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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
Thrombomodulin
endothelial mediator that keeps thrombin activity local at the site of injury
26
Pro-coag endothelial mediators
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
27
Exogenous causes of decreased AT
CBP | heparin therapy
28
Exogenous causes of decreased Protein C and/or S
``` warfarin therapy estrogen therapy liver disease nephrotic syndrome acute thrombosis ```
29
Exogenous cause of increased vWF release
DDAVP
30
Vit K dependent proteins include:
-factors II, VII, IX, and X, protein C & S
31
APTT measures?
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
PT measures?
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
INR measures?
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
Clotting factors are synthesized where?
- Endothelial cells - megakaryocytes - liver via hepatocytes
35
ACT measures?
Activated clotting time - normal 70-120 sec - therapeutic range for anticoagulation being 150-600 sec. -uses: high heparin concentrations used during cardiac surgery
36
TEG measures?
- 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
Normals TEG
``` R time = 5-10 K time = 1-3 Angle = 50-70 degrees MA = 50-70 Lysis = < 8% ```
38
TEG treatment for abnormals
``` Long R time = FFP Long K type = Cryo Low angle = Cryo Low MA = platelets or DDAVP Lysis = TXA, amicar ```
39
Genetic pro-coagulation issues
- inherited antithrombin deficiency - prothrombin G20210A mutation - Factor V Leiden - Dysfibrinogememia - protein C deficiency - lipoprotein(a) - tPA abnormalities
40
Acquired pro-coagulation issues
- antiphospholipid antibodies - blood stasis - cancer - DIC - HIT
41
Genetic anti-coagulation issues
``` Hemophilia A (VIII) Hemophilia B (IX) vW disease other factor deficiencies ```
42
Acquired anti-coagulation issues
- thrombocytopenia - liver or renal failure - dilutional coagulopathy - anticoagulant/antiplatelet therapy
43
Universal donor
O-
44
Universal acceptor
AB+
45
Acute hemolytic reaction
- 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
TRALI
- 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
TACO
- 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
Heparin activity dependent on:
antithrombin III
49
Heparin MOA
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
Heparin MOA
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
Drugs that target IIa
Bound with AT: UFH Argatroban, Bivalirudin, Dabigatran, Lepirudin
52
S/S of HIT
- 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
Protamine
- 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
LMWH drugs
- enoxaparin, dalteparin - molecular weight 4-5000 - more Xa activity than IIa - uses: VTE prophylaxis - route: SQ - elimination: depends on renal fxn.
55
LMWH drugs
- enoxaparin, dalteparin - molecular weight 4-5000 - more Xa activity than IIa - uses: VTE prophylaxis - route: SQ - elimination: depends on renal fxn.
56
Fondaparinux
- 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
Bivalirudin
``` DTI IV only t1/2 25 min uses: PCIs in pts with HIT, PTCAs, pts with HIT stop 4 hrs before surgery ```
58
Argatroban
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
Lepirudin & Desirudin
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
Warfarin
``` 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
Preferred lab evaluation for warfarin
PT/INR - since 3 of the 4 inhibited factors (II, VII, X) are measured by PT goal: INR 2-3
62
Preferred lab evaluation for warfarin
PT/INR - since 3 of the 4 inhibited factors (II, VII, X) are measured by PT goal: INR 2-3
63
Oral Direct Factor Xa Inhibitors
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
Oral DTIs
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
Reversal of anticoagulants: FFP
- 4 units - risk include transfusion risks & volume overload - not able to restore INR to baseline
66
New anticoagulants - when to stop before surgery?
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
New anticoagulants - when to stop before surgery?
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
Reversal of anticoagulants: activated VII & PCCs
"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
Platelet Inhibitors
Aspirin Thienopyridines: Clopidogrel, prasugrel, ticagrelor Dipyridamole Dextran Platelet Glycoprotein IIb/IIIa antagonists: abciximab, tirofiban, eptifibatide

Anesthesia Fast Facts (24 decks)

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