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cornelius 2 > lecture #1 > Flashcards

lecture #1 Flashcards

1
Q

what is primary hemostasis mediated by

A

platelets

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2
Q

platelets adhere to disrupted vessel wall via

A

receptor Ib

VWF

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3
Q

platelets adhere to one another by

A

IIb/IIIa

fibrinogen

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4
Q

two arachidonic acid vasoconstrictors

A

TXA2

PGs

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5
Q

what gets released from platelet storage granules

A

ADP, serotonin (platelet agonists)
VWF, factor V
heparin binding proteins factor IV
PDGF, TGF-b, TPO

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6
Q

platelet surface proves site for…

A

generation of thrombin

subsequent fibrin formation

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7
Q

Extrinsic system

A

tissue factor exposed to blood

TF + VII leads to activation of VII

FT-VIIa activates X

Xa convertes prothrombin (II) to thrombin (IIa) (you need factor V as a cofactor for this)

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8
Q

where is prothrombin conversion most efficient

A

presence of a phospholipid surface such as an activated platelet

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9
Q

alternate pathway

A

factor IX activated by TF-VIIa complex

factor IXa and cofactor VIII activate X (thrombin)

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10
Q

third coagulation pathway

A

factor X activates XI

XIa activates IX…leads to additional factor Xa formation

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11
Q

what does thrombin do

A

converts fibrinogen to fibrin

activates coagulation factors and cofactors

strong activator of platelet aggregation

mediates fibrinogen cleavage

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12
Q

what is the ultimate step in the coagulation cascade

A

Crosslinking of fibrin by factor XIII

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13
Q

what are 3 natural anticoagulation mechanisms

A

tissue factor pathway inhibitor

protein C

antithrombin III

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14
Q

what does protein C do

A

along with cofactor protein S, protein C degrades cofactors V and VIII

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15
Q

what is protein C activated by

A

thrombomodulin

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16
Q

what does antithrombin III do

A

forms complexes and inactivates thrombin and Xa

**strongly enhanced by heparin!

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17
Q

where are tPA and uPA found? what activates their release?

A

found in endothelial cells

released by stimuli including hypoxia, acidosis

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18
Q

how is fibrinolysis inhibited

A

activator inhibitors (PAIs)

circulating protease inhibitors (antiplasmin)

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19
Q

type I VWF

A

reduced concentration of VWF

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20
Q

type II VWF

A

dysfunctional VWF

IIa: defect in GP-Ib binding

IIb: gain of function in GP-Ib, excessive binding

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21
Q

type III VwF

A

absent VWF (homozygous)

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22
Q

what corrects type I and IIa VWF and how does it work

A

desmopressin

promotes VWF release from weibel palade bodies

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23
Q

what is contraindicated for IIb VWF?

A

desmopressin

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24
Q

after surgery on VWF pt how long should you continue desmopressin tx or replacement of transfused factors

A

4-7 days

initial clotting mostly platelet dependent! coagulation disease results in late rebleeding after fibrinolysis

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25
Q

pts with factor VIII levels of greater than ____% will rarely spontaneously bleed but will have problems after surgery

A

5%

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26
Q

hemophilia A: what percentage have anti FVIII antibodies?

A

10-15%, this is real bad

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27
Q

mild to moderate hemophilia A tx

A

DDAVP

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28
Q

MOA DDAVP

A

releases endogenous factor VIII from liver sinusoids and endothelial cells

also releases VWF resulting in transient increase in FVIII

MONITOR!

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29
Q

severe hemophilia A tx

A

FVIII transfusion

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30
Q

hemophilia B what factor is missing

A

F IX

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31
Q

Protein C and S deficiency puts you in what state

A

hypercoaguable

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32
Q

Factor V Leiden

A

their factor V resists being broken down by protein C, HYPERCOAG

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33
Q

factor V leiden present in ____% of north american caucasians

A

5%

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34
Q

thrombocytopenia in liver failure patients a result of..

A

portal hypertension, and associated splenomegaly

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35
Q

model for end stage liver disease score based on (3):

A

serum bilirubin

serum creatinine

INR

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36
Q

if your MELD score is 40+ chances of survival?

A

71.3% dead in three months

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37
Q

why do patients with renal failure bleed more

A

impaired platelet adhesion, aggregation, release

low hematocrit

38
Q

what test to order for renal failure patients

A

platelet function assay

39
Q

tx for renal disease patients with increased bleeding

A

desmopressin

40
Q

life span of platelets

A

10 days

41
Q

how long do you have to wait after termination of aspiring use to restore adequate platelet function

A

5-7 days

42
Q

most important adverse affects of aspirin

A

bleeding

hemorrhagic gastritis/ulceration

43
Q

should you discontinue aspirin for most dental procedures

A

no

44
Q

plavix metabolism

A

15% becomes active form in liver

45
Q

half live of plavix

A

8 hours but effects last a platelets lifetime (binds irreversibly to P2Y12ADP receptor)

46
Q

is combo of clopidogrel and aspirin better than aspiring alone for cardiac patients

A

yes

47
Q

which results in more clinical bruising/bleeding: aspirin or clopidogrel

A

cloppy

48
Q

should you discontinue clopidogrel for dental shit

A

not usually

49
Q

which P2Y12 blocker has a less variable response than clopidogrel

A

ticlopidine (not a prodrug)

50
Q

ticlopidine onset vs clopidogrel

A

ticlopine faster but does not last as long–reversible binding

51
Q

which drug increases adenosine

A

ticlopidine

52
Q

is dipryamidole effective for preventing thromboembolic dz

A

not proven in literature

53
Q

what are the most potent inhibitors of platelet aggregation

A

glycoprotein IIb/IIIa inhibitors

54
Q

MOA IIb/IIIa inhibitors

A

competitive inhibitors for fibrinogen binding

55
Q

IV or oral for IIb/IIIa inhibitors

A

IV (oral does not work)

56
Q

full effect of coumadin therapy in how many days

A

2-3 days

57
Q

full restoration of normal coagulation after stopping coumadin

A

at least 3-5 days

58
Q

why does dose-effect relationship vary widely with individuals for coumadin therapy

A

changes in binding to albumin

variable vitamin K intake

variable clearance by liver

must monitor closely! INR

59
Q

who is at risk for coumadin induced skin necrosis

A

people with low levels of protein C to begin with (net pro coagulant state results)

60
Q

dabigatran brand name

A

pradaxa

61
Q

revaroxaban brand name

A

xarelto

62
Q

apixaban brand name

A

eliquis

63
Q

edoxaban brand name

A

savaysa

64
Q

do factor Xa inhibitors require monitoring

A

no (not affected by diet , liver function etc)

65
Q

onset and half life of Xa inhibitors

A

rapid onset (2-3 hrs)

short half life (8-12 hrs)

66
Q

is there a test you can use to determine effect of Xa inhibitors

A

no

67
Q

should you discontinue Xa inhibitors prior to surgery

A

yes 1-2 days beforehand (longer in renal patients)

ask prescriber first of course

68
Q

dabigatran reversal agent MOA

A

praxbind (idarucizamab)

monoclononal antibody

reverses anticoagulation immediately, peak in four hours, wears off after 24 hrs

used in emergency situations

69
Q

what should you not give to someone with fructose intolerance

A

praxbind (has sorbitol in solution)

70
Q

what is andexanet alfa

A

factor Xa decoy protein, reverses anticoagulation in less than 5 mins (apixiban, rivaroxaban)

71
Q

PER977

A

non specific agent for anti Xa and anti-thrombin agents (heparin)

72
Q

effect of heparin after IV administration is…..

A

immediate

73
Q

heparin must be given orally or parenterally

A

parenterally

74
Q

low molecular weight heparins vs unfractioned

A

more predictable bio availability and clearance

much longer half life (but not as easily adjustable)

75
Q

fondaparinux is what type of molecule

A

pentasaccharide

for DVT/PE tx

anti-factor Xa

76
Q

when does heparin induced thrombocytopenia show up

A

5-7 days if patient has never had heparin

can be immediate if pt has had heparin before

77
Q

long term use of heparin consequence

A

osteopenia

less with LMWH

78
Q

signs that might point to defect in coagulation

A

abnormal bruising

petechiae

splenomegaly

79
Q

should you run coagulation tests for ppl with negative med hx and normal physical exam

A

no not unless youre doing like brain surgery

80
Q

is platelet function testing clinically relevent

A

not really

81
Q

how does PT/INR test work

A

mixture of calcium and thromboplastin is added to citrated blood, measure how long it takes to get a clot

82
Q

PT value reflects what pathway

A

TF-VIIa

83
Q

normal PT time

A

12 plus or minus 2 seconds

84
Q

PT is prolonged by deficiencies in

A

factor VII

factor X

factor V

prothrombin

fibronogen

85
Q

is INR useful for NOACs

A

no

86
Q

normal PTT time

A

25-40 seconds

87
Q

what factor deficiencies will not be detected by PTT test

A

VII, XIII

88
Q

prolonged aPTT indicates

A

use of heparin

antiphospholipid ab (lupsus)

coag factor deficiency

sepsis (coag factor consumption)

ab against coagulation factors

89
Q

is bleeding time a good test

A

no, poor sensitivity and specificity

poorly reproducible

technique dependent

90
Q

how is platelet function measured nowadays

A

PFA-100 test (measures platelet response to collagen/ADP/epi)

start with reaction to collagen/epi. if normal cool. if abnormal, try with collagen/ADP.

91
Q

if the collagen/ADP is normal after having an abnormal collagen/EPI test….

A

means patient is taking aspirin

if both abnormal you have platelet disfunction prob

92
Q

gold standard for measuring lately function

A

platelet agggregometry

stuff about light beams and stuff

tests a lot of agonists (ADP, collagen, ristocetin, AA)

cornelius 2 (6 decks)

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