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Phase 1 > Ch. 7 Hemostasis > Flashcards

Ch. 7 Hemostasis Flashcards

1
Q

Describe the difference between primary and secondary hemostasis

A

Primary - interactions between platelets and endothelium which lead to a platelet plug
Secondary - a cascade of proteolytic reactions involving coag factors that lead to the generation of fibrin polymers to stabilize those platelet plugs

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2
Q

What is the lifespan of a platelet in a dog or cat?

A

6-8 days

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3
Q

Where does thromboxane A2 come from?

A

platelets synthesize thromboxane from arachidonic acid, which is mediated by COX 1

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4
Q

Where do platelets adhere?

A

either to endothelial collagen via the platelet glycoprotein VI receptor
OR
to collagen bound vWF via the glycoprotein Ib receptor

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5
Q

What do platelets release to recruit more platelets?

A

Thromboxane A2 and adenosine diphosphate (ADP)

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6
Q

What is platelet integrin αIIbβ3 receptor?

A

agonist binding to this receptor leads to a conformational change in the receptor which exposes more binding domains for fibrinogen

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7
Q

What is thrombopoeitin?

A

Made in the liver, stimulates platelet production

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8
Q

What aids in platelet adhesion to each other?

A

Collagen & vWF
Weak binding to subendothelium
Activation of integrin αIIbβ3

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9
Q

What aids in platelet activation?

A

Membrane flipping

Shape change

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10
Q

What is the common pathway of secondary hemostasis?

A

Activation of factor X to Xa
Xa with cofactor Va will activate prothrombin (II) to thrombin (IIa)
Thrombin will then cleave fibrinogen to fibrin

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11
Q

What pathway does PT coag test?

A

The extrinsic (so tissue factor when in presence of platelet phospholipid in calcium coverts VII to VIIa) and common

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12
Q

What pathway does aPTT coag test?

A

Intrinsic (so XII converting XI to XIa, then XIa plus VIIIa plus platelet phospholipid and calcium converting X to Xa) and common

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13
Q

What does the cell based model of coagulation reflect:

A
  1. tissue factor is the primary physiologic initiator of caogulation (contact activation playing no role in vivo)
  2. coagulation is localized and controlled by cellular surfaces

Coagulation occurs in three overlapping phases: initiation (on tissue factor bearing cells), amplification, and propagation (on platelets)

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14
Q

What is the initiation phase of the cell based model of coagulation

A

basically the tissue factor initiated (or considered extrinsic) pathway that will generate small amounts of thrombin
VII and tissue factor (aka factor III) will bind together and then activate X
Factor X will combine with Va to make small amounts of thrombin

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15
Q

What occurs in the propagation phase of the cell based model of coagulation

A

activated platelets express high affinity for binding sites for coag factors
XI binds and is activated by thrombin
XIa will then activate IX
IXa will complex with VIIIa to activate X (which is basically the intrinsic pathway)
Xa and Va will make complexes to activate prothrombin

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16
Q

What are three inhibitors of platelet reactivity within the normal endothelium?

A

Prostacyclin (PGI2)
Ectoadenosine diphosphatase (ecto-ADPase)
Nitric oxide

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17
Q

Which COX pathway is predominant in endothelial cells?

A

COX 2

*COX 1 predominant in platelets

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18
Q

How does prostacyclin inhibit platelet reactivity?

A

limits platelet response to thromboxane

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19
Q

how does ecto-ADPase inhibit platelet reactivity?

A

metabolizes ADP, which is an agonist of platelet activation

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20
Q

How does nitric oxide inhibit platelet reactivity?

A

NO is produced by endothelial cells
it diffuses into platelets and decreases the intracellular Ca2+ flux, which will suppress the conformational change in the integrin αIIbβ3 receptor (the receptor becomes a binding site of fibrinogen)

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21
Q

What are the three natural anticoagulant pathways

A

antithrombin
activated protein C
tissue factor pathway inhibitor

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22
Q

How does antithrombin act?

A

It is a circulating alpha 2 globulin made by the liver
Inactivates coag proteins, most notably by inactivating thrombin and Xa
Also will inactivate VII, IX, XII, XII and kallikrein
Its rate of inhibition is even greater when it is working with heparin
It also inhibits neutrophil adherence

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23
Q

How does activated protein C inhibit coagulation

A

It is activated by the thrombin-thrombomodulin complex
protein C along with its cofactor protein S will inactivate V and VIII –> slows rate of thrombin formation
Also enhances fibrinolysis via inactivation of plasminogen activator inhibitor 1 (PAI-1)
Also limits inflammatory responses and decreases endothelial cell apoptosis

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24
Q

How does Tissue factor pathway inhibitor regulate coagulation?

A

binds to and inactivates factor Xa

this complex will then bind to VIIa-TF complex and inactivate them all

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25
Q

How is plasminogen converted to plasmin (a degrader of fibrin)

A

either by tissue type plasminogen activator
or
urokinase type plasminogen activator

These activators are controlled by activator inhibitors. The most important is plasminogen activator inhibitor 1 which is stored in platelet alpha granules and released upon platelet activation

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26
Q

What are the major inhibitors of the fibrinolytic system?

A

Plasminogen activator inhibitor 1
thrombin activatable fibrolysis inhibitor
alpha 2 antiplasmin

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27
Q

What is the normal range of a BMBT in dog and cat

A

Dog - less than three minutes

cat - 34-105 seconds

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28
Q

What is a BMBT testing?

A

reflects in vivo primary hemostasis

prolonged with thrombocytopenia, thrombopathia, and vasculopathy

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29
Q

How much of a factor must be deficient for PT or APTT to be prolonged?

A

about 25-30%

PT is very sensitive to vitamin K deficiency/antagonism

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30
Q

What does activated clotting time measure? ACT test

A

evaluates intrinsic and common pathways

less sensitive than APTT

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31
Q

What do fibrin split product tests measure?

A

these measure fibrin degradation products - elevated concentrations indicate increased fibrinolysis and/or fibrinogenolysis
May be elevated with DIC or thromboembolism, neoplasia, IMHA, hepatic failure, sepsis, SIRS, heat stroke, trauma, GDV, warfarin tox, hemorrhage, PLN, cushings, heart failure - not very specific!

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32
Q

What do D dimers indicate?

A

They indicate the activation of thrombin and plasmin and are specific for active cogulation and fibrinolysis
Very sensitive and more specific than fibrin split products but still not very specific

33
Q

How decreased must fibrinogen be to prolong PT, APTT, or ACT?

A

severely as in less than 50-100mg/dL
fibrinogen concentrations are determined by the thrombin clot time
it is an acute phase protein so concentrations may be elevated with inflammation

34
Q

What is R (reaction time) on a TEG

A

represents the time of latency from the test initiation until the beginning of fibrin formation (an increase in the amplitude of 2 mm)

35
Q

What is the clotting time (K) on a TEG

A

This is the time to clot formation and measured from R to an amplitude of 20 mm

36
Q

What is the angle (alpha) on a TEG?

A

it is the rapidity of fibrin accumulation and cross linking
Dependent largely on fibrinogen
The slope from R to K

37
Q

What is MA on a TEG?

A

maximum amplitude - the strength of a clot

38
Q

What are the four technical causes of surgical bleeding

A
  1. inadequate repair of vessels or vascular structures that have been opened
  2. occult or undiagnosed injury to the vascular system
  3. damage to organs or structures within the operative field
  4. damage during surgery or post op to organs or structures remote from the surgical site
39
Q

What theories explain how acute traumatic coagulopathies are made?

A

DIC with a hyperfibrinolytic phenotype
enhanced thrombomodulin thrombin protein C
catecholamine induced endothelial damage

40
Q

What six factors will influence the development of acute traumatic coagulopathy?

A
  • tissue injury - initiates coagulation, elevated thrombin then activates protein C
  • hypoperfusion
  • inflammation - proinflammatory cytokines like TNF alpha, IL1, IL6 will enhance anticoagulation and hyperfibrinolysis
  • acidemia - increases fibrinogen degradation and impairs coag factor activity
  • hypothermia - platelets are very temp sensitive
  • hemodilution - fibrinogen is the first factor that becomes critically reduced

the last three are more going to result in trauma induced coagulopathy

41
Q

What components does fresh frozen plasma contain?

A

all the hemostatic factors including the coag factors, vWF, albumin, globulins, and natural anticoagulants too
contraindicated in heparin coagulopathy

42
Q

What components are high in frozen (stored) plasma?

A

highest in factors II, VII, IX, and X

43
Q

What components are high in cryoprecipitate?

A

factors VIII, vWF, fibrinogen, fibrinectin

This is made from FFP’s heavier proteins

44
Q

What components are high in cryosupernatent

A

the plasma that remains after cryoprecipitate is removed so it is high in all but vWF, VIII, fibrinogen, and fibronectin

45
Q

What plasma transfusion products would be appropriate for a dog with vWF deficiency?

A

fresh frozen plasma

cryoprecipitate

46
Q

What plasma products would be good for a patient with low protein?

A

fresh frozen plasma

cryosupernatent

47
Q

what are the best products for platelet increase?

A

platelet rich plasma or platelet concentrate

48
Q

Properties of Desmopressin

A

desmopressin, or DDAVP, is a syntehtic vassopresin that works on V2 receptors to release vWF which increases platelet function as well as release VIII and plasminogen from the endothelium
Assists in vWF type 1 disease but not type 2 or 3

49
Q

What are epsilon aminocaproic acid and tranexemic acid?

A

these are antifibrinolytics that are lysine analogues
they block the binding and activation of plasminogen
they also have some antiinflammatory effect by inhibiting interleukin

50
Q

How long should you wait before taking a patient on aspirin to surgery?

A

discontinue and wait 7-10 days
verify you are in the clear with a BMBT
Use platelet transfusion or desmopressin if bleeding occurs

51
Q

How long should you wait before taking a patient on NSAIDs to surgery

A

at least 24 hours

use platelet transfusion if bleeding occurs

52
Q

How long should you wait before taking a patient on clopidogrel to surgery

A

discontinue and wait 7-10 days
verify you are in the clear with a BMBT
Use platelet transfusion or desmopressin if bleeding occurs

53
Q

How long should you wait to take a patient on unfractionated heparin to surgery

A

at least 6 hours
check with APTT or TEG
use protamine with uncontrolled bleeding

54
Q

How long should you wait to take a patient on low molecular weight heparin to surgery

A

at least 24 hours
check via anti factor Xa or a TEG
use protamine with uncontrolled bleeding

55
Q

How long should you wait before taking a patient on warfarin to surgery?

A

3-7 days
verify via PT or TEG
give plasma or vitamin K for uncontrolled bleeding

56
Q

What breeds are overrepresented in type II vWF deficiency

A

this is uncommon and reported in german shorthair and wirehaired pointers
usually results in severe bleeding
a disproportionate loss of high molecular weight multimers
type 1 by contrast is just low levels

57
Q

What breeds have familial forms of type 3 vWF deficiency been reported in

A

it is almost a complete absence of vWF and has been reported in shelties, scotties, chesapeake bay retrievers, and dutch kooikers

58
Q

Why are platelet transfusions more effective in thrombocytopathic than penic patients?

A

For thrombocytopenic patients, a large tranfusion must be performed to elevate the levels and then those platelets dont last long. Only a few days with fresh whole blood or PRP (which is a large volume) or about 15 min with lypholized platelets.
Thrombocytopathic patients, however, benefit from platelet transfusions because the transfused platelts will help initiate hemostasis and then the natural defective platelets are able to aid once the process begins

59
Q

What breed of cat has a reported rare combined deficiency of vitamin k dependent coag factors (II, VII, IX, X)

A

Devon rex

60
Q

Which coag (PT or APTT) will be prolonged in hemophilia A and B patients

A

prolonged APTT

61
Q

what is the most common coag factor deficiency in cats?

A

factor XII
it is common but usually asymptomatic because it is involved in contact factor activation but is not essential for in vivo hemostasis - it will prolong APTT and usually is diagnosed incidentally

62
Q

What enzyme helps recycle vitamin K

A

vitamin K epoxide reductase

63
Q

Where does the body get its vitamin k

A

vitamin k is a fat soluble vitamin produced by colonic bacteriafrom ingeted vitamin K1

64
Q

What factors increase the risk for percutaneous liver biopsy associated hemorrhage

A

in the dog, plt less than 86,000 and any prolongation of PT

in the cat, APTT prolongation more than 1.4 times

65
Q

What is virchow’s triad

A

abnormalities of blood vessel (endothelial injury)
abnormalities of blood flow (vascular stasis)
abnormalities of blood constituents that promote hemostasis (hypercoagulability)

66
Q

how does low protein lead to platelet hyperaggregability

A

hypoalbuminemia increases thromboxane synthesis

67
Q

What is protein c role in hemostasis

A

The protein C system provides important control of blood coagulation by regulating the activities of factor VIIIa (FVIIIa) and factor Va (FVa), cofactors in the activation of factor X and prothrombin, respectively.

68
Q

What conditions are associated with canine thromboembolism formation

A 
PLN
Neoplasia
IMHA
necrotizing pancreatitis
Cushings or steroids
cardaic disease (endocarditis and heartworm)
sepsis
diabetes mellitus
69
Q

What do cancer cells express and produce that can increase the risk of a thromboembolism

A

tissue factor

cancer procoagulant which activates factor X

70
Q

what is the westermark sign

A

it is a sign of regional oligemia which is an uncommon but reasonably specific finding for PTE
appears as areas of increased radiolucency representing hypovascular lung regions distal to the occlusion

71
Q

what is the only laboratory marker with clinical utility in the diagnosis of PTE in humans

A

D dimers and we think it likely is helpful in dogs too

72
Q

What is the mechanism of unfractionated heparin

A

5000 to 30,000 daltons
potentiation of antithrombin activity, which leads to inactivation of coag factors, especially thrombin and X
also releases tissue factor pathway inhibitor
decreases blood viscosity
decreases platelet function
increases vascular permeability

73
Q

What is the mechanism of low molecular weight thrombin

A

4000 to 6500 dalton
will inhibit factor X far more than thrombin
must be assessed by anti factor X assay because APTT will not be reliable
lesser effects on platelet function
needs more frequent dosing than unfractionated

74
Q

what is the mechanism of warfarin

A

vitamin k antagonist that alters the synthetsis of vitamin k dependent coag factors II, VII, IX, and X
also will alter proteins C and S synthesis
during the first 24-48 hours of administration, only short half life (VII and protein C) are affected

75
Q

What kind of drug is rivaroxaban, apixaban, and edoxaban?

A

direct factor X inhibitors

76
Q

WHat kind of drug is dabigatran

A

a direct thrombin inhibitor

77
Q

what is the mechanism of aspirin

A

causes irreversible functional defect in platelets by inactivating COX 1 which then means that thromboxane production is decreased
But endothelial cells can still make new COX 1 and then can make more prostacyclin so overall effect may be blunted

78
Q

What is the mechanism of clopidogrel

A

thienopyridine clopidogel requires hepatic metabolism to acquire antiplatelet activity
its active metabolies will irreversibly block ADP binding on the platelet surface
This then prevents activation of alphaIIbBeta3 integrin receptor, fibringogen binding, and sustained aggregation
onset of action takes 2 days and reaches staeady state after 5-7
also irreversible so it lasts for the life of a platelet

79
Q

What inflammatory processes lead to increased risk of DIC

A

TNF alpha, IL 1, and IL 6 are initiators of DIC
cytokines damage microvascular endothelium and induce the expression of tissue factor which activates VII-TF pathway
protein c leves decline rapidly as a result of consumption
cytokines also stimulate plasminogen activator inhibitor 1 so that means the fibrinolytic system is also suppressed

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