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Tim's CP Board Review > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Amyloidosis - Factor, test

A 
X (decreased)
Thrombin time (increased)
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2
Q

Conditions affecting vWF levels

A

Increased: Acute phase reaction, OCPs, pregnancy, neonates
Decreased: Type O blood group

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3
Q

Protein S

A

Carrier of protein C.

In turn 60% bound to C4BP.

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4
Q

Reptilase time

A

Snake venom (Batroxobin) from Bothrops snake&raquo_space; Directly cleaves fibrinogen. Unlike thrombin time, not sensitive to heparin.

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5
Q

Time-dependent prolongation on mixing study

A

fVIII inhibitor

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6
Q

Platelet aggregation - Phases

A

1st phase: ADP release

2nd phase: More ADP release, TXA2 release.

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7
Q

Bernard-Soulier

A

CD42 (Gp1b/V/X)&raquo_space; Macrothrombocytopenia

Impaired aggregation with ristocetin

Decreased response to thrombin-induced aggregation

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8
Q

Glanzmann’s thrombasthenia

A

GPIIb (CD41) / IIIa (CD61) abnormality. Normal platelet count.

No aggregation except with ristocetin.

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9
Q

Alpha-granule deficiencies

A 
Gray platelet (retain P-selectin)
Quebec platelet (excess u-PA degrades granule)
Paris-Trousseau
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10
Q

Dense-granule deficiencies

A

Chediak-Higashi
Wiskott-Aldrich
Hermansky-Pudlak

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11
Q

Storage pool deficiencies - Testing

A

No second wave on aggregation.

Diminished responses to collagen, arachidonic acid

Note: Both of above also true of aspirin effect

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12
Q

vWD - I, III

A

I - Autosomal dominant. Mild, treatable with DDAVP. Normal multimers.

III - Autosomal recessive. Total absence.

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13
Q

vWD - 2A, 2B, plt-type

A

2A - Most common after I. Very few large multimers. Low activity:antigen ratio. Acquired forms resemble this.

2B - Rare. Exon 28 abnormality&raquo_space; increased Gp1b affinity. Few large multimers. Abnormal RIPA. DDAVP will cause thrombocytopenia.

Plt-type - Gp1b on platelet has higher affinity for vWF. Abnormal RIPA. Fewer multimers. Distinguish with cryo challenge

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14
Q

vWD - 2N, 2M, Plt-type

A

2N - Abnormal fVIII binding site, presents like Hemophilia A.

2M - Decreased Gp1b binding affinity. Very low activity.

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15
Q

Hemophilia A - Congenital & acquired

A

Congenital: Usually intron 22 inversion. XLD, can be seen in women in Turner, homozyg, lyonization

Acquired: Rare, elderly with new bruising

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16
Q

Minor hemophilias

A 
Hemophilia C (factor XI, jews, autosomal. No recombinant available)
fIX (anaphylaxis with repletion)
f12 (maybe thrombogenic?)
f7 (maybe also thrombogenic?)
f13
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17
Q

Dysfibrinogenemias

A

Qualitative dysfunction, only partially corrects on mixing due to competitive inhibition.

Diagnose with thrombin time (more sensitive than reptilase time)

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18
Q

Alpha-2 antiplasmin deficiency

A

Test: SLOW euglobulin clot lysis. Normal other coags.

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19
Q

TTP/HUS

A

Normal PT, PTT, fibrinogen, D-dimer. Platelet-rich clots.

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20
Q

Heparin resistance

A

AT-III deficiency

Increased heparin clearance or binding

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21
Q

Homocysteinemia

A

Endothelial dysfunction

Lens dislocation, peripheral neuropathy, maybe low folate?

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22
Q

Hypercoagulability of pregnancy

A

General increase in all factors
Decrease in protein S
APC resistance
Venous stasis

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23
Q

Platelet collagen receptors

A 
GPVI (major, plays signaling role, deficiency in Japanese)
Integrin a2b1 (GpIa/IIa)
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24
Q

Wiskott-Aldrich

A

XLD

Thrombocytopenia, eczema, immunodeficiency

Cytoskeletal abnormality, impaired signal transduction

Low IgM, high IgE and IgA

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25
Q

VASP

Cone & Plate analysis

A

VASP: Flow-based method, gold-standard for P2Y12 inhibitor effect.
Cone & Plate: In vitro method studying shear-induced adhesion. Affected by Hct, plt count, meh,.

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26
Q

May-Hegglin
Chediak-Higashi
Fechtner

A

May-Hegglin - Dohle-like bodies in neutrophils. MYH9
Chediak-Higashi - Peroxidase+ granules in many leukocytes
Fechtner - May Hegglin + Alport syndrome

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27
Q

Congenital amegakaryocytosis

A

MPL gene mutation

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28
Q

Specimen types in coag testing

A

Most: Citrated plasma (3.2% NaCit)
Flow: Whole blood
Plt agg: Platelet rich and poor plasma (still collect in blue top)

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29
Q

PFA-100: Patterns

A

ASA: Col/Epi prolonged, Col/ADP normal
Plavix: Variable, both may be prolonged
BSS, GT: Both prolonged

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30
Q

ITP targets

A

Usually GpIIb/IIIa or Ib/V/X

31
Q

IIb/IIIa inhibitors

A

Abciximab (Fab fragments)
Tirofiban (nonpeptide)
Eptifibatide (oligopeptide)

32
Q

Plavix

A 
Blocks P2Y12 (irreversibly)
Prodrug, activated by 2C19
33
Q

Scott syndrome

A

Disorder of flippase
Abnormal Annexin V on flow
Shortened PT

34
Q

TXA2 metabolites

A

Metabolized to TxB2, then to 11-dehydroTxB2 in urine.

35
Q

Plt aggregation - Types, agonists

A

Types: Turbidometric (gold standard), impedance, lumiaggregometry

Agonists: Col, ADP, Epi, AA, Thrombin, TRAP, Ristocetin, U44619

36
Q

Aggregometry - Aspirin, plavix

A

Aspirin: Impaired TXA2 production. No second wave after ADP/Epi agonism.

Plavix: No first wave with ADP agonist.

37
Q

Falsely elevated plt count on hematology analyzer

A

Red cell fragments (schistocytes, AML)

Microorganisms

38
Q

NAIT

A

Usually due to HPA-1a > 4b (Asian) antibodies. Treat with maternal platelets.

Ddx: Maternal ITP with placental transfer (mom should be thrombocytopenic)

39
Q

Fonio method

A

To estimate platelet count, multiply the number of platelets seen on a 1000x field by 20.

40
Q

Plt histogram

A

Right skew

41
Q

ITP Tx

A

Steroids, IVIG

Second-line: Rituximab, other immunosuppressants

42
Q

PAR-1

PAI-1

A

PAR-1 - Thrombin receptor on platelets

PAI-1 - Plasminogen activator inhibitor (serpine antifibrinolytic protein on…endothelium?)

43
Q

Jackass platelet trivia

A

10^11 produced per day

7-10d lifespan

44
Q

Clinical presentation of platelet-type and coagulation-type bleeding

A

Platelet-type: Mucocutaneous bleeding, excessive bleeding from minor trauma

Coagulation-type: Deep or delayed bleeding, bruising, hemearthroses

45
Q

TPO agonists

A

eg Romiplostim, eltrombopag

May cause bone marrow fibrosis (reticulin deposition)

46
Q

Weibel-Palade bodies

A

Contain vWF, P-selectin

47
Q

VitK dependent factors.

What conditions affect these?

A

2, 7, 9, 10, C, S

Warfarin, antibiotics, IBD

48
Q

Factor half-lives

A

fVII - 6hrs (shortest)
fVIII - 12hrs
fIX - 24hrs
fXIII - week (longest)

49
Q

NovoSeven

A

Activated factor 7, can be used as bypass agent. Very short lived.

50
Q

Factor dosing

A

fVIII - Bw(kg) x %change, divided by 2.

fIX - Bw(kg) x %change

51
Q

Pharmacogenetics of warfarin

A

VKORC polymorphisms may confer resistance

Metabolized by CYP2C9

52
Q

Early activators of intrinsic pathway

A

HMWKgen activates fXII which activates pre-kallikrein.

HMWKgen deficiency does NOT correct on mixing aPTT.

53
Q

fXIII treatment

A

Cryoprecipitate

Corifact (recombinant fXIII)

54
Q

Brill-Edwards regression

A

Relates aPTT to anti-Xa activity (0.3-0.7 goal)

55
Q

Indications for thrombophilia testing

A

Thrombosis <50yo
Unusual thromboses
Recurrent thromboses
Primary family member with thrombophilia

56
Q

APC resistance
Protein C assay (functional)
Protein S assay (functional)

A

APC resistance: Spike APC into patient plasma, look for expected prolongation of clotting
Protein C assay: Use protein C activator (not APC itself)
Protein S assay: Also spikes APC, looking for expected prolongation of clotting

57
Q

AT3 Testing

A

Chromogenic reagent is normally generated by thrombin. Add heparin and patient sample (AT). Normally, chromogenic substance should not be generated.

58
Q

Causes of decreased AT3

A

Liver disease
Nephrotic syndrome
Thrombosis? IBD? Pregnancy?

L-asparaginase

59
Q

APCR elevation

A 
Factor V leiden
Any inhibitors (LAC, heparin)
Factor deficiencies
60
Q

DRVVT

A

Protac snake venom activates protein C. More protein C prolongs clotting time.

Used as screening test for LAC.

61
Q

Purpura fulminans

A

Deficiency of protein C, as seen in DIC, newborns, warfarin without bridging, and homozygous C deficiency.

62
Q

INR calculation

ISI calculation

A

(PT / geomean) ^ ISI

ISI is slope of reference PT means to lot PT means

63
Q

Heparin side effects

A

Bleeding

Osteoclast activation, osteoblast suppression&raquo_space; osteoporosis

64
Q

Protamine

A

Arginine rich, positively charged antidote to UFH > LMWH

65
Q

Liver transplant phases

A

Anhepatic stage: Activation of fibrinolysis, loss of factors&raquo_space; BLEEDING
Postreperfusion: Correction o fibrinolysis, slow replenishment of factors, but plt sequestration
Postoperative: HYPERCOAGULABLE

66
Q

Heparin cofactor II

A

Minor target of heparin (adjunctive to AT3). Inactivates only IIa.

67
Q

Factors produced exclusively in liver, or not in liver at all

A

Only made in liver: PAI-1, Plasminogen

Not made in liver: vWF,

68
Q

Josso loop

A

In vivo activation of factor IX by TF-VIIa complex

69
Q

At what dilution would an 8-bethesda inhibitor reduce activity by 75%?

A

1: 4 - 25% residual ***
1: 8 - 50% residual
1: 16 - 75% residual

70
Q

TFPI

Thrombomodulin

A

TFPI - Inhibits TF-VIIa complex

Thrombomodulin - Activates protein C, has minor procoagulant and anti-inflammatory functions

71
Q

Germline RUNX1 mutation

A

Thrombocytopenia, increased risk of AML

72
Q

Chromogenic factor X

A

For warfarin monitoring of patients with LAC.

73
Q

Activated clotting time (ACT)

A

Uses whole blood and a contact activator.

For very high heparin levels (eg, bypass)

Takes >100 sec to result

74
Q

Heparin assay

A

Titrate heparin using protamine

Tim's CP Board Review (16 decks)

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