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ACVECC > Coagulation/transfusion > Flashcards

Coagulation/transfusion Flashcards

1
Q

Major cross match

A

mixing of donor RBCs and recipient serum

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2
Q

Minor Cross Match

A

donor plasma and recipient RBCs

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3
Q

Tenase vs prothrombinase complexes

A

Tenase: FIXa + PS + FVIIIa

Prothrombinase: FVa + PS + FXa

PS: activated serine protease
Occur on platelet surface

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4
Q

Anticoagulant properties of endothelial cells

A
  • Heparin sulfated proteoglycans –> bind AT –> inactivates thrombin
  • Negative charge
  • Thrombomidulin: binds with thrombin –> activates protein C–> aProC+ aProS–> irreversibly cleave FVa + FVIIIa–> no more thrombin generation

AND aProC-ProS –> inactivates PAI-1 (resuling in creased fibrinolysis)

  • TFPI –> irreversibly binds FXa –> Making TFPI, FXa, FVIIa, TF complex –> prevent further activation/formation of thrombin
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5
Q

Virchows triad

A

3 areas of predisposition of thrombotic Disease

  1. Endothelial dysfunction
  2. Hypercoaguability of blood
  3. Blood stasis/altered blood flow
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6
Q

Function of thrombin

A

thrombin = FII

Propagation
- activates plt, FXIa & FVa
-Cleaves vWF off FVIII–> FVIIIa & increased platelets

Amplification
- Binds thrombomodulin on EC surface –> activates TAFI & aPrC–> aPrC + PrS
- Cleaves fibrinopeptide A from fibrinogen –> fibrin

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7
Q

Prothrombinase complex

A

FXa + FVa –> activates thrombin

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8
Q

INtrinsic Tenase

A

FIXa + FVIIIa

  • Binds on platelet surface (propogation)
  • Generates F Xa on surface
    *50x more efficient at activating FX than extrinsic tenase
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9
Q

Extrinsic Tenase

A

FVIIa + TF (initiation)

-Activates small amounts FIX & X
-Activates more FVII

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10
Q

Dense granule contents

A
  • ADP
  • ATP
  • Histamine
  • Epinephrine
  • Serotonin
  • Calcium ions
  • polyphosphates
  • Sphingosine - 1- phosphate

Pneumonic: CAN: cations, Amines (hist, epi, sero) & nucleotides (ATP, ect)

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11
Q

Alpha granules

A

Platelet function test (pneumonic)

  • PDF: platelet derived growth factor
  • P selectin
  • Fibronectin
  • FI, FV, FVIII, vWF
  • Fibrinolytics: PAI-1, TAFI
  • TGF & endostatin –> proangiogenesis
  • beta thromboglobulin
  • Mitogens: IGF-1, VEGF = wound healing
  • Cytokines: IL-8, PF4
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12
Q

Lysosomes

A

-Released from platelets - unclear role
- Need more agonists to release
- Acid hydrolases: glucorinadase, cathepsins, aryl sulfatase, galactosidase, elastase, collagenase

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13
Q

Subendothelial procoagulant macromolecules

A

-vWF
- Fibronectin
- Fibulin
- Laminin
- Thrombospondin

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14
Q

Actions of CIRCULATING vWF

A
  • Primary source is Endothelial cells
  • Binds:

collagen
GPIb-alpha
Itself!!

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15
Q

GPIba

A
  • Platelet tethering to subendothelial vWF
  • leads to formation of platelet monolayer
  • bindings of platelet, collagen and vWF
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16
Q

α2bβ3

A

Platelet integrin –> activated by intracellular calcium

  • Binds:
    Fibrinogen/fibrin bound
    vWF
    If activated, can bind soluble fibrin
  • May form bridges with fibrinogen in middle between activated platelets
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17
Q

P2Y1

A

Platelet receptor

Agonist:
ADP

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18
Q

P2Y12

A

Platelet receptor

Agonist:
ADP

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19
Q

TPalpha & TPbeta

A

Platelet receptor

Agonist:
TXA2

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20
Q

PAR1

A

Platelet receptor

Agonist:
Thrombin

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21
Q

PAR4

A

Platelet receptor

Agonist:
Thrombin

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22
Q

Alpha2A

A

Platelet receptor

Agonist: epinephrine

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23
Q

IP

A

Platelet receptor

Agonist: PGI2

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24
Q

Causes of hypotension

A
  1. Decreased Preload
    - Hypovolemia –> address underlying problem & give IVF
    - Obstructive (Mes Volvulous, GDV, pericardial effusion, PTE, pleural space disease)
    –> centesis, relieve obstruction, thrombolysis, IVF
  2. Decreased Contractility
    - Primary: valve disease, cardiomyopathy, arrhythmias–> treat with primary inotrope, antiarrhythmic, treat CHF
    - Secondary: SIRS, electrolyte abnormalities, hypoxia, acidosis/alkalosis –> treat with inotrope and underlying disease
  3. Decreased systemic vascular resistance
    - drug/toxin –> treat with pressors, IVF, treat underlying issues
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25
Q

Determining metHgb presence

A
  • blood chocolate brown
  • Drop blood on white paper - If >10% metHgb wil be brown
  • co-oximeter definitive
  • Saturation Gap
    –> SpO2 to PaO2 - >5% difference
    If MetHgb >30% –> SpO2 plateaus 85%
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26
Q

Allergic transfusion reactions

A

Type I Hypersensitivity Reactions (IgE + Mast Cells)
- Occurs within 4 hours
- Diagnosis based off signs:
–> Cutaneous: urticaria, angioedema, pruritis
–> Respiratory (cats): stridor, dyspnea, wheezing, hypoxia
–> Cardiovascular: drop BP, syncope

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27
Q

Transfusion associate dyspnea

A

Acute transfusion reaction characterized by developement of acute respiratory distress during or within 24 hrs of transfusion where TACO, TRALI, allergic reaction, & underlying pulmonary disease have been ruled out

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28
Q

TACO

A
  • acute, nonimmunologic reaction
  • Secondary to increase in blood volume mediated by blood transfusion characterized by acute resp distress & hydrostatic pulmonary edema
  • Occurs within 6 hours of transfusion
  • Rads or echo confirm LA hypertension or volume overload
  • Responds to diuretics
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29
Q

TRALI

A
  • within 6 hours
  • Noncardiogenic pulmonary edema–> acute hypoxemia with evidence of
  • Secondary to Ag-Aby complexes in the lungs
30
Q

TRALI Type I

A
  • No Risk factors for ARDS with:
    – Acute onset defined by hypoxemia (P/F </=300 or SpO2 <90% on room air), bilateral pulmonary edema, no evidence left atrial hypertension on echo
    – Pulm signs within 6 hrs of transfusion
    –No alternative risk factor for ARDS
31
Q

TRALI type II

A
  • Risk factor of ARDS but no diagnosis of ARDS with:

–Acute onset defined by hypoxemia, bilateral pulmonary edema, no LA hypertension
- Pulmonary signs within 6 hrs of transfusion
- Stable respiratory status 12 hrs prior to trnasfusion

32
Q

Immunologic transfusion reaction

A

Adverse reaction to transfusion of blood or blood component due to response of the patient’s immune system

33
Q

Nonimmunologic transfusion reaction

A

Adverse reaction to transfusion of blood or blood component caused by physical or chemical changes to blood cells or product, contamination or secondary to the volume transfused

34
Q

Acute Transfusion Reaction

A

Adverse reaction to blood, blood compnents or plasma derivatives that occur within 24 hours of administration

35
Q

Delayed Transfusion Reaction

A

Adverse reaction to blood, blood components or plasma derivatives beyond 24 hours

36
Q

IMputability

A

Probability that an identified probable cause was the active cause of adverse event after investigation of adverse transfusion event completed

37
Q

Causes of thrombocytopenia

A
  1. Decreased Production: cytotoxic drugs, idiopathic, myelopathies
  2. Increased destruction: ITP
  3. Peripheral utilization: DIC, vasculitis, hemorrhage, cancer, infection
  4. Sequestration: splenomegaly
38
Q

RBC inclusions

A

Mycoplasma
Babesia

39
Q

Monocyte & Neutrophil inclusions

A

Erlichia
Histoplasmosis
Hepatozoon
Leishmania

40
Q

Nonregenerative Anemia differentials

A
  • <2-3 days
  • Inflammatory disease
  • Iron Deficiency: microcytic hypochromic
  • Acanthocytes: liver disease
  • Increased nRBC, no polychromasia: lead toxicitiy & FeLV
  • FeLV: macrocytic, normochromic
  • Renal disease: Dacroctster, ovalocytes
41
Q

List of POssible transfusion reactions

A

Febrile nonhemolytic
Resp (TACO, TRALI, TAD)
Allergic Reactions
Hemolytic (acute vs delayed)
Delayed serologic trans reaction
Transfusion transmitted infection
Hypocalcemia (citrate tox)
Tran-related hyperammonemia
Hypotensive trans reaction
Post trans purpura
Trans assd Graft vs host Dz

42
Q

Causes of MetHb/ Heinz body anemia

A
  • Allium
  • Propylene glycol
  • Zinc
  • Methylene blue
  • crude oils
  • moth balls (naprinthalene)
  • Repeated propofol (cats)
  • Phenylhydrazine –> mushrooms
  • Vitamin K3(menadione)
  • Methionine (cats)
  • Copper (dogs)
43
Q

Causes of erythrocyte oxidation

A
  • Methgb
  • Acetaminophen
  • Topical benzocaine metabolites
  • Skunk Musk
  • Nitrates, nitrites (nitroglycerin, nitroprusside) –> NO decreased metHb reductase function
  • Methgb Reductase deficiency
  • Hydroxycarbide (chemo)

**SHANT make meth

44
Q

Types of cell membrane receptors

A

Ligand gated: coupled to an ion channel

INtracellular protein: signal to intracellular

45
Q

Anticoagulant elements of endothelial glycocalyx

A
  1. glycosaminoglycans (GAGs)
  2. Proteoglycans
  3. Glycoproteins
  4. Heparin factor II
  5. Thrombomodulin
  6. Tissue factor pathway inhibitor (TFPI)
  7. +/- nitric oxide
46
Q

Prothrombotic elements of endothelial glycocalyx

A
  1. decreased GAGs –> compromised function of anticoagulants in glycocalyx
  2. large monomers vWF–> platelet aggregation
  3. Tissue factor and micro-particle exposure
47
Q

FFP

A

Plasma that has been separated from RBC and frozen within 24 hours of collection
Storage: -30C for 1 year
- Contains: coag factors, anticoags, alpha macroglobs, albumin, fibrinogen. & fibronectin

  • Dose to increase COP: 22.5 ml/kg plasma to increase serum albumin by 0.5g/dL (not possible to meet this)
48
Q

Frozen Plasma

A
  • Either FFP stored> 1 year OR plasma kept at room temp > 8 hrs
  • Does not contain labile clotting factors ( V & VIII) & FXI7
  • Contains: F II, VII, IX & X, & alpha macroglobs, albumin, fibrinogen. & fibronectin
49
Q

Cryoprecipitate

A
  • Created by slowly thawing and centrifuging FFP
  • Storage </=-30C for 12 mo from FFP collection
  • Supernatant (CPP) is discarded - remaining is CRYO
  • Contains: vWF, F VIII, FXIII, fibrinogen & fibronectin
  • Indications: active hemorrhage secondary to vWD or Hemophilia A or preop to affected patients
50
Q

CryoPoor precipitate (CPP)

A
  • Supernant removed after centrifuging FFP
  • Storage </=-30C for 12 mo from FFP collection
  • Contains albumin, globulin, antithrombin, ProteinC, Protein S, & F II, VII, IX & X
  • Contains mean albumin in CPP > than both FFp and Cryo
51
Q

Albumin

A
  • INdicated with acute, severe and progressive hypoalbuminemia (<1.5 g/dl) due to treatable illness like trauma, sepsis, or extensive surgical intervention
  • Albumin plays role in wound healing, antioxidan, free radical scavenger, & transport agent and in preserving normal platelet function
  • Calculate via findings patients albumin deficit
52
Q

Whole Blood

A
  • Storage conditions: immediately transfuse or stored 24 hrs at room temp with continuous gentle agitation
    -Contains: RBC, WBCs, PLTs, coag factors, albumin, globs
    Indicated: massive hemorrhage, thrombocytopenic/pathic anemia, coagulopathic anemia
53
Q

Stored whole blood or Cold whole blood

A

Storage:
SWB: 2-6C for 28-35 days
CWB 2-6 for 21 days

Containes: RBC, PLTs, coag factors, but gradual loss of labile coag factors (VIII & V)

54
Q

pRBCs

A

Storage: 2-6C for 35-42 days

Dosage:
pRBC ml = PCV rise (%) desired x 1.5 x BW (kg)

OR

(desired PCV- patient PCV)/donor PCV x volume blood (ml/kg) x BW (kg)

dog blood volume 90 ml/kg; cat 60 ml/kg

55
Q

Liquid plasma (LP), refridgerated plasma (RP)

A
  • Storage: 2-6C for 14 days
  • Contains: coag factors, fibrinogen 20% decrease over 14 days but remains within reference range; labile factors also decline over 14 days but still good coag activity
56
Q

PRP (platelet rich plasma)

A
  • Created through soft spin of FWB at22C
  • Storage: immediately use or stored at room temp with continuous gentle agitation up to 5 days
  • Contains: platelets (mean yeild from FWB to PRP is ~78%), clotting factors
  • Dose one unit/10kgs
57
Q

PC (platelet concentrate)

A
  • Storage: immediately use or stored at room temp with continuous gentle agitation up to 5 days or can add to DMSO and freezer store for 6mo-1 yr
58
Q

Indication of consumptive coagulopathy

A

drop in circulating platelet count or >/= 20% prolongation aPTT

59
Q

Mechanisms of hypercoaguability

A
  1. Endothelial disturbances(causing procaog state)
  2. Increased Procaoguable elements (TF, platelet activation, MPs, NETs
  3. Decreased endogenous anticoags (AT, ProC & TFPI primarily)
  4. Decreased fibrinolysis (decreased tPA)
60
Q

TFPI

A

“Tissue factor pathway inhibitor”
- inhibits fVIIa-TF complex & fXa (all of extrinsic pathway)
- released from endo cells primarily but also platelets, mononucs, vascular smooth m and cardiac myocytes, fibroblasts & megakaryocytes

61
Q

Protein C

A

inhibits fVa & VIIIa
- activated (APC) when trace amounts thrombin bind TM on endothelium of microcirculation
- In presence of protein S APC inhibitions of Va & VIIIa is accelerated by 20x
- Protein C system less functional during inflammation due to decreased hepatic synthesis of Protein C & S, inflamm cytokines effect endothelium and TM which inhibits activation of ProC

62
Q

Antithrombin

A
  • inhibits thrombin and FXa, less so F XIIa, XI, IXa & fVIIa-TF complex
  • Most effects when bound to heparin sulfate and/or exogenous heparins
  • Decreased in systemic inflammation or critical illness by consumption (increased thrombin production), decreased production (neg acute phase pro) or degradation by norepi
63
Q

WHat is considered a massive transfusion

A

Transfusion of blood products totalling an estimated entire blood volume in 24 hours, 50% blood volume in 3-4 hours or administration at 1.5 ml/kg/min over 20 min

  • Chelation may results in hypocalcemia and hypomagnasemia –> administer through diff IVC than blood
64
Q

What factors affected by glutamic acid?

A
  • FII, VII, IX & X
  • ProteinC
  • Protein S
  • Protein Z

Glutamic acid residues allow binding of the protein to membrane surface via interactions btw calcium and negatively charged phospholipids.
** Require carboxylation by the vitamin K cycle in the liver**

65
Q

PT tests for….

A

Extrinsic and common pathways

  • TF + FVIIa
  • FX, V, II, XIII, & Fibrin
66
Q

aPTT tests for

A

Intrinsic and common pathways

  • XII, XI, IV, VIII
  • X, V, II, XIII, fibrin

**ACT also tests these pathways

67
Q

Mechanisms of hypercoaguable state of illness

A
  1. Endothelial disturbances (decreased GAGs, endothelial activation by TNF𝛂, bradykinin, thrombin, histamine, and vascular endothelial growth factor leading to release of weibel palade bodies)
  2. Increased procaog elements (increased TF on monos & macs & neoplastic cells, TF perpetuates inflammation via activating NFKb → increased production TNF𝛂, increased microparticle release from apoptotic cells, NETs for antimicrobial purposes may have procoag effects)
  3. Decreased Anticoag elements (decreased AT due to consumption, degraded by norepi and neg acute phase protein, TNF𝛂 downregulates TM –> decreased protein C activation, AND elastase from endotox activated neus cleaves TM from endo cells, decreased TFPI due to decreased Protein S which acts as cofactor for FXa inhib)
  4. Perterbations in fibrinolysis (TNF𝛂 & IL-1𝛃 cause delayed but sustained increase of PAI-1 compared to tPA → increased plasminogen → DEcreased fibrinolysis and persistence of thrombi
68
Q

Other blood types canine

A

DEA 3, 4, 5, 7

  • DEA 3(-) 30% pop have alloantibodies - 94% pop is DEA 3-
  • DEA 4(+) >99% pop so sensitization rare
  • DEA 5 naturally occuring alloantibody ~10% pop
  • DEA 7 expressed in 10-55^ of dogs, but conflicting info on any alloantibodies

DEA 3,5,7 + blood to sensitized DEA 3, 5 ,7 - recipient will cause delayed clearance of transfused cells within 3-5 days

Kai 1 & 2 no naturally occuring alloaby

Dal agn prevelence ~93% dogs

69
Q

Reported benefits of leukoreduction

A
  • Decreased FNTRs
  • Decreased inflamm mediatory
  • Decreased alloimmunization against WBC and plt antigens
  • Decreased microagglutination
  • Prevention transfusion related immunomodulation
  • Decreased post-op infections
  • Decreased microparticle formation
  • Improved RBC function/survival
70
Q

Recommendations for moderate to severe transfusion reactions

A
  1. stop transfusion
  2. Diphenhydramine (+/- steroid but may be detrimental)
  3. 1/3-1/2 shock dose if no concern for TACO
  4. Epi 0.01 mg/kg IV if severe anaphylactic
  5. Monitoring
    - If moderate baseline parameters q 30-60 min (if do not resolve discard donor blood)
    - If severe q 5 min
  6. Fruther diagnostics:
    - check recipient PCV and u/a
    - if severe check chem on recipient
    - Check unit PCV (hemolysis), gram stain and culture if indicated
71
Q

Storage lesions

A
  • micro-vesicle formation (hypercoaguable)
  • Free Hgb - NO scavenger may lead to hypertension (contribute to MODS) & hypercoaguability
  • Free Fe –> possible increased oxidative stress
  • Cytokine accumulation
  • Ammonia accumulation
72
Q

WEIBEL PALADE BODIES CONTAIN

A
  • vWF
  • FVIII
  • IL 8
  • P Selectin

ACVECC (10 decks)

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