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MS2 Unit2 > Tranfusion Lectures - Sheet2 > Flashcards

Tranfusion Lectures - Sheet2 Flashcards

1
Q

Mixing pt RBCs w. anti A/B/D(Rh) is what type of basic testing

A

Froward Testing

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2
Q

Mixing pt plasma w. A and B RBCs is what type of basic testing

A

Reverse testing

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3
Q

Mixing pt plasma w. screening O cells s what type of basic testing

A

Antibody Screen for non ABO Abs

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4
Q

What blood type is the universal donor for RBC? for Plasma?

A
  • O;

- AB

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5
Q

tranfusions reactions present what sx (4)? and result in?

A
  • fever, chills, SIRS, flank pin

- kidney damage, death

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6
Q

hemolytic dz in fetus and newborns results in (4)

A

hemolysis
anemia
hyrdops fatalis
death

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7
Q

whole blood can be fractionated via pharesis into what volumes of RBCs, plasma, and plt

A

350 mL RBC
200 mL plasma
350 mL plt

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8
Q

RBC admin is pt specific, and given primarily to____

A

↑ O2 carrying capacity (correct anemia)

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9
Q

5 factors affecting target Hgb?

A
  1. PMH of cardiac dz/stoke
  2. chronic anemia (leukema, chemo, renal failure, ∆Hb)
  3. Active bleeding/coagulopathy
  4. Cardiac hypoxia (angina)
  5. Neural hypoxia (SYncope/TIA)
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10
Q

A problem of stored blood is ____

A

hyperviscocsity (↓ pliability + tissue perfusion)

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11
Q

plts undergo a conformation change in GPIIb-IIIA to bind to

A

fibrinogen (–> plt crossbridging)

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12
Q

after activation, content release from ____ in plts –> cytoskeletal changes

A

𝛂 granules

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13
Q

How are plt’s stored?

A

5 days at RT with gentle agitation (afterward ↑ microbial growth)

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14
Q

If plt are cold they are considered

A

activated (cold = activated)

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15
Q

How are RBCs stored?

A

21-42 days at 4C

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16
Q

plt cut off to avoid spontanous bleeding

A

6K (10K is prophylactic std)

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17
Q

what are the transfusion guidlines for prophx; active bleeding/surgical hemostasis; neurosurgery?

A

prophx <10K
active bleeding/surgical hemostasis <50K
neurosurgery <100K

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18
Q

ITP, TTP, HIT, HUS (hemolytic uremic syndrome), bleeding due to coagulopahty, and prophylactic transfusion without bleeding are common mistakes made with what blood component?

A

plt (plt transfusion increases risk for thrombosis)

TTP + HIT = contraindication (Hypercoag states w/ plt consumption + risk for stroke)

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19
Q

when should you replace coag or anticoag factors? (2)

A

when pt is bleeding or at risk for bleeding (invasive procedure)

PT > 20
INR > 1.8
PTT > 44

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20
Q

should you give plasma if: prophx tx of severe liver dz

A

if no bleeding, no!

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21
Q

should you give plasma if: nurittional support or oncotic/fluid support

A

no!

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22
Q

should you give plasma if: heparin reversal

A

no, give protamine sulfate!!! (heparin potenztions ATIII –> ↑ PTT)

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23
Q

should you give plasma if: single factor defc’s

A

no!; factor concentrates available for PCC, rVIIa, VIII, IX, vWF, ATIII, C1inh (=hereditary angiodema)

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24
Q

Cryoppt (7-15 mL/U) usually containts ___ firbrinogen and ____ of FVIII; how much should be given to adults?

A

250 mg fibrinogen
80-120 U FVIII (+ vWF + FXIII)
5-10 pooled units for adults (prepooled cropppt = 5 U)

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25
Q

For Hypofibrinogenemia (<100 mg/dL) or dysfribrinogenemia (asympto) what do you give?

A

Cryoppt (less common for vWF dz or VIII defc)

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26
Q

Warfarin blocks the enzyme ____

A

vit K reductase (-/-> vitK regeneration to carboxylate 2,7,9,10 C and S)

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27
Q

What 3 types of inactive factor concentrates are there ?

A
  1. Prothrombin complex conc (Kcentra, Profilnine, 2-7-9-10-C+S)
  2. Single factor concentrate (FVIII)
  3. vWF (w/øFVIII)
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28
Q

Profilnine is composed of what 3 factors

A

2-9-10

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29
Q

K centra has how many factors?

A

4 factors in Kcentra

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30
Q

Factor VIII defc (ø synth) is also known as ____ and is mild, sever, and critical at what percentages of FVIII expression?

A

Hemophilia A (A-ght)

asympto > 30% expression
mild = 5-30%
severe = 1-5%
Critical <1%

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31
Q

What 2 types of active factor concentrates are there ?

A

Coagulation factors Novo7 (FVIIa) + FEIBA (Factor 8 Inh Bypassing Activity)

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32
Q

What is FEIBA? how does it work

A

non active 2-9-10 + active F7

–> coagulation via extrinsic + common pathways

33
Q

whats the major risk of FEIBA

A

thrombotic potential! (use for critical bleeding)

34
Q

who is FEIBA best for?

A

designed for pts with anti F8 Abs

35
Q

after a procedure, pt presents w/Fever, chills, rigors, impending sense of doom. Exam shows flank pain and SIR. Tests show ↑ free Hb (serum and urine) and kidney tubule damage; ↓haptoglobin, ↑LDH + bili; ⊕DAT(direct combs). CBC shows poor ↑Hgb/Hct. Dx?

Tx?

A

Hemolytic Transfusion Rxn (↑hb + ↓haptoglobin + ↑LDH/bili = RBC damage)

Tw hydration (flush kidneys) + supportive care (most likely clerical error)

36
Q

in Hemolytic Transfusion Rxn, ↑ free Hb binds with _____ which forms methemoglobin –> cytokine release (IL8 IL6) –> fever chills, SIRS. Decrease in this compound also leads to what phenomenon?

A

NO (nitric oxide);

↓NO –> hypercoagulability (+ ↑vasc tone)

37
Q

Acute HTR sx onset is due to ____ vs a delayed HTR onset due to _____

A

high Ab titer (acute);

low Ab titer (delayed)

38
Q

Plasma transfused with cytokines (IL1, IL6, TNF𝛂), which causes a hypothalamic response in the pt (shivering, VasoC, fever). What is the Dx?

Tx?

A

Febrile non-hemolytic transfusion (ø free Hb)

Tw with antipyretics/tylenol (± self-limited)

39
Q

Pt with PMH of CHF, COPD is in for another infusion; after procedure exhibits profuse pulmonary edema after a spike in BP (volume overload). The infusion seemed to have lead to ↑ BNP (atrial pressure) and cardiac failure. Dx ?

A

TACO (Transfusion-assc circulatory overoad; tw LASIX = diuretics + hydration)

run transfusions slower in the future

40
Q

After a procedure, pt presents with acute + severe hypoxia, shortness of breath reactive htn, and a sudden drop in BP. CXR shows diffuse consolidation (white out). The medical team intubates to avoid death and AVOIDS plasma rich units! Dx?

A

TRALI (Transfusion-related acute lung injury; ↓BP dt hypovolemia; diuretics would worsen)

41
Q

Tranfusion of room tempt plt results in ↑temp (fever) and dramatic tachycardia (HR > 120)

A

Bacterial Contamination (looks like SIRS/sepsis)

4C RBCs = cold growing bact,Yersinia enterocolotica

42
Q

This transfusion reaction can result in hives (trunk and head involvment) or anaphylactice shock + organ dysfunction. Tx?

A

Allergic Transfusion rxn

Tw supportive care, Benadryl, corticosteroids

43
Q

How should you tx a pt with IgA defc or a pt with repeated allergic rxns?

A
  • give IgA⊖ blood products (most common immunodefc)

- premedicate w. Benedryl

44
Q

2 causes of allergic transfusion rxn

A
  1. rcp IgE Ab recognize allergen –> amst cells release histamine
  2. Donor histamine –> vasoD + vasc permb in rcp endoth cells
45
Q

Post transfusion purpura results bc of Abs mouned against _____ on donor plt

A

HPA-1a (aka PLA-1 or CD61)

Ab response –> immune destruction of donor AND pt plts

46
Q

After a procedure, pt has very low plt count, and diffuse purpura and some eccymoses on skin. to avoid bleeding thiasis how should you treat the pt? (2)

A

IVIG or plasmapharesis

47
Q

HPA-1a is an antigentc site on ____

A

GPIIIa rcp on plt

48
Q

anti HPA-1a Abs cross the placenta and causes

A

neonatal alloimmune thrombocytopenia

49
Q

Pt presents with severe chest hip and lower back pain shortly after a procedure. The pain stopped shortly after transfusion; and the pt was given supportive care? Dx?

A

Pain Tranfusion (unknown mechanism, comes and goes within an hour)

50
Q

vWF forms multimers (plt aggregation/binding/F8 stabzn) and is cut by _____ into smaller, functional multimers

A

ADAMTS13 (results in TTP)

51
Q

Explain the mechanism for ADAMTS13 defc TTP

A

Anti-ADAMTS13 Ab/congenital defect –> ↓ ADAMTS13 –> HMW vWF multimers + wide spread thromboses –> (thrombocytopenia) plt consumption + RBC destruction + deformation (shistocytes)

52
Q

The process of removing blood, centrifuging components –> removing selected components –> and returnign blood to the pt via continue cycle (1.5-4 hrs)

A

Apharesis (= take away; sequential depletion )

maximum removal of bad factor with min SEs (series of 5 works best)

53
Q

For what condition is Apharesis not ideal

A

Guillon Barre (treat underlying sx)

54
Q

Anticoag that binds ATIII and potientiates its activiey on X and II

A

heparin (HIGH bleeding risk)

55
Q

Anticoag that chelates ionized Ca (= required for 8-9a and 10-5a activity)

A

Citrate

56
Q

benefit of citrate as an anticoag

A

spontaneous reversal

57
Q

con of citrate as an anticoag (2)

A
  1. hypocalcemia (∆membrane potential –> parasthesia/twiching/cardiac defects/GI)
  2. metabolic alkalosis (contra for kidney failure)
58
Q

toa void thick (jello) consistency blood use

A

plasma exchange with door plasma

59
Q

the intent of TTP treatment

A

removal of HMW vWF, anti ADAMTS13 Ab; replace w/ functional ADAMTS13

↓chance of clotting, hemolysis, ↑plt count

60
Q

ET usually usually has what mutations?

A

JAK2, CALR, MRL

otw isolated high plt (>400K) = reactive thromocytosis or p/splenectomy

61
Q

Differential of high Hb (3)

A
  1. 2˚plycythemia (COPD, CO poisoning form smoking, ∆Hb)
  2. P.vera (∆Jak2 or BFU form (øEPO)
  3. p/splenectomy
62
Q

CML mutations are ____ (2)

A

acquired + somatic (not germline)

63
Q

Myeloproliferative disorders can lead to _____ (2)

A

Acute leukemia or marrow failure (↑ plt–> myelofibrosis = reactive endpt)

64
Q

Post hot shower pruritis?

A

p.vera

65
Q

painful red hands or feet with normal pulses

A

erythromelaliga (ET dt ↑ plt count)

66
Q

Carefully palpate for spleen in _____ position if suspecting MPN

A

right lateral decubitis

67
Q

This drug provides folate rescue when fiven with methotrexate

A

Leucovorin

68
Q

Methotrexate inhibits what enzyme

A

DHFR (dihydrofolate reductase)

69
Q

GEfitinib, CEtuximab and ERlotinib both do what?

A

inhibit EGFR tyrosine kinase (EGFR+ cancer)

70
Q

Imatinib and Nilotinib both inh ___?

A

ABL kinase (tx CML)

71
Q

Bevacizumab is a monoclonal Ab against ___?

A

VEGF

72
Q

This drug inh Ribonucletoide reductase (key enzyme for DNA precursors)

A

Hydroxyurea (hydRRRoxyurea)

73
Q

give ____ with ATRA to abate leukocyte activation syndrome (30% of cases)

A

Prednisone (corticosteroids for immunosuppression)

74
Q

↑glutathione production may cause resistance to what class of cancer drugs?

A

alkylators

75
Q

VemuRAFenib and DabRAFenin are both known to inhibit

A

BRAF+ cancers

76
Q

Ipilimumab is a known ___ inh

A

CTLA4 inh

77
Q

Trametinib is a ____ inh

A

MEK inh

78
Q

A known side effect of Vemurafenib is

A

QT interval prolongation (ventricular arrythmia [fatal]; contraindicated in long QT syndrome, electrolyte abnormalities, and other QT prolongation drugs)

79
Q

Temozolomide and methotrexate are not prodrugs that require enzymatic conversion (T/F)

A

true

MS2 Unit2 (8 decks)

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