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Heme / Onc > SM_259b: Acquired Coagulation Disorders > Flashcards

SM_259b: Acquired Coagulation Disorders Flashcards

1
Q

____, ____, ____, and ____ interplay to achieve normal hemostasis

A

Vascular integrity, platelet function, clotting proteins / coagulation, and fibrinolysis interplay to achieve normal hemostasis

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2
Q

Describe conditionns resulting from issues with vascular integrity

A

Vascular integrity issues

  • Telangiectasias
  • Allergic purpura: Henoch-Schonlein purpura
  • Atherosclerotic disease
  • Rheumatologic disease: vasculitis
  • Weak connective tissue: steroids, senile purpura
  • Vascular infiltration: AML
  • Mechanical issues
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3
Q

Describe quantitative defects in platelets

A

Quantitative defects in platelets

  • Autoimmune, medications, sequestration, consumption
  • > 50k: minimal risk of bleeding
  • 20-50k: minimal risk of spontaneous bleeding, high risk of surgical bleeding
  • <20k: variable risk spontaneous bleeding, consider comorbidities
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4
Q

Describe qualitative defects in platelets

A

Qualitative defects in platelets

  • Immune mediated
  • Toxins: uremia
  • Medications: aspirin, clopidogrel, ticlopidine, eptifibatide, high dose beta-lactams
  • Other acquired defects: myelodysplastic syndrome, acquired von Willebrand’s disease
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5
Q

Third phase of hemostasis is ___

A

Third phase of hemostasis is coagulation

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6
Q

Describe causes of acquired coagulopathy

A

Causes of acquired coagulopathy

  • Associated with bleeding: Vitamin K deficiency, liver disease, disseminated intravascular coagulation, drug-induced, inhibitors of coagulation factors (acquired hemophilia), abnormal fibrinolysis, essential thrombocytosis
  • Associated with clotting: antiphospholipid syndrome, liver disease, disseminated intravascular coagulation, drug-induced, polycythemia, nephrotic syndrome, and essential thrombocytosis
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7
Q

___ and ___ are causes of acquired coagulopathy associated with both bleeding and clotting

A

Liver disease and disseminated intravascular coagulation are causes of acquired coagulopathy associated with both bleeding and clotting

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8
Q

Vitamin K is a ___

A

Vitamin K is a co-factor in enzymatic post-translational modifications of specific factors

  • Changes N-terminal glutamic acid residues into gamma-carboxyglutamic acids (G1a): Ca2+ chelation, allows binding to phospholipids
  • Procoagulants: factors II, VII, IX, X
  • Anticoagulants: Protein C and S
  • Factor synthesis mainly hepatic
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9
Q

Vitamin K sources are ___ and ___

A

Vitamin K sources are diet (leafy green vegetables) and intestinal flora

  • Severe malnutrition can lead to Vitamin K deficiency
  • Antibiotics and malnutrition can lead to Vitamin K deficiency
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10
Q

Vitamin K is ____ and absorbed in the ____

A

Vitamin K is fat soluble (bile acids) and absorbed in the termianl ileum

  • Malabsorption syndromes can lead to Vitamin K deficiency
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11
Q

Vitamin K deficiency occurs in ____ and bleeding occurs because of non-administration of Vitamin K deficiency at birth or parental refusal

A

Vitamin K deficiency occurs in newborns and bleeding occurs because of non-administration of Vitamin K deficiency at birth or parental refusal

  • Presentation
    • Early: maternal use of drugs, with ICH
    • Classic: as GI bleeding or bleeding from venipuncture in 1st week of life
    • Late: between 3 weeks and 8 months of life, can progress to ICH
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12
Q

Describe treatment of acquired Vitamin K deficiency

A

Acquired Vitamin K deficiency treatment

  • No overt bleeding: oral Vitamin K
  • Overt bleeding: Vitamin K, plasma products such as FFP or PCC
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13
Q

Low levels of ____, ____, ____, and ____ are present in Vitamin K deficiency

A

Low levels of Factrs II, VII, IX, and Protein C are present in Vitamin K deficiency

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14
Q

Describe normal functions of liver

A

Normal hepatic function

  • Synthesis of all coagulation factors
  • Synthesis of inhibitors of coagulation
  • Thrombopoietin synthesis
  • Clearance of activated hemostatic proteins and inhibitor complexes from circulation
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15
Q

Describe platelet effects in liver disease

A

Platelet effects in liver disease

  • Quantitative: decreased levels
  • Qualitative: decreased aggregation
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16
Q

____ including ____, ____, and ____ lead to bleeding in coagulopathy of liver disease

A

Clotting factor abnormalities including decreased synthesis, decreased Vitamin K absorption, and decreased fibrogen synthesis / dysfibrinogenemia lead to bleeding in coagulopathy of liver disease

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17
Q

___ including ___ and ___ leads to clotting in coagulopathy of liver disease

A

Decreased production of anticoagulants such as antithrombin III and protein C and S leads to clotting in coagulopathy of liver disease

  • Decreased production and increased consumption of antithrombin III
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18
Q

Fibrinolysis is ____ in liver disease

A

Fibrinolysis is increased in liver disease

  • Decreased clearance of tPA -> increased levels
  • Decreased levels of plasminogen, a2-plasmin inhibitor, Factor XIII, thrombin activatable fibrinolytic inhibitor
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19
Q

aPTT is ____, PT is ____, platelets are ____, and fibrinogen is ____ in liver disease

A

aPTT is prolonged, PT is prolonged, platelets are low, and fibrinogen is low in liver disease

  • However, bleeding and thrombosis occur at the same time
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20
Q

Liver disease coagulopathy treatment involves ____

A

Liver disease coagulopathy treatment involves focus on active bleeding or clotting as they occur

  • Do not treat the lab values
  • Blood products: > 50k platelets, FFP, cryoprecipitate, Vitamin K
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21
Q

2-year old boy admitted to PICU with transaminitis and direct hyperbilirubinemia. Platelet count is 90,000/mm3.

____ will be elevated in coagulopathy of liver failure

A

2-year old boy admitted to PICU with transaminitis and direct hyperbilirubinemia. Platelet count is 90,000/mm3.

PT will be elevated in coagulopathy of liver failure

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22
Q

Describe disseminated intravascular coagulation

A

Disseminated intravascular coagulation

  • Systemic process involving both thrombosis and hemorrhage
  • Exposure of blood to procoagulants
  • Circulating fibrin
  • Concurrent fibrinolysis
  • Depletion of clotting factors and platelets
  • End organ damage
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23
Q

Describe coagulation in DIC

A

Coagulation in DIC

24
Q

Describe bleeding in DIC

A

Bleeding in DIC

25
Q

Describe acute DIC

A

Acute DIC

  • Decompensated intravascular coagulation
  • Depletion of platelets, fibrinogen, prothrombin, clotting factors
  • FDP generation: hemostasis interference
  • Clinically: bleeding diathesis
  • Can also see microangiopathic hemolytic anemia
26
Q

Describe chronic DIC

A

Chronic DIC

  • Liver compensates for clotting factor consumption
  • Bone marrow compensates for platelet loss
  • Clinically see more thrombotic manifestations
  • Malignancies (except APML)
27
Q

Describe causes of DIC

A

DIC causes

  • Infection / sepsis: bacterial and nonbacterial
  • Tissue damage: surgery or trauma
  • Cancer
  • Obstetrical complications
28
Q

Describe how infection / sepsis causes DIC

A

Infection / sepsis causes DIC

  • Both bacterial and nonbacterial
  • Shock -> decreased blood flow and tissue damage -> thrombin generation
  • Impaired hepatic perfusion -> decreased removal of activated procoagulants
29
Q

Describe how tissue damage causes DIC

A

Tissue damage causes DIC

  • Surgery or trauma (particularly head trauma)
  • Release of tissue enzymes and phospholipids from damaged tissue
30
Q

Describe how cancer causes DIC

A

Cancer causes DIC

  • TF expression by circulating tumor cells
  • Cancer procoagulant
31
Q

Describe how obstetrical complications cause DIC

A

Obstetrical complications cause DIC

  • > 50% of cases due to amniotic fluid embolus or abruptio placenta (release of thromboplastin-like material)
32
Q

Describe clinical presentation of acute DIC

A

Clinical presentation of acute DIC

  • Usually profound bleeding w/ ischemic tissue injury
  • Petechiae / ecchymosis, oozing from lines / mucosal surfaces
  • Microangiopathic hemolytic anemia
  • Shock
  • Hyperbilirubinemia: hemolytic anemia, liver dysfunction / shock liver
  • Thromboembolic phenomena
  • AKI: microthrombi in afferent arterioles w/ cortical ischemia, hypotension -> ATN
  • Pulmonary hemorrhage / ARDS
  • CNS hemorrhag
33
Q

Describe clinical presentation of chronic DIC

A

Clinical presentation of chronic DIC

  • Tend to be thrombotic complications
  • Can be both arterial and venous
  • Malignancy is most common cause
34
Q

DIC is diagnosed ___

A

DIC is diagnosed clinically with aid of some labs

  • Lab values depend on rapidity of evolution and ability of normal systems to compensate
  • Moderate-severe thrombocytopenia (< 100)
  • Fibrinolysis: FDP and D-dimer elevations
  • Prolonged PT and PTT
  • Fibrinogen usually low
35
Q

Describe treatment of DIC

A

DIC treatment

  • Treat underlying cause
  • Blood product used only if bleeding
36
Q

Compare and contrast Vitamin K deficiency, liver disease, and DIC

A

Vitamin K deficiency, liver disease, and DIC

37
Q

You are consulting on an elderly woman in the hospital who is admitted with a severe pneumonia and bacteremia. She is on broad spectrum antibiotics but is oozing from venipuncture sites and has widespread ecchymosis. She has elevated PT, PTT, and low platelets. You suspect she has DIC.

Need ___ for diagnosis of DIC

A

You are consulting on an elderly woman in the hospital who is admitted with a severe pneumonia and bacteremia. She is on broad spectrum antibiotics but is oozing from venipuncture sites and has widespread ecchymosis. She has elevated PT, PTT, and low platelets. You suspect she has DIC.

Need increased D-dimers for diagnosis of DIC

38
Q

Describe pathologic inhibitors of coagulation

A

Pathologic inhibitors of coagulation

  • Circulating antibodies directly inhibit clotting proteins
  • Associated with clinical bleeding syndrome
  • Acquired FVIII inhibitors occur in a few situations: all antibody in congenital hemophilia A, autoantibodies
39
Q

Describe acquired FVIII inhibitor

A

Acquired FVIII inhibitor (autoantibodies)

  • IgG specific to FVIII: most epitopes specific for A2 and C2, no interference w/ vWF
  • Symptoms: easy bruising / bleeding, large muscle hematomas, GI / GU bleeding
40
Q

Describe normal hemostasis

A

Normal hemostasis

41
Q

Describe labs for acquired FVIII inhibitor

A

Labs for acquired FVIII inhibitor

  • Low factor VIII activity: undetectable
  • Prolonged PTT: normal PT
  • No correction on 1:1 mixing study
42
Q

Describe the mixing test

A

Mixing test

43
Q

Describe labs for acquired FVIII inhibitor

A

Labs for acquired FVIII inhibitor

  • Quantify titer of Ab with Bethesda assay (BU): low titer inhibitors ≤ 5 BU
44
Q

Describe treatment of acquired Factor VIII inhibitors

A

Acquired Factor VIII inhibitors treatment

  • Bleeding if low titer: desmopressin trial, FVIII concentrates
  • Bleeding if low titer: prothrombin complex concentrates, recombinant FVIIa
  • Eradication of antibody: immunosuppressives (steroids, cytoxan), rituximab

May spontaneously resolve but relapse is common

45
Q

Describe differences in congenital and acquired hemophilia

A

Congenital and acquired hemophilia

46
Q

He has ____

A

He has low Factor VIII activity level

47
Q

Describe where phospholipids are involved in the coagulation cascade

A

Phospholipids are involved in the coagulation cascade

48
Q

Describe antiphospholipid antibodies

A

Antiphospholipid antibodies

  • Autoantibodies directed against anionic phospholipids and plasma proteins: B2 glycoprotein I and prothrombin are antigen targets, antibodies are lupus anticoagulant / anticardiolipin antibody, and B2 glycoprotein antibody
49
Q

Antiphospholipid antibodies can interfere with ___

A

Antiphospholipid antibodies can interfere with normal clotting times

  • Lupus anticoagulant is a common cause of elevated PTT
  • Does not confer a bleeding risk but associated with thrombosis
50
Q

Describe pathophysiology of antiphospholipid syndrome

A

Antiphospholipid syndrome pathophysiology

  • Complex interplay of endothelial cells, monocytes, platelets, and complement
  • Increase tissue factor, thromboxane, complement activation -> procoagulant state
  • Second hit may lead to clinical thrombosis: often other cardiovascular risk factors
51
Q

Describe cells involved in antiphospholipid syndrome

A

Antiphospholipid syndrome

  • Endothelial cells: antiphospholipid antibodies recognize B2 glycoprotein I bound to endothelium -> binding -> endothelial activation -> expression of adhesion molecules and upregulation of tissue factor
  • Monocyte activation: upregulation of tissue factor, cytokine production
  • Platelet activation: increase glycoprotein 2b-3a production and thromboxane A2 production
52
Q

Describe clinical manifestations of antiphospholipid syndrome

A

Clinical manifestations of antiphospholipid syndrome

  • Venous thrombosis (most common)
  • Arterial thrombosis
  • Adverse pregnancy outcomes: recurrent miscarriage, preterm birth, preeclampsia and placental insufficiency, intrauterine growth restriction
  • Other: thrombocytopenia, hemolytic anemia, livedo reticularis, cognitive deficits, cardiac valvular disease
53
Q

Antiphospholipid antibodies can ___, ___, and ___

A

Antiphospholipid antibodies can interfere with normal clotting times, be transiently detected, and found in association with autoimmune conditions

54
Q

Describe differences in antiphospholipid antibody and acquired hemophilia

A

Antiphospholipid antibody and acquired hemophilia

55
Q

Antiphospholipid syndrome diagnosis involves ___ and ___

A

Antiphospholipid syndrome diagnosis involves at least 1 clinical and 1 lab criteria

56
Q

Catastrophic antiphospholipid antibody syndrome is ___

A

Catastrophic antiphospholipid antibody syndrome is life-threatening with ≥ 3 organs involved

  • Plasma exchange to decrease antiody load may be helpful
57
Q

Most appropriate lab test is ___

A

Most appropriate lab test is aPTT mixing study

Heme / Onc (41 decks)

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