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MDTI > Hemostasis and Thrombosis > Flashcards

Hemostasis and Thrombosis Flashcards

1
Q

Thrombocytopenia

A
  • low platelet count
  • ID: petichial hemorrhage, ecchymosis, fever, nausea, vomiting, epistaxis, platelet count
  • causes: medications that impair marrow function, peripheral destruction, decreased production, portal hypertension and splenomegaly
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2
Q

Thrombocytopenia- Heparin-induced (HIT)

A
  • Heparin complexes with platelet factor 4 –> IgG Ab response –> FC binds to FCgiia activation of platelets –> thrombosis
  • ID: PF4 ELISA, medium reduction in platelet count (usually no bleeding)
  • Tx: stop heparin, provide lepirudin NOT warfarin b/c of warfarin necrosis
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3
Q

Warfarin necrosis

A
  • warfarin blocks vitamin k –> inhibition of protein C, VII, II, IX, X–> protein C and VII have shorter half lives and are inhibited more strongly –> cant inhibit 5,8 –> coagulative state –> thrombosis –> gangrene
  • Tx: stop warfarin, provide Vitamin K, provide heparin for first few days before starting warfarin, FFP/Protein C provision
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4
Q

Thrombocytopenia- Idiopathic/Immune/ITP

A
  • IgG antibodies directed against platelet GP IIB/IIIA or Ib9 –> opsonophagocytosis by splenic macrophages –> Thrombocytopenia –> bleeding
  • ID: no splenomegaly, bleeding, by exclusion
  • Tx: corticosteroids or IVIg, splenectomy, immunosuppression, anti-D, TPO agonist
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5
Q

Thrombocytopenia-Thrombotic thrombocytopenic purpura/TTP

A
  • disseminated microthrombi
  • cause: deficiency or inhibition of ADAMTS13 –> accumulation of vWF multimers –> long strands snare platelets –> shear stress in microcirculation –> hemolysis
  • ID: Pentad: fever, anemia (MAHA), thrombocytopenia, renal failure, neurologic symptoms
    • ADAMTS13 >5% + shiga toxin = HUS
    • ADAMTS13 >5% = aHUS
    • ADAMTS13 <5% = TTP
  • Tx: plasmapheresis, immunosuppressants
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6
Q

von Willebrand Disease

A
  • poor platelet adhesion and decreased stabilization of factor VIII
  • vWF produced in endothelium and stored in Palade bodies
  • in absence of vWF –> Factor VIII degraded rapidly
  • Type 1: low vWF of all sizes
    • mostly asymptomatic/ epistaxis
  • Type 2: qualitative functional defects–> lack high molecular weight multimers
    • abnormal multimers
  • Type 3: deficiency of vWF and Factor VIII –> profound hemorrhage
  • ID: aPTT increased, NO muscle/joint bleeding
    • quantity: vWF antigen assay
    • function: ristocetin cofactor
    • Factor VIII level
    • function: gel electropheresis-multimer analysis
  • Tx: DDAVP stimulates endogenous VWF release
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7
Q

aPTT

A
  • evaluates intrinsic pathway
  • longer w/deficiencies in 1, 5, 8, 9, 10, 11, 12
    • long aPTT due to 12, PK, HMWK may not matter in vivo
  • longer in hemophilia, von willebrand disease, DIC, antiphospholipid antibody, heparin, factor inhibitors
  • Mixing test
    • dissapear –> factor deficiency
    • still prolonged –> factor inhibitor (heparin, antibody, factor specific)
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8
Q

PT

A
  • measure of extrinsic/common pathway–>often reported as INR to standardize reagants
  • prolonged by deficiency in 1, 2, 5, 7, 10
  • also prolonged in warfarin, DIC, liver faiulre
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9
Q

Bleeding- Vitamin K

A
  • Vitamin K needed for production of 2, 7, 9, 10, C, S –> lengthen PTT and PT if deficient
  • warfarin necrosis due to relative half lives of C and 7 vs other factors lead to hypercoagulable state b/c of reduced inhibition of 5 and 8
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10
Q

Thrombin

A
  • circulates as prothrombin
    • -> cleaves to thrombin by X
  • cleaves fibrinogen to fibrin
  • activates platelets
  • induces TF synthesis
  • activates 5, 8, 9, 11
  • binds to thrombomodulin to induce protein C negative feedback
  • generated during
    • inflammation
    • infection
    • hemostasis
    • endothelial damage
    • platelet activation
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11
Q

Antithrombin

A
  • inactivates contact phase: 2, 9 10, 11, 12, kallikrein, plasmin
  • activity increased by heparin –> inactivates 2, 10
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12
Q

Fibrinolysis

A
  • cross-linked fibrin clots ensare proenzyme plasminogen –> converted to plasmin by plasminogen activator from endothelial cells –> lyses into d-dimers
  • activation promoted by
    • plasminogen activator
    • thrombin
    • urokinase
  • Tx modality: recomb t-Pa used to promote fibrinolysis
    • increases risk of secondary hemorrhage
      *
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13
Q

D-dimers

A
  • fibrinolysis split product
  • indicative of
    • DIC
    • DVT
    • PE
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14
Q

Coagulopathy-Hemophilia

A
  • A: deficiency in 8
  • B: deficiency in 9
  • C: deficiency in 11
  • Acquired A: auto-antibody = aPTT not resolved with mixing test
  • ID: long PTT, bleeding, factor assay//mimicked by vW disease
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15
Q

Coagulopathy-Liver Disease

A
  • liver produces 1, 2, 4, 5, 6, 7
  • ID: extended PT
  • causes: hepatitis, EBV, CMV, HSV, parvo, acetaminophen, methanol, isoniazid, chronic disease
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16
Q

Coagulopathy-Dilutional

A

reduction in platelets and clotting factors due to RBC transfusion without plasma replensihment

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17
Q

Coagulopathy-DIC

A
  • cytokines, endotoxins–> release of TF–> microthrombtic condition that consumes coagulation proteins, inhibitors, and platelets –> paradoxical bleeding
  • causes: cancer, preeclampsia, trauma, burns, infections, liver disease, snake bites, viral hemorrhagic fever
  • ID: low platelets, low fibrinogen, prolonged PT, less prolonged PTT, positive D-dimer
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18
Q

Coagulopathy-Factor V Leiden

A
  • hereditary thrombophilia that alters the inactivation site used by Protein C–> ongoing thrombin production –> DVT
  • ID: aPTT with and without protein C
  • Tx: prophylactic anticoagulation
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19
Q

Coagulopathy-Antithrombin deficiency

A
  • prolonged circulation of activated factors –> thromboembolic events (especially mesentery)
    • Type 1: reduced levels of normal AT
    • Type 2: abnormal AT: thrombin binding site defects, heparin binding site defects,thrombin and heparain binding site defects
  • ID:
    • antigen assay-levels
    • functional assay
    • both reduced in type 1, function only in type 2
  • heparin-resistant
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20
Q

Coagulopathy-Protein C deficiency

A
  • associated with warfarin-induced skin necrosis and neonatal purpura fulminans
  • converts to active form by thrombin when bound to thrombomodulin
  • Type 1: reduced level
  • Type 2: functionally abnormal
  • ID:
    • antigen assay
    • functional assay
    • both down in type 1
    • functional down in type 2
21
Q

Coagulopathy-Antiphospholipid Syndrome/Lupus anticoagulant

A
  • antibodies to ß2 gp I and cardiolipin –> inhibition of Protein C, increased cleavage of prothrombin, etc. –> thrombosis
  • ID: lupus anticoagulant assay, anti-cardiolipin ELISA
22
Q

Tissue Factor

A
  • initiating event in the hemostatic response to injury
  • present in the vascular wall where it is expressed on the surface of vascular smooth muscle cells, activated monocytes and, in some disease states, endothelial cells composed of an apoprotein and phospholipid
  • anchored to the cell membrane by a transmembrane domain and a short cytoplasmic domain.
23
Q

Prothrombinase complex

A

5, 10, Calcium, phospholipids catalyze cleavage of prothrombin to thrombin

24
Q

F1.2

A

small peptide thrown off during thrombin formation –> measure of thrombin formation

25
Q

Contact Phase

A
  • in absence of TF –> coagulation in presence of charged particles
  • minimal role in humans –> deficiencies in 12, PK, HMWK have little effect
  • deficiency in 11 is important because part of positive thrombin feedback loop
26
Q

Hemostatic balance is dependent on

A
  • fibrin deposition
  • platelet plug
  • anti-coagulant
  • fibrin lysis
27
Q

Platelet

A
  • small, discoid, anucleate, 10 day lifespan
  • megakaryocyte derived
  • TPO–> signal megarakyocyte to produce platelets –> platelets bind TPO and reduce signal –> regulation
28
Q

Platelet fate

A
  • form clots
    • platelet aggregation
      • adhesion (e.g. vWF)
      • thrombin
      • ADP
      • TxA2
      • Caclium
    • phospholipid acceleration of fibrin formation
  • cleared in spleen
29
Q

Glanzmann’s thrombasthenia

A

platelets do not express AIIbß3 –> no aggregation

30
Q

Bernard-Soullier

A

platelets lack GP1b receptor for VWF

31
Q

Storage Pool Deficiency

A

platelets are missing secretory granules

32
Q

Procoagulant PF3 Deficiency

A

platelet surface unable to promote clotting because of missing Pn

33
Q

Thrombus Identification

A
  1. Lines of Zahn
  2. ID of site of attachment of thrombus to vessel wall
34
Q

Lines of Zahn

A
  • layers of platelet/fibrin and RBC–> alternating pink and red layers
  • represent dynamic thrombotic process
  • firm clots formed before death
  • usually visible in large arteries
35
Q

Postmortem clots

A

currant jelly and chicken fat appearance from stasis postmortem resulting in local collection of clotting factors

36
Q

Distinguishing between liver failure and vitamin K deficiency

A
  • Both will prolong PT more than aPTT
  • mixing test will correct clotting time
  • factor assays can differentiate the two
    • vitamin k = 2, 7, 9, 10 reduced
    • liver failure = also 5 reduced, 8 increased
37
Q

Pregancy increases risk of left-side VTE because

A

left iliac vein compressed by right iliac artery due to increased flow

38
Q

Coagulopathy-Protein S deficiency

A
  • cofactor for protein c
  • Type 1: reduced levels of normal
  • Type 2: functionally abnormal
  • Type 3: reduce levels of normal S but normal level of total S
  • ID:
    • total S
    • free S
    • functional assay
    • all down: type 1
    • functional down: type 2
    • free S and functional down: type 3
39
Q

Neonatal purpura fulminans

A
  • rare condition due to homozygous protein C deficiency
  • purpura and necrosis due to thormbosis of cutaneous vessels on first day of life
  • Tx: anticoagulation and donor protein C
40
Q

Coagulopathy-Prothrombin mutation

A

GOF mjutation that incrases prothrombing levels –> increased VTE risk

41
Q

Heparin

A
  • large amount of GAG and small protein core
  • synthesized by mast cells found throughout body
  • unfractionated/standard - mixture of sizes –> activates AT3 –> inactivates 2, 9, 10, 11, 12
  • LMWH - pentasaccharaide–> activates AT3 –> only inactivates 10
    • useful b/c of longer halflife, kinetics, lower risk of thrombocytopenia
42
Q

Anti-platelet agents

A
  • Receptor antagonists
    • ADP receptor P2Y12
  • Signaling blockers
    • TxA2 formation (Cox 1 inhibitors)
    • Increase cAMP
  • Integrin AIIbB3 antagonists
43
Q

Hyperemia

A
  • Local increased blood volume
  • Increased arterial inflow blood due to dilation
  • “Redder” tissue (erythema)
44
Q

Congestion

A
  • Passive process resulting in local increase venous blood volume (from organ outflow)
  • “Blue” tissue
    • Liver in right heart failure (nutmeg liver)
    • Lung in left heart failure
  • Often associated with edema but usually no infarction
45
Q

Virchow’s Triad

A
  • Endothelial injury
  • Hypercoagulable State
  • Abnormal Blood Flow (e.g. stasis, turbulence)

–> contribute to thrombosis

  • red = venous
  • white = arterial
46
Q

Thrombi fates

A
  1. resolution
  2. propagation
  3. embolization
  4. organization/recannalization
47
Q

Infarction

A
  • ischemic necrosis of tissue due to occlusion of
    • arterial blood supply
    • venous drainage
48
Q

White infarcts occur in

A

solid organs suffering arterial infarction with single blood supply

49
Q

Red infarcts occur in

A

venous infarction, solid organs with dual blood supplies, and white infarcts with reperfusion

MDTI (10 decks)

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