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Health Assessment - Autumn > Coag Part 2 > Flashcards

Coag Part 2 Flashcards

1
Q

CKD patients display a baseline anemia due to:

A

-lack of erythropoietin
-platelet dysfunction (due to uremic environment)

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2
Q

What 2 things are shown to shorten bleeding times in CKD?

A

-dialysis
-correction of anemia

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3
Q

Treatment of platelet dysfunction in CKD:

A

-Cryoprecipitate (rich vWF)
-DDAVP
-Conjugated estrogen given pre-operatively for 5 days

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4
Q

What is DIC?

A

-disseminated intravascular coagulation

-pathological hemostatic response to tissue factor/7a complex causing excessive antagonism of the extrinsic pathway-which overwhelms the anticoagulant mechanism-generates intravascular thrombin

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5
Q

What 2 things become depleted during widespread microvascular thrombotic activity, causing multi=organ dysfunction?

A

-coagulation factors
-platelets

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6
Q

What can precipitate DIC?

A

-trauma
-amniotic fluid embolus
-malignancy
-sepsis
-incompatible blood transfusion

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7
Q

What lab finding are found with DIC:

A

-decreased platelets
-prolonged PT/PTT/Thrombin time
-increased soluble fibrin and fibrin degradation products

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8
Q

Management of DIC:

A

correct underlying condition and administer appropriate blood products

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9
Q

What is trauma-induced coagulopathy?

A
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10
Q

What is a common cause of trauma-related death?

Why causes coagulopathies to occur?

A

-uncontrolled hemorrhage

-acidosis, hypothermia, and/or hemodilution

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11
Q

What is Trauma-induced coagulopathy?

A

-independent acute coagulopathy seen in trauma patients-thought to be related to activated protein C decreasing thrombin generation

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12
Q

What is the driving force for protein C activition?

A

Hypo-perfusion

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13
Q

What happens to endothelial glycocalyx, which contains proteoglycans?

A

It degrades due to the protein C activation

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14
Q

What does proteoglycan-shedding result in?

A

Auto-heparinization

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15
Q

What does platelet dysfunction contribute to?

A

increased bleeding

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16
Q

The most common inherited prothrombotic diseases are caused by a mutation in _______ or ____

A

-factor V

-PT

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17
Q

What does factor V leidin mutation lead to ?

A

-leads to activated protein C resistance

-present in 5% caucasian population

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18
Q

What does prothrombin mutation cause?

A

Increased PT concentration-leading to hypercoagulation

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19
Q

What is thrombophilia?

A

-inherited or acquired predisposition for thrombotic events

-manifests as venous thrombosis

-highly susceptible to virchow’s triad

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20
Q

What is virchows triad again?

A

-blood stasis
-endothelial injury
-hypercoagulability

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21
Q

What is antiphospholipid syndrome?

A

autoimmune disorder with antibodies against the phospholipid-binding proteins in the coagulation system

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22
Q

What is antiphospholipid syndome characterized by?

What do people with this syndrome often require?

A

-characterized by recurrent thrombosis and pregnancy loss

-often require life-long anticoagulants

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23
Q

What factors greatly increase the risk of thrombosis in people with antiphospholipid syndrome?

A

-oral contraceptives
-pregnancy
-immobility
-infection
-surgery
-trauma

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24
Q

Heparin-Induced Thrombocytopenia:

A

-mild to moderate thrombocytopenia associated with heparin

-occurs 5-14 days after heparin treatment

-it’s an autoimmune response occurring in up to 5% of pts receiving heparin

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25
Q

What does HIT result in?

A

platelet count reduction as well as activation of the remaining platelets and potential thrombosis

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26
Q

If a patient has received a prior heparin dose, thrombocytopenia or thrombosis may occur within __ day(s) of subsequent dose.

A

1 day of subsequent dose

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27
Q

Risk factors for HIT:

A

-women
-pts receiving high heparin doses such as with cardiopulmonary bypass
-increased risk with unfractionated heparin compared to LMWH

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28
Q

What to do if HIT is susprected:

A

-D/C heparin
-convert to an alt. anticoagulant
-warfarin is CONTRAINDICATED b/c it decreases protein C and S synthesis

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29
Q

What is the HIT diagnosis confirmed with?

A

-HIT antibody testing

-antibodies are typically cleared from circulation in 3 months

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30
Q

PT info:

A

-prothrombin time: plasma is mixed with tissue factor and the number of seconds is measured until a clot forms

-assess integrity of extrinsic and common pathways

-used to monitor vit K antagonists like warfarin

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31
Q

What factor deficiencies does PT reflect?

A

Factor 1, 2, 5, 7, 10

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32
Q

What factors are vit K dependent?

A

Factors 2, 7, and 10

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33
Q

aPTT info:

A

-activated partial thromboplastin time

-measures seconds until clot forms after mixing plasma with phospholipid, Ca++, and an activator of the intrinsic pathway

-assess integrity of intrinsic and common pathways

-may be used to measure effect of heparin

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34
Q

What specific deficiencies is the aPTT test more sensitive towards?

A

Factor 8 and 9

35
Q

Anti-factor Xa activity assay:

A

-aka “Factor Xa inhibition test” plasma combined with Xa and an artificial substrate that releases a colorimetric signal after factor Xa is cleaved

-provides assessment of heparin’s anticoagulant effect

-also used to assess effect of LMWH, fondaparinux, and factor Xa inhibitors

36
Q

Platelet Count:

A

-standard component of coagulation testing

-normal= >100,000 platelets/microliter

-POC testing available

37
Q

ACT:

A

-activated clotting time: variation of whole blood clotting time w/ addition of a clotting activator to accelerate clotting time

-addresses intrinsic and common pathways

-used to measure responsiveness to heparin

-normal: 107 +/- 13 seconds
-POC analyzers available

38
Q

Heparin Concentration Measurement:

A

-protamine-concentration is the MOST popular POC method to determine perioperative heparin concentration

-1 mg protamine will inhibit 1 mg heparin

-this test estimates plasma heparin concentration

39
Q

What happens as amount of protamine in heparin blood increases?

A

-as increasing amts of protamine are added to heparinized blood, time to clot DECREASES until protamine concentration > heparin concentration

40
Q

Viscoelastic Coagulation Tests:

A

-measures all aspects of clot formation from early fibrin generation to clot retraction and fibrinolysis-coag diagrams generated

-allows for more precise blood product administration

41
Q

Diagrams generated from viscoelastic coag tests:

A

-TEG: thromboelastogram

-ROTEM: rotational thromboelastometry

42
Q

TEG Diagram Image:

A
43
Q

R time:

A

-time to start forming clot

-5-10 min= normal

-prob with coag factors

-Tx: FFP

44
Q

K time:

A

-time until clot reaches a fixed strength

-1-3 min= normal

-fibrinogen prob

-Tx: cryo

45
Q

Alpha angle:

A

-speed of fibrin accumulation

-53-72 seconds= normal

-prob with fibrinogen

-tx: cryo

46
Q

Maximum amplitude (MA):

A

-highest vertical amplitude of the TEG

-50-70 min= normal

-prob with platelets

-Tx: platelets and/or DDAVP

47
Q

Lysis at 30 minutes: (LY30)

A

-% of amplitude reduction 30 min after maximum amplitude

-0-8%= normal

-prob with excess fibrinlysis

-Tx: TXA or aminocaproic acid

48
Q

What do platelet inhibitors do and what are the 3 main classes?

A

inhibit platelet aggregation and/or adhesion

-COX inhibitors
-P2Y12 receptor antagonists
-Platelet GIIb/IIa R antagonists

49
Q

COX inhibitors:

A

-block Cox 1 from forming TXA2-which is important in platelet aggregation

-ASA: anti-platelet effects x7-10 days after d/c
-NSAIDs: anti-plt effect x3 days

50
Q

P2Y12 receptor antagonists:

A

-inhibit P2Y12-R-preventing GIIb/IIIa expression

-plavix: anti-plt effects x7 days after d/c
-ticlopidine: anti plt effects x14-21 days after d/c
-ticagrelor and cangrelor: short acting, <24 hr activity

51
Q

Platelet GIIb/IIIa R antagonists:

A

-prevent vWF and fibrinogen from binding to GIIb/IIIa-R

-abciximab, eptifibatide, tirofiban

52
Q

Vitamin K antagonists:

A

-inhibit synthesis of vit-K dependent factors (2, 7, 9, 10, protein C and S)

53
Q

Warfarin:

A

-most common vit K antagonists

-DOC for valvular Afib and valve-replacements

-long halflife:40 hrs-can take 3-4 days to reach therapeutic INR of 2-3

-usually requires heparin until therapeutic effected achieved

-monitor PT/INR freq.

-reversible with Vit K

54
Q

How does heparin work?

A

It binds to antithrombin which DIRECTLY inhibits soluble thrombin and Xa

55
Q

Unfractionated Heparin:

A

-short half life, given IV

-fully reversible with protamine

-close monitoring required

56
Q

LMWH:

A

-longer halflife, dosed BID SQ

-no coag testing needed

-protamine only partially effective

57
Q

Fondaparinux:

A

-much longer halflife (17-21 hr), dosed once/day

-protamine not effective

58
Q

How do direct thrombin inhibitors work?

A

They bind and block thrombin in both soluble and fibrin-bound states

-hirudin, argatroban, bivalirudin, and dabigatran

59
Q

What’s random about hirudin?

A

naturally found in leeches lol

60
Q

Argatroban:

A

-synthetic, reversible binds to thrombin-HL 45 min

-monitored intraop with PTT or ACT

61
Q

Bivalirudin:

A

-synthetic, shortest HL of direct thrombin inhibitors

-DOC for renal or liver impairment

62
Q

Dabigatran (Pradaxa):

A

-1st direct oral anticoagulant

-direct thrombin inhibitor approved for CVA prevention and non-valvular A-fib

63
Q

Direct oral anticoagulants (DOACs):

A

-newer class, introduced in past 10 yrs

-have more predictable PK/PD

-fewer drug interactions and fewer embolic events, intracranial hemorrhages, and lower mortality than warfarin

-dosed daily w/o lab monitoring

-efficacy similar to warfarin-not much shorter HL

64
Q

What are examples of Xa inhibitors?

A

-Rivaroxaban (Xarelto)
-Apixaban (Eliquis)
-Edoxaban (Savaysa)

65
Q

Thrombolytics:

A

-used to dissolve blood clots
-may be given IV or directly into site of blockage

66
Q

What are most thrombolytics?

A

-Most are serin proteases that convert plasminogen to plasmin-breaks down fibrinogen to fibrin

67
Q

The 2 categories of thrombolytics:

A

-fibrin-specific: altepase (tPA), Reteplase, and Tenecteplase

-non-fibrin-specific: Streptokinase **not widely used d/t allergic reactions

68
Q

Surgery is CONTRAINDICATED within ___ day(s) of thrombolytic treatment.

A

-10 days

69
Q

List of Absolute and Relative Contraindications for Thrombolytics

A

-absolute: vascular lesions, severe-uncontrolled HTN, recent cranial surgery or trauma, brain tumor, ischemic stroke < 3 months, and active bleeding

-relative: ischemic stroke >3 months, active peptic ulcer, current use of anticoagulant drugs, pregnancy, prolonged/traumatic CPR <3 weeks prior, major surgery < 3 weeks prior

70
Q

What are procoagulants?

A

-used to mitigate blood loss

-2 classes: antifibrinolytics and factor replacements

71
Q

Antifibrinolytics:

A

2 subclasses: lysine analogues and a SERPIN

-lysine analogues: epsilon-aminocaproic acid (EACA) and TXA: binds and inhibits plasminogen from binding to fibrin-impairing fibrinolysis

-SERPIN: aprotinin (removed from market d/t renal and cardio toxicity)

72
Q

Factor Replacements:

A

-Recombinant VIIa (RfVIIa): increase thrombin generation via intrinsic and extrinsic paths

-Prothrombin complex concentrate (PCC): contain vit K factors

-fibrinogen concentrate: derived from pooled plasma, standard concentration

-cryo and FFP: cheaper and contain more coag factors, but less specific composition

73
Q

Preop guidelines for warfarin:

A

-low risk pts should d/c 5 days prior to surgery and restart 12-24 hrs postop

-high risk pts should stop 5 days prior and bridge w/ UFH or LMWH

74
Q

Preop guidelines for heparin:

A

-UFH d/c’d 4-6 hr prior to surgery and resumed (NO bolus) > 12 hr postop

-LMWH d/c’d 24 hour prior to surgery and resumed 24 hr postop

75
Q

Preop guidelines for Aspirin:

A

not as defined

-moderate/high risk pts: current recc is to continue ASA

-low risk pts: stop 7-10 days prior to surgery

76
Q

Preop guidelines for pts post-coronary stent placement:

A

-bare metal stents: delay elective surgery 6 wks after placement

-drug-eluding stents: delay elective surgery 6 months after placement

77
Q

Graph for neuraxial anesthesia on anti-coags:

A

-no restrictions for NSAID and Heparin SQ BID

78
Q

What may be required for excessive bleeding or emergent surgery?

A

Warfarin reversal

79
Q

Prothrombin complex concentrates for the DOC for what?

A

emergent coumadin reversal (though HL is short)

80
Q

Concurrent ____ __ is required to restore carboxylation of vit K dependent factors by the liver for more sustained correction

A

Concurrent vitamin K

81
Q

Do reversal agents exist for direct thrombin inhibitors?

A

No reversal for most, but not a horrible thing b/c HL is relatively short

-exception: DOAC Dabigatran (Pradaxa) does have an antidote-Idarucizumab

82
Q

What can DOAC factor Xa inhibitors by reversed by?

A

Andexanet-a derivative of factor Xa

83
Q

Master List of Common Anticogulants:

A

Health Assessment - Autumn (6 decks)

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