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Anesthesia Fast Facts > Transfusion/Coags > Flashcards

Transfusion/Coags Flashcards

1
Q

Inflammation / Arachidonic Acid pathway

A
  • tissue injury or irritation releases phospholipase A2
  • Phospholipase A2 converts phospholipids from the cell membrane into arachidonic acid
  • Arachidonic acid is converted to prostaglandin G2 and then to H2 by COX 1&2 (or to leukotrienes by 5-LOX)
  • Prostaglandin H2 is converted to Thromboxane A2 (which contributes to platelet aggregation) and prostaglandins by COX 1, and prostaglandins by COX 2
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2
Q

NSAID categories

A

Selective COX 1 inhibitors (aspirin, ketorolac)

Non-selective COX inhibitors (naproxen, ibuprofen)

Selective COX 2 inhibitors (celecoxib)

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3
Q

MOA for NSAIDS r/t antiplatelet therapy

A

-inhibition of COX 1 & then also TxA2

asa = irreversible
ibuprofen = reversible
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4
Q

AA pathway Prostaglandins

A

Both prostaglandins are converted from AA by COX 1. (COX 2 only converts PGI2)

Thromboxane A2 (TxA2) - in platelets
-pro-coagulation

Prostacyclin (PGI2) - in the endothelium
-anti-coagulation

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5
Q

How are steroids anti-inflammatory?

A

They inhibit phospholipase A2

which inhibits the AA pathway (aka, Before COX/LOX)

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6
Q

Thromboxane A2

A

TXa2
will promote thrombosis by vasoconstriction (also bronchoconstriction, can cause prinzmetal angina) & platelet aggregation

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7
Q

Prostacyclin

A

PGI2

work as anticoag by promoting vasodilation and inhibit platelet aggregation

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8
Q

Why do NSAIDS cause pulm problems for people with asthma or COPD?

A

Blocking COX pathway increases the amount of AA moving towards LOX pathway, producing more leukotrienes.

Leukotriene B4 - chemotaxis agent (recruits neutrophils)
Leukotriene C4, D4, E4 - bronchoconstriction

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9
Q

High dose vs low dose aspirin

A

low dose - antiplatelet

high dose- analgesic, anti-inflammatory, antipyretic

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10
Q

Two general steps of hemostasis

A
  1. primary - formation of temporary platelet plug

2. secondary - coagulation cascade leading to stabilization by a fibrin clot

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11
Q

Platelet activation

A
  • receptors on plt bind to exposed damaged blood vessel wall along with vWF that is from the endothelium
  • once adhered, plt surface receptor changes promoting plt aggregation
  • plts have fibrinogen receptors (IIb/IIIa) & fuse with local fibrinogen
  • aggregated plts expose surface factors & release granules that then activate the coagulation cascade
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12
Q

4 Stages of Coagulation Cascade

A

Initiation
Amplification
Propagation
Stabilization

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13
Q

Coagulation Cascade: Initiation (aka old extrinsic pathway)

A
  • Damage to the vessel and tissue releases a protein called Tissue Factor
  • TF binds to factor VIIa forming the VIIa/TF complex
  • this complex activates factor X and IX
  • Xa causes prothrombin (II) to activate to thrombin (IIa)
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14
Q

Coagulation Cascade: Amplification

A

-IIa activates V, VIII/vWF, and XI on the surface of platelets

  • activation of VIII/vWF causes them to dissociate & vWF helps platelets adhere to cells expressing TF
  • activation of XI by IIa explains why XII isn’t required for normal hemostasis
  • XIa activates IX, IXa joins with the previously activated/released VIIIa to form the IXa/VIIIa complex
  • that complex activates X to Xa
  • activated Va is a cofactor to Xa
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15
Q

What happens in the absence of VIIIa or IXa?

A

the initiation of coagulation is normal but amplification/propagation is altered. They will clot but they develop bleeding in muscle and joints due to low TF expression.

(hemophilia A or B)

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16
Q

Coagulation Cascade: Propagation

A
  • Xa + Va join with Ca++ and PL [aka prothrombinase complex] to catalyze prothrombin (IIa) to thrombin (IIa)
  • large amounts of local thrombin is responsible for the cleavage of fibrinogen into fibrin which then strengthens/consolidates platelet plug
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17
Q

Tenase complexes

A

“Tenase” refers to factor complexes which activate, factor X through enzymatic cleavage to Xa

BOTH the extrinsic (factor VIIa/TF) and intrinsic (factors IXa/VIIIa) tenase complexes produce factor Xa (which is the major producer of thrombin which cleaves fibrinogen into fibrin.

Fibrin is the end goal of the cascade.

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18
Q

Factor XIII

A

Released by activated platelelets

mechanically stabilizes the formation of cross-linked fibrin mesh and generation of a stable hemostatic plug and protects it from fibrinolysis

XIII is activated by thrombin and Ca++

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19
Q

Four natural anticoagulants released by endothelium are involved to control the spread of coagulation activation

A

tissue factor pathway inhibitor (TFPI)
protein C (PC)
protein S (PS)
antithrombin (AT)

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20
Q

Thrombin activates endothelial Protein C and Protein S which then?

A

thrombin activates protein C which binds protein S, and together they function as a critical anticoagulant by inhibiting factor Va and factor VIIIa

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21
Q

Platelet aggregation and the AA pathway

A

AA is released from the cell membrane of the plt

AA –> COX 1 –> Txa2 –> vasoconstriction & platelet aggregation

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22
Q

tissue factor pathway inhibitor (TFPI)

A
  • -plasma lipoprotein secreted by endothelium

- slows/inhibits the extrinsic pathway by inhibiting the TF/VIIa/Xa/Ca complex

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23
Q

tissue plasminogen activator (tPA) as an enzyme

A

endothelial protein

it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown & fibrinolysis

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24
Q

tissue plasminogen activator (tPA) as a drug

A
  • uses: embolic or thrombotic stroke
  • can be inhibited by plasminogen activator inhibitor (PAI-1)
  • the antidote for tPA in case of toxicity is aminocaproic acid.
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25
Q

Thrombomodulin

A

endothelial mediator that keeps thrombin activity local at the site of injury

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26
Q

Pro-coag endothelial mediators

A

TF, vWF, plasminogen activator inhibitor (PAI)-1, and PARs

  • PAI-1 prevents plasmin generation and fibrinolysis, or clot cleavage.
  • PARs further signal platelet and a host of other responses by thrombin and other inflammatory mediators
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27
Q

Exogenous causes of decreased AT

A

CBP

heparin therapy

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28
Q

Exogenous causes of decreased Protein C and/or S

A 
warfarin therapy
estrogen therapy
liver disease
nephrotic syndrome
acute thrombosis
29
Q

Exogenous cause of increased vWF release

A

DDAVP

30
Q

Vit K dependent proteins include:

A

-factors II, VII, IX, and X, protein C & S

31
Q

APTT measures?

A

Activated partial thromboplastin time

  • INTRINSIC and common pathways
  • affected by XII, XI, VIII (X, V, II, I)
  • normal is 25-38 seconds

-uses: screen for hemophilia A and B, detect clotting inhibitors, warfarin and other agents with vitamin K antagonist activity, or activity r/t hepatic dysfunction, heparin therapy, DTIs like argatroban & bivalirudin

32
Q

PT measures?

A

Prothrombin time

  • EXTRINSIC and common pathways
  • affected by factors VII (X, V, II, I)
  • normal 11-13 seconds

-uses: warfarin therapy, long-term anticoagulant therapy

33
Q

INR measures?

A

PT normalized due to the fact that different hospitals use different lab machines that cause varying results in PT

INR standardizes the results of PT
-normal 0.8-1.2

34
Q

Clotting factors are synthesized where?

A
  • Endothelial cells
  • megakaryocytes
  • liver via hepatocytes
35
Q

ACT measures?

A

Activated clotting time

  • normal 70-120 sec
  • therapeutic range for anticoagulation being 150-600 sec.

-uses: high heparin concentrations used during cardiac surgery

36
Q

TEG measures?

A
  • thromboelastography TEG
  • Coagulation time represents the onset of clotting
  • Clot formation time and angle both represent the initial rate of fibrin polymerization
  • Maximal clot firmness is a measure of the maximal viscoelastic strength of clot.
  • Lysis time is used for the diagnosis of premature lysis or hyperfibrinolysis.
37
Q

Normals TEG

A 
R time = 5-10
K time = 1-3
Angle = 50-70 degrees
MA = 50-70
Lysis = < 8%
38
Q

TEG treatment for abnormals

A 
Long R time = FFP
Long K type = Cryo
Low angle = Cryo
Low MA = platelets or DDAVP
Lysis = TXA, amicar
39
Q

Genetic pro-coagulation issues

A
  • inherited antithrombin deficiency
  • prothrombin G20210A mutation
  • Factor V Leiden
  • Dysfibrinogememia
  • protein C deficiency
  • lipoprotein(a)
  • tPA abnormalities
40
Q

Acquired pro-coagulation issues

A
  • antiphospholipid antibodies
  • blood stasis
  • cancer
  • DIC
  • HIT
41
Q

Genetic anti-coagulation issues

A 
Hemophilia A (VIII)
Hemophilia B (IX)
vW disease 
other factor deficiencies
42
Q

Acquired anti-coagulation issues

A
  • thrombocytopenia
  • liver or renal failure
  • dilutional coagulopathy
  • anticoagulant/antiplatelet therapy
43
Q

Universal donor

A

O-

44
Q

Universal acceptor

A

AB+

45
Q

Acute hemolytic reaction

A
  • ABO incompatible
  • occurs 1:30,000
  • occurs in first 15 min of transfusion
  • S/Ss: Agitation, N&V, dyspnea, fever, flushing, hypotension, tachycardia, Hemoglobinuria
  • Can cause: Renal failure from ATN or DIC
46
Q

TRALI

A
  • Inflammatory response: neutrophils lodging in pulmonary microcirculation which then release pro-inflammatory substances
  • leading to Pulmonary vascular injury, leakage & pulmonary edema
  • Acute onset within 6 hours following transfusion
  • bilat infiltrates
  • ARDS
  • hypoxemia
47
Q

TACO

A
  • Transfusion associated circulatory overload
  • 6% incidence in ICU patients
  • Acute onset dyspnea, HTN, tachy, tachypnea, volume overload, rales, high JVD
  • Similar to TRALI, echo differentiates
48
Q

Heparin activity dependent on:

A

antithrombin III

49
Q

Heparin MOA

A

enhances the reactions of antithrombin III

-ATIII inhibits Xa and thrombin (and also XIa & IXa)

  • high negative electrostatic charge of heparin also attracts and binds the AT/heparin complex to thrombin –> therefore the size of the heparin molecule affects whether it inhibits thrombin or not.
  • HMWH/UFH inhibits Xa and thrombin
  • LMWH inhibits Xa
50
Q

Heparin MOA

A

enhances the reactions of antithrombin III

-ATIII inhibits Xa and thrombin (and also XIa & IXa)

  • high negative electrostatic charge of heparin also attracts and binds the AT/heparin complex to thrombin –> therefore the size of the heparin molecule affects whether it inhibits thrombin or not.
  • HMWH/UFH inhibits Xa and thrombin
  • LMWH inhibits Xa
51
Q

Drugs that target IIa

A

Bound with AT: UFH

Argatroban, Bivalirudin, Dabigatran, Lepirudin

52
Q

S/S of HIT

A
  • severe thrombocytopenia (sudden 50% drop in platelet count)
  • thrombotic events (DVT, VTE, PE, MI, CVA)
  • develops after 4 to 5 days of heparin therapy
  • Also hypotension, pulm HTN, tachycardia after IV heparin bolus
  • anaphylaxis

-caused by heparin antibodies

53
Q

Protamine

A
  • reverses heparin anticoagulation
  • positive charge binds to heparins negative charge and forms a complex that is then inactivated and cleared by system

Dose: 1mg / 100 units of circulating heparin

54
Q

LMWH drugs

A
  • enoxaparin, dalteparin
  • molecular weight 4-5000
  • more Xa activity than IIa
  • uses: VTE prophylaxis
  • route: SQ
  • elimination: depends on renal fxn.
55
Q

LMWH drugs

A
  • enoxaparin, dalteparin
  • molecular weight 4-5000
  • more Xa activity than IIa
  • uses: VTE prophylaxis
  • route: SQ
  • elimination: depends on renal fxn.
56
Q

Fondaparinux

A
  • synthetic lab created anticoagulant that works at heparin site on AT
  • inhibits Xa (NO IIa)
  • uses: DVT, PE prophylaxis for patients with HIT
  • route: SQ (also IV)
  • elimination: depends on renal fxn
57
Q

Bivalirudin

A 
DTI
IV only
t1/2 25 min
uses: PCIs in pts with HIT, PTCAs, pts with HIT
stop 4 hrs before surgery
58
Q

Argatroban

A

DTI
IV only
t1/2 40-50min
uses: PCI in HIT pts, VTE prophylaxis in pts with HIT
elimination: hepatic* so can be used in pts with renal failure
stop 4 hrs before surgery

59
Q

Lepirudin & Desirudin

A

t1/2 - long, stop 24 hours before surgery

  • IRREVERSIBLE DTIs
  • Lepirudin IV - used for HIT and prevention of VTE
  • Desirudin SQ - used for VTE in THA,TKAs, PTCA
60
Q

Warfarin

A 
Vitamin K antagonist (II, VII, IX, X)
dose: 1-10 mg
route: oral (also IV)
onset 8-12 hrs & peak 36-72 hrs
-highly protein-bound
-metabolized and excreted in bile and urine 
uses: VTE, prevention of stroke in pts with valves or afib, pts who are hypercoagulable
D/C 3 days preop
61
Q

Preferred lab evaluation for warfarin

A

PT/INR - since 3 of the 4 inhibited factors (II, VII, X) are measured by PT

goal: INR 2-3

62
Q

Preferred lab evaluation for warfarin

A

PT/INR - since 3 of the 4 inhibited factors (II, VII, X) are measured by PT

goal: INR 2-3

63
Q

Oral Direct Factor Xa Inhibitors

A

Rivaroxaban (Xarelto)
Apixaban (Eliquis)

uses: DVTs, PE, reduce reoccurrence of DVT/PEs, risk reduction of stroke in afib
caution: neuraxial anesthesia catheters should not be removed until more than 18 hrs after last admin of rivaroxaban

64
Q

Oral DTIs

A

ximelagatran (withdrawn from market dt liver toxicity)

dabigatran etexilate (pradaxa)
-uses: risk reduction of stroke in pts with afib, DVT/PE in pts who have been treated with IV coags for 5-10 days, and risk reduction in DVT/PE pt
65
Q

Reversal of anticoagulants: FFP

A
  • 4 units
  • risk include transfusion risks & volume overload
  • not able to restore INR to baseline
66
Q

New anticoagulants - when to stop before surgery?

A

Procedures with
= low risk - 48 hrs
= medium to high risk - 5 days

-pts at high thrombotic risk can be bridged with LMWH or UFH

67
Q

New anticoagulants - when to stop before surgery?

A

Procedures with
= low risk - 48 hrs
= medium to high risk - 5 days

-pts at high thrombotic risk can be bridged with LMWH or UFH

68
Q

Reversal of anticoagulants: activated VII & PCCs

A

“Prothrombin complex concentrate” contains factors II, IX, and X, and variable amounts of factor VII concentrate

  • mixed success
  • Rivaroxaban reversed with ~ 50 IU/kg
  • dabigatran minimally
69
Q

Platelet Inhibitors

A

Aspirin
Thienopyridines: Clopidogrel, prasugrel, ticagrelor
Dipyridamole
Dextran
Platelet Glycoprotein IIb/IIIa antagonists: abciximab, tirofiban, eptifibatide

Anesthesia Fast Facts (24 decks)

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