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ABSITE > Fiser Chaper 2. HEMATOLOGY > Flashcards

Fiser Chaper 2. HEMATOLOGY Flashcards

1
Q

Intrinisic pathway

A

-Exposed collagen, prekallikrein, HMW kininogen, factor 7

–> activate 11

–> activate 9, then add 8

-> activate X, then add V

–> contvert prohrombin (2) to thrombin

-> thrombin converts fibrinogen to fibrin

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2
Q

Extrinisic pathway

A

Injured cells: tissue factor + 7

  • > convert prothrombin to thrombin
  • > thrombin converts fibrinogen to fibrin
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3
Q

Prothrombin complex

A

10, 5, calcium, platelet facotr 3, prothrombin

Forms on platelets

Catalyzes the formation of thrombin

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4
Q

What is the convergent point for intrinsic and extrinsic pathways

A

X

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5
Q

Tissue factor pathway inhibitor does what?

A

Inhibits factor 10

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6
Q

Factor13 does what?

A

Helps crosslink fibrin

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7
Q

Fibrin dose what?

A

Binds GpIIb/IIIa molecule to link platelets together and form platelet plug

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8
Q

Thrombin does what?

A

Key to coagulation

COnverts fibrinogen to fibrin and fibrin split products

Activates 5 and 13, and platelets

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9
Q

Key to normal AC?

A

Antithrombin III

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10
Q

What does AT-III do?

A

Key to anticoagulation

Binds and inhibits Thrombin

Also inhibits 9, 10, 11

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11
Q

How does heparin work?

A

Activates AT-III (up to 1000x normal activity)

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12
Q

Protein C and S

A

Both vitamin K dependent

C: decreades 5and 8 and fibrinogen

S: protein Ccofactor

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13
Q

Fibrinolysis needs what?

A

Tissue plasminogen activator: released from endothelium and converts plasminogen to plasmin

–> Plasmin degrades factors 5, 8, fibrinogen, fibron

–> lose platelet plug

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14
Q

Alpha-2 antiplasmin

A

Natural inhibitor of plasmin, released from endothelium

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15
Q

Shortest half life factor?

A

7

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16
Q

Only factor not synthesized in liver?

A

8 (endothelium)

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17
Q

Vit K dependent factors

A

2, 7, 9, 10, C and S

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18
Q

How long does vit k take?

A

6 hours to have effect

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19
Q

How long does FFP take?

A

Immediate, lasts 6 hours

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20
Q

Half life of RBCs, platelets, PMNs

A

RBCs: 120 days

Platelets: 7 days

PMNs: 1-2 days

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21
Q

PGI2

A

prostacyclin

from endothelium

decreases platelet aggregation and promotes vasodilation

antagonist to TXA2

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22
Q

TXA2

A

Thromboxane

From platelets

Increases platelets aggregation and vasoconstriction

Triggers release of calciumin platelets –> exposes GpIIb/IIIa receptor and causes platelet-to0platelet binding; platelet-to-collagen binding also occurs (Gp1b receptor)

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23
Q

Cryoprecipitate

A

highest conc of vWF-8; also has fibrinogen

used in vWF disease and hemophilia A

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24
Q

FFP

A

all coag factors, C, S, AT-III

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25
Q

DDAVP and conjugated estrogens

A

Cause release of 8 and vWF from endothelium

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26
Q

PT

A

measures 2, 5, 7, 10, fibrinogen; best for liver synthetic function

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27
Q

PTT

A

measures most factors except 7 and 13 (so does NOT pick up factor 7 def)

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28
Q

ACT goals

A

Activated clotting time

150-200 sec for AC

> 460 for cardioplum bypass

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29
Q

MCC surgical bleeding

A

Incomplete hemostasis

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30
Q

MCC congenital bleeding disorder

A

vWF disease

Types 1 (MCC) and 2 are AD, 3 (severe) is autosomal recessive

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31
Q

vWF

A

Links Gp1b receptor on platelets to collagen

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32
Q

vWF disease labs

A

INR/PT normal

PTT normal or abnormal

Prolonged bleeding time (ristocetin test)

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33
Q

vWF disease types

A
  1. MCC, reduced vWF quantity, tx recombinant 8:vWF, DDAVP, cryo
  2. defect, vWF molecule not working well, tx recombinant 8:vWF, cryo
  3. absent (rare), tx recombinant 8:vWF, cryo; DDAVP WILL NOT WORK
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34
Q

Hemophilia A

A

8 deficiency

sex-linked recessive

need levels 100% preop

80-100% for 10-14 days after surgery

prolonged PTT, normal PT

factor 8 crosses placenta so newborns may not bleed at circumcision

Join bleed: DO NOT ASPIRATE: tc ice, ROM exercises, factor 8 concentrate or cryo

Epistatxis or ICH or hematuria: tx recombinant factor 8 or cryo

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35
Q

Hemophilia B

A

9 deficiency

sex-linked recessive

need level 100% preop

30-40% for 2-3 days after surgery

prolonged PTT, normal PT

Tx recombinant factor 9 or FFP

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36
Q

Factor 7 deficiency

A

Prolonged PT/INR, normal PTT

Tx: recombinant factor 7 or FFP

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37
Q

Bruising, epistaxis, mucosal bleeding, petechiae, purpura

A

Platelet disorder (acquired thrombocytopenia, Glanzmann’s thrombocytpoenia, Bernard Soulier thrombocytopenia, Uremia)

38
Q

Acquired thrombocytopenia causes

A

H2 blockers

Heparin

39
Q

Glanzmann’s thrombocytopeniais a deficiency in what?

A

GIIIb/IIa receptor (so platelets cannot bind to each other)

Fibrin normally links the GpIIb/IIIa receptors together

Tx: platelets

40
Q

Bernard-soulier thrombocytopenia is a deficiency in what?

A

Gp1b receptor (platelets cannot bind to collagen)

vWF normally bind Gp1b to collagen

Tx: Platelets

41
Q

Uremia causes what?

A

Inhibits platelet function

Tx: HD first, DDAVP, platelets

42
Q

HIT is due to what?

A

Antiplatelet antibodies (IgG PF4 ab)

Causing platelet destruction (can also cause aggregation and thrombosis)

White clot

LMWhas a decreased risk of causin HIT

Tx: Stop heparin, start argatroban (DTI)

43
Q

DIC

A

Decreased platelets and fibrinogen; high fibrin split products and D-dimer; prolonged PT and PTT

44
Q

DIC often initiated by waht factor?

A

Tissue factor

45
Q

How long before surgery do patients need to stop asa? plavix? warfarin?

A

7 days

46
Q

Aspirin MoA

A

Inhibits COX in platelets and decreases TXA2

Irreversible because platelets lack dNA so cannot resynthesize COX

47
Q

Clopidegril MoA

A

ADP receptor antagonist

Tx: platelets

48
Q

Prostate surgery effects on coag?

A

Can release urokinase, which activate plasminogen causing thrombolysis

Tx: E-aminocaproic acid (amicar)

49
Q

Does normal circumcision rule of bleeding disorder?

A

No

50
Q

Tooth extraction or tonsillectomy in history good way to tell bleeding risk?

A

Yes picks up 99% of patients with bleeding disorder

51
Q

Epistaxis is common in what coag disorder?

A

vWF and platelet disorders

52
Q

MCC congenital hypercoag disorder

A

Factor V LEiden: resistanceto activated proctein C, defect is on factor V

Tx: Heparin and warfarin

53
Q

Hyperhomocysteinemia tx

A

B12 and folic acid

54
Q

Prothrombin gene defect G20210A tx

A

Heparin and warfarin

55
Q

Protein C or S def treatment

A

Heparin and warfarin

56
Q

AT-III deficiency tx

A

Heparin does NOT work (heparin activates AT-III)

Can develop after prvious heparin exposure

Tx: Recombinant AT-III concentrate or FFP (highest conc of AT-III), followed by heparin and warfarin

57
Q

Dysfibrinogenemia, dysplasminogenemia tx

A

Heparin and warfarin

58
Q

PV

A

Defect in platelet function, can get thrombosis

Keep Hct<48, platelets <400 before surgery
Tx: phlebotomy and asa

59
Q

Anti-phospholipid antibody syndrome

A

Not all have SLE

Get high PTT but hypercoagulable

Caused by cardiolipin and lupus anticoagulant abs

60
Q

High PTT but hypercoagulable

A

Anti-phospholipid ab syndrome

61
Q

Dx of antiphospholipid ab syndrome

A

Prolonged PTT, not corrected with FFP

Positive Russell vipor venom time

False-positive RPR test for syphilis

62
Q

Antiphospholipid ab syndrome tx

A

Heparin and warfarin

63
Q

MCC acquired hypercoagulability

A

Tobacco

Other: malignancy, inflammatory states, IBD, infection, OCP, pregnancy, RA, postop patients, myeloproliferative disorders

64
Q

Hypercoagulability from cardiopulmonary bypass is due to what?

A

Hageman factor (Factor 12) activation

Tx: Heparin to prevent

65
Q

Who is especially susceptible to warfarin induced skin necrosis?

A

Protein C deficiency

Protein C and S have shortest half life, so these anticoag factors first decrease before the coag factors decrease

Tx: Heparin

66
Q

Virchow’s triad

A

Stasis, endothelial injury, hypercoagulability

67
Q

Key element in development of arterial thrombosis

A

Endothelial injury

68
Q

Postop DVT tx for 1st,2md and 3rd postop DVT

A

1st: 6 months warfarin
2nd: 1 yr warfarin

3rd or significant PE: lifelong warfarin

69
Q

Who with a DVT gets a Greenfield filter?

A

Patients with contraindication to AC

Documented PE while on AC

Free-floating DVT in IVF, iliofemoral, or deep femoral

Recent pulmonary embolectomy

70
Q

Treatment of PE

A

Heparin (thrombolytics no improvement in survival) or suction catheter-based intervention

If patient in shock despite massive inotropes and pressors, go to OR

71
Q

Most common source of PE

A

iliofemoral

72
Q

Procoagulant agents (anti-fibrinolytics)

A

E-aminocaproic acid (amicar): inhibits plasmin (which inhibits fibrinolysis), used in DIC, persistent bleeding after cardiopulm bypas, thrombolytic overdose, prostate surgery

73
Q

Anticoagulation agents

A

Warfarin

SCDs

Heparin

LMWH

Argatroban

Bivalirudin

Hirudin

Ancrod

74
Q

Warfarin MoA

A

Inhibits vit-K dep DECARBOXYLATION of glutamin acid residues on vit-K dep factors

75
Q

SCD MoA

A

Improves venous return but also induced fibrinolysis with compression (releast of tPA fromendothelium)

76
Q

Heparin MoA

A

Binds and activates AT-III (1000x more activity)

77
Q

What can you use to reverse heparin?

A

Protamine (binds heparin)

Cross-reacts with NPH insulin or previous protamine exposure

1% get protamine reaction (hypotension, bradycardia, decreased heart function)

78
Q

Heparin halft life

A

60-90 min

79
Q

How is heparin cleared?

A

Reticuloendothelial system

80
Q

Side effects of longterm heparin

A

Osteoporosis, alopecia

81
Q

What AC to use in preg?

A

Heparin (does not cross placental barrier, while warfarin does)

82
Q

LMWH

A

Enoxaparin, fondaparinux

Lower risk of HIT

Binds and activates AT-III but increases neutralization of just Xa and thrombin

NOT reversed with protamine

83
Q

Argatroban MoA

A

Reversible DTI

Metabolized by liver

Half life 50 min

Used in HIT

84
Q

Bivalirudin (Angiomax) MoA

A

Reversible DTI

Metabolized by proteinase enzymes in blood

Half life 25 min

85
Q

Hirudin (Hirulog; from leeches)

A

Irreversible DTI

MOST POTENT DIRECT INHIBITOR OF THROMBIN

High risk for bleeding complications

86
Q

Ancrod

A

Malayan pit viper venom

StimulatestPA release

87
Q

Thrombolytics

A

Streptokinase
Urokinase
tPA

88
Q

Thrmbolytic MoA

A

Activate plasminogen

Need to follor fibrinogen levels: <100 associated with increased risk and severity of bleeding

89
Q

Tx for thrombolytic OD

A

E-aminocaproic acid (amicar)

90
Q

CI to thrombolytics (tPA, urokinase, streptokinase)

A

Absolute: active internal bleeding, recent CVA or neurosurgery <3 mo, intracranial pathology, recent GIB

Major: recent surgery/organ bx/obstetric delivery <10 days ago, left heart thrombus, active peptic ulcer, recent major trauma, uncontrolled HTN, recent eye surgery

Minor: Minor surgery, recept CPR, A fib with mitral valve disease, bacterial endocarditis, hemostatic defects (renal or liver disease), diabetic hemorrhagic retinopathy, pregnancy

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