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p2 year > immunology therapeutics > Flashcards

immunology therapeutics Flashcards

1
Q

stages of immunosuppression for SOT

A

1) pre-transplant induction
2) day 0: transplant
3) post-transplant induction and maintenance overlap
4) maintenance

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2
Q

SOT maintenance treatment options

A

normal protocols
1) TAC + MMF/EC-MPS + prednisone –> most patients
2) CYA + MMF/EC-MPS + prednisone

minimized protocols
3) low dose TAC + regular dose MMF/EC-MPS
4) low dose CYA + regular dose MMF/EC-MPS

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3
Q

how long is a patient on maintenance immunosupression?

A

the lifetime of the organ –> probably their whole life unless the transplanted organ dies

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4
Q

induction agent options

A
  • ATG (anti-thymocyte globulin) (Thymoglobulin)
  • IL-2 receptor blockers (anti-CD25 mAb): basiliximab (Simulect), daclizumab (Zenapax)
  • Anti-CD52 mAb: alemtuzumab (Campath)
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5
Q

immunosuppression drugs are…

A

narrow therapeutic range drugs

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6
Q

immunosuppression drugs have more ___ variability

A

inter-subject –> very extreme!

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7
Q

CNIs

A
  • tacrolimus
  • cyclosporine
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8
Q

CNI MoA

A

block calcineurin activation -> prevents NFAT (nuclear factors of activated T cells) transcription factor production -> prevents signal 1 -> prevents further propagation of naïve T cell specification and production –> therefore, fewer immune cells to mount attack on organ

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9
Q

immunomodulator

A

agents that can have both positive (inc) and negative (dec) impacts on the immunesystem

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10
Q

immunostimulant

A

agents that inc the immune response

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11
Q

immunoadjuvants

A

used in combination with antigen administration to enhance that antigen’s immune system impact
- ex: MDP (muramyldipeptide)

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12
Q

immunosuppressants

A

agents that can reduce the immune response
- ex: all the drugs we talk about with SOT!

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13
Q

biological response modifiers (BRMs)

A

immunomodulators that are endogenous –> CSFs, ILs, IFN, MDP ; are potent immunopharmacology

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14
Q

immunopotentiator

A

agent that boosts a failing immune system (an immunostimulant)
- ex: immunoglobulin (antibody)

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15
Q

measles definition and presentation

A

*example of artifically acquired active immunity (adaptive immunity)
- respiratory disease caused by virus
- rash, fever, cough, runny nose, Koplik spots (blue-white spots in mouth), tight clusters of red spots, starts at hairline and moved down
- symptoms 10-12 days after exposure, very contangious 4 days before and after rash
- for school, children need MMR vaccine

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16
Q

tetanus definition and presentation

A
  • aka “lockjaw”
  • bacterial infection by Clostridium tetani spores (soil, dust, animal feces)
  • spores enter a deep flesh wound -> produce tetanospasmin toxin *not contagious
  • muscle spasms start in jaw and progress, fever, sweating, HA, impaired swallowing
  • DTap -> Tdap -> Td (every 10 yrs for adult dose)
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16
Q

cyclosporine AEs (in order of prevalence)

A
  1. hyperlipidemia
  2. nephrotoxicity
  3. tremor, HA
  4. HTN
  5. hyperglycemia, gingival hyperplasia, hirsutism, diarrhea, vomiting
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17
Q

tacrolimus AEs (in order of prevalence)

A
  1. diarrhea, nausea
  2. nephrotoxicity
  3. tremor, HA
  4. insomnia
  5. hyperglycemia, hyperlipidemia, HTN
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18
Q

drugs that inhibit 3A4 and p-gp for CNIs

A

*inc trough, inc AUC
- CCB: verapamil, nicardipine
- antifungals: fluconazole
- antibiotics: clarithromycin, erythromycin
- protease inhibitors: indinavir, ritonavir, boceprevir
- gastric acid suppressors: omeprazole, antacids
- grapefruit juice –> naringin in large amounts

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19
Q

drugs that induce 3A4 and p-gp for CNIs

A

*dec trough, dec AUC
- antibiotics: rifampin, nafcillin, rifabutin
- antifungal: caspofungin, terbinafine
- anticonvulsants: carbamazepine, oxcarbazepine, phenobarbital, phenytoin
- others: octreotide, ticlopidine, orlistat
- herbals: St. John’s wart, Echinacea

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20
Q

types of mycophenolic acid

A
  • mycophenolate mofetil (MMF)
  • mycophenolic acid sodium (MPS)
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21
Q

which MPA has less GI AE

A

MPS

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22
Q

which MPA is a pro drug

A

MMF

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23
Q

which MPA is regular release? delayed release?

A

regular: MMF
delayed: MPS

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24
Q

MPA dose comparison

A

1000mg MMF (prodrug) = 720mg MPS (active) (either the brand or generic)

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25
Q

which drugs do you do TDM for?

A
  • CNI !
  • MPA - controversial, only use if AEs or monitoring compliance
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26
Q

short-acting glucocorticoids

A
  • cortisone (pro-drug)
  • hydrocortisone
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27
Q

intermediate-acting glucocorticoids

A
  • prednisone (pro-drug)
  • prednisolone
  • triamcinolone
  • methylprednisolone
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28
Q

long-acting glucocorticoids

A
  • dexamethasone
  • betamethasone
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29
Q

equivalent glucocorticoid doses

A

cortisone: 25mg
hydrocortisone: 20mg
prednisone: 5mg
methylprednisolone: 4mg
dexamethasone: 0.75mg

**potency

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30
Q

best glucocorticoid dosing

A

one AM dose

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31
Q

glucocorticoid AEs

A

(steroids)
- striae
- ecchymoses (bruise really easily)
- avascular necrosis
- cataracts
- changes in behavior, cognition, memory

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32
Q

itraconazole DDI with CNIs

A

inhibit 3A4 and pgp -> inc CNI AUC

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33
Q

verapamil DDI with CNIs

A

inhibit 3A4 and pgp -> inc CNI AUC

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34
Q

ritonavir DDI with CNIs

A

inhibit 3A4 and pgp -> inc CNI AUC

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35
Q

phenytoin DDI with CNIs

A

induce 3A4 and pgp -> dec CNI AUC

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36
Q

cyclosporine DDI with MPA

A

dec EHC -> dec conversion of MPAG to MPA -> dec MPA AUC

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37
Q

prednisone AEs

A
  • hyperlipidemia
  • hyperglycemia
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38
Q

MPA AEs

A
  • vomiting
  • diarrhea
  • leukopenia
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39
Q

thymoglobulin is what type of immunosuppressant?

A

depleting induction therapy

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40
Q

alemtuzumab is what type of immunosuppressant?

A

depleting induction therapy

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41
Q

IL-2 receptor blockers (basiliximab, daclizumab) are what type of immunosuppressant?

A

non-depleting induction therapy

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42
Q

thymoglobulin MoA

A

polyclonal Ab

block CD2, CD3, CD4, and CD8 -> T cell depletion -> prevent lymphocyte activation and proliferation against allograft

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43
Q

after a SOT, a patient is considered…

A
  • immunocompromised
    AND
  • having secondary immunodeficiency due to immunosuppressive drugs
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44
Q

types of cytokines

A
  • pro-inflammatory
  • regulatory
  • hematopoietic growth factors, colony stimulating factors (CSF)
  • interferons
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45
Q

1) pro-inflammatory cytokines

A
  • IL-1
  • TNF
  • CSF
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46
Q

2) regulatory cytokines –> up or down regulate immune activity

A
  • interleukins (IL-1, IL-2, IL-4, IL-6, IL-12)
  • tumor necrosis factor (TNF-alpha, TNF-beta)
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47
Q

3) hematopoietic growth factors or CSFs

A
  • granulocyte CSF (G-CSF)
  • granulocyte-monocyte CSF (GM-CSF)
  • erythropoietin (RBC CSF)
  • IL-3 multi-lineage CSF
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48
Q

4) interferon

A
  • IFN-alpha
  • IFN-beta
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49
Q

interferon

A

inhibits viral replication, released by our immune cells to protect others

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50
Q

IL-1

A

source: macrophage, fibroblast, endothelial cell

action:
- activate T and B cells
- hematopoietic growth factor
- induce inflammation

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51
Q

IL-2

A

source: CD4+ TH1 cells

action: activate T, B, and NK cells

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52
Q

IL-4

A

source: CD4+ TH2 cells, mast cells, basophils, eosinophils

action:
- B and T cell growth factor
- activate macrophage
- inc IgE
- bone marrow precursor proliferation

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53
Q

IL-6

A

source: CD4+ TH2 cells, macrophages, mast cells, fibroblasts

action:
- B and T cell growth factor
- hematopoietic growth factor
- inc inflammation

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54
Q

TNF-alpha

A

source: macrophages, NK cells, T cells, B cells, mast cells

action:
- activate neutrophils, endothelial cells, lymphocytes, liver cells -> produce acute phase proteins/reactants

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55
Q

TNF-beta

A

source: T cells

action:
- destroy tumor cells

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56
Q

IFN-alpha

A

source: monocytes

action:
- antiviral
- activate NK cells, macrophages
- upregulate MHC I

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57
Q

IFN-gamma

A

source: T cells, NK cells

action:
- activate macrophage, NK cells
- upregulate MHC I and II

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58
Q

what is a immunoglobulin

A

antibody

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59
Q

GM-CSF inc

A

neutrophils AND monocytes

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60
Q

G-CSG inc

A

neutrophils ONLY

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61
Q

GM-CSF AE

A

fever, diarrhea

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62
Q

which G-CSF is peglyated

A

Neulasta –> dec AE

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63
Q

functions of endogenous antibodies

A
  • activate complement
  • cause opsonization of antigen (in order to digest it)
  • directly neutralize virus or toxin
  • AB dependent cytotoxicity of cell –> prime antigen and cause destruction (via phagocytosis bc antigen is attached to phagocyte and binds microbe)
  • direct antimicrobial action –> generates oxidants
  • reduce damage of inflammation for host
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64
Q

which immunoglobulin(s) crosses the placenta and therefore protects fetuses?

A

IgG

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65
Q

which immunoglobulins fix complement

A

IgM, IgG

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66
Q

limitations of MoAb

A
  • limited production
  • antigenic modulation
  • chronic impact on immune system –> can inc infections, cancer
  • HAMA reactions
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67
Q

primary (congenital) immunodeficiency

A

genetic defects resulting in impaired maturation or function of immune system components
- ex: severe combined immunodeficiency (SCID)

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68
Q

SCID

A

severe combined immunodeficiency
- defects in T or B cell functions and maturation

a primary immunodeficiency (congenital)

68
Q

SCID

A

severe combined immunodeficiency
- defects in T or B cell functions and maturation

a primary immunodeficiency (congenital)

68
Q

SCID

A

severe combined immunodeficiency
- defects in T or B cell functions and maturation

a primary immunodeficiency (congenital)

69
Q

secondary (acquired) immunodeficiency

A

non-genetic and acquired over lifetime

70
Q

causes of secondary immunodeficiency

A

developed countries: cancer, anti-neoplastic therapy, irradiation, IMMUNOSUPPRESSION THERAPY

developing countries: environment, malnutrition, advanced age, chronic diseases

71
Q

what are the clinical risks of neutropenia?

A

inc in opportunistic infections

72
Q

cluster of determination definition

A

a classification of lymphocytes based on the specific cell surface markers and the number of sites
- use to monitor: AIDS, leukemia, SOT, SLE, bone marrow transplant

73
Q

CD3

A

all T lymphocytes (helper and cytotoxic)

74
Q

CD4

A

helper T lymphocytes, either TH1 or TH2

75
Q

CD8

A

cytotoxic/suppressor T lymphocytes

76
Q

CD20

A

B lymphocytes

77
Q

CD25

A

activated T lymphocytes, B lymphocytes, IL-2 receptor chain (Tac)

78
Q

CD56

A

NK cells

79
Q

deficiency in the immunes system can…

A

inc infection risk

80
Q

how to measure CELL MEDIATED (T cell) immunocompetency

A

measure cell mediated immunity and T lymphocytes
*intradermal administration of common recall antigens

81
Q

common recall antigens

A
  • candida albicans
  • mumps
  • tuberculin (PPD)
  • trichophyton
82
Q

cylex immune cell assay

A

measures suppression of CD4 lymphocytes

83
Q

total immunoglobulins (Ig) measure

A

measures B cell function via serum protein electrophoresis (SPEP)
- primary or secondary immunodeficiencies
- measures: IgG, IgM, IgG, IgE, IgD

if IgM –> active infection
if IgG –> later/memory Ag, therefore hepatitis

84
Q

complement system measures

A

humoral response -> AG lysing, opsonization

85
Q

SOT rejection mediated by

A

T-cells (cell mediated)

86
Q

another name for self-antigens

A

auto-antigens

87
Q

immunologic tolerance

A

state in which an individual is incapable of developing an immune response to a specific antigen
**good –> stops us from reacting to all antigens

88
Q

self-tolerance

A

lack of responsiveness to an individual’s own body antigens
**good –> needed to allow us to not attack our own cells and tissues

89
Q

systemic lupus erythematosus presentation and MoA

A
  • autoimmune disorder; autoantibodies against nucleic acid, erythrocytes, coagulation proteins, lymphocytes, platelets
  • inc in women, 15-45yrs
  • complement activated, AG-AB complexes formed and deposited in organs of vasculature system
  • chronic and acute inflammation
  • due to reduced suppression of immune system B cells
  • butterfly rash
90
Q

discoid lupus erythematosus

A

severe inflammation, scarring, rashes on face scalp ears –> butterfly rash

91
Q

SLE treatment

A

belimumab (Benlysta)
- B cell depletion –> balances out the upregulated/overactive B cell production in SLE

92
Q

which cytokine receptor can inc or dec immune activity and is the concept for RA drug therapy

A

soluble cytokine receptors

93
Q

basic classifications of hypersensitivies

A

adaptive immunity:
- humoral:
type I: immediate (anaphylactic)
type II: cytotoxic
type III: immune complex mediated
- cell mediated:
type IV: cell mediated

94
Q

allergy

A

immunologic responses to environmental or endogenous antigens that can result in disease or hypersensitivity and be clinically harmful

95
Q

autoimmunity

A

disturbance in immunologic tolerance –> initiates a response against auto-antigens

could also say a disturbance with self-tolerance

96
Q

alloimmuntiy

A

immune system of host mounts immunologic response to tissue of another individual
- transplant, transfusion

97
Q

clinical features of hypersensitives (allergic drug reactions)

A
  • no correlation with pharmacologic properties (not due to the drug’s MoA)
  • requires an induction period on primary exposure (will not happen on the first interaction with the drug)
  • occurs with doses below therapeutic range
  • small proportion of population
  • disappears when therapy stops, reappears when small doses of structurally similar therapy starts
  • may be able to desensitize
98
Q

predisposing factors to hypersensitivity reactions

A
  • female, adult
  • Hx of asthma, allergic rhinitis, atopic dermatitis –> may be more severe than other patients
  • AIDS, Epstein-Barr, lymphocytic leukemia
  • previous allergy to similar drugs
  • topical drug administration –> greatest sensitization risk vs oral is least
99
Q

onset of hypersensitivity depends on

A
  • original immunologic insult -> prevention, follow up treatment
  • genetics -> predisposition or not
  • specific immunologic reaction –> chronic vs acute, any remaining consequences
  • host risk factors –> primary immunodeficiency, secondary immunodeficiency
100
Q

immunodeficient patients are more/less at risk for hypersensitivity reactions

A

more

101
Q

secondary immunodeficiency causes

A
  • immunosuppressive therapy
  • irradiation
  • chronic diseases: CKD, liver disease, cancer, transplantatio, SLE
  • malnutrition
102
Q

components of a detailed drug history

A
  • prior allergic and medication encounters
  • nature/severity of reaction
  • other medical problems
  • temporal relationship between drug and reaction (dose, date, duration, time, treatment)
  • prior exposure of same or structurally related medications after reaction
  • effect of drug discontinuation –> if it lingered maybe more of a disease than a hypersensitivity
  • treatment response
  • prior diagnostic testing or re-challeneg
  • route of administration
  • preservatives or additives in the formulation
103
Q

anaphylaxis presentation

A
  • respiratory depression
  • laryngeal edema
  • hypotension
  • cardiovascular collapse
104
Q

allergen

A

an immunogen (antigen) that results in an allergic reaction

105
Q

atopic allergies

A

genetic tendency to develop allergic diseases –> includes atopy

106
Q

atopy

A

heightened immune responses to common allergens; conditions include:
- asthma and allergic
- food allergies
- specific drugs
- insect venom

107
Q

if penicillin allergy, avoid

A

carbapenems

108
Q

if aminopenicillin (amoxicillin, ampicillin) allergy, avoid

A
  • cefadroxil
  • cephalexin
  • cefaclor
  • cefprozil
109
Q

if penicillin allergy, can use

A

aztreonam

110
Q

which drugs can you use desensitization for

A

penicillin, co-trimoxazole

111
Q

which antibodies mediate type i hypersensitivies

A

IgE

112
Q

which antibodies mediate type ii and iii hypersensitivies

A

IgG

113
Q

which hypersensitive can impact the fetus?

A

ii and iii bc only IgG can cross placenta!

114
Q

symptoms of hemolytic anemia of newborn

A
  • hemolytic anemia (bilirubin inc, jaundice)
  • high output HF (death)
  • enlarged liver and spleen
  • generalized swelling
  • impaired platelets (petechial (facial) hemorrhaging)
115
Q

minimal organ involvement

A

drug induced lupus (iii)

116
Q

elevated ANA titer, SS-DNA, ESR

A

drug induced lupus (iii)

117
Q

serum sickness

A

iii
- generalized reaction
- exogenous antigen

118
Q

drug-induced lupus

A

iii
- endogenous antigen

119
Q

arthus reaction

A

iii
- localized reaction

120
Q

agents that cause acute serum sickness

A
  • animal serums (polyclonal antibodies)
  • bee venom injections
  • cefaclor
  • ciprofloxacin
  • insulin from animal sources
  • iron dextran
  • IVIG
  • MoAB
  • penicillins
  • sulfonamides
121
Q

causes of anergy

A
  • elderly
  • severe debility
  • disseminated TB (spread throughout body)
  • HIV
  • IMMUNOSUPPRESSIVE TREATMENT
  • glucocorticoid therapy
  • recent viral infection
  • immunization
122
Q

anergy

A

absence of CELL MEDIATED immune response

123
Q

number one cause of SJS or TENS

A

drugs!

4-12 days after exposure!!!

124
Q

drug causes of SJS or TENS

A
  • sulfa drugs: cotrimoxazole, sulfasalazine
  • other antibiotics: aminopenicillins, fluoroquinolone, cephalosporins
  • anti-epileptics: phenytoin, carbamazepine, phenobarbital, valproate, lamotrigine
  • other drugs: piroxicam, allopurinol
125
Q

SJS

A

less than 10%

126
Q

TEN

A

greater than 30%

127
Q

SJS/TEN

A

15-30%

128
Q

how long does it take for AGEP to develop

A

3 weeks after exposure

129
Q

most frequent drug causes of AGEP

A
  • aminopenicillins
  • sulphonamides
  • quinolone
  • hydroxychloroquine
  • terbinafin
  • diltiazem
130
Q

drug induced fever mostly caused by

A

biologics –> therefore need pre-treatment to prevent!!

131
Q

immunosuppressive drug monitoring

A
  • patient risk factors
  • drug PK (exposure, …)
  • graft function
  • drug PD (outcomes, AEs)
  • pharmacogenomics
132
Q

secondary (acquired) immunodeficiency (SAID)

A

immune system deficiencies acquired throughout life that are NOT due to genetic/congenital immune disorders

133
Q

SAID risks

A
  • inc typical and opportunistic infection –> more severe
  • inc in risk of tumors –> remove immunosurveilance of atypical cells that could become cancers
134
Q

common causes of SAID and mechanism of cause

A
  • HIV infection –> deplete CD4 cells
  • irradiation and chemo –> dec bone marrow leukocyte precursors
  • IMMUNOSUPPRESION FOR GRAFT REJECTION AND INFLAMMATORY DISEASES –> deplete or functionally impair lymphocytes
  • bone marrow cancers –> reduce site of leukocyte development
  • protein-calorie malnutrition –> inhibit lymphocyte maturation and function
  • spleen removal –> dec phagocytosis of microbes
135
Q

what to check when taking labs for TDM

A
  • compliance
  • dose
  • exact timing of last dose

**PATIENT CANNOT TAKE MEDS THE MORNING OF GETTING LABS DRAWN –> bc is then a peak not a trough!!!

136
Q

CNI MoA

A

inhibit calcineurin –> prevent signal 1 –> prevent cell DNA proliferation for replication of T cell

137
Q

MPA MoA

A

interfere with T cell nucleotide synthesis –> prevent more T and B cells from being committed and proliferating and therefore attacking graft
- anti-proliferative drug

138
Q

post-transplant induction and start of maintenance therapy CNI dosing

A

AVOID FULL DOSES
- cause renal vasoconstriction and slower function of renal graft –> not good immediately post transplant

139
Q

induction therapy overall strategy/MoA

A

block T cell, or other immunologic, activation at the time of graft placement

140
Q

induction therapy advantages

A
  • improve early graft function
  • prevent graft rejection
  • improve graft survival
141
Q

induction therapy disadvantages

A
  • inc cost
  • inc risk of cytomegalovirus (CMV)
  • inc risk of post-transplantation lymphoproliferative disease (PTLD) –> bc dec immunosurveillance of atypical cells
142
Q

factors affecting CNI PK

A
  • fat content in meals
  • time post-transplant –> early post transplant = inc absorption
  • type of organ transplant
  • compromised GI function –> diarrhea dec absorption
  • bioavailability of dosage forms -> generally low
  • DDIs
143
Q

which CNI more potent

A

TAC

144
Q

which CNI more F

A

CYA

145
Q

which CNI longer half life

A

TAC

146
Q

IR TAC

A

Prograf

147
Q

ER TAC

A

Astagraf XL
Envarsus

148
Q

IV TAC

A

IV Prograf

149
Q

oral CYA

A

modified:
Neoral
Gengraf

non-modified:
Sandimmune

150
Q

IV CYA

A

non-modified:
Sandimmune

151
Q

which MPA is a prodrug

A

CellCept (MMF)

152
Q

which MPA is regular release

A

CellCept (MMF)

153
Q

which MPA is enteric coated

A

Myfortic (EC-MPS)

154
Q

which MPA is delayed release

A

Myfortic (EC-MPS)

155
Q

MMF:MPS dose ratio

A

1000mg MMF : 720mg MPS
prodrug : active

156
Q

nephrotoxicity, think

A

CNI

157
Q

severe GI side effects, think

A

MPA

158
Q

MPA DDIs that dec MPA AUC due to EHC

A
  • CYA
  • cholestyramine, bile and resins
  • antibiotics (norfloxacin metronidazole, cipro, augmentin, rifampin)
159
Q

MPA DDIs that inc MPA AUC due to EHC

A
  • TAC
160
Q

factors impacting MPA PK

A
  • time after transplant
  • DDIs
  • EHC –> concurrent CNI effects
  • other disease states –> adjust for renal dosing
  • food
  • ethnicity
  • genetic polymorphisms
161
Q

post transplant complications

A

post-transplant…
- HTN
- opportunistic infections
- DM
- HLD
- osteoporosis
- lymphoproliferative disorder (dec immunosurveillance)

162
Q

glucocorticoid DDIs: inhibit gluco –> inc AUC

A
  • oral contraceptives
  • estorgens
  • macrolide antibiotics (erythromycin, clarithromycin)
  • ketoconazole
  • isonazid
  • naproxen
  • CYA
163
Q

glucocorticoid DDIs: inc hypoK

A
  • diuretic
  • amphotericin B
164
Q

glucocorticoid DDI: induce gluco –> dec AUC

A
  • phenytoin
  • phenobarbital
  • rifampin
  • carbamazepine
  • edphedrin
165
Q

glucocorticoid DDI: drugs that gluco induces their metabolism –> dec these drug AUCs

A
  • CYA
  • TAC
  • MPA
166
Q

glucocorticoid DDIs: dec steroid absorption –> dec AUC of gluco

A
  • cholestyramine
  • antacids
167
Q

glucocorticoid AEs

A
  • striae
  • ecchymoses
  • avascular necrosis
  • cushings –> adrenal atrophy
  • dyslipidemia
  • change in behavior, cognition
  • GI bleed, ulcer
  • delayed wound healing
  • bone necrosis
  • cataracts
  • glaucoma
  • hyperglycemia
  • HLD
  • child growth suppression

p2 year (9 decks)

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