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Anatomic Pathology Board Review > COAGULATION > Flashcards

COAGULATION Flashcards

1
Q

biologic half-life of factor IX and why do we care?

A

*Inherited factor deficiency –> Hemophilia B
*we replace factor IX to treat this disorder
*18-24 hours
*Targets of 50% are desirable for joint bleeding, dental procedures, hematuria, and gastrointestinal bleeding.
*Higher targets of 100% are desirable for soft tissue hematomas, intracranial hemorrhage, and surger

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2
Q

What should you expect after replacement therapy for factor IX deficiency?

A

The half-life of factor IX is 18 to 24 hours, which means a loading dose should be provided and then a maintenance dose (usually one half the loading dose) administered every 24 hours.
***Administration of recombinant factor IX can have 60% to 80% recovery because of the rapid extravascular distribution of the factor after administration.

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3
Q

coagulation factors XII, XI, IX, X

A

INTRINSIC pathway
*Intrinsic pathway leads to formation of tenase complex (FIXa:FVIIIa:FX:PL:Ca²⁺), where key event is factor X being cleaved to factor Xa

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4
Q

tenase complex

A

Intrinsic pathway leads to formation of tenase complex (FIXa:FVIIIa:FX:PL:Ca²⁺), where key event is factor X being cleaved to factor Xa

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5
Q

prothrombinase complex:

A

*Formation of prothrombinase complex: Factor Xa combines with factor Va, factor II (prothrombin), and Ca²⁺ on PL surface (platelet membrane phosphatidylserine in vivo)
*Assembled in this complex, factor II (prothrombin) is cleaved to factor IIa (thrombin)

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6
Q

Factor II

A

prothrombin
*Formation of prothrombinase complex: Factor Xa combines with factor Va, factor II (prothrombin), and Ca²⁺ on PL surface (platelet membrane phosphatidylserine in vivo)
Assembled in this complex, factor II (prothrombin) is cleaved to factor IIa (thrombin)

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7
Q

Vitamin K dependent factors

A

1972, completely strange
*10, 9, 7, 2, Proteins C and S
*X, IX, VII, II

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8
Q

What ‘additives’ in hemostasis TESTING are needed to start intrinsic pathway?

A

Factor XII, prekallikrein, and HMWK are required to initiate intrinsic pathway but are not associated with bleeding disorders

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9
Q

PT, aPTT, and the intrinsic pathway

A

PT is *insensitive to intrinsic factor deficiencies
aPTT is more sensitive to intrinsic factor deficiencies
Prolonged aPTT with normal PT reflects certain deficiencies
Factor VIII
Factor IX
Factor XI
Factor XII
PK
HMWK

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10
Q

What is HMWK in hemostasis?

A

High-molecular-weight kininogen (HMWK or HK) is a circulating plasma protein which participates in the initiation of blood coagulation
*contact activation

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11
Q

In what conditions is aPTT performed?

A

aPTT is performed on PPP (platelet poor plasma) obtained from anticoagulated whole blood
3.2% sodium citrate in 1:9 anticoagulant-to-whole blood ratio is needed
**No other anticoagulant is acceptable

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12
Q

3.2% sodium citrate in 1:9 anticoagulant-to-whole blood ratio

A

Anticoagulant setup for aPTT
*nothing else will work
*sensitive to intrinsic cascade

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13
Q

What are the steps of the aPTT?

A

Aliquot of PPP is incubated to 37°C with aPTT reagent
aPTT reagent contains source of phospholipid (e.g., cephalin) and contact activator (e.g., silica, kaolin)
Clotting is initiated by recalcifying plasma using calcium chloride
Time from initiation to clot detection is measured in seconds
Clots can be detected using optical (e.g., spectrophotometry), impedance, mechanical, and original tilt tube method (visual observation in test tube)

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14
Q

Normal range aPTT

A

aPTT range is approximately 24-36 sec
*normal PT and elevated aPTT means there’s probably an intrinsic cascasde problem

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15
Q

1/2 life of factor VIII

A

The half-life of factor VIII is 12 hours
*we can replace this in inherited factor VIII deficiency
or acquired for that matter (vWD)

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16
Q

Dosing of recombinant factors

A

*depends on 1/2 life
* recombinant factor VIIa is dosed every 2 hours, factor VIII every 12 hours, and factor IX every 24 hours.
*factor XIII has longest 1/2 life (200 hours)

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17
Q

warfarin induced skin necrosis

A

*associated with inherited protein C or S deficiency
*skin lesions after starting a patient on warfarin

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18
Q

What does activated protein C do?

A

Activated protein C (APC) is released from receptor, binds with its cofactor (protein S), and cleaves factor Va and VIIIa to its inactive forms, Vi and VIIIi, respectively

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19
Q

What does a protein C deficiency mean clinically?

A

*> 7x increase in risk of venous thromboembolism (VTE), particularly in deep veins of lower extremities
*Recurrent fetal loss
*Warfarin-induced skin necrosis–> rapid skin necrosis, mostly on extremities, breasts, trunk, and penis

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20
Q

How do you diagnose protein C deficiency?

A

Functional assays should be performed first
If low functional activity detected, antigen assay should be performed to detect type 2 protein C deficiency
Tests for protein C deficiency should not be ordered during acute thrombotic episode or while patient is on warfarin

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21
Q

What’s type1 vs type2 protein C deficiency?

A

Type 1
Most common
Quantitative decrease in normally functioning protein C due to missense or nonsense mutations (most common), promoter mutations, or frameshift deletions or insertions
Type 2
Point mutation causes qualitative decrease in protein C activity

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22
Q

What do thrombin/thrombomodulin and protein C have in common?

A

IIa (thrombin) will, in conjunction with thrombomodulin, release and activate protein C where it’s bound to endothelial surface

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23
Q

How do you ‘acquire’ protein c deficiency?

A

*Due to decreased synthesis: Liver disease, warfarin treatment
Due to increased consumption: Sepsis, disseminated intravascular coagulation, major surgery
**Severe form of protein C deficiency can be seen in patients with meningococcemia

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24
Q

DDX for protein C deficiency

A

Protein S deficiency (cofactor for protein C)
Antithrombin deficiency
Dysfibrinogenemia

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25
Q

dense granules of platelets

A

Dense granules contain calcium, magnesium, and pyrophosphate.
*also known as dense bodies

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26
Q

alpha granules platelets

A

α-granules contain PDGF, β-thromboglobulin, factor V, P-selectin, fibrinogen, vWF, PF4, and other proteins.

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27
Q

Absent or abnormal α- and dense granules…

A

Absent or abnormal α- and dense granules can lead to abnormal platelet function, such as in gray platelet syndrome and Hermansky-Pudlak syndrome, respectively.

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28
Q

Hermansky-Pudlak syndrome

A

Absent or abnormal α- and dense granules can lead to abnormal platelet function, such as in gray platelet syndrome and Hermansky-Pudlak syndrome, respectively.

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29
Q

gray platelet syndrome

A

Absent or abnormal α- and dense granules can lead to abnormal platelet function, such as in gray platelet syndrome and Hermansky-Pudlak syndrome, respectively.

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30
Q

Bernard-Soulier (BS) syndrome

A

*inherited platelet defect
BS syndrome is associated with a defect of the membrane GPIb-IX-V complex.
*initial platelet adhesion

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31
Q

Wiskott-Aldrich syndrome

A

Wiskott-Aldrich syndrome is associated with defects in platelet signal transduction and maintenance of the cytoskeleton.

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32
Q

Quebec platelet syndrome

A

Quebec platelet syndrome is associated with a defect of the α-granules.

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33
Q

Chediak-Higashi syndrome

A

Chediak-Higashi syndrome is associated with a defect of the β-granules.
*dense granules - fewer, bigger, contain ADP and epi and ATP (signaling cascadae specifically for other platelets)
*alpha granules contain pro-coag factors for NOT platelets specifically

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34
Q

Weibel-Palade bodies of endothelial cells

A

vWF and P-selectin are stored in Weibel-Palade bodies.
Weibel-Palade bodies store vWF and P-selectin. vWF participates in primary hemostasis by binding platelets to the subendothelium and also stabilizes factor VIII in the plasma. P-Selectin participates in leukocyte adhesion.
*ALSO, tPA is stored there

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35
Q

plasminogen activator inhibitor 1 activity means what?

A

PAI-1 is a serine protease inhibitor (serpin) that regulates fibrinolysis by inhibiting tPA and urokinase.
*tPA tPA activates plasminogen to plasmin. Plasmin degrades fibrinogen and fibrin to its degradation products.

with excess PAI-1 activity, tPA doesn’t function as well and you don’t breakup clots

36
Q

Glanzmann thrombasthenia

A

Glanzmann thrombasthenia is associated with a defect of GPIIb/IIIa.
*no agonists will cause aggregation, but ristocetin will cause incomplete aggregation

Absent or markedly impaired aggregation to all agonists except Ristocetin. Ristocetin-induced agglutination shows only primary wave - aggregation cannot occur because fibrinogen cannot bind.
Afibrinogenaemia gives similar results.

37
Q

Paris-Trousseau/Jacobsen syndrome

A

Paris-Trousseau/Jacobsen syndrome is characterized by the presence of giant α-granules.
*defect in alpha-granules and release
*alpha granules contain PDGF, β-thromboglobulin, factor V, P-selectin, fibrinogen, vWF, PF4, and other proteins.

38
Q

How does heparin work?

A

Heparin causes anticoagulation by binding with antithrombin (antithrombin III), resulting in the inactivation of thrombin and factor Xa.

39
Q

How can someone have heparin resistance?

A

Heparin causes anticoagulation by binding with antithrombin (antithrombin III), resulting in the inactivation of thrombin and factor Xa.
**Deficiency of antithrombin (congenital or acquired) or high levels of factor VIII or fibrinogen (acute-phase reactants) may result in heparin resistance (i.e., subtherapeutic aPTT despite receiving high-dose heparin). Anti–factor Xa activity may be useful under such circumstances to measure the response to heparin.

40
Q

why might a neonate have an isolated prolonged aPTT?

A

*you need to use age-appropriate reference intervals for newborns, their coag system isn’t ‘mature’
*Clotting factors with lower levels in young children than in adults include the vitamin K–dependent factors (II, VII, IX, and X), as well as factors V, XI, and XII, prekallikrein, and high-molecular-weight kininogen.

41
Q

What factors are about the same btw adult and child?

A

Clotting factors with similar or higher levels in young children than in adults include fibrinogen, factor VIII, and vWF.

42
Q

Which platelet receptor is activated by thrombin?

A

The most potent activator of platelets is mediated by the thrombin–PAR-1 interaction.

43
Q

When testing for vWD, you see Normal response to all agonists, with increased response to low-dose ristocetin

A

This pattern is seen in type 2B and platelet-type (pseudo) von Willebrand Disease

44
Q

what is Light transmission aggregometry (LTA)?

A

Light transmission aggregometry (LTA) can be used to detect platelet dysfunction by measuring changes in light transmission in citrated platelet-rich plasma when known platelet agonists are added. When the agonist is added, initially the discoid-to-spheroid shape change of the platelets causes decreased light transmission; then, as the platelets aggregate, the light transmission increases. Because platelets have receptors for different agonists on their surface, testing aggregation with a panel of agonists can help identify the platelet defect.

45
Q

What mediates inter-platelet aggregation?

A

GPIIb-IIIa receptor on platelets binds to fibrinogen and vWF to mediate platelet-platelet interactions
*

46
Q

Something needs to happen to a circulating platelet so that it binds more tightly…

A

GPIIb-IIIa must become activated and undergo conformational change before it is able to bind to fibrinogen and vWF
Signaling process responsible for activation of GPIIb-IIIa is referred to as “inside-out” signaling
Signaling that is initiated by binding of GPIb-V-IX complex to vWF leads to activation of GPIIb-IIIa
Several agonists are able to cause activation of GPIIb-IIIa
ADP
Thrombin
Collagen
Epinephrine
Arachidonic acid and its metabolites (i.e., thromboxane A₂)
Serotonin
Platelet-activating factor
*essentially, you need vWF to bind, and you need other platelets to release their granules (cascade)

47
Q

protein S deficiency results in…

A

Failure of APC to inactivate factors Va and VIIIa
*clotting

48
Q

AT deficiency results in…

A

Failure to inhibit factor IIa, factor Xa, and other activated factors
*clotting

49
Q

how does hemolysis affect anti-Xa assay?

A

Hemolysis interferes with measurement of the signal emitted by the assay and leads to falsely low anti-Xa activity.
*the same thing in hyperbilirubinemia

50
Q

What disease state would increase anti-Xa activity of LMWH?

A

Renal disease (LMWH is renally cleared)

51
Q

How does LMWH assert it’s effect?

A

Low-molecular-weight heparin (LMWH) is an anticoagulant that accelerates the inhibition of factor Xa by the natural anticoagulant antithrombin.

52
Q

When do you need to monitory LMWH?

A

*you usually don’t
*anti–factor Xa (anti-Xa) assay can be used when LMWH activity monitoring is necessary.
*Monitoring with the anti-Xa assay is indicated at extremes of age, renal impairment, extremes of weight, and pregnancy.

53
Q

Which pre-analytic variables can falsely alter your anti-Xa assay results?

A

Preanalytic variables can increase or decrease the anti-Xa activity. (this test is used to determine your dosage of anti-coagulation)
*Hemolysis (decrease),
* hyperbilirubinemia (decrease),
* lipemia (increase),
* delay in sample analysis (decrease)
**Acute phase reactants (e.g., factor VIII) and increased heparin-binding proteins can decrease the anti-Xa activity of the LMWH.

54
Q

Prolonged TT and normal reptilase time suggest…

A

Prolonged TT and normal reptilase time suggest presence of heparin
**TT (you start reaction by adding in thrombin) initiates clotting by cleaving fibrinopeptides A and B from fibrinogen, which leads to fibrin formation
Presence of heparin inhibits thrombin and prevents release of fibrinopeptides A and B
**Reptilase time uses reptilase snake venom, which cleaves fibrinopeptide A and leads to fibrin formation
Reptilase cleaves fibrinopeptide A, which leads to fibrin formation (it does the job of thrombin in a heparin-independent/resistant way)
***Reptilase is insensitive to heparin inactivation

55
Q

Prolonged TT and prolonged reptilase time suggest…

A

Prolonged TT and prolonged reptilase time suggest afibrinogenemia, hypofibrinogenemia, or dysfibrinogenemia

56
Q

How does the anti-Xa assay work?

A

**Anti-Xa assay is measured in U/mL of Xa inhibition
**Test is performed on patient platelet-poor plasma
1) Excess antithrombin and factor Xa are added to patient sample
2) Heparin in the sample binds to antithrombin and inactivates factor Xa added to sample
3) Factor Xa that is not inhibited by heparin:antithrombin is available to cleave a chromogenic signal on a substrate
Substrate is designed to mimic factor Xa cleavage site on prothrombin
4) Chromogenic signal is measured by spectrophotometry at specific wavelength
**Heparin activity is inverse proportional to signal detected
High heparin activity → lower residual factor Xa → less chromogenic substrate cleavage → lower signal

57
Q

Platelets are not aggregating with ristocetin…

A

*Bernard-Solier
platelets from patients with BS syndrome aggregate with physiologic agonists, but do not aggregate when induced with ristocetin. In the absence of GPIb/IX/V, isoantibodies against GPIb can form, leading to ineffective responses to platelet transfusions.
*BS syndrome is an autosomal recessive disorder caused by genetic lesions in GPIb/IX/V complex such that platelets do not adhere to vWF.

58
Q

What happens in Bernard-Solier syndrome?

A

BS syndrome is an autosomal recessive disorder (platelet aggregation) caused by genetic lesions in GPIb/IX/V complex such that platelets do not adhere to vWF.

BS syndrome shows thrombocytopenia with giant platelets, a lack of ristocetin-induced platelet aggregation, and a decreased response to thrombin-induced aggregation

59
Q

What anticoagulant causes platelet clumping?

A

*pseudothrombocytopenia
*EDTA
*use Na citrate tubes

60
Q

How does a lab diagnose Lupus Anticoagulant?

A

*LAC
*There is no single test that identified every LAC/aPL; instead, a combination of tests must be performed.
Screening test:

Prolonged phospholipid-based clotting test, such as aPTT.

Additional prolonged screening test, such as dRVVT or PCT.

Mixing study 1:1 with normal pooled plasma that does not correct.

Then, you need to prove heparin isn’t in there, and confirm phospholipid DEPENDENCE by adding tons of phospholipid to remove inhibitor

61
Q

What does aspirin do to platelets?

A

Aspirin irreversibly inhibits cyclooxygenase, which leads to impaired TxA2 production, and platelet aggregation is inhibited. The secondary wave of aggregation is usually missing after ADP or epinephrine agonists. Collagen aggregation is impaired.
***Ristocetin aggregation is unaffected.

62
Q

What assay uses Chromogenic amidolytic methodology?

A

Anti-thrombin activity
*Chromogenic amidolytic assays measure the functional activity of AT.
*Excess thrombin is added to patient plasma with heparin.
*AT will then inactivate thrombin, leaving a residual amount of thrombin.
*A thrombin substrate is added, and the cleavage product is measured.
*AT activity is inversely proportional to the residual thrombin. The assay can also be factor Xa based because AT also inhibits factor Xa.

63
Q

What’s the difference between AT deficiency types?

A

Type I AT deficiency is a decreased level of functionally normal AT. Antigen assays would be low, and functional assay would be low (i.e., quantitative defect).

Type II AT deficiency is a functionally abnormal AT present in normal quantities. Antigen assays would be normal, and functional assay would be low (i.e., qualitative defect).

64
Q

aPTT is allowed to incubate for 10 minutes before starting it (adding calcium) in a mixing study. This corrects the patient’s prolongued aPTT (isolated, he has normal PT). What is going on?

A

Complete normalization of prolonged aPTT following prolonged incubation is characteristic of prekallikrein deficiency and is caused by autoactivation of factor XII (activation of factor XII by factor XIIa).

65
Q

How does a Protein S assay work? (PTT based)

A

PTT-based protein S assays are performed by diluting patient plasma with protein S-deficient plasma.
*Fixed amounts of APC and factor Va are added. Prolongation of the PTT is proportional to the amount of protein S in the sample (low protein S → less factor Va inactivated → shorter PTT).
*super short PTT is seen in protein S deficiency

66
Q

how is protein C activity measured?

A

Protein C activity can be measured using a Russell viper venom–based or aPTT-based assay. An activator of protein C is added to plasma, such as the snake venom Protac, to convert the protein C to APC. Increased APC will then inactivate factors Va and VIIIa, prolonging the Russell viper venom time (RVVT) or aPTT in these assays. Therefore, the more protein C, the more factors Va and VIIIa are inactivated, and the more prolonged the aPTT or RVVT will be.

67
Q

An isolated aPTT in the setting of clinical bleeding can be caused by…

A

An isolated aPTT in the setting of clinical bleeding can be caused by factor VIII, factor IX, and factor XI deficiencies.
*most common is factor VIII, then IX, then XI

68
Q

hemophilia A

A

Factor VIII deficiency, inherited
*Hemophilia A is inherited in an X-linked recessive manner so that males are affected more than females. Females can develop hemophilia A by inheriting two affected alleles, having Turner syndrome (XO), or having skewed lyonization.
*severe (<1%)
*mild (5-30%)

69
Q

In coag, what is the Bethesda Assay?

A

The Bethesda assay standardizes the measurement of factor VIII (FVIII) inhibitors (i.e., titer) using a FVIII neutralization assay.
*One Bethesda unit (BU) is defined as the amount of inhibitor that results in 50% residual FVIII activity in a test mixture.
*Alternatively, it can be thought of as the amount the inhibitor in the sample must be diluted in order to recover 50% activity. *The Bethesda assay is an aPTT-based assay, and interference with aPTT can lead to false-positive and false-negative results. For example, heparin and lupus anticoagulants are also inhibitors and will prolong the aPTT (false-positive result).
*Non-neutralizing antibodies will lead to a false-negative result.

70
Q

vWD type 2M

A

Type 2M is a qualitative deficiency caused by loss-of-function mutations in the GpIba binding site on vWF.
*High-molecular-weight multimers are normal.
*Expected test results for type 2M:
*vWF:RCo < 30%;
*vWF:Ag < 30%;
*FVIII low or normal;
*RCo/Ag < 0.5-0.7;
*high-molecular-weight multimer analysis decreased with normal distribution.

71
Q

vWD type 2B

A

Type 2B is a qualitative deficiency caused by an increased affinity for platelet GpIb.
*High-molecular-weight multimers are absent.
*Expected test results for type 2B: vWF:RCo < 30%; vWF:Ag < 30%; FVIII low or normal; RCo/Ag < 0.5-0.7; and high-molecular-weight multimer analysis decreased.

72
Q

vWD type 2N

A

Type 2N is caused by a mutation in the FVIII binding site, resulting in markedly decreased binding affinity for FVIII and therefore increased clearance and low circulating levels of FVIII.
*High-molecular-weight multimers are normal.
*Expected test results for type 2N: vWF:RCo 30-200%; vWF:Ag 30-200; FVIII low; RCo/Ag normal; and high-molecular-weight multimer analysis decreased with normal distribution.

73
Q

vWD type 2A

A

Type 2A is a qualitative deficiency of vWF caused by defective high-molecular-weight multimer assembly, resulting in decreased high-molecular-weight and intermediate-molecular-weight multimers. Expected test results for type 2A: vWF:RCo < 30%; vWF:Ag < 30%; FVIII low or normal; RCo/Ag, < 0.5-0.7; and high-molecular-weight multimer analysis decreased.

74
Q

vWD type 1

A

Type 1 is a quantitative deficiency of von Willebrand factor (vWF). Patients have vWF antigen and activity < 30%. High-molecular-weight multimers are present but in decreased amounts. Expected test results for type 1: vWF:RCo < 30%; vWF:Ag < 30%; FVIII low or normal; RCo/Ag normal; and high-molecular-weight multimer analysis decreased with normal distribution.

75
Q

what’s RIPA used for?

A

RIPA (ristocetin-induced platelet aggregation) is mainly used to diagnose type 2B VWD
* It is generally done using low-concentration ristocetin (usually < 0.6 mg/mL). At this low concentration, ristocetin does not cause VWF binding and platelet aggregation. If it does cause, it shows that the respective individual has either type 2B or mutations in the platelet VWF receptor.

76
Q

What is vWF:RCo

A

Assay to measure vWF activity
vWF:RCo is the Gold standard
*Measures ability of vWF to agglutinate platelets in response to ristocetin
*low in type 2vWD subtypes (qualitative problems)

77
Q

The hallmark of HIT…

A

The hallmark of HIT is an otherwise unexplained thrombocytopenia beginning 4 to 14 days after heparin administration. Thrombocytopenia can present with a platelet count less than 100 to 150 × 103 /μL or can present as a 30% to 50% decrease in platelet count from the preheparin baseline.
*HIT antibodies can develop in response to both unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH). Due to its smaller molecular size, LMWH has a decreased capacity to bind to PF4 tetramers and generate HIT antibodies. Patients treated with LMWH are 2 to 3 times less likely to develop HIT antibodies than are patients treated with UFH.

78
Q

What are the DISadvantages of SPAs (multiplexed beads in HLA testing for HLA antibodies)

A

-Inability to distinguish harmful complement fixing antibodies from non–complement fixing ones
-Inability (using the standard SPA procedures) to identify antibody isotypes other than IgG
-Inability to detect antibodies to non-HLAs

79
Q

What are the advantages of SPAs (multiplexed beads in HLA testing for HLA antibodies)

A

SPAs, which use beads coated with specific antigens (usually HLAs), have several advantages, including the following:
-Excellent sensitivity
-Ability to resolve antibody specificity (if an anti-HLA antibody)
-Immunity to interference from most monoclonal antibody therapies currently used since those target antigens are not coated onto the beads

80
Q

The only factors SIMILAR between children and adults

A

Clotting factors with similar or higher levels in young children than in adults include fibrinogen, factor VIII, and vWF.

*the rest are DECREASED in kids (especially vitamin K dependent factors)

81
Q

what does tPA do?

A

tPA activates plasminogen to plasmin. Plasmin degrades fibrinogen and fibrin to its degradation products.

82
Q

hyperhomocysteinemia

A

Endothelial cell toxicity and disruption of vascular hemostatic mechanisms

83
Q

Protease-activated receptor 1 (PAR-1)

A

*target on platelets for thrombin
*thrombin is a VERY strong platelet activator
*The most potent activator of platelets is mediated by the thrombin–PAR-1 interaction.

84
Q

LTA for BS or vWD

A

Absent or markedly reduced platelet agglutination with Ristocetin.
*agonists still work fine

85
Q

Storage Pool Disorder OR Platelet Release Defect

A

Primary aggregation only with ADP, adrenaline and collagen and only partial agglutination with Ristocetin suggesting a failure of granule release or a deficiency of platelet granules.

86
Q

Aspirin [or defects in the COX pathway]

A

Absent aggregation to Arachidonic acid.
Primary wave aggregation only with ADP.
Decreased or absent aggregation with collagen.

Anatomic Pathology Board Review (7 decks)

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