Graft versus host disease Flashcards

1
Q

Organ systems involved in acute GVHD

A
  • Rash
  • GI tract (high concentration of WBCs)
  • Liver
  • nausea and emesis
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2
Q

RF’s

A
  • High HLA disparity
  • Donor and recipient gender disparity
  • Unrelated donor
  • Intensity of transplant conditioning regimen
  • peripheral-blood stem-cell graft
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3
Q

Acute GVHD timing

A

Can occur at any point but most commonly in early post-transplant period (first couple months)

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4
Q

Description of rash in acute GVHD

A

Maculopapular

**see photos online

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5
Q

Presentation of GI involvement with GVHD

A

Diarrhea (can be severe) + abdominal pain

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6
Q

Lab abnormalities of acute GVHD

A

rising serum bili

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7
Q

Diagnosis

A

1) Clinical if presentation consistent (classic rash, rising bili)
2) Sometimes, ddx is less clear and you need bx of skin or GI tract

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8
Q

Key concept of treating GVHD

A
  • Treatment requires suppression of donor T cells, but these same cells are responsible for immunologic effect on tumor, so you need to balance benefit of treating GVHD with harming of decreasing GVT effect .
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9
Q

Approach to treatment depends on

A

Grade of GVHD

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10
Q

Grade I GVHD management

A

1) Topical steroids

2) Optimize or restart prophylaxis

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11
Q

Grade II or higher GVHD management

A

Systemic steroids + oral steroids if GI involvement

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12
Q

GVHD prophylaxis for ablative allo HCT

A
  • calcineurin inhibitor (Cyclosporine or tacrolimus) + MTX
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13
Q

Presentation of chronic GVHD

A
  • skin involvement (lichen planus or scleroderma)
  • dry oral mucosa
  • GI tract (ulceration)
  • rising bilirubin
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14
Q

skin findings in acute vs. chronic

A
acute = maculopapular rash
chronic = lichen planus or scleroderma
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15
Q

organ systems involved in chronic GVHD

A

skin (most common)
liver
GI tract
**lungs

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16
Q

More advanced skin stage of acute GVHD presentation

A

Blistering and ulceration

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17
Q

GVHD prophylaxis for reduced intensity HCT

A

Cyclophosphamide

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18
Q

New, evolving approach to GVHD prophylaxis

A
  • post transplant cyclophosphamide
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19
Q

What is Grade I GVHD?

A

Rash less than 1/4 of BSA + NO liver or GI involvement

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20
Q

Management of steroid refractory acute GVHD?

A
  • No standard therapy (most don’t work and mortality rate is high, bad prognosis)
  • ruxolitinib is FDA approved
21
Q

Standard prednisone dosing for acute GVHD

A

1 mg/kg

22
Q

Pathogen patients are at highest risk of early on after transplant

A

bacteria

23
Q

Bacterial pathogen patients are at highest risk of later on after transplant

A

encapsulated bacteria

24
Q

bacterial prophylactic medicifications

A

fluoroquinolones (levoquin)

25
Q

encapsulated bacteria ppx for patients with chronic GVHD

A

Bactrim

26
Q

What is pentamidine used for?

A

PCP ppx

27
Q

Patients who are at highest risk of CMV reactivation

A

Seropositive patient, seronegative donor

28
Q

How to monitor for CMV in seropositive patient

A

PCR q2 weeks until 1 year post-transplant

29
Q

When acute GVHD typically occurs

A
  • early transplant period

- within 19 days of HCT

30
Q

RF’s for acute GVHD

A
  • HLA mismatch or unrelated donor
  • gender disparity (female donor to male recipient)
  • lack of prophylactic GVHD regimen (MTX, cyclosporine)
31
Q

Acute vs chronic GVHD in terms of timing

A
Acute = within 100 days
Chronic = any time
32
Q

RF’s for chronic GVHD

A
  • older age of donor or recipient
  • prior acute GVHD
  • seropositive CMV in donor or recipient
33
Q

Description of rash in chronic GVHD

A
  • resembling lichen planus or scleroderma + areas of hypo or hyperpigmentation
34
Q

other clinical features of chronic GVHD

A
  • dry oral mucosa with ulcerations
  • dry eyes
  • esophageal webs or strictures
  • fasciitis or joint strictures
35
Q

incidence of chronic GVHD in post-transplant patients

A
  • very high (around 50%)
36
Q

acute GVHD timeframe

A

Less than 100 days

37
Q

acute GVHD clinical features

A

rash + diarrhea and nausea + LFT abnormalities

38
Q

Other common prophylaxis regimens

A
  • cyclosporine

- methotrexate

39
Q

Grade II or higher generally speaking

A
  • liver or GI tract involvement or skin involvement that is greater than 50% of body surface area
40
Q

Clinical features of gastrointestinal tract involvement in GVHD

A
  • usually presents with lower tract symptoms (diarrhea and abdominal pain), but may also present with nausea, vomiting, and anorexia
41
Q

Stage 3 means

A
  • rash greater than 50% BSA
  • bili 6.1-15
  • Stool greater than 7 episodes per day
42
Q

Stage 4 means

A
  • bili greater than 15
  • severe abdominal pain with or without ileus or bloody stool
  • rash: bullous formation or desquamation
43
Q

stem cell graft type that is a risk factor for chronic GVHD + why

A
  • peripheral stem cell graft (higher number of T cells in peripheral blood compared to a bone marrow graft)
44
Q

pulmonary manifestation of chronic GVHD

A

bronchiolitis obliterans

45
Q

RF’s for development of chronic GVHD

A
  • high degree of HLA mismatching
  • Older age of donor and/or recipient
  • donor and recipient gender disparity
  • alloimmunization of donor (history of pregnancy, transfusions)
  • peripheral blood as stem cell source
  • previous splenectomy
  • CMV seropositivity (donor or recipient)
  • donor EBV virus seropositivity
46
Q

HCT donors for which acute GVHD is more common

A
  • matched unrelated donors
  • female donors (more often alloimmunized due to pregnancy)

- haploidentical donors

47
Q

MDS pathophys

A
  • blood cells remain in an immature stage within the bone marrow, never developing into mature cells.
  • eventually, marrow may be filled with blast cells suppressing normal cell development
48
Q

Second line for chronic GVHD

A

ibrutinib

49
Q

Second line for acute GVHD

A

jakafi