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Block 7 Week 4 > Coagulation-Freeman > Flashcards

Coagulation-Freeman Flashcards

1
Q

(blank) pathway is the main system that causes clotting

A

Extrinsic pathway

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2
Q

Why do you get hypercoag because of factor V Leiden?

A

In this disorder, the Leiden variant (form) of factor V cannot be inactivated (switched off) by activated protein C, and so clotting is encouraged

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3
Q

What does normal factor 5 do?

A

APC binds to factor V and cleaves it into 2 inactive fragments

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4
Q

(blank) thrombophilia is a genetically inherited disorder of blood clotting. It is a variant (mutated form) of human factor V that causes an increase in blood clotting (hypercoagulability)

A

Factor V Leiden

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5
Q

In the normal person, factor V functions as a cofactor to allow factor (blank) to activate an enzyme called thrombin. Thrombin in turn cleaves fibrinogen to form fibrin, which polymerizes to form the dense meshwork that makes up the majority of a clot. Activated protein C (aPC) is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V.

A

Xa

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6
Q

What is the incidence of factor V leiden?

A

3-8%

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7
Q

What is the risk of hypercoagulable in heterozyg of factor V leiden?

A

8X

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8
Q

What is the risk of hypercoagulable of homozy factor V leiden?

A

20X

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9
Q

What do heparins do?

A

bind to Anti thrombin III to block Xa

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10
Q

What is the key to degrading clots or preventing them?

A

inhibiting fibrin formation

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11
Q

(blank) and (blank) can cause vasoconstriction

A

epi and nicotine

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12
Q

What are the two components in flow dynamics?

A

mechanical and chemical

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13
Q

What are the components for flow dynamics?

A

prior sites of thrombus
compression (obesity)
chemical (nictone, vasoconstricting agents)

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14
Q

What are the modifiable factors for coagulation?

A
  • Obesity
  • Sedentary life-style
  • Travel
  • BCPs
  • Pregnancy
  • Surgery (elective)
  • Smoking
  • Prior DVT
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15
Q

What are the unmodifiable factors for coagulation?

A
  • factor V leiden
  • prothrombin gene mutation
  • malignancy
  • surgery (emergent)
  • chronic illness
  • lupus anticoagulant
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16
Q

The body need how many risk factors to clot?

A

4 (the body has a near perfect system to prevent clotting)

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17
Q

In acute thrombogenesis, what should you give patients?

A

7-10 days of full heparinization (LMWH) (regardless of coumadin levels)

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18
Q

What are the vit-K dependent factors?

A

2,7,9,10

Protein C/S

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19
Q

What is the 1/2 life of factor X?

What is the 1/2 life of protein C?

A

48H
6H
***notice that protein C has shorter half life so you might get a hypercoag state)

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20
Q

When can you initiate coumadin?

A

at time of heparin-> course of coumadin is based on etiology of thrombogenic event

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21
Q

(blank) anticoagulants may be seen at time of acute thrombotic events (acute phase reactants).

A

Lupus anticoagulants (LA)

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22
Q

Repeat serology is recommeneded (blank) months after acute events prior to making long-term therapeutic coumadin decisions.

A

3

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23
Q

Lupus anticoagulant is actually a (Blank)

A

pro-coagulant (misnomer)

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24
Q

If you have LA in vitro, what will you see?

A

prolonged PTT

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25
Q

If you have LA in vivo, what will you see?

A

procoagulant

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26
Q

If your patient has HIT what should you give them?

A

agatroban

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27
Q

What are the 2 types of HIT?

A

Type I and Type II

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28
Q

What is this:
modest, transient decrease in platelets 2/2 heparin-induced platelet agglutination. Self-limited; plt counts can return to normal while heparin is continued.

A

Type I HIT

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29
Q

What is this:
a drug-induced, immune-mediated response 2/2 abs directed against heparin-plt factor 4 complex that results in 50% or greater drop in platelet counts. Severe thrombocytopenia w/ bleeding is rare!

A

HIT (type II)

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30
Q

Severe hit involves heparain and what clotting factor?

A

factor 4

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31
Q

What is the major problem with HIT?

A

the creation of a prothrombic state which can occur even after heparin has been discontinued

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32
Q

When do you typically see HIT?

A

in major surgery where large volumes of heparin are required (CABG) -> less commonly seen in medical patients

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33
Q

When should you be thinking about HIT?

A

in all recently hospitalized patients returning w/ acute thrombosis w/ in 1-2 weeks of their hospital stay

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34
Q

If you see thrombocytopenia AND thrombosis what should you be thinking?

A

HIT

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35
Q

How do you test for HIT?

A

radiolabeled platelet-serotonin release assay

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36
Q

How do you treat HIT?

A

direct thrombin inhibitors to treat the thrombosis

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37
Q

The incidence of hit is 10X greater in patients treated with (blank) than in those receiving (blank)

A

unfractionated heparin

LMWH’s

38
Q

HIT is higher among (blank) patients than (Blank), particularly orthopedic surgery

A

surgical

medical

39
Q

T or F

HIT is uncommon among pediatric, obstetrical patients and awa patients receiving hemodialysis

40
Q

Thrombosis w/ declining platelets is seen in (blank) percent of patients w/ recent hospitalization

41
Q

(blank) is used to reverse heparin and it is better at reversing UFH, than LMWH

A

protamine sulfate

42
Q

What causes DIC?

A

widesprea activaton of the clotting cascade causing a consumption of clotting factors and platelets w/ resultant bleeding

43
Q

Why can you get end-organ damage because of DIC?

A

Microvascular compromise 2/2 to thrombin formation results in tissue ischemia w/ resultant end-organ damage, particularly liver and kidneys

44
Q

If patient has been in DIC too long what do you do?

A

dont use heparin cuz its too late

45
Q

What causes activation of the coag cascade?

A

Endotoxin
IL-1
TNF

46
Q

(blank) is released in response to exposure to these or other cytokines

A

TF (tissue factor)

47
Q

DIC is triggered by diseases that promote the expression of (blank)

A

tissue factor

48
Q

What can cause DIC?

A
  • gram (-) septicemia
  • damaged cerebral tissue
  • APL awa other liquid/solid malig
  • placental tissue from obstetric catastrophies
  • snake venoms
  • acute hemolytic transfusion rxns
  • hypotension
  • major tissue damage (trauma, burns, hypothermia)
49
Q

Is DIC more common than HIT?

50
Q

What are the lab findings in DIC?

A

-prolonged PT/PTT or both
-thrombocytopenia
-decreased fibrinogen levels
-increased D-dimer
(seen in hospitaliized ICU patients a lot)

51
Q

How do you treat DIC?

A

fix underlying condition

use supportive therapy (maintain platelets greater than 100K and fibrinogen greater than 100)

52
Q

Pnts going in for liver transplants need to be (blank)

A

anticoagulated

53
Q

What are caues of bleeding (5)

A
  1. trauma
  2. infections
  3. drugs
  4. disorders of coag (platelet disorder, factor disorders)
  5. disorders of organ systems (renal, liver, hematopoietic, CABG- coronary artery bypass graft)
54
Q

What drugs can be associated with bleeding?

A 
GP IIb/IIIa inhibitors(Plavix)
	COX I inhibitors(ASA)
	Heparin
	Coumarins
	OTC
	    *Ginko
	    *Ginseng (can cause bleeding)
55
Q

T or F

Acquired disorders of platelet fxn are common but rarely assoc. w/ clinically relevant bleeding

56
Q 
GP1b causes (blank). 
GP11b/IIIa causes (blank)
A

adhesion

aggregation

57
Q

Gp1b binding induces (Blank) expression

A

GpIIb/IIIa

58
Q

(blank) is stored at the endothelium in the weible palade bodies

59
Q

How do you treat bleeding caused by renal failure?

A

DDAVP (desmopressin)

60
Q

What can cause prolonged PT?

A

malnutrition
liver disease (decreased synthesis of vit K factors)
coumadin

61
Q

What can cause prolonged PTT?

A
  • lupus anticoagulant/ acquired factor inhibitors
  • vWD
  • Factor VIII/IX deficiency or inhibitor
  • Heparin
62
Q

Can you give DDAVP to vWD type IIB?

A

no because you lack factor 8 and DDAVP works by acting on factor 8

63
Q

What is von willebrand dz?

A

factor 8 deficiency

64
Q

How do you inherit vWD?

A

autosomal dominant

65
Q

What kind of deficiency is vWD type 1?

A

Quantitative deficiency

66
Q

What kind of deficiency is vWD type 2?

A

Qualitative deficiency

67
Q

What kind of deficiency is vWD type 3?

A

Total deficiency

68
Q

How do you acquire vWD?

A
  • lymphoproliferativd disorders
    * Monoclonal gammopathies
    * MPS, particularly ET (essential thrombocytosis)
    * Mechanical (Heidi’s Syndrome)
69
Q

Factor 8 can be thought of as 2 distince molecules. what are they?

A

factor 8 vWD

factor 8 hemophilia

70
Q

Factor 8 vWD has 2 major roles in hemostasis, What are they?

A

a. carrier protein for F VIII h

b. platelet adhesion to sites of vascular injury (Ib-IX-V receptor) & the subendothelial matrix.

71
Q

Factor 8 hemophilia is a (blank)

A

procoagulant

72
Q

What factors are involved in the intrisic pathway?

A

12, 11, 9, 8, 10

73
Q

What factors are involved in th extrinsic pathway?

A

7, 8,9, 10

74
Q 
What is this:
autosomal dominant
clinically, mucosal "oozing" after surgery or trauma
-activity;
mild>20%
moderate > 10-20%
Severe > <10%
75
Q

What is this:
x-linked disorder
-clinically, spontaneous hemarthroses
-A, B (factor IX: christmas)

A

Hemophilia

76
Q

How do you treat mild cases of vWD?

A

DDAVP (IV)

AND factor 8

77
Q

How do you treat children with vWD that experience mild playground injuries or women w/ heavy menses

A

DDAVP (nasal spray)

AND factor 8

78
Q

What is the disease called that is deficient in GpIIb-IIIa?

A

Glanzmann’s Thrombasthenia

79
Q

What is the disease called that is deficient in GpIb?

A

Bernard-Soulier Syndrome

80
Q

What is Heydes Syndrome?

A

syndrome of aortic valve stenosis resulting in GI bleeding. It is due to the induction of von Willebrand disease type IIA by the valvular stenosis

81
Q

(blank) stimulates the release of von Willebrand factor (vWF) from the Weibel Palade bodies of endothelial cells, thereby increasing the levels of vWF

82
Q

What is this:
A syndrome caused by aortic valve stenosis resulting in GI bleeding @ sites of colonic angiodysplasia w/exaggeration of bleeding 2/2 mechanical destruction of ultra-large von Willebrand factor molecules(acquired vWD).

A

Heydes syndrome

83
Q

In inherited TTP, the (blank) gene is faulty

84
Q

(blank) is a metalloproteinase involved in the normal processing of von Willebrand factor.

85
Q

What is this:

platelet activation leads to microvascular fibrin deposition and thrombocytopenia associated with hemolysis

A

autoantibody-mediated TTP

86
Q

What are the clinical manifestations of TTP?

A

neurological dysfunction, renal insufficienct, and fever, MSA;s, microangiopathic HA, thrombocytopenia

87
Q

How do you treat TTP?

A

plasmapheresis (w/out treatment results in death)

88
Q

What are the lab like in TTP?

A

anemia/ thrombocytopenia
increased LDH
increased Serum creatinine
p.s. schistocytes

89
Q

If you see thrombocytopenia and shistocytes what should you do?

A

start treating for TTP before the quintad appears

90
Q

How can you get acquired ADAMTS-13 abs?

A 
E. coli
idiopathic (40%)
autoimmune disease/ infection
drugs
blood diarrhea prodrome
pregnancy. post partum 
hematopoetic cell transplantation

Block 7 Week 4 (7 decks)

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