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DD & BL Unit III / Final Exam > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Tissue factor

A

TF is a membrane protein on fibroblasts and other cells in the vessel wall; it is exposed to the blood with endothelial injury

TF binds activated, circulating VIIa in order to begin the extrinsic coagulation cascade

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2
Q

Tenase

A

Cofactor VIII supports IXa and X; X becomes activated to Xa

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3
Q

Prothrombinase

A

Cofactor V supports Xa and II; II becomes activated to IIa

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4
Q

Vitamin K-dependent proteins

A

II, VII, IX, X

Protein C, Protein S

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5
Q

Role of Vitamin K in coagulation

A

Factors II, VII, IX, and X undergo vitamin K-dependent gamma carboxylation of glutamic acid in the liver; this reaction oxidizes vitamin K, which must be reduced by Vitamin K oxidoreductase in order to continue synthesizing functional clotting factors

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6
Q

Warfarin - Mechanism

A

Factors II, VII, IX, and X undergo carboxylation of N-terminal glutamates by enzymes that are Vitamin K-dependent; without this carboxylation they are unable to bind Ca2+ and are non-functional

Vitamin K undergoes redox during this reaction and the recycling of Vitamin K to its reduced, active form by Vitamin K Reductase is inhibited by Warfarin, resulting in depletion of Vitamin K and active coagulation factors

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7
Q

Tissue Factor Pathway Inhibitor (TFPI)

A

Binds and inhibits Tenase and free, activated Xa

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8
Q

Antithrombin (AT3)

A

Binds and inhibits thrombin, as well as factors Xa and XIa

This binding interaction is enhanced by heparin

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9
Q

Protein C System

A

Thrombomodulin (TM) activates PC to APC; APC binds PS as a co-factor to cleave and inactivate Va and VIIIa

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10
Q

Tissue Plasminogen Activator (TPA)

A

Converts plasminogen to plasmin; plasmin cleaves fibrin to fibrin split products (FSPs) and Dimers

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11
Q

Plasminogen activator inhibitor-1 (PAI-1)

A

Binds and inhibits tissue plasminogen activator (TPA), preventing the formation of plasmin and inhibiting fibrinolysis

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12
Q

TF-VIIa

A

Converts X to Xa and IX to IXa

Results in the production of a small amount of thrombin

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13
Q

Propagation Phase

A

Production of Xa (by Tenase) and Thrombin (by Prothrombinase)

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14
Q

Role of Thrombin in Amplification

A

Thrombin activates co-factors VIII and V

Thrombin also activates XI

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15
Q

Mechanism of fibrin cross-linking

A

Factor XIIIa is activated by thrombin to covalently cross-link fibrin, leading to formation of a “hard clot”

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16
Q

Contents of Platelet Dense Granules

A 
ATP
ADP
Ca2+ 
Histamine
Serotonin
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17
Q

Contents of Platelet Alpha Granules

A

Procoagulant proteins - fibrinogen, factor V, vWF
Platelet activation factors
Platelet-derived growth factor

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18
Q

Contents of Platelet Lysosomal Granules

A

Acid hydrolases

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19
Q

GPIa/IIa

A

Binds Collagen in the exposed sub-endothelium at the site of vascular injury

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20
Q

GPIIa-IIIb

A

Binds vWF in the sub-endothelium at the site of vascular injury

Also binds fibrinogen to cross-link platelets

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21
Q

GPIb

A

Binds vWF in the exposed sub-endothelium at the site of vascular injury

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22
Q

Platelet Adhesion

A

Platelets adhere to the injured surface and build at temporary clot by virtue of binding interactions:

GPIba binds vWF
GPIIb/IIIa binds Fibrinogen
GPIa/IIa binds collagen

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23
Q

Platelet Activation

A

Interaction of the extracellular, soluble agonists thrombin, thromboxane A2, and ADP with their respective GCPRs in the platelet membrane signal calcium influx that results in secretion of alpha and dense granule contents; calcium also activates the conversion of arachidonic acid to TXA2 via COX1

End result of agonist binding is a conformational change in the platelet to expose GPIIa/IIIb binding sites for fibrinogen

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24
Q

Platelet aggregation

A

Platelet adhesion & binding of soluble agonists converts GPIIa-IIIb to a high-affinity state where it can bind fibrinogen and vWF; GPIIa-IIIb bound to fibrinogen acts as a bridge to lace platelets together into a mesh; locally, thrombin acts to convert fibrinogen to fibrin, stabilizing the platelet mesh

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25
Q

Mechanisms by which endothelial cells inhibit coagulation (3)

A
  1. Secreting a heparin-like molecule to suppress coagulation cascade activity
  2. Expressing thrombomodulin which, when bound to thrombin, activates Proteins C and S
  3. Secretion of NO and prostacyclin, inhibitors of platelet activation
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26
Q

Immune thrombocytopenic purpura ITP)

A

Caused by the production of auto-antibodies directed against platelet antigens, leading to their removal by macrophages of the RE system

May be acute or chronic

Acute onset is often preceded by viral infection and presents as petechiae and nosebleeds

Chronic is often associated with other auto-immune disorders (SLE, RA, HIV)

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27
Q

Treatment for ITP (4)

A

Corticosteroids - suppress inappropriate immune response to platelets

IVIG - Blocks Fc receptors on splenic macrophages

Splenectomy - prevents sequestration and destruction of opsonized platelets

Rituximab - anti CD20, depletes B cells

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28
Q

Alloimmune thrombocytopenia

A

Production of antibodies against platelet antigens not present on the patient’s own platelets

Occurs in the setting of a patient receiving platelet transfusions, or in a neonate through passive transfer of maternal IgG alloantibodies across the placenta to attack fetal platelets

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29
Q

Thrombotic thrombocytopenic purpura (TTP)

A

Due to mutation in or antibodies against the ADAMTS13 protein that normally functions to digest vWF; as a result, large vWF multimers are released from endothelial cells in the setting of damage; these large vWF multimers mediate platelet adhesion and aggregation forming diffuse platelet plugs in small arterioles

Presents as renal insufficiency, mental status changes, thrombocytopenia

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30
Q

Von Willebrand Disease - Types

A

The most common congenital bleeding disorder; 3 types:

Type I - Partial quantitative deficiency of vWF
Type II - Partial qualitative deficiency of vWF
Type III - Total absence of vWF

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31
Q

Pathophysiology of Von Willebrand Disease

A

vWF facilitates platelet adhesion to injured vascular endothelium and also serves as a carrier protein for Factor VIII

Deficiency of vWF leads to defects in platelet aggregation and plug formation (primary hemostasis) as well as in fibrin deposition (secondary hemostasis) due to decreased Factor VIII levels

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32
Q

Diagnosis of Von Willebrand Disease

A

vWF antigen measures quantity of vWF present; decreased in Type I and absent in Type III vWD disease

vWF Ristocetin Cofactor Activity measures activity of vWF present; decreased in Type I and II, absent in type III vWF disease

PFA elevated (ADP & Epi)

Decreased VIII levels

Prolonged PTT

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33
Q

Treatment of von Willebrand Disease

A

DDAVP - enhances release of vWF from endothelial stores; effective for treatment of Type I disease only

Factor VIII replacement

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34
Q

Bernard-Soulier Syndrome

A

Autosomal recessive disorder caused by decreased expression of GPIb on the platelet surface, leading to defective adhesion and bleeding

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35
Q

Afibrogenemia

A

Inherited mutation in fibrinogen; causes defects in primary hemostasis due to inability of fibrinogen to cross-link GPIIb-IIIa in platelet aggregation; also causes defects in secondary hemostasis due to lack of fibrinogen for formation of cross-linked fibrin clots

Patients present with platelet-type mucosal and cutaneous bleeding as well as deep muscle hematomas more characteristic of coagulation defects

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36
Q

Platelet Function Analyzer (PFA)

A

In vitro measure of platelet sensitivity to agonists collagen/epinephrine and collagen/ADP; elevated PFA (epi) indicates aspirin effect whereas elevation in both epi and ADP assays suggests true finding of deficient platelet activity

37
Q

PT/INR

A

Calcium and thromboplastin (an extract of TF) are added to patient plasma; time to clotting is measured in seconds

Thromboplastin potency varies by manufacturer so the PT is “normalized” such that INR = 1 is normal by definition

Prolonged with deficiencies of the extrinsic and common pathways: Factor VII, X, V, II, and Fibrinogen; also prolonged with Vitamin K deficiency / Warfarin

38
Q

Thrombin TIme

A

Excess thrombin is added to plasma to measure the procoagulant activity of fibrinogen; deficiencies or abnormalities of fibrinogen prolongs the thrombin time

Heparin and the presence of fibrin split products also prolongs the thrombin time

39
Q

Activated Partial Thromboplastin Time (aPTT)

A

Surface activating agent and phospholipid is added to plasma; time to clotting is measured in seconds; useful to detect defects in the intrinsic pathway: Factors VIII, IX, XI, and XII

Does not measure the activity of Factor VII

Sensitive to inhibition by heparin and fibrin split products

40
Q

Hemophilia A

A

Most common cause of severe bleeding tendency; caused by X-linked deficiency of Factor VIII

Elevated PTT is the only abnormal screening test

May be mild (>10% activity), moderate (2-5% activity, bleed after trauma), or severe (<1% factor activity, spontaneous bleeding)

Treatment: Recombinant Factor VIII

41
Q

Hemophilia B

A

10x less common than Hemophilia A; caused by X-linked deficiency of Factor IX

Elevated PTT is the only abnormal screening test

May be mild (>10% activity), moderate (2-5% activity, bleed after trauma), or severe (<1% factor activity, spontaneous bleeding)

Treatment: Recombinant Factor IX

42
Q

Hemophilia C

A

Autosomal recessive condition caused by Factor XI deficiency; factor levels usually >5%, spontaneous bleeding is rare

PTT is prolonged

43
Q

Factor VII Deficiency

A

Autosomal condition; may cause severe bleeding similar to Hemophilia A and B

Only PT is prolonged; PTT is normal

44
Q

Role of liver disease in coagulopathy

A

Decreased liver function leads to decreased Vitamin-K dependent carboxylation of Factors II, VII, IX, and X; these factors affect the PT more than the PTT so coagulation tests usually show a prolonged PT with relatively normal PTT

Patients may also have consumption of platelets due to hypersplenism

45
Q

Disseminated Intravascular Coagulation (DIC)

A

Coagulation cascade is pathologically activated within the vascular system; fibrin and platelet microthrombi form and block capillaries, causing tissue infarct; at the same time, some factors and platelets are consumed to the point of multiple coagulation factor deficiencies, resulting in hemorrhage

46
Q

Lab findings associated with DIC

A

Long PTT - usually reflects non-specific inhibition by fibrin split products; Factor VIII deficiency can also prolong PTT

Long PT/INR - caused by Factor V deficiency

Low fibrinogen due to formation of microthrombi

Low AT3 and plasminogen due to activation of fibrinolytic processes

47
Q

Lupus Anticoagulant

A

IgG antibody directed against phospholipidin the platelet or endothelial cell membrane; the antibody binds up the phospholipid added to the PTT test, causing prolonged PTT in vitro - however, the antibody actually causes thrombotic disorders in vivo by interactig with platelet phospholipid membranes, increasing platelet adhesion and aggregation

48
Q

Diagnosis of Antiphospholipid Antibody Syndrome (APS)

A

Mixing normal plasma with the plasma from a patient with the lupus anticoagulant will not correct the PTT because the antibody is still present

However, if the patient’s plasma is first mixed with a source of phospholipid, the lupus anticoagulant will be absorbed out of the patient’s plasma by the phospholipid and a repeated PTT will show partial correction

49
Q

Familial hypercoagulable state (Thrombophilia)

A

Autosomal dominant conditions caused by Antithrombin III deficiency, protein C deficiency, or protein S deficiency

Heterozygous patients usually present after puberty with recurrent venous thrombotic disease; homozygous is usually fatal at birth

50
Q

Factor V Leiden - 2 Mechanisms

A

Most common inherited predisposition to hypercoagulability, due to autosomal dominant mutation of the Factor V gene

  1. Increased coagulation: Normally, thrombin cleaves V into Va and Protein C cleaves Va into Vi; the Factor V Leiden mutation eliminates a cleavage site for Protein C, producing a Va that is partially resistant to proteolytic cleavage; more Va is available in the clotting cascade to further activate thrombin
  2. Decreased anticoagulation: Normal factor V, cleaved at the right position, is a cofactor together with protein S for protein C; protein C cleaves Va and VIIIa; lack of normally cleaved V decreases the anticoagulant property of protein C
51
Q

Mechanism of a 1:1 mixing study

A

Used to distinguish clotting factor deficiency from the presence of an inhibitor of coagulation, (LA, anti-VIII)

Patient and control plasma are mixed and PTT is assayed: if the PTT corrects immediately, then a factor deficiency is likely; if the PTT doesn’t correct immediately, than a coagulation inhibitor is responsible, likely LA

Next, patient and control plasma are incubated at 37 degrees for two hours and PTT is assayed; if PTT stays corrected, then a factor deficiency is diagnosed; if the PTT does not stay corrected, then specific Factor VIII deficiency (acquired Hemophilia A, antibody-mediated) is likely; the antibody in the patient’s plasma has bound and inhibited the normal Factor VIII

52
Q

Differential DIagnosis of Long PTT - Patients who bleed

A 
Hemophilia A
Hemophilia B 
Acquired Hemophilia (usually VIII deficiency) 
Severe con Willebrand Disease 
Heparin in sample 
Fibrin split products in sample
53
Q

Differential Diagnosis of Long PTT - Patients who do not bleed

A

Factor XII deficiency

Lupus anticoagulant

54
Q

Bleeding complications in hemophilia

A

Soft tissue hematomas
Joint bleeding
CNS bleeds - leading cause of death
Retroperitoneal or psoas bleeds

55
Q

Differential of PT more prolonged than PTT

A

Liver disease
Vitamin K deficiency
Warfarin
Rat Poison Ingestion

56
Q

Differential of PTT more prolonged than PT

A

DIC

57
Q

Unfractionated Heparin - Pharmacokinetics

A

Not absorbed from GI tract; must be given IV or sub-cutaneous; does not cross placenta

Poor bioavailability and short half-life; dose response is unpredictable

58
Q

Low Molecular Weight Heparin (LMWH) - Pharmacokinetics & Uses

A

Given subcutaneously with better bioavailability and longer half life than unfractionated; requires less monitoring, used for outpatient treatment

59
Q

Fondaparinux (Arixtra)

A

Synthetic pentasaccharide corresponding to the minimal sequence in heparin for binding AT3

60
Q

Heparin - Mechanism

A

Heparin binds to AT3, increasing the natural activity of AT3

Heparin containing at least 18 saccharide units binds to the antithrombin/thrombin complex, inhibiting it

LMWH and Fondaprainux do not inhibit thrombin but selectively bind to and inactivate Factor Xa by AT3

61
Q

Heparin - Adverse Effects

A

Bleeding - anticoagulant effect of Heparin disappears within hours of discontinuation; can be neutralized by protamine sulfate in life threatening situations

Heparin-induced thrombocytopenia syndrome (HIT) - platelet count decreases by >50%, 5-10 days after heparin; caused by production of antibodies to platelet/heparin complexes; antibodies bind and activate platelets, resulting in a prothrombotic state

62
Q

Alternative anticoagulant therapies for patients with heparin-induced thrombocytopenia

A

Direct thrombin inhibitors:

Argatroban
Lepirudin

63
Q

Warfarin - Pharmacokinetics

A

Good oral absorption and bioavailability

Slow onset of action - full anti-thrombic effect not achieved until existing coagulation factors in circulation are removed (5 days)

64
Q

Warfarin - Adverse Effects

A

Hemorrhage - discontinuation of drug + administration of Vitamin K; reversal takes 24-48 hours while new coagulation factors are synthesized

DDIs with drugs that increase anti-coagulation effect: aspirin, antibiotics that decrease vitamin K synthesis by intestinal microbes, phenytoin (displaces Warfarin from plasma proteins)

DDIs with CYP450 inducers (barbituates, rifampin) and inhibitors (cimetidine)

Cannot be used in pregnancy - crosses placenta, is teratogenic

65
Q

New Oral Anticoagulants

A

Direct Thrombin or Xa inhibitors

Advantages: Rapid onset of action, absence of DDIs, does not require monitoring

Disadvantages: Contraindicated in kidney disease, GI bleeding, short half-life, cost, no antidote

66
Q

t-PA (Alteplase)

A

Recombinant tissue plasminogen activator; converts plasminogen to plasmin, which breaks down fibrin clots into fibrin degradation products

Given by bolus injection with prolonged half life

Adverse effects: Hemorrhage, allergic reaction

67
Q

Aspirin

A

Inhibitor of platelet products

Irreversibly inactivates COX1 in platelets, preventing TXA2 formation

68
Q

ADP Receptor Antagonists

A

Thienopyridines - Clopidogrel (Plavix), Ticlopidine

Oral agents that bind irreversibly to ADP receptor (P2Y12) on platelets, blocking platelet activation; this inhibits secretion of alpha granules and blocks expression of adhesion proteins GPIIb/IIIa

69
Q

Thienopyridines - Pharmacokinetics

A

Absorbed as pro-drug and metabolized to active intermediate in the liver; slow onset of action with maximum

Bind irreversibly to platelets; effects last for the duration of the platelet life span (7-10 days)

70
Q

Ticagrelor

A

Oral analog that binds reversibly to the ADP receptor P2Y12; more rapid action than thienopyridines since it does not require metabolic activation

Greater platelet inhibition than clopidogrel

71
Q

Inhibitors of platelet adhesion

A

GPIIb/IIIa inhibitors block the receptor binding site for fibrinogen, preventing platelet aggregation

Ex: Abciximab - mAb fragment against GPIIb/IIIa

72
Q

Virchow’s Triad

A
  1. Decreased blood flow (venous stasis)
  2. Inflammation of the blood vessels (vessel wall damage)
  3. Intrinsic alterations in the nature of the blood itself (hypercoagulability)
73
Q

Pathogenesis of Pulmonary Embolism

A

Caused by part of a thrombus that breaks off and travels through the major veins, past the right heart, and into pulmonary artery circulation until it becomes lodged; de-oxygenated blood cannot reach the lung tissue past the thrombus and gas exchange is reduced

Compensatory vasoconstriction in the vessels supplying the blocked part of the lung may lead to increased pulmonary vascular resistance and to right ventricular heart failure

74
Q

Signs and symptoms of PE

A 
Dyspnea
Tachypnea
Tachycardia
Chest Pain 
Diminished capacity for exercise
Syncope
Cardiac Arrest
Sudden Death
75
Q

White thrombi

A

Composed mostly of aggregated platelets, containing small amounts of fibrin and few red cells; occur mostly in the arterial system causing ischemia and infarction of downstream tissues

76
Q

Red Thrombi

A

Composed primarily of fibrin containing numerous red cells; occur mostly in the venous system causing impaired venous return of blood leading to edema and dilation of superficial veins

77
Q

D-dimer assay

A

D-dimers are formed when cross-linked fibrin is degraded by plasmin through fibrinolysis

D-dimer has high negative predictive value - a negative D-dimer assay rules out DVT

However, a positive D-dimer assay does not definitively diagnose a DVT as there are other causes of positive D-dimer

78
Q

Diagnosis of PE

A

Chest CT with venous contrast

Ventilation-Perfusion scan

79
Q

Prothrombin gene mutation

A

Second most common inherited predisposition to hypercoagulability, caused by an autosomal dominant overexpression mutation in the prothrombin gene leading to elevated levels of plasma prothrombin

80
Q

Antithrombin deficiency

A

Autosomal dominant inherited predisposition to hypercoagulability; 2 types:

Type I - quantitative deficiency
Type II - qualitative deficiency (decreased ability to bind heparin)

Most patients are heterozygous with ~50% normal levels of AT3 and 40x increased risk of thrombosis; homozygous deficiency is fatal in utero

May exhibit heparin resistance, since heparin acts by binding AT3

81
Q

Protein C deficiency

A

Inherited predisposition to hypercoagulability, inherited in an autosomal dominant fashion; heterozygotes have ~50% normal protein C levels and 31x increased risk of thrombosis; homozygous deficiency is fatal in utero

Warfarin decreases the already low protein C levels more rapidly than it does the procoagulant factors, exacerbating the basal hypercoagulable state

82
Q

Protein S deficiency

A

Inherited predisposition to hypercoagulability inherited in an autosomal dominant fashion;

83
Q

Use of Heparin and Warfarin in acute DVT/PE

A

Heparin inactivates activated clotting factors, particularly IXa, Xa, and XIIa, by enhancing the activity of AT3; should be used for minimum 5 days and until Warfarin is fully therapeutic

Warfarin is used to prevent additional clots; it does not treat the acute clot and cannot be given alone for treatment of an acute event; reduction of vitamin-K dependent factors takes at least 4-5 days

84
Q

Unfractionated Heparin - Mechanism

A

Unfractionated heparin binds AT3 in combination with either Xa or Thrombin (IIa); it therefore accelerates the normal activity of AT3 to inactivate factor Xa and thrombin

85
Q

Low Molecular Weight Heparin - Mechanism

A

LMWH binds AT3 in combination with factor Xa, increasing the activity of AT3 in deactivating Xa

LMWH does not bind thrombin

86
Q

Anti-Phospholipid Antibody Syndrome (APL, APLS)

A

Characterized by venous or arterial thrombotic or obstetric complication caused by antibodies

Diagnosed by the presence of anti-phospholipid antibodies (anticardiolipin, Lupus anticoagulant, or Beta2glycoprotein-I) on 2 or more occasions at least 12 weeks apart

87
Q

Pseudo-thrombocytopenia

A

An in vitro artifact resulting from platelet agglutination via antibodies when the calcium content of serum is decreased by blood colleciton in an EDTA (anti-coagulated) tube for CBC

A CBC result showing thrombocytopenia should always be confirmed by looking at the smear

88
Q

Gray Platelet Syndrome

A

Autosomal recessive disorder caused by deficiency of platelet alpha granules; characterized by mild bleeding disorder

89
Q

Lab abnormalities in DIC

A

Prolonged PT
Greatly prolonged PTT - due to presence of FSPs
Prolonged TT - due to low fibrinogen and presence of FSPs
Low platelet count
Increased FSPs
Increased D-Dimer

PTT is increased relatively much more than PT

DD & BL Unit III / Final Exam (7 decks)

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