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ACE Review - Hematology Flashcards

(90 cards)

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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
citrate toxicity. what happens to the pulse pressure
decrease pulse pressure
26
citrate toxicity. why is there a decrease in pulse pressure
beause the myocardium is depressed
27
citrate toxicity. what happens to the pressures in the heart with citrate toxicity
back flow...leading to increase left ventricle end diastolic pressure, and increase cvp
28
citrate toxicity. what has more citrate, whole blood or ffp
both have the same
29
citrate toxicity. what is more likely to get citrate toxicity when infusing...whole blood or ffp
ffp, because it is easier to infuse faster than blood
30
citrate toxicity. what is the treatment
calcium chloride infusion
31
transfusion. what is the most common viral infection by transfusion
cmv
32
transfusion. what is the second common viral infection by transfusion
hep b
33
transfusion. what is the third common viral infection by transfusion
west nile
34
transfusion. what is the fourth most common viral infection by transfusion
hep c
35
transfusion. what is the fifth most common viral infection by transfusion
hiv
36
transfusion. what is the most common complication of tx
mistransfusion.
37
transfusion. what is mistransfusion.
transfusing the wrong abo blood or also...transfusing when the patient is not indicated for transfusion
38
transfusion. what is the most common cause of death related to tx
TRALI
39
transfusion. what products are assoc with TRALI the most
ffp or platelets bc those have the most amount of plasma
40
transfusion. what is suspected to be in plasma that causes TRALI
antibodies
41
transfusion. what antibodies in particular are thought to be responsible for TRALI
antineutrophil antigen ANTIBODY and antihumanleukocyte ANTIBODY
42
transfusion. what kind of donor is suspected to have more of these antibodies in their plasma if they donate blood.
female donors tend to have more of these antibiodies...mainly multiparous female donors
43
transfusions. what is the MOA of hemolytic transfusion reaction
the patient has antibodies toward the donated blood
44
transfusions. what antibiodies of the recipient is most likely the cause for hemolytic transfusion reaction
antiA or antiB antibodies of the recipient toward the blood
45
transfusions. when possibly can a hemolytic transfusion reaction occur
it can even happen up to 3-10 days after transfusion
46
transfusion. why is there a possible delay in onset of hemolytic transfusion reaction in some patients
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
transfusion. what are the symptoms of hemolytic transfusion reaction
in a patient under general anesthesia. you can see hypotension and hemoglobinuria.
48
transfusions. what is the most common cause of sepsis
plateletes because it is stored at room temperature
49
transfusions. does leukocyte reduction effect the risk for allergic reaction.
no...not at all..leukocyte reduction does not have any MOA for allergic reaction reduction
50
vitamin K. what factors of coag is made by this
2 , 7, 9, 10, and protien c and s
51
vitamin K. what can antibiotics do to its absorption
bacterial flora process the vitamin K...so killing off the flora with prolong antibiotic use may cause coaguloopathy in the patient
52
vitamin K deficiency. what lab increase do u see
prothrombin time (pt)
53
vitamin K deficiency. how long does it take to replace vitamin k
6-24 hours
54
vitamin K deficiency. what are the routes it is given
oral or IM....iv can be done but there have been deaths by giving it iv
55
vitamin k deficiency...how is it treated acutely
ffp
56
vwd. von willowbrands disease. what coagulopathic disease is it like
it is like hemophilia A
57
vwd. how is vwd like hemophiilia 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
vwd. how is it classified.
into phenotypes numbered 1, 2, and 3
59
vwd. why is it important to classify phenotypes
because the treatments are based on it
60
vwd. what is phenotype 1
it is a quantitative decrease in vwf, but only partial
61
vwd. what is phenotype 2
it is a qualitative decrease in vwf
62
vwd. what is phenotype 3
it is a severe to complete lack in vwf
63
vwd. what is speical about phenotype 3
it is autosomal recessive where as 1 and 2 are autosomal dominant
64
vwd. what is different between phenotype 1 and 2's treatment
phenotype 1 can be treated with ddavp where phenotype 2 is treated with factor 8-vwf concentrates
65
vwd. what is the risk with the treatment that vwd phenotype 3 get
they can get the concentrates for a while and develop alloantibiodies to their treatment
66
vwd. what is the treatment for those of phenotype 3 who develop alloantibodies
factor 8 concentate
67
vwd. what is the treatment if factor 8 concentrate becomes problematic for phenotype 3 pts
activated factor 7 concentrates aka VIIa
68
vwd. what is the first thing to treat a phenotype 3
first. always aim for using factor 8-vwf concentrates
69
vwd. what is the second line treatment if factor 8-vwf concentrates dont work
platelete concentrates....in non alloantibiodies pts.
70
vwd. how is ddavp given
it can be given nasal or iv q24 hrs...but can develop tachyphylaxis after first dose
71
vwd. when do u see the effects of ddavp
within 30 mins
72
vwd. how long does ddavp effect last
8-10 hrs
73
vwd. cant you give cryo for these pts???
no because of risk of infections from viral contaminates are greater than the benefits from cryo
74
vwd. cant you give ffp to these pts?
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
febrile transfusion. how do u classify them
hemolytic and non hemolytic
76
febrile transfusion. what is the most cmmon cause for nonhemolytic
donor wbc or cytokines
77
febrile transfuion. what is the most commo cause for hemolytic
abo incompatibility
78
methhemoglobinemia. what genetic mutation can cause this
nadph reductase deficiency can cause this
79
methhemoglobinimeia. what is the best way to diagnose it
co-oximitry (abg)
80
methhemoglobinemia. what local anes can cause it
prilocaine, benzocaine
81
methhemoglobinemia. what antipsycotic can cause it
phenytoin...but not clinically significant
82
methhemoglobinemia. what antihypertensive can cause it
nitroglycerine and nitroprusside.
83
methhemoglobinemia. what malarial drug can cause it
dapsone
84
methhemoglobinemia. what sulfur drugs can cause it
sulfonamides
85
ptt. what does that stand for
activated partial thromboplastin time
86
ptt. what pathway
intrinsic
87
ptt. what factor does it not cover
factor 7
88
ptt. if you dont fill up the whole test tube, is the ptt prolonged or shortend
prolonged bc there are less factors compared to a norm
89
coagulation factors. what coag factor has the shortest half life
factor 7
90
coagulation factor. if factor 7 has the shortest half life...what can u use it for
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

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