ACE Review - Hematology Flashcards

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1
Q

What factor is defficient in hemophilia a

A

Factor eight

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2
Q

What should be given to hemophilia a patient

A

Preop factor eight as well as factor 810 to 14 days post operative

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3
Q

How is hemophilia a patient’s treatment postoperatively Different for bone surgeries

A

They may require factor 8 4 To6 weeks postoperatively

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4
Q

When will Recombinant factor 8 not be sufficient to treat hemophilia a patient

A

When they develop anti-Body inhibitors

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5
Q

What is the Treatment for patients with antibody inhibitors in hemophilia a patient

A

Factor Seven a

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6
Q

Argatroban. What is the mechanism of action

A

it is a direct thrombin inhibitor

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7
Q

agatroban. how is it cleared

A

liver…significantly

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8
Q

agatroban. what is the half life

A

forty five minutes

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9
Q

agatroban. what do u use to monitor it

A

ptt

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10
Q

agatroban. what can be used to reverse it

A

nothing…just time, usually afte 2 hours

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11
Q

Hemophilia a. What are the severity levels

A

Mild moderate and severe

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12
Q

Hemophilia a. What is mild

A

6-30% of normal factor 8 levels…these patients usually do not show signs of bleeding

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13
Q

Hemophilia a. What is moderate

A

1-5%. These patients do not spontaneously bleeding but will during surgery or trauma

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14
Q

Hemophilia a. What is severe.

A

Less than 1% normal functioning factor 8. These patients bleed spontaneously

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15
Q

Hemophilia a. What is chronic treatment

A

Recombinant factor 8 to achieve 3% of normal levels

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16
Q

Hemophilia a. What severity patient needs recombinant factor 8 before surgery.

A

All..all hemophiliacs need need 100% factor levels before surgery.

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17
Q

Hemophilia A. When is factor 7a used for treatment

A

In severe hemophiliac A patients who have developed antibodies to factor 8 recombinant

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18
Q

Hemophilia A. How long after surgery should factor 8 be continued.

A

For most non ortho surgeries…at least 10-14 days

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19
Q

Hemophilia a. For ortho surgeries,,.how long should factor 8 be continued

A

4-6 weeks

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20
Q

Hemophilia a. Is it a contraindication for neuraxial block

A

No…but appropriate levels of factor 8 needs to be documented before the procedure

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21
Q

Sickle cell disease. What predisposes to sickling.

A

Hypoxemia, hypothermia, dehydration, acidosis, vascular stasis, infection.

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22
Q

citrate toxicity. what is the t wave ekg change

A

flattened t waves

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23
Q

citrate toxicity. what is the qt interval ekg change

A

prolong qt

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24
Q

citrate toxicity. what is the most common sign

A

hypotension

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25
Q

citrate toxicity. what happens to the pulse pressure

A

decrease pulse pressure

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26
Q

citrate toxicity. why is there a decrease in pulse pressure

A

beause the myocardium is depressed

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27
Q

citrate toxicity. what happens to the pressures in the heart with citrate toxicity

A

back flow…leading to increase left ventricle end diastolic pressure, and increase cvp

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28
Q

citrate toxicity. what has more citrate, whole blood or ffp

A

both have the same

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29
Q

citrate toxicity. what is more likely to get citrate toxicity when infusing…whole blood or ffp

A

ffp, because it is easier to infuse faster than blood

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30
Q

citrate toxicity. what is the treatment

A

calcium chloride infusion

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31
Q

transfusion. what is the most common viral infection by transfusion

A

cmv

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32
Q

transfusion. what is the second common viral infection by transfusion

A

hep b

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33
Q

transfusion. what is the third common viral infection by transfusion

A

west nile

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34
Q

transfusion. what is the fourth most common viral infection by transfusion

A

hep c

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35
Q

transfusion. what is the fifth most common viral infection by transfusion

A

hiv

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36
Q

transfusion. what is the most common complication of tx

A

mistransfusion.

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37
Q

transfusion. what is mistransfusion.

A

transfusing the wrong abo blood or also…transfusing when the patient is not indicated for transfusion

38
Q

transfusion. what is the most common cause of death related to tx

A

TRALI

39
Q

transfusion. what products are assoc with TRALI the most

A

ffp or platelets bc those have the most amount of plasma

40
Q

transfusion. what is suspected to be in plasma that causes TRALI

A

antibodies

41
Q

transfusion. what antibodies in particular are thought to be responsible for TRALI

A

antineutrophil antigen ANTIBODY and antihumanleukocyte ANTIBODY

42
Q

transfusion. what kind of donor is suspected to have more of these antibodies in their plasma if they donate blood.

A

female donors tend to have more of these antibiodies…mainly multiparous female donors

43
Q

transfusions. what is the MOA of hemolytic transfusion reaction

A

the patient has antibodies toward the donated blood

44
Q

transfusions. what antibiodies of the recipient is most likely the cause for hemolytic transfusion reaction

A

antiA or antiB antibodies of the recipient toward the blood

45
Q

transfusions. when possibly can a hemolytic transfusion reaction occur

A

it can even happen up to 3-10 days after transfusion

46
Q

transfusion. why is there a possible delay in onset of hemolytic transfusion reaction in some patients

A

because some recipients have anti Rh or antiKidd antibodies that are so low in amount that when they are given blood with those antigens..the body takes time to build up enough antibodies that can cause the hemolysis

47
Q

transfusion. what are the symptoms of hemolytic transfusion reaction

A

in a patient under general anesthesia. you can see hypotension and hemoglobinuria.

48
Q

transfusions. what is the most common cause of sepsis

A

plateletes because it is stored at room temperature

49
Q

transfusions. does leukocyte reduction effect the risk for allergic reaction.

A

no…not at all..leukocyte reduction does not have any MOA for allergic reaction reduction

50
Q

vitamin K. what factors of coag is made by this

A

2 , 7, 9, 10, and protien c and s

51
Q

vitamin K. what can antibiotics do to its absorption

A

bacterial flora process the vitamin K…so killing off the flora with prolong antibiotic use may cause coaguloopathy in the patient

52
Q

vitamin K deficiency. what lab increase do u see

A

prothrombin time (pt)

53
Q

vitamin K deficiency. how long does it take to replace vitamin k

A

6-24 hours

54
Q

vitamin K deficiency. what are the routes it is given

A

oral or IM….iv can be done but there have been deaths by giving it iv

55
Q

vitamin k deficiency…how is it treated acutely

A

ffp

56
Q

vwd. von willowbrands disease. what coagulopathic disease is it like

A

it is like hemophilia A

57
Q

vwd. how is vwd like hemophiilia A

A

because VWF is made in endothelia cells and act as the factor 8 protien carrier. if there i s a deficiency in vwf, factor 8 will functionaly decrease

58
Q

vwd. how is it classified.

A

into phenotypes numbered 1, 2, and 3

59
Q

vwd. why is it important to classify phenotypes

A

because the treatments are based on it

60
Q

vwd. what is phenotype 1

A

it is a quantitative decrease in vwf, but only partial

61
Q

vwd. what is phenotype 2

A

it is a qualitative decrease in vwf

62
Q

vwd. what is phenotype 3

A

it is a severe to complete lack in vwf

63
Q

vwd. what is speical about phenotype 3

A

it is autosomal recessive where as 1 and 2 are autosomal dominant

64
Q

vwd. what is different between phenotype 1 and 2’s treatment

A

phenotype 1 can be treated with ddavp where phenotype 2 is treated with factor 8-vwf concentrates

65
Q

vwd. what is the risk with the treatment that vwd phenotype 3 get

A

they can get the concentrates for a while and develop alloantibiodies to their treatment

66
Q

vwd. what is the treatment for those of phenotype 3 who develop alloantibodies

A

factor 8 concentate

67
Q

vwd. what is the treatment if factor 8 concentrate becomes problematic for phenotype 3 pts

A

activated factor 7 concentrates aka VIIa

68
Q

vwd. what is the first thing to treat a phenotype 3

A

first. always aim for using factor 8-vwf concentrates

69
Q

vwd. what is the second line treatment if factor 8-vwf concentrates dont work

A

platelete concentrates….in non alloantibiodies pts.

70
Q

vwd. how is ddavp given

A

it can be given nasal or iv q24 hrs…but can develop tachyphylaxis after first dose

71
Q

vwd. when do u see the effects of ddavp

A

within 30 mins

72
Q

vwd. how long does ddavp effect last

A

8-10 hrs

73
Q

vwd. cant you give cryo for these pts???

A

no because of risk of infections from viral contaminates are greater than the benefits from cryo

74
Q

vwd. cant you give ffp to these pts?

A

no…bc ffp contains so low concentration of factor 8 and vwf that you need to give massive amounts…concentrates of these factors is beter

75
Q

febrile transfusion. how do u classify them

A

hemolytic and non hemolytic

76
Q

febrile transfusion. what is the most cmmon cause for nonhemolytic

A

donor wbc or cytokines

77
Q

febrile transfuion. what is the most commo cause for hemolytic

A

abo incompatibility

78
Q

methhemoglobinemia. what genetic mutation can cause this

A

nadph reductase deficiency can cause this

79
Q

methhemoglobinimeia. what is the best way to diagnose it

A

co-oximitry (abg)

80
Q

methhemoglobinemia. what local anes can cause it

A

prilocaine, benzocaine

81
Q

methhemoglobinemia. what antipsycotic can cause it

A

phenytoin…but not clinically significant

82
Q

methhemoglobinemia. what antihypertensive can cause it

A

nitroglycerine and nitroprusside.

83
Q

methhemoglobinemia. what malarial drug can cause it

A

dapsone

84
Q

methhemoglobinemia. what sulfur drugs can cause it

A

sulfonamides

85
Q

ptt. what does that stand for

A

activated partial thromboplastin time

86
Q

ptt. what pathway

A

intrinsic

87
Q

ptt. what factor does it not cover

A

factor 7

88
Q

ptt. if you dont fill up the whole test tube, is the ptt prolonged or shortend

A

prolonged bc there are less factors compared to a norm

89
Q

coagulation factors. what coag factor has the shortest half life

A

factor 7

90
Q

coagulation factor. if factor 7 has the shortest half life…what can u use it for

A

you can use it to monitor liver function because its decrease can tell u early on, relative to other factors, if there is liver disfunction