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BTK Review 2024 > Heme Onc > Flashcards

Heme Onc Flashcards

1
Q

PTT measures all coagulation factors except which?

A

VII

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1
Q

PT/INR measures which coagulation factors?

A

II, VII, IX, X

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2
Q

Which coagulation factors are not synthesized int he liver?

A

VIII and vWF

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3
Q

What does cryo contain and when should it be used?

A
  • contains FVIII, vWF, fibrinogen
  • use for hemophilia A, vWD, and hypofibrinogenemia
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4
Q

What does FFP contain?

A

all coagulation factors and some fibrinogen

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5
Q

What is the most common congenital bleeding disorder?

A

von willebrand’s disease

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6
Q

What are the three types of vWD?

A
  • type I: partial quantitative
  • type II: qualitative
  • type III: complete quantitative
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7
Q

How are the three types of vWD treated?

A
  • type I: desmopressin or cryo
  • type II: desmopressin or cryo
  • type III: FVIII or cryo
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8
Q

Which type of vWD doesn’t respond to desmopressin?

A

type III since desmopressin enhances vWF function and type III is the complete absence of the factor

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9
Q

What are hemophilia A and B?

A
  • hemophilia A: FVIII absent
  • hemophilia B: FIX absent
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10
Q

How are hemophilias treated?

A
  • A: recombinant FVIII, cryo, desmopressin
  • B: recombinant FIX, FFP
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11
Q

What is FVL mutation?

A

a mutation in factor V, which prevents the binding of protein C, leading to hypercoagulability

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12
Q

How does antithrombin III deficiency present? How is it treated?

A
  • hyper coagulability without response to heparin
  • treat with ATIII concentrate or FFP and heparin heparin bridge to therapeutic anticoagulation
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13
Q

How do you treat patients with hyperhomocysteinemia?

A

folate and B12

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14
Q

Describe the presentation, pathophysiology, and treatment of anti-phospholipid syndrome.

A
  • history of lupus, DVTs, recurrent pregnancy losses
  • labs show a prolonged PTT but are hyper-coagulable
  • caused by antibodies to cardiolipin and lupus anti-coagulant
  • treat with a heparin bridge to lifelong warfarin
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15
Q

What is the specific reversal agent for Xarelto and Eliquis?

A

andexxa

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16
Q

What is the generic name for praxbind?

A

idarucizumab

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17
Q

How does heparin work?

A

it potentiates antithrombin III, making it 1000x more effective

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18
Q

What are the side effects of protamine?

A

hypotension and bradycardia

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19
Q

How do you test for HIT?

A
  • start with PF4 antibodies
  • confirm with a serotonin release assay
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20
Q

How do you monitor the effectiveness of lovenox?

A

measure factor Xa levels

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21
Q

How does warfarin work?

A

it inhibits a protein, VKORC, that activates vitamin K, preventing creation of vitamin-K dependent coagulation factors

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22
Q

Which anticoagulation is teratogenic and contraindicated during pregnancy?

A

warfarin

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23
Q

How does dabigatran work?

A

it is a direct thrombin (FII) inhibitor

24
Q

How does andexxa work?

A

it acts as a decoy receptor for factor Xa inhibitors

25
Q

How does tPA work?

A

it activates plasminogen to break down fibrinogen

26
Q

How is tPA reversed?

A

with aminocaproic acid

27
Q

What are absolute contraindications to tPA administration?

A
  • active internal bleeding
  • recent CVA or neurosurgery
  • intracranial mass/pathology
  • recent GI bleed
28
Q

What are relative contraindications to tPA administration?

A
  • surgery within 10 days
  • recent organ biopsy
  • recent delivery
  • recent major trauma
  • uncontrolled hypertension
29
Q

What is MHC I?

A

a human leukocyte antigen present on all nucleated cells expresses intra-cellular antigens to active CD8 cytotoxic T cells

30
Q

How do natural killer cells work?

A

they recognize and destroy cells that either lack self-MHC or are bound with antibodies

31
Q

Describe a type I hypersensitivity reaction.

A

IgE binds to mast cells and basophils, triggering a release of histamine, serotonin, and bradykinin

32
Q

Describe a type II hypersensitivity reaction. Give two examples.

A
  • antibody mediated
  • IgG or IgM binds cell triggering destruction via cytotoxic T cell or complement system
  • examples include ABO incompatibility and hyper acute rejection
33
Q

Describe a type III hypersensitivity. Give two examples.

A
  • immune complex deposition
  • antigen-antibody complexes are deposited in tissue leading to complement activation and neutrophil attack
  • SLE or serum sickness
34
Q

Describe a type IV hypersensitivity reaction. Give two examples.

A
  • delayed-type
  • APCs present antigen to CD4 cells, activating macrophages
  • examples are PPD and contact dermatitis
35
Q

Describe the four types of hypersensitivity reactions with examples.

A
  • type I: IgE mediated
  • type II: antibody mediated (ABO incompatibility or hyper acute rejection)
  • type III: immune complex deposition (SLE or serum sickness)
  • type IV: delayed/CD4 (PPD or contact dermatitis)
36
Q

Which HLA classes are most important for recipient/donor matching?

A

HLA-A, B, and DR

37
Q

Describe the timing, mechanism, and management of hyperacute rejection.

A
  • less than 1 hr
  • mediated by preformed antibodies that activate complement cascade
  • treat with emergent re-transplantation
38
Q

Describe the timing, mechanism, and management of accelerated rejection.

A
  • days
  • sensitized T-cells respond to donor HLA, much like a cellular acute rejection
  • treat with increased immunosuppression or pulse steroids
39
Q

Describe the timing, mechanism, and management of acute cellular rejection.

A
  • weeks to months
  • T cells respond to donor HLA
  • treat with increased immunosuppression or pulse steroids
40
Q

Describe the timing, mechanism, and management of acute humoral rejection.

A
  • weeks to months
  • antibodies form to donor antigens
  • treat with pulse steroids, antibodies, or plasmapharesis
41
Q

Describe the timing, mechanism, and management of chronic rejection.

A
  • months to years
  • T cells and antibody formation
  • treat with increased immunosuppression or re-transplantation
42
Q

How does mycophenolate work? What are the side effects?

A
  • inhibits de novo purine synthesis to inhibit T cell growth
  • can cause GI upset and pancytopenia
43
Q

How do the following work:
- cyclosporine
- tacrolimus
- sirolimus

A
  • a calcineurin inhibitor which decreases cytokine production
  • inhibits FK binding protein which decreases cytokine production
  • inhibits mTOR to limit T and B cell responses to IL-2
44
Q

Sirolimus is associated with what side effect?

A

interstitial lung disease

45
Q

How does thymoglobulin work?

A

its a polyclonal antibody against T cell antigens

46
Q

Why do transplant patients get started on Bactrim?

A

for PJP ppx

47
Q

What is the treatment for post-transplant lymphoproliferative disorder?

A

decrease immunosuppressive therapy, rituximab

48
Q

What is the treatment for CMV in a transplant patient?

A

ganciclovir

49
Q

What is the treatment for EBV in a transplant patient?

A

decrease immunosuppression

50
Q

Which coagulation factor has the shortest half life?

A

F VII

51
Q

What are the main steps of the coagulation cascade?

A
  • FXa activates thrombin (FII)
  • thrombin converts fibrinogen to fibrin
52
Q

How does antithrombin III work?

A

it binds and inhibits thrombin, preventing conversion of fibrinogen to fibrin and thus activation and cross linking of platelets

53
Q

What is the most common inherited hypercoagulable disorder?

A

Factor V Leiden mutation

54
Q

What is the first immune cell to arrive at the site of an injury?

A

neutrophils

55
Q

What is the most common antibody in the spleen?

A

IgM

56
Q

Which antibody type can cross the placental barrier and provides immunity to newborns?

A

IgG

57
Q

What is the most common malignancy following transplant?

A

squamous cell carcinoma

58
Q
A

BTK Review 2024 (19 decks)

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