15: Transplant Flashcards

1
Q

When is engraftment first evident in a transplant patient? How long does that typically take?

A

When new white blood cells, red blood cells and platelets being to appear in the patient’s blood. Usually not until week 2-3 post infusion.

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2
Q

What are the 3 types of HCT? Describe them each.

A

Autologous HCT - uses patient’s own stem cells, collected before the conditioning regimen. Mainly used for NHL, HL, MM

Syngeneic HCT - using identical twin stem cells – rare for obvious reasons

Allogeneic HCT - used stem cells from a donor. Mainly used for acute/chronic leukemias, NHL, and marrow diseases like Aplastic Anemia. This can have several types.

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3
Q

What are the different types of Allogeneic HCT?

A

Matched related Donor
Matched unrelated Donor (MUD)
mismatched unrelated Donor
half-matched related Donor (Haploidentical or Haplo)
Umbilical cord blood

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4
Q

What are the different conditioning regimens for transplant?

A

It requires either cytotoxic chemo, TBI (total body irradiation) or both

High-Dose or myeloalative regimens – combo of chemo to ablate bone marrow that requires stem cell infusion in order to rebuild the bone marrow

Nonmyeloablative regimens – chemo that cause minimal cytopenias, so patient doesn’t need stem cell infusion

Reduced intensity conditioning (RIC) — less intense chemo or TBI (or both) that causes prolonged cytopenia, resulting in need for stem cell infusions

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5
Q

What mechanism does the RIC or nonmyeloablative regimens (aka lower dosage) for conditioning rely on for full disease eradication? When/why would these be used?

A

graft-versus-tumor (GVT) effect – response in which the infused graft stem cells attack and kill remaining cancer cells that weren’t killed by the conditioning.

Often used in older patients, have been heavily pretreated, or have comorbidities and unable to tolerate high-dose

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6
Q

What’s the typical timeline for neutrophil engraftment by transplant type?

A

Auto — 10-12 days

Allo —
MRD/MUD with peripheral blood and Haplo — 14-16 days
MRD/MUD with bone marrow — 19-21 days
Umbilical cord blood — 21 days

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7
Q

What type of diet should patients be on post transplant?

A

Food Safety Diet – reduce risk of foodborne illness
Really restrictive diets are not supported by evidence. Foodborne illness is rare in first year post transplant if patients follow guidelines:

AVOID
raw/undercooked meat (including game), fish, shellfish, poultry, eggs, sausage and bacon
avoid raw tofu, unless pasteurized
lunch meats unless heated until steaming
unpasteurized dairy
blue-veined cheeses, uncooked soft cheeses, mexican-style soft cheeses, cheese containing chili peppers and uncooked vegetables
refrigerated smoked seafood and pickled fish
fresh salad dressings that contain raw eggs or above cheeses
unwashed raw or frozen fruits/veg and those with visible mold
all raw vegetable sprouts
unpasteurized fruit/vegetable juice
well water unless boiled for 15-20 minutes and consumed within 48 hours

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8
Q

How long are HSCT patients on the required diet?

A

Food Safety Diet

auto – about 90 days post transplant
allo – until off immunosuppressive therapy, which varies by health care facility and type of match. Usually at least 3-6 months, could be longer

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9
Q

How does being underweight or overweight impact survival?

A

underweight — increased risk of relapse, poor overall survival

overweight — increased risk for nonrelapse mortality. Also at increased risk for GVHD.

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10
Q

What are the typical oral/GI complications of transplant?

A

These are frequent. Conditioning regimens side effects typically start to diminish as engraftment begins.

These are commonly taste loss, nausea, early satiety and mucositis.

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11
Q

What method is used to reduce the risk of mucositis in high-dose conditioning regimens?

A

Cryotherapy – the placement of ice chips in the mouth during infusion-with melphalan helps reduce mucositis by decreasing blood flow and exposure to chemo. This is a great tool to use since up to 80% of patients develop this.

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12
Q

Describe SOS or Sinusoidal Obstructive Syndrome

A

The effect of chemo causes sinusoidal endothelial and hepatocyte damage that triggers a cascade of events leading to narrowing and occlusion of hepatic venules, fibrosis, and hepatocyte necrosis. This causes decreased hepatic outflow, portal HTN, ascites and hepatomegaly, and cause cause multiorgan failure and death.

Usually occurs within first few weeks of transplant and incidence varies widely to 0-60% based on transplant type, diagnostic criteria used and population risk factors. Has a high mortality rate exceeding 80%.

Medical management using diuresis, sodium restriction, renal replacement therapy (HD or CRRT), pain management and use of defibrotide.

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13
Q

What two main lab issues can occur with transplant and why?

A

Hyperglycemia – usually by meds, typically prednisone, or by use of TPN. Usually during the neutropenic phase for HCT, causing delays in neutrophil recovery, function, and increased risk for infection/prolong engraftment time and risk for acute GVHD.

Renal impairment – could be chemo, TBI, nephrotoxic meds like antibiotics, SOS, intravascular volume depletion and sepsis. Nutrition should work to max nutrition support within fluid allowance, correcting electrolyte imbalance and maintain sufficient intravascular volume.

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14
Q

What is a major source of morbidity and mortality for patients receiving HCT?

A

Infection – bloodstream infections, pneumonia and GI infections like C Diff are the most common. TPN/PN could be another source concern.

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15
Q

What do about half of all patients develop within the first 100 days? What different forms can it take?

A

Clinically Significant Cytomegalovirus (CSV)

CMV enteritis - nonspecific GI that can cause ulcerations anywhere along the GI tract. Diagnosed via biopsy to rule out other causes.

CMV gastritis - often causes severe epigastric pain

CMV esophagitis - present at odynophagia and dysphagia

CMV colitis - may cause diarrhea, abd pain, anorexia, and fever

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16
Q

Define GVHD

A

Graft-vs-host disease is a T-cell meditated immunologic reaction to engrafted lymphoid cells against the host tissues. Risk increases as donor source is less matched—unrelated and mismatched donors are at higher risk.

17
Q

When does Acute GVHD typically occur and where

A

Typically within first 100 days, however if it is persistent, reoccurs, or is late-onset acute.

Effects skin (75%), Liver (20%), and GI tract (50%)

18
Q

What are the clinical manifestations of gut GVHD? How long can symptoms last?

A

N/V
anorexia
food intolerance
abd pain
voluminous diarrhea and cramping if the lower GI tract is involved

for weeks to months

19
Q

What is the rate of malnutrition/wt loss in GVHD patients?

What are underlying causes?

A

14-43% of patients

villous atrophy, mucosal ulcerations, secretory dysfunction, osmotic factors, rapid passage and EPI. Intestinal protein losses and fat malabsorption are also characteristic of GI GVHD.

20
Q

What are the Nutrition support recommendations for HCT? What patients should it be considered for?

A

EN is now recommended as first-line NS during HCT for patients who are malnourished or have inadequate intake than expected to be prolonged. This applies to GVHD because of the emerging research for gut microbiome helping the immune system.

Undergoing allo HCT and have functional GI tract
Malnourished before auto or allo transplant

21
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Declomethasone
dipropionate

A

Dysgeusia
Oral Candidiasis

22
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Budesonide

A

Xerostomia

23
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Calcineurin inhibitors (cyclosporine, tacrolimus)

A

N/V

Low Mg, High K+, renal insufficiency, food-drug interaction (grapefruit/bergamot/bitter orange/pomegranate)

24
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Methotrexate

A

N/V
Anorexia
Mucositis
Diarrhea

renal and hepatic changes

25
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Mycohenolate mofetil

A

D/C/abd pain/N

Interaction with dietary Ca and with Mg/Iron supplements
should be taken on empty stomach

26
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Sirolimus

A

Hypertriglyceridemia

27
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Prednisone

A

Dyspepsia
Hyperphagia

Insulin resistance, hyperglycemia, edema, Low K+ and Phos, High Lipids, Skeletal muscle catabolism, osteoporosis, growth retardation in children

28
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Extracorporeal
photopheresis

A

Low Ca
IV fluids might needed for adequate hydration
may not be possible with significant hypertriglyceridemia (lipemic serum blocks ultraviolet light)

29
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Psoralen and ultraviolet irradiation

A

N
Hepatotoxicity

30
Q

Therapies for prevention/treatment of GVHD and their side effects/nutrition concerns:

Ursodiol

A

N/V/D/Dyspepsia

31
Q

When should TPN/PN be used for HCT?

A

patients with the following:
severe mucositis (>grade 3)
ileus
intractable vomiting
GVHD with more than 1 L of stool/day (grades 3 and 4)
inability to place an NGT
significant intolerance of EN
Refusal of feeding tube placement

32
Q

Phase 1 of Diet Progression for GVHD

A

Bowel Rest

GI cramping
Large volume/watery diarrhea >500 ml/d
Depressed serum albumin
severely reduced transit time
SBO or diminished bowel sounds
N/V

NPO with IV

33
Q

Phase 2 of Diet Progression for GVHD

A

Intro to Oral Feeding

min GI cramping, Diarrhea <500 ml/hr, improved transit time, infrequent N/V

Isotonic/low-residue/low-lactose fluids + IV

34
Q

Phase 3 of Diet Progression for GVHD

A

Intro to Solids

min/no cramping, formed stool

Allow intro to solid foods containing min lactose, low fiber, low fat, low total acidity, no gastric irritants + IV

35
Q

Phase 4 of Diet Progression for GVHD

A

Expansion of diet

min/no cramping, formed stool

add foods with low lactose, low fiber, low total acidity, no gastric irrtants; if stools indicate fat malabsorption, prescribe low fat diet. IV as needed

36
Q

Phase 5 of Diet Progression for GVHD

A

Resumption of regular diet

No cramping, normal stool, normal transit time, normal albumin

progress to regular diet, adding in acid/fiber/lactose in various orders per pt tolerance and preference. If no steatorrhea, fat restriction should be slowly lifted. D/C IV

37
Q

Survivorship Concerns with HCT

A

Chronic GVHD

Osteoporosis (prevalence is as high as 50% as early as 1 year post transplant)

Vit D Deficiency/Insufficiency

Growth/development for kids

Metabolic syndrome

cardiometabolic changes

iron overload (multiple RBC transfusions)–iron supplement/MVI with iron should be avoided