Transfusions Flashcards

1
Q

If R time is elevated on a TEG we give?

A

FFP

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2
Q

TEG parameters;

A
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3
Q

When do we give platelets on a TEG?

A

If MA is depressed

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4
Q

MC type of transfusion reaction?

A

Febrile non-hemolytic transfusion reaction

2/2 circulating recipient antibodies to donor leukocytes —> get cytokine release

Can occur during the transfusion or up to 4 hrs after, assc with fever, chills/rigors

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5
Q

Leading cause of transfusion related fatality in the US?

A

TRALI

2/2 neutrophil mediated damage to pulmonary vasculature

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6
Q

Where is VWF made?

A

Stored and release from endothelial cells of blood vessels and megakaryocytes of bone marrow

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7
Q

MOA of TPA?

A

Convert plasminogen to plasmin

When using TPA, monitor the fibrinogen levels, levels <150 are high risk for bleeding (normal levels of fibrinogen at 200-400)

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8
Q

What can we use to reverse bleeding after TPA use?

A

TPA converts plasminogen to plasmin, which breaks down fibrin to fibrin degradation products

Cryoprecipitate is first line therapy; repletes fibrinogen, however, if unable, aminocaproic acid can be used to stop TPA

Aminocaproic acid binds to lysine residues on thrombolytics preventing further thromoblysis

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9
Q

What does FFP contain?

A

Clotting factors 2, 7, 9, 10

Lasts 6 hrs, works within 30 mins

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10
Q

Why are platelets the most frequently contaminated blood product?

A

Stored at room temp

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11
Q

Reversal for heparin?

A

Protamine sulfate

1- 1.5 mg/per 100 units of heparin

MC adverse effect of heparin is hypotension

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12
Q

How does DDAVP work in uremic coagulopathy?

A

Increases release of VWF from endothelium which helps increase platelet aggregation activation

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13
Q

What lab parameters do we see with VWD?

A

Normal platelets, normal PT

Abnormal bleeding time

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14
Q

X linked recessive disorder caused by deficiency of factor 8?

A

Hemophilia A

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15
Q

Tx for hemophilia A?

A

Recombinant factor 8

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16
Q

TEG parameters;

A
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17
Q

MOA of aspirin?

A

Irreversible inhibitor of cyclo-oxygenase in platelets, thus prostaglandins can’t be formed

Platelets become dysfunctional over their entire 7 day span

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18
Q

Gold standard for diagnosing HIT?

A

Serotonin release assay

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19
Q

Reversal for direct Xa inhibitors like Eliquis (apixaban) and Xarelto (rivaraxaban)?

A

Adenexet alfa

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20
Q

Dabigatran ?

A

Direct thrombin inhibitor

Reversal is: Praxabind (idarucizumab)

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21
Q

Most common hereditary blood clotting disorder?

A

VWD

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22
Q

Tx for type I VWD in pts undergoing surgery what can we use as prophylaxis?

A

Desmopressin

If desmopressin fails can use cryoprecipitate or VWF/Factor 8

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23
Q

What does cryoprecipitate contain?

A

VWF
Factor 8/13/fibronectin

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24
Q

MOA of clopidrogel?

A

Plavix

Irreversible platelet inhibitor

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25
Q

MC inheritable hypercoagulable disorder?

A

Factor V Leiden

Factor V gets altered and it can’t be inactivated by activated Protein C——> propensity to clot

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26
Q

Type I hypersensitivity rxn?

A

Anaphylaxis

Binding of antigens to IgE—-> mast cell and eosinophil degranulation

Release of vasoactive substances leads to vasodilation

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27
Q

Type II hypersensitivity rx?

A

Cytotoxic mediated

Ig attached to surface antigen with subsequent complement fixation

Graves and Hashimoto’s thyroiditis

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28
Q

Type III hypersensitivity rxn?

A

Circulating antigen-antibody complexes with subsequent complement fixation

Serum sickness

These immune complexes deposit into joints, kidneys, vessels

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29
Q

Type IV hypersensitivity rxn?

A

Cell mediated immunity

Contact dermatitis- poison ivy

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30
Q

MC type of transfusion rxn is febrile non-hemolytic transfusion reaction; and is caused by?

A

Recipient antibodies to donor leukocytes, causing release of cytokines

Pts experience fevers, chills, rigors

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31
Q

This immunosuppression medication has been shown to increase wound dehiscence rates;

A

Sirolimus (mTOR inhibitor)

32
Q

SE of cyclosporine?

A

Gingival hyperplasia and hrisutism

33
Q

How can we identify someone with hemophilia A?

A

X-linked recessive with deficiency in Factor 8

These pts usually have a prolonged PTT that normalizes with a mixing study, they also have a normal PT and bleeding time

34
Q

How can we reverse thrombolytic therapy?

A

Use aminocaproic acid

Binds to lysine residues on thrombolytics (tPA) and inactivates them

35
Q

MOA of tacrolimus and cyclosporine?

A

Binds to FK506-binding proteins which inhibit the enzyme calcineurin

When calcineurin is inhibited, you get decreased IL-2, and other cytokine production which leads to decreased T-cell function

36
Q

SE of cyclosporine?

A

Nephrotoxicity

37
Q

MOA of mycophenolate?

A

Inhibits de novo purine synthesis

SE: nausea/vomiting/diarrhea

38
Q

Hyper acute graft rejection?

A

Occurs mins to hrs after transplant

Preformed recipient antibodies to donor antigens

You see intramuscular thrombosis and graft necrosis

39
Q

First line tx for post-transplant lymphoproliferative d/o?

A

Rituximab; monoclonal antibody to CD20

40
Q

MOA of vincristine?

A

Binds to tubulin and inhibits microtubule formation, disrupts formation of mitotic spindle

41
Q

Syndrome of vascular calcification, thrombosis, and painful chronic skin necrosis seen in ESRD;

A

Calciphylaxis

USually fatal

Punch biopsy confirms dx

42
Q

What is graft v host disease?

A

WBCs in the donated marrow (stem cells) recognize the recipient (host) as foreign

The transplanted cells then attack the hosts’ cells

Involves both T/B cells

Pts present with GI sxs and maculopapular rash on palms of hands

43
Q

What lab values normally seen with VWD?

A

Abnormal bleeding time

Normal PT & platelet count

44
Q

Major side effects of mycophenolate mofetil?

A

Diarrhea and leukopenia (inhibits de novo purine synthesis)

45
Q

Type I and Type III VWD:

A

Type 1; partial quantitative defect; tx is desmopressin

Type 3; severe quantitative defect; tx is VWF concentrates or Factor 8 replacements

46
Q

Gold standard to diagnose HIT?

A

Serotonin release assay

47
Q

Anaphylaxis after a transfusion is a result of?

A

IgA deficiency usually

Pts present with hypotension, flushing, wheezing, angioedema

48
Q

How does an acute hemolytic transfusion reaction as a result of ABO incompatibility result?

A

Fever, chills, flank pain and oozing from IV sites

49
Q

Which pts do we bridge with heparin?

A
50
Q

MC cause of mortality after a transfusion is?

A

TRALI

51
Q

MC transfusion rxn?

A

Febrile, non-hemolytic transfusion rxn

Can occur up to 4 hrs of tx

52
Q

Cause of TRALI?

A

Neutrophil mediated damage to pulmonary microvasculature

53
Q

MOA of tissue plasminogen activators?

A

Convert plasminogen to active plasmin

Plasmin then breaks down fibrin into fibrin degradation products causing lysis

Fibrinogen levels normally at 200-400

54
Q

What does plasmin do?

A

Active clot inhibitor

Normally chills as plasminogen (inactive); gets converted to plasmin by urokinase/streptokinase

Plasmin then breaks down fibrinogen and fibrin

55
Q

Coag parameters seen with VWD?

A

Abnormal bleeding time

Normal PT
Normal platelets

56
Q

Direct Factor Xa inhibitors?

A

Apixaban (Eliquis)

Rivaraxoban (Xarelto)

Antidote is adnexent-alpha

57
Q

Direct thrombin inhibitor?

A

Dabigatran

Tx is idaricuzumab

58
Q

Prolonged R-time?

A

Give FFP (need coagulation factors)

59
Q

We use thrombolytics, like urokinase, and pt is now bleeding; what’s the reversal agent for thromoblytics?

A

Aminocraproic acid

Binds to lysine residues on thrombolytics; inactivates them

60
Q

Gold standard for diagnosis of HIT?

A

Serotonin release assay

61
Q

IgG antibodies to platelet factor 4?

A

HIT

62
Q

X linked recessive d/o affecting Factor 8?

A

Hemophilia A

63
Q

What parameters do we see with hemophilia A?

A

X-linked recessive

Prolonged PTT that normalizes with a mixing study
Normal PT
Normal bleeding time

64
Q

Elevated R-time on TEG?

A

Prolonged time to clot formation

Tx—-> FFP

65
Q

K time and a-angle are issues with ?

A

Fibrinogen

Tx—-> cryoprecipitate

66
Q

VWD:

A

Most common inherited bleeding disorder
Deficiency in vWF: platelets don’t aggregate as well
See secondary deficiency of factor VIII

67
Q

VWF levels and therapy:

A

VWF levels of 30-50; give DDAVP and TXA

VWF levels less than 30; give recombinant vWF and Factor VIII

68
Q

How does TXA work?

A

Lysine derivative that blocks lysine binding sites on plasminogen

69
Q

What kind of transfusion products do we use in transplant pts?

A

Leukoreduced blood

Decreases risk of rejection

Decreases risk of CMV infection

70
Q

Drug eluding stents?

A

Delay elective surgery for at least 6 months

71
Q

Stages of decubs:

A

1; skin in tact, non-blanching erythema
2; epidermis and partial dermis
3; full thickness skin down to subq fat
4; exposed bone, tendon, muscle

Unstagable

72
Q

Hyper acute rejections;

A

Preformed antibodies by recipient to donor

Occurs within minutes to hours

Cross matching blood is a way to mitigate this

73
Q

Common cancers after transplant;

A

Non melanoma skin cancer MC

PTLD second most common

74
Q

What does acute rejection look like?

A

Few days to few months post-op

See lymphocyte infiltration, membrane damage, apoptosis of graft cells

75
Q

Absolute contraindication to living donor nephrectomy?

A

T1 DM

76
Q

B cell mature into plasma cells which make abs; what helps B cells become plasma cells?

A

IL-5 and IL-6

77
Q

What is thymoglobulin?

A

Polyclonal antibodies against T lymphocytes