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Board Review 2020 > Coagulation Phys > Flashcards

Coagulation Phys Flashcards

1
Q

What is the difference between the cell based model and the traditional model?

A

Traditional: two pathways operate semi-independent distinct, redunt interactions between factors and cells are limited
Cell based model: Plasma does not clot therefore cells invovled

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2
Q

What is the extrinsic pathway of coagulation

A

Tissue Damage —> Tissue factor + Ca –> FVIIa with Ca + Phospholipid –> FXa

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3
Q

What is the intrinsic pathway of coagulation

A

Damaged vessel –> FXII —> FXI + Ca —-> FIX w/ FVIII + Ca + plt phospholipid —> FX

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4
Q

What are the Vitamin K factors and why is one more likely decreased?

A

Thrombin (II), FVII, IX, X

FVII shortest 1/2 life 4-6 hrs

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5
Q

What Coagulation factors are tested in PT

A

Extrinsic and common pathway

Added to TF, phospholipid, and Ca

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6
Q

What coagulation factors are tested in PTT

A

Intrinsic and common

Added to contact activator and phospholipid and Ca

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7
Q

In the cell based model of coagulation what is the initiation phase:

A

‘Spark’ Tissue factor exposed to endothelium to circulating FVII forms complex with Ca
Extrinsic factor tenase complex activates FXa w/ FV get thrombin formation
Tissue factor inhibitor inhibits Extrinsic factor tenase complex

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8
Q

In the cell based model of coagulation what is the amplification phase

A

Thrombin burst: Activation and aggregation of platelets
Thrombin activates FVIII which binds with FIX to make intrinsic factor tenase complex—> FX with Ca
50-100 times more thrombin

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9
Q

In the cell based model of coagulation what is the propagation phase

A

Dependent on platelets: Leads to fibrin deposition

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10
Q

What are the procoagulation effects of thrombin

A

FV, Fibrin, FXI, FXIII, TAFI

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11
Q

What are the anticoagulation effects of thrombin

A

Plasmin, Protien C (by binding with thrombomodulin)

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12
Q

How does uremeic thrombocytopathy affect coagulation

A

Increased thrombosis, increased fibrin activation of P-selectin, abnormal release of microparticles

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13
Q

What is the pathway of fibrinolysis

A

tPA (tissue plasminogen activator) Released from vascular endothelial cells binds and activates plasminogen to plasmin
Plasmin molecules bineds to lysine residues on fibrin

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14
Q

What is the difference in FDPs and D-dimers

A

FDPs- are fibrin and cross-linked fibrin

D-Dimers- only cross-linked

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15
Q

What are the regulators of fibrinolysis

A

Plasminogen activator inhibitor-1 (PAI-1)
Alpha 2 Antiplasmin
Thrombin-activated Fibrionlysis inhibitor (TAFI)

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16
Q

What does Plasminogen activator inhibitor 1 do

A

inhibits tPA and uPa

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17
Q

What does alpha 2 antiplasmin do

A

Forms complex with plasmin

Prevents plasminogen into active clot

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18
Q

What does Thrombin-activated fibrinolysis inhibitor do

A

Down regulates fibrinolysis prevents palsmin from binding fibrin

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19
Q

What is the difference between primary and secondary hyperfibrinolysis

A

Primary: quantitative /qualitative abnormalities in regulation of fibrionlysis
Secondary: hyperactivity of normal fibrinolysis due to other coagulation abnormaliteies

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20
Q

What is the difference in TEG versus Rotem

A

TEG: Cup moves around stationary pin
ROTEM: Pin moves around stationary cup

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21
Q

What is the treatment for low fibrin

A

cyroprecipitate

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22
Q

How is hyperfibrinolysis develop with cavitary effusions

A

Anticoagulant environment, mesothelial cells secrete tPA and uPA, increase local expression of Protien C
Systemic due to reabsorption of hyperfib fluid via thoracic duct

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23
Q

How does hyperfibrinolysis develop with hepatic failure?

A

decreased hepatic production of alpha 2 atniplasmin

decreased clearance of plasminogen activators and plasmin

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24
Q

What is the MOA of EACA and TXA

A

Lysine analogues competitively bind c-terminal lysine sties on plasminogen
Plasmin formation is inhibited

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25
Q

What are platelets, how long til mature

A

anucleate cytoplasmic fagments from megakaryocytes

Mature in 3-5 days, life span 5-7 days

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26
Q

What are 4 key features of platelets for coagulation

A

Phospholipd membraned with high density regulated adhesive receptors
Cytoskeleton with contractile proteins
dense tubular system equest/release Ca
Secretory granules

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27
Q

What are the types of platelet secretory granules and what is included

A

Alpha granules: fibrinogen, P-selectin, Factor V, FXI, growth factors, VWF
Dense granules: released for mass platelet attraction
ADP, Epiniphrine, serotonion, histamine, calcium

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28
Q

How does platelet adhesion occur

A

Subendothelial collagen exposed with vascular injury
GPV1 or GP1b-IX-V receptor w/ VWF
alpha 2b Beta 2 (GP2B3A) intrigren with VWF

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29
Q

Where is VWF produced and stored

A

Produced by endothelial or megakaryocytes
Stored in weibel-palade bodies
Also prevents degredation of FVII

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30
Q

Which VWF has the higher affinitiy for platelets

A

Larger

31
Q

What occurs in activation to lead to increased platelet binding

A

Adhesion triggers intracellular signaling to
alpha 2bB3 to high affinity for further adhesioin
membrane flipping exposing phosphaltidylserine creating a neg charge (scrambalase)
Contractile protein change shape to incrase surface area
Dense granules
TXA2 Potent platelet agonist stimulated by AA and Cox

32
Q

What occurs in platelet aggregation

A

Adhesion of activated platelets to each other using receptor bound fibrinogen

33
Q

What are the normal inhibitory mechanism of platelet activation and aggregation

A

Endothelial cells relase ADPase, prostacyclins: inhibit platelet activation
Negatively charged glycocosaminoglycans release nitric oxide to inhibit aggregation

34
Q

What are the three types of VW disease

A

1: low multimers of all sizes
2: variable concentrations, absence of large size
3: marked reduction/absence of all sizes

35
Q

What are three tests of platelet function

A 
PFA-200: adhesion under shear stress
Light transmission aggegometry
Electrical impedance (muultiplate):
36
Q

What is the MOA of coagulapothay with rattle snake envenomation

A

Local: Metalloprotienases damage extracellular matrix proteins mostly collagen
Phospholipase A2, protein C, antithrombin, and FV denaturation
Leads to decreased platelets, consumptive coagulatoapthy

37
Q

What is the MOA of uremic bleeding

A

Primary hemostasis
Platelet secretion defects abnormal vessel wall interaction
Increase platelet inhibitors, uremic toxins

38
Q

How does anemia result in hypercoagulable viscoelastic testing

A

Increase of clotting factors per volume of RBCs

39
Q

What is the MOA of Rivaroxabain

A

Directly inhibits factors Xa

Renal and biliary excretion

40
Q

What is the MOA of Warfarin

A

Vitamin K antagonist

FII, VII, IX, X

41
Q

What is the MOA of unfractionanted heparin

A

Increase activity of antithrombin 3
Inhibit Xa and IIa (thrombinogen)
Inhibits thrombin formation

42
Q

What is the MOA of LMWH

A

Binds AT3, Higher impact on Xa vs. IIa

43
Q

What is the MOA of daltparin

A

Binds AT3, Higher impact on Xa vs. IIa

44
Q

What is the MOA of Enoxaparin

A

Binds AT3, Higher impact on Xa vs. IIa

45
Q

What is the MOA of protamine

A

Postive cationic that forms a salt with heparin

46
Q

What is the MOA of clopidogrel

A

ADP irreversible P2Y12 inhibitor

Platelet activation inhibitior

47
Q

What is the MOA of Aspirin

A

Irreversible inhibition of TXA2 formation

Inhibits platelet activation

48
Q

What is the MOA of NSAID in coagulation

A

Reversible inhibition of TXA 2 Formation inhibits platelet activation

49
Q

What is the proposed MOA of Yunnan biayo

A

enhanced expression of surface glycoprotiens on platelets under condition of stimulation

50
Q

What are the eitologies of aortic thrombosis in dogs

A

Disregulation mechanisms– Increase generation of prothombotic elements
Inhibition of anticoagulation mechanisms
Inhbition of thrombolysis via fibrinolytic system

51
Q

What is virchawos triad in aortic thrombosis in dogs

A

alterations in flow
endothelial damage
Hypercoagulable states

52
Q

Name 10 underlying disease process that have been reported with ATE

A

PLN, PLE, HypoT4, Hypo adrenal, hyperadrenal, Immune mediated disease, DM, neoplasia, steroid administration, endocardiosis, PDA endocarditis, Spiroceria

53
Q

What is the difference between arterial and venous clots

A

Arterial: high shear, VWF, Platelet rich, Tx with platelet inhibitors
Venous: low shear, fibrinogen, RBCs, WBCs, Fibrin, anticogulants

54
Q

How does PLN lead to ATE in dogs

A

Loss of antithrombin 3 in kidneys

55
Q

How does TRALI occur after blood transfusion

A

antibiodies in donor plasma agains antigens present in reciepnt leukocytes (why leukoreduction might not help)

56
Q

What are 7 factors that make IMHA patients hypercoagulable

A

excessive platelet activation
TF expression of microparticles
Sequestation of nitric oxide
Cytokine induce endothelial TF expression
Monocyte activation of TF expession
TF expressing microparticles derived from monocytes bind to endothelium
Phosphatidylserine exposing particles released from platelets

57
Q

How does oxidative hemolysis lead to anemia

A

denaturation of hemoglobin leads to heinz body formation
Methehemoglobinemia
Felines more susceptible due to sulfhydroxyl groups

58
Q

How does Zinc lead to anemia

A

Intravascular hemolysis

Pennies after 1982, bolts, screws, skin products

59
Q

How does endogenous heparin sulfate work and where is it found

A

On glycocalyx. Works with antithrombin to inhibit II and X

60
Q

What are eicosanoids

A

Signaling molecules generated following release of arachadonic acid from phospholipid bilayers of cells especially platelets and immune cells

61
Q

What are the canine dog blood types

A

DEA 1.1, 1.2, 1.3, 3, 4, 5, 7

Dahl

62
Q

Which blood type is most common and which is most immunogenic in dogs

A

1.1 most immunogenic

Alloantibiotied against 7 highest

63
Q

What is leukoreduction

A

Filter the blood to remove WBCs (platelets) prior to storage

64
Q

What is cryopriciptate

A

Contains FVIII, VWF, Fibrinogen, and FXIII

65
Q

What disease processes if cryopreciptate used for and what is it better than FFP for

A

VWD and hemophillia

More effective at increasing BMBT in VWD

66
Q

Define Massive transfusion- at least three

A

1 blood volume in 24 hrs
50% of blood volume in 3 hrs
150% of blood volume regardless of time
1.5 ml/kg/min of blood products for 20 minutes

67
Q

What shock index in dogs is likely to result in transfusion after blunt trauma

A

SI > 1.43

71% resulted in transfusions

68
Q

Define the blood vicious cycle of ATC

A

bleeding –> resuscitation –> dilutional and hypothermia –> coagulopathy —> bleeding

69
Q

What are complications of massive transfusions

A

Transfusion reactions
Hypocalcemia (citrate from blood or failure of liver to break down citrate)
Hypomagnesemia
HyperK (increase K in RBC supernate
Hypothermia
metabolic alkalosis— citrate broken down to bicarb
Metabolic acidosis— units have low pH

70
Q

Name immunologic transfusion reactions state if delayed or acute

A

Hemolytic -acute
Fever- acute
Uticareia - acute
Transfusion realted immunomodulation (TRIM) - delayed

71
Q

Name acute non immunologic transfusion reactions (9)

A 
TACO
Vomiting
ARDS
Infectious disease
citrate toxicity
TRALI
Dilutional thrombocytopenia
embolism
Hemosiderosis (iron overloade
72
Q

In hemolytic transfusion reactions what is the mechanism

A

Type II hypersenstivity

Steroids/antihistamines won’t prevent

73
Q

In febrile non hemolytic reactions what is the mechanism

A

cytokines and WBCs in donor unit

Steroids and antihistamines won’t prevent

Board Review 2020 (37 decks)

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