Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Immunology > transplant > Flashcards

transplant Flashcards

1
Q

autotransplantation

A

transplant tissue from one part of the body to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

allotransplantation

A

transplant tissue from one person to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

orthotopic transplant

A

transplanted organ is placed in the same location at the original organ (heart, lung, liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

heterotopic transplant

A

transplanted organ is placed in a different location as the original organ (pancreas, kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which organs can have deceased or living donors

A

kidney, liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which organs can have deceased donors only

A

heart, lung, pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does the immune system identify “self”

A

a self marker (MHC) labels the body’s cells as a friend

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does the immune system identify “non-self”

A

it recognizes an antigen as foreign and treats it as a foe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do HLA molecules act in transplant

A

they are markers that determine compatibility of tissue for transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MHC class I

A

found on all nucleated cells. presents antigenic peptides to CD8+ T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MHC class II

A

restricted expression on antigen presenting cells
presents antigenic peptides to CD4+ T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Type A blood

A

can only have A or O blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type B blood

A

can only have B or O blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Type AB blood

A

universal recipient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type O blood

A

universal donor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do patients develop antibodies to other HLAs

A

transfusion, pregnancy, other organ transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

sensitization is generally defined as PRA > __%

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

recipient risk factors for rejection

A

black race, highly sensitized, previous transplant, young age, prior pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

when does hyperacute rejection occur

A

immediately (in the OR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the mechanism by which hyperacute rejection occurs

A

activation of complement through antibody-mediated interactions– results in inflammation & microvascular thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how to prevent hyperacute rejection

A

screening: ABO, HLA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

treatment of hyperacute rejection

A

retransplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

when does acute cellular rejection occur

A

can occur at any time after transplant but most common in the first 12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the mechanism by which acute cellular rejection occurs

A

recognition of foreign antigen leads to T- cell activation
cytokines are produced: CD8, NK and B cells are recruited and causes damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the clinical presentation of acute cellular rejection

A

depends on organ transplanted:
kidney- abrupt change in SCr
liver- abrupt change in LFTs
heart- decrease in cardiac output or ejection fraction
lung- change in pulmonary function/breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

management of acute cellular rejection

A

best treatment is prevention
pharmacologic therapy: corticosteroids (prednisone, methylprednisolone), lymphocyte depletion (antithymocyte globulin, alemtuzumab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the general definition of antibody mediated rejection

A

a form of allograft rejection triggered by the production of antibodies directed toward donor HLA molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

in antibody mediated rejection, what do the donor specific antibodies activate

A

the complement: attaches to and pokes holes into the allograft (membrane attack complex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are some therapy targets for antibody mediated rejection

A

proteasome inhibition (stop plasma cells from making antibodies)
cellular depletion (get effector cells out of circulation)
inhibit signals (IL-6)
inhibit complement cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the calcineurin inhibitors

A

cyclosporine and tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the ultimate action of calcineurin inhibitors

A

block cytokine transcription by inhibiting calcineurin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

true or false: you can substitute sandimmune for neoral or gengraf

A

FALSE: the bioavailability of cyclosporine depends on the formulation and you CANNOT substitute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

different brand names of cyclosporine and their absorption

A

sandimmune: high variability. <10% up to 89% bioavailable. depends on enterohepatic recirculation
neoral, gengraf: 30% bioavailable, more consistent absorption, less dependent on bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

effects of food on the calcineurin inhibitors

A

high fat meal decreases absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

cyclosporine causes drug interactions because of being _____ substrate

A

CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

cyclosporine elimination is extensive in the ____

A

bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

cyclosporine adverse effects

A

think c for cyclosporine and c for cosmetic: acne, hirsutism, gingival hyperplasia
as well as:
nephrotoxicity and neurotoxicity- dose limiting
hypertension
hyperlipidemia
hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CYP3A4 inhibitors will ______ cyclosporine levels. is this reaction immediate or delayed?

A

increase
interaction happens quick because the protein is already there and you just inhibit it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

CYP3A4 inducers will ____ cyclosporine levels. is this reaction immediate or delayed?

A

decrease
interaction is delayed because you have to make new proteins, takes a couple weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

cyclosporine interaction with OATP substrates

A

cyclosporine inhibits OATP and increases the OATP substrate concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

IV doses of cyclosporine are ____ PO doses

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

counseling point for cyclosporine

A

maintain consistent administration with meals
don’t care if you eat or not just do it consistently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

TDM for cyclosporine

A

narrow therapeutic window: methods are trough, AUC, peak monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

with extensive and intermediate CYP3A5 metabolizers, _____ doses of tacrolimus are needed

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

with poor CYP3A5 metabolizers, _____ doses of tacrolimus are needed

A

standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

tacrolimus absorption

A

bioavailability 30%, erratic and variable absorption– decreased with high fat meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

tacrolimus side effects

A

nephrotoxicity (dose limiting): hyperkalemia, hypomagnesemia
neurotoxicity (dose limiting): headache, tremor, insomnia, seizure
hypertension
hyperlipidemia
hyperglycemia
pruritis
cosmetic- alopecia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

tacrolimus drug interactions

A

decreased GI absorption with cationic compounds
CYP3A4 inducers decrease TAC levels, inhibitors increase TAC levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

IV doses of tacrolimus are ___ of PO doses

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

TDM for tacrolimus

A

narrow therapeutic window: trough concentrations are easiest to measure but may not correlate with efficacy/toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

which transplant drugs are purine analogs

A

mycophenolic acid, azathioprine, mercaptopurine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the basic mechanism of mycophenolic acid

A

to block T and B cell proliferation and activity. does so by inhibiting IMPDH to block purine nucleotide synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

adverse effects of mycophenolic acid

A

bone marrow suppression and GI toxicity are dose limiting
progressive multifocal leukoencephalopathy (PML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

drug interactions with mycophenolic acid

A

decreased GI absorption with cationic compounds, decreased elimination with acyclovir and ganciclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

mycophenolate mofetil dose of 500 mg correlates to mycophenolic acid dose of ____

A

360 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

TDM for mycophenolic acid

A

controversial; AUC monitoring most widely used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

bioavailability of mycophenolate

A

depends on formulation:
MMF 94%; rapidly converted to MPA
MPA 72%: protected by enteric coating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

mechanism of azathioprine and mercaptopurine

A

block de novo and salvage pathways for purine synthesis; suppresses T>B cells, anti-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

2 enzymes responsible for azathioprine/mercaptopurine metabolism

A

TPMT to inactive & active metabolites
xanthine oxidase to inactive metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

azathioprine/mercaptopurine side effects

A

bone marrow suppression (dose limiting)
GI toxicity (less than MPA)
alopecia, hepatitis, pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

azathioprine/mercaptopurine drug interactions

A

xanthine oxidase inhibitors (allopurinol, febuxostat) decrease metabolism and increase toxicity of azathioprine. requires decrease azathioprine doses to 1/3 or 1/4 of the usual dose but generally avoid the combination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

TDM for azathioprine/mercaptopurine

A

TPMT activity
monitor CBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

name the pyrimidine synthesis inhibitor

A

leflunomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

leflunomide mechanism

A

ultimately blocks T and B cell proliferation and activity by blocking pyrimidine nucleotide synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

leflunomide side effects

A

bone marrow suppression, GI side effects, alopecia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

leflunomide drug interaction

A

bile acid sequestrants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

leflunomide PO dosing requires ____

A

loading dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what drugs are the mTOR inhibitors

A

sirolimus and everolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

mechanism of the mTOR inhibitors

A

inhibiting mTOR which is what moves the cell from G1 to S phase. ultimate activity is blocking response to IL-2 and effects on cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

mTOR inhibitors: how does their absorption compare

A

sirolimus is erratic and variable (14% solution to 27% tablets)
everolimus is more consistent (30%)

both are impacted by high fat meals, highly distributed in WBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

mTOR inhibitor side effects

A

bone marrow suppression
GI toxicity
wound dehiscence
hyperlipidemia
proteinuria
pulmonary infiltrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

mTOR inhibitors drug interactions

A

CYP3A4 inducers decrease
CYP3A4 inhibitors increase

with cyclosporine, you have to take sirolimus 4 hours after it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

mTOR inhibitors: which one requires a loading dose

A

sirolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

mTOR TDM

A

narrow therapeutic window: measure by whole blood assay and monitor by trough

75
Q

which drug is folic acid antagonist

A

methotrexate

76
Q

methotrexate mechanism

A

inhibits dihydrofolate reductase to interfere with DNA synthesis and cell proliferation

77
Q

methotrexate bioavailability

A

higher doses are associated with lower bioavailability
Doses <30 mg/m2= 90% BA
Doses >40 mg/m2= 17% BA

78
Q

methotrexate side effects

A

bone marrow suppression
GI toxicity
alopecia
nephrotoxicity
hepatotoxicity
cardiotoxicity

79
Q

methotrexate drug interactions

A

overlapping toxicities, albumin displacement

80
Q

higher doses of methotrexate are often given with ____

A

leucovorin rescue

81
Q

methotrexate doses are based on ___

A

BSA

82
Q

methotrexate TDM

A

generally based on therapeutic response

83
Q

which drug is the alkylating agent

A

cyclophosphamide

84
Q

cyclophosphamide mechanism

A

reacts with nitrogen atoms on purine bases, forms cross links in DNA, ultimately interferes with DNA synthesis and cell proliferation

85
Q

cyclophosphamide side effects

A

bone marrow suppression
GI Toxicity
alopecia
amenorrhea
cardiotoxicity
pulmonary toxicity/fibrosis

86
Q

very broad: glucocorticoid versus mineralocorticoid effects of corticosteroids

A

glucocorticoid: immune system, anti-inflammatory, metabolic, central nervous system, and bone metabolism effects
mineralocorticoid: kidneys (waste potassium and hold on to sodium)

87
Q

effects of glucocorticoids on the innate immune system

A

decrease expression of adhesion molecules (the little feet that get the cells where they want to go- site of inflammation)

88
Q

effects of glucocorticoids on the acquired immunity

A

at high doses (>100 mg prednisone): T cells, direct cytotoxicity

blocks expression of pro-inflammatory genes and increases expression of anti-inflammatory genes

89
Q

glucocorticoid SIDE effects on immune system

A

increasing incidence of infection

90
Q

anti-inflammatory actions of glucocorticoids

A

blocks release of arachidonic acid and COX-2 to block the pro-inflammatory prostaglandins and decrease inflammation

91
Q

side effects of the anti-inflammatory actions of glucocorticoids

A

GI upset, bleeding, ulcers

92
Q

anabolic effects of glucocorticoids

A

increase gluconeogenesis in liver
reduce protein stores in cells except liver

93
Q

catabolic effects of glucocorticoids

A

increase lipolysis
inhibit uptake of glucose
inhibit protein synthesis
increase mobilization of fatty acids

94
Q

side effects of the metabolic actions of glucocorticoids

A

hyperglycemia and hyperlipidemia
impaired wound healing
buffalo hump: deposits of fat in neck and torso

95
Q

effects of glucocorticoids on the central nervous system

A

increases CNS excitability

96
Q

side effects of glucocorticoids on the central nervous system

A

insomnia
mania
mood disorders
impaired cognition
increased appetite

97
Q

effects of glucocorticoids on bone metabolism

A

decrease calcium
inhibit osteoblasts
decrease calcium absorption from intestines
increase calcium excretion from kidneys

98
Q

side effects of glucocorticoids on bone metabolism

A

hypocalcemia, osteopenia/osteoporosis

99
Q

mineralocorticoid actions

A

promotes sodium reabsorption and potassium excretion

100
Q

side effects of mineralocorticoid actions

A

hypernatremia: water retention, truncal obesity, hypertension
hypokalemia: dysrhythmia

101
Q

in summary: short term side effects of corticosteroids

A

sodium & water retention
psychosis
mood changes
poor wound healing
insomnia
hyperglycemia
GI upset
increased appetite

102
Q

in summary: long term side effects of corticosteroids

A

hypertension
hyperglycemia
weight gain
adrenal suppression
cataracts
osteoporosis
acne
GI ulcers

103
Q

_______ has the most mineralocorticoid activity

A

fludrocortisone

104
Q

______ has the most anti-inflammatory activity

A

dexamethasone

105
Q

corticosteroid dosing for transplant rejection vs maintenance

A

rejection: methylprednisolone 250-1000 mg IV daily x 3 days
maintenance: tapered over months to a low maintenance dose of 5-10 mg prednisone daily

high dose for short course, low dose for long course

106
Q

symptoms of adrenal insufficiency

A

hypotension
decreased appetite
weight loss
fatigue
inability to mount response to stress

107
Q

what causes iatrogenic adrenal insufficiency

A

HPA axis suppression from long term administration of supratherapeutic corticosteroids: negative feedback inhibits production of CRH and ACTH so body does not produce endogenous cortisol

108
Q

how to prevent iatrogenic adrenal insufficiency

A

slowly taper steroids
decrease steroid dose by 10-20% every 1-2 weeks

109
Q

what is the purpose of induction immunosuppression

A

to prevent T-cell mediated immune activity at the time of graft introduction: decrease incidence of acute cellular rejection, delay initiation of maintenance immunosuppression

110
Q

for induction immunosuppression: what is depleting vs non-depleting agent

A

depleting: cause LYSIS of T cells (thymoglobulin and alemtuzumab)
non-depleting: inhibit T cell activity (Basiliximab)

111
Q

thymoglobulin adverse effects

A

thrombocytopenia
leukopenia & infection
hyperkalemia
respiratory distress
tachycardia
fever, chills

112
Q

alemtuzumab adverse effects

A

thrombocytopenia
leukopenia & infection
hyperkalemia
hypotension
fever, chills

113
Q

basiliximab adverse effects

A

none– well tolerated!

114
Q

time of effects for induction agents

A

thymoglobulin & alemtuzumab: 6-12 months
basiliximab: 3-6 months

115
Q

pre-medication for induction

A

thymoglobulin and alemtuzumab: required acetaminophen, diphenhydramine, corticosteroid

not needed for basiliximab

116
Q

which EBV serostatus gives the highest risk of PTLD

A

D+/R-

117
Q

rejection risk based on age

A

young>elderly
more active immune system

118
Q

rejection risk based on sex

A

female>male

119
Q

rejection risk: pregnancy?

A

sensitizing event: increases antibodies

120
Q

rejection risk based on race

A

black patients highest risk, more likely to have CYP3A5 mutation leading to tacrolimus rapid metabolism

121
Q

rejection risk based on PRA

A

high PRA> low PRA
high means more antibodies against donor pool

122
Q

what are some “sensitizing events”

A

pregnancy, blood transfusion, prior transplantation

123
Q

rejection risk based on organ type: lowest risk to highest risk

A

liver<kidney<heart<lung< small bowel

124
Q

which organ types typically require long term steroids

A

lung & small bowel

125
Q

goals of maintenance immunosuppression

A

prevent acute cellular and antibody mediated rejection

126
Q

what drugs are in the maintenance immunosuppression toolbox

A

calcineurin inhibitors
antimetabolites
mTOR inhibitors
corticosteroids
belatacept

127
Q

preferred calcineurin inhibitor for maintenance

A

tacrolimus

128
Q

cell cycle inhibitors use in pregnancy?

A

mycophenolate is contraindicated in pregnancy.
azathioprine is used in pregnancy.

129
Q

timing with mTOR inhibitors

A

need to wait 90 days from transplant to initiate due to impaired wound/anastomosis healing

130
Q

benefits of mTOR inhibitors?

A

benefit in malignancy and viral infections

131
Q

what is belatacept mechanism of action

A

binds CD80/86 on antigen presenting cells which prevents second signal required for T cell activation

132
Q

belatacept adverse effects

A

mostly well tolerated, some infusion related like HTN, HA, NVD, edema

*PTLD risk and fungal/viral infections

133
Q

contraindications of belatacept

A

EBV high risk patients (D+/R-)

134
Q

ALL cases of acute cellular rejection should receive ____

A

steroids

135
Q

treatment of initial rejection episode in acute cellular rejection

A

methylprednisolone 1000 mg IV x 3 doses

136
Q

treatment of refractory or recurrent rejection episode in acute cellular rejection

A

lymphodepleting agents: thymoglobulin, alemtuzumab

137
Q

treatment of antibody mediated rejection

A
  1. remove antibodies: plasmapheresis
  2. inhibit new antibody production: IVIG
  3. inhibit/deplete B cells: rituximab, carfilzomib, bortezomib, daratumma
  4. inhibit/deplete T cells: corticosteroids, thymoglobulin
  5. inhibit C5 to prevent formation of MAC: eculizumab
138
Q

drug of choice for PJP

A

sulfamethoxazole/trimethoprim

139
Q

bactrim coverage

A

PJP, toxoplasmosis, listeria, nocardia

140
Q

bactrim dosing PJP

A

DS MWF or SS daily
renal dose adjustments

141
Q

bactrim adverse effects

A

increased SCr, photosensitivity, hyperkalemia

142
Q

bactrim drug interaction

A

warfarin

143
Q

use bactrim alternatives if __

A

sulfa allergy, hyperkalemia

144
Q

bactrim alternatives

A

dapsone, atovaquone, pentamidine

145
Q

dapsone disadvantages

A

covers only PJP, requires G6PD testing prior to initiation

146
Q

atovaquone advantages/disadvantages

A

covers PJP and toxoplasmosis
ok in sulfa allergy or G6PD deficiency

146
Q

pentamidine disadvantages

A

inhaled, high rates of bronchospasm

146
Q

nystatin prevents ___

A

thrush

147
Q

fluconazole prevents ___

A

candida spp infections

148
Q

voriconazole prevents ____

A

candida and aspergillus spp infections

149
Q

nystatin side effects and counseling

A

GI effects
shake well prior to using
no food/drink for 10 minutes before/after

150
Q

fluconazole side effects

A

QT prolongation, LFT elevations, GI effects

151
Q

fluconazole drug interactions

A

CYP3A4 inhibitor (increases CNI and mTOR levels)

152
Q

voriconazole side effeccts

A

LFT elevations, photosensitivity, hallucinations, blurred vision, QT prolongation

153
Q

voriconazole drug interactions

A

strong CYP3A4 inhibitor: decrease CNI dose by 50-75% upon starting

154
Q

acyclovir covers ____

A

HSV prophylaxis

155
Q

letermovir covers ____

A

CMV prophylaxis

156
Q

ganciclovir & valganciclovir cover ____

A

HSV & CMV prophylaxis/treatment

157
Q

acyclovir side effects

A

headache, neurotoxicity, nephrotoxicity, thrombocytopenia

158
Q

ganciclovir & valganciclovir side effects

A

leukopenia, thrombocytopenia, AKI, GI

fetal risk: avoid in pregnancy and breastfeeding

159
Q

letermovir side effects

A

headache GI

160
Q

letermovir drug interactions

A

moderate CYP3A4 inhibitor
cyclosporine: inhibits letermovir metabolism

161
Q

most common indications for a kidney transplant and which one is #1

A

1 is diabetes

others: hypertension, glomerulonephritis, cystic kidney disease

162
Q

which HLA antigens are used for matching a kidney transplant

A

A, B, C, DR, DP, DQ

163
Q

how does HLA matching affect kidney transplant outcomes

A

6 antigen match= best outcomes & least rejection
0-5 antigen match= not as good of a chance

164
Q

what is the significance of the kidney donor prognosis index

A

calculates risk of graft failure based on DONOR factors
age, ht/wt, race, HTN, DM, cause of death, SCr, HCV, DCD

165
Q

how does the cPRA affect the kidney transplant waitlist

A

the higher the number= the more reactive the patient is and the more chance they will have antibodies to the donor antigen. anything over a 20% is a high risk

166
Q

how does living kidney donor affect kidney transplant outcomes

A

we can transplant patients much sooner instead of waiting for a deceased donor
living donor kidney is better: higher GFR

167
Q

most common indication for adult liver transplantation

A

alcoholic liver disease

168
Q

most common indication for pediatric liver transplantation

A

biliary astresia

169
Q

you can donate part of your liver?

A

yes it is the only organ that can regenerate itself

170
Q

do the majority of liver transplant recipients receive induction immunosuppression?

A

NO!

171
Q

what maintenance immunosuppression regimen is most common in liver transplant recipients?

A

tacrolimus, mycophenolate, and a steroid

172
Q

who has the lowest incidence of acute rejection in liver transplant recipients

A

ages 65+

173
Q

what is MELD a predictor for

A

90 day mortality

174
Q

components of MELD-BNa score

A

SCr, bili, INR, Na

175
Q

components of child pugh score

A

albumin, bili, INR, ascites, encephalopathy

176
Q

components of PELD score & who it applies to

A

Kids <12: age, size, albumin, bili, INR

177
Q

most common indications for lung transplant

A

IPF, COPD, cystic fibrosis

178
Q

the ______ assesses pre transplant urgency & post transplant survival to determine lung allocation offers

A

Lung CAS

179
Q

median survival for lung transplant is _____ compared to most other transplanted organs

A

shorter

180
Q

_____ is common in the first year after lung transplant

A

ACR

181
Q

primary limitation to long-term survival after lung transplantation is _____

A

CLAD (chronic lung allograft dysfunction)

Advanced Immunology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions