmonary hypertension may arise with what?
    chronic emboli that are reorganized over time.
  213. Systemic embolism is usually due to?
  214. Where does systemic embolism most commonly arise?
    in the left heart and travels down systemic circulation to occlude flow to organs, most commonly lower extremities
Card Set:
2013-06-03 17:10:56

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