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Immunology And Infectious Diseases > Exam 1: Immunology, Hypersensitivity, SOT, Immunosuppression > Flashcards

Exam 1: Immunology, Hypersensitivity, SOT, Immunosuppression Flashcards

1
Q

What is Polyclonal ABs?

A

ABs harvested from 1000 patients (animal or human) with various B cells. Increased risk of hypersensitivity reaction due to lack of purity/specificity.
Artificial Passive immunity.

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2
Q

What is an example of a Type I hypersensitivity?

A

Anaphylaxis

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3
Q

What immunoglobulin/cells mediate the anaphylactic reaction

A

IgE, B/plasma cells, macrophages

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4
Q

What is the IMMEDIATE treatment (Rx) for anaphylaxis?

A

Epinephrine 1:1000 IM/SQ every 15-20 mins until respiratory relief
Oxygen treatment

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5
Q

What is the LATE treatment (Rx) for anaphylaxis?

A

25-50 mg diphenhydramine (parenteral)
Anti-H2 receptor blocker (ie. Cimetidine, famotidine)
Hypotension = IV fluids
IV hydrocortisone to reduce recurrence risk

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6
Q

Penicillin Type 1 hypersensitivities are fairly common. What other class of drug should we be careful using? What overlapping element causes the cross reactivity?

A

Cephalosporines
The side chain moieties of the beta lactam cause reactivity

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7
Q

What is an example of complement-mediated lysis (type 2 hypersensitivity)?

A

ABO mismatched blood transfusion

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8
Q

What is an example of macrophage-mediated phagocytosis (type 2 hypersensitivity)? What immunoglobulin is this mediated by?

A

Erythroblastosis fetalis
From the IgG opsonization

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9
Q

When a mother is administered Rho-Gam, what is the Rh0D Ig actually doing?

A

Binds to the Rh0 positive RBCs of the fetus and protects them from the mother’s anti-Rh0 antibodies.

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10
Q

What is an example of and exogenous Ag-caused type 3 hypersensitivity? An endogenous Ag-caused T3 hypersensitivity?

A

Exogenous = Gluten allergy, Serum Sickness*
Endogenous = Drug-induced Lupus

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11
Q

What agents may cause serum sickness? (10)

A

Animal serums
Bee venom
Cefaclor
Insulin
Iron dextran
IV Ig
mAb
Penicillins
Sulfonamides

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12
Q

What drugs may cause Drug-Induced Lupus?

A

Hydralazine
Procainamide
Isoniazid
Quinidine
TNF-a inhibitors

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13
Q

What treatments (Rx) should be used for contact dermatitis?

A

Topical steroids (hydrocortisone)
Antihistamines
Topical immunomodulators (ie. TAC)
Systemic steroids (last line; many AEs)

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14
Q

How do we test for anergy when conducting a TST/Tuberculin PPD?

A

Do a control skin test (candida/mumps) - if either are positive, then no anergy

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15
Q

What are the cutoffs between TEN, SJS/TEN and SJS?

A

SJS = affects <10% body surface area
SJS/TEN = affects 15-30% body surface area
TEN = affects >30% body surface area

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16
Q

What drugs may cause SJS/TEN?

A

Sulfa drugs
Some antibiotics (ampicillin/amoxicillin, fluoroquinolones, cephalosporins)
Anti-epileptics
Etc: allopurinol, piroxicam

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17
Q

What subtype is SJS/TEN?

A

Type IV-C hypersensitivity

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18
Q

What non-Rxs may trigger SJS/TEN?

A

Infections
Viruses
Vaccines
Graft v Host disease

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19
Q

What is AGEP?

A

Type IV-D hypersensitivity
Rapid appearance of small pustules and erythema followed by desquamation of skin
Unclear physiology, 90% caused by drugs

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20
Q

What drugs cause “allergy-like” reactions?

A

Beta Lactams
Sulfonamides
Anticonvulsants
Additives (dyes, parabens)
Biological
Chemo agents
Aspirin/NSAIDS**

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21
Q

Name the 3 lymphocyte proliferation inhibitors

A

Mycophenolate Mofetil (MMF)
Mycophenalic Acid (MPS)
Azathioprine [older]

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22
Q

What are the 3 stages of immunosuppressive therapy?

A
  1. Induction
  2. Maintenance
  3. Rejection
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23
Q

Explain the pre-transplant Rx therapy regimen

A

One induction agent (depleting/non-depleting)
IV bolus methylprednisolone
Mycophenolic Acid dose (MMF/MPS)

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24
Q

Explain the post op INDUCTION (days 0-7) Rx therapy regimen

A
  • A few doses induction agent (depleting/non-depleting) then D/C
  • IV methylprednisolone —> convert to ORAL prednisone taper
  • Mycophenolic Acid dosing
  • Initiate low dose CNI
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25
Q

Explain the maintenance therapy regimen (SOT)

A
  • Mycophenolic acid dosing
  • CNI dose continuously titrated by TDM
  • Prednisone taper cont.

Monitor allograft function + AEs

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26
Q

What CNI+Steroid Taper is MOST COMMONLY used?

A

Tacrolimus + MMF/EC-MPS + Prednisone

(Can either use mycophenolate mofetil OR enteric coated Mycophenolic Sodium)

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27
Q

What 6 conditions cause secondary (acquired) immunodeficiency?

A

Spleen removal
HIV
Immunosuppressive for graft rejection**
Protein-calorie malnutrition
Radiation/chemotherapy
Bone marrow dysfunctional from cancers

“SHIP R&B”

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28
Q

What are the IMMEDIATE release Tacrolimus drugs? Can we substitute them out?

A

Prograf**
+ generics

NOT substitutable

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29
Q

What are the EXTENDED release Tacrolimus drugs? Can we substitute them out?

A

Astagraf XL**
Envarsus**
IV Prograf = continuous infusion

Not interchangeable/subtitutable

30
Q

What are the Cyclosporine drugs? Which two can we substitute with each other?

A

Neoral* [BID]
Gengraf* [BID]
Sandimmune (po) [QD]
Sandimmune IV [may cause anaphylaxis, last resort]

  • = modified CYA, MAY SUBSTITUTE
31
Q

What are the adverse effects of cyclosporine? (4 maj, 4 min)

A

Hyperlipidemia**
Nephrotoxicity**
Tremor, headache**
HTN**
Hyperglycemia
Gingival hyperplasia
Hirsutism
Diarrhea, vomiting

32
Q

What are the adverse effects of tacrolimus? (4 maj, 3 min)

A

Diarrhea, nausea**
Nephrotoxicity**
Tremor, headache**
Insomnia**
Hyperglycemia
Hyperlipidemia
HTN

(All minor ones start w “hyper”)

33
Q

CNIs are metabolized by CYP3A4s. What are some CYP3A4 INHIBITORS?

A

CCBs
Antifungals (-zole)
Antibiotics [clarithromycin, erythromycin]
Protease Inhibitors (-vir)
Gastric acid suppressors (PPIs, H2RAs, etc)
Grapefruit juice (naringin)

34
Q

CNIs are metabolized by CYP3A4s. What are some CYP3A4 INDUCERS?

A

Antibiotics [rifampin, rifabutin]
Antifungal [caspofungin]
Anticonvulsants [phenytoin, phenobarbital, carbamazepine, oxcarbazepine]
Herbals [St. John’s Wort]
Others = octreotide, orlistat

35
Q

Finish the phrases on CNI PK:
CYA and TAC exhibit _______ kinetics
______ concentration monitoring is state of practice

A

Linear kinetics
Trough

36
Q

Mycophenolate Mofetil is _____ release
Mycophenolic Acid Sodium is ______ release
Which is a prodrug? Can they be interchanged?

A

MMF = regular release, PRODRUG
MPS = delayed release

Not interchangeable

37
Q

What is the MOA for MPAs?

A

Mycophenolic acids inhibit enzyme IMPDH which interferes with the purine metabolism required for T lymphocyte proliferation.

38
Q

While not interchangable, what is the RATIO between MMF and EC-MPS? **

A

1000mg MMF : 720 mg EC-MPS

39
Q

How do some drugs have enterohepatic recirculation with MPAs? (4 drugs)

A

Cyclosporine = INHIBITS MRP2, reduces MPA AUC (MPA less effective)

Tacrolimus = minimal inhibition of MRP, lower daily dose needed for equal MPA effect (EHC)

Cholestyramine/Bile Acid Reducers = reduced MPA AUC

Antibiotics = reduced MPA AUC

40
Q

What drugs are renally cleared and thus interact with MPA?

A

Acyclovir
Ganciclovir
Co-trimoxazole

41
Q

How do COCs and MPA interact?

A

MPA decreases levonorgestrel AUC significantly

42
Q

MPA may alter the albumin binding of which 2 drugs?

A

Phenytoin
Aspirin

43
Q

Which drug class may increase MPA metabolism?

A

Glucocorticoids

44
Q

Name the adverse effects of mycophenolic acids?

A

GI: N/V, diarrhea, dyspepsia
Hematologic: leukopenia, neutropenia, anemia, thrombocytopenia
Opportunistic infections
CNS: dizziness, insomnia, headache
Cardiovascular

45
Q

What effect does glucocorticoid therapy have on the HPA axis?

A

As cortisol concentrations increase, it functions as a negative feedback on hypothalamic and pituitary hormones.

46
Q

What is the interchange ratio between prednisone and methylprednisolone?

A

5:4 (Prednisone:Methylprednisolone)

47
Q

What are some metabolic inhibitors of glucocorticoids? (6)

A

Macrolide antibiotics (erythromycin, clarithromycin)
Oral contraceptives
Conjugated estrogens
Ketoconazole
Naproxen
Isoniazid
Cyclosporine*

48
Q

What are some metabolic inducers of glucocorticoids? (5)

A

Phenytoin
Phenobarbital
Rifampin
Carbamazepine
Ephedrine

49
Q

What are some drugs that are metabolically inhibited BY glucocorticoids? (3)

A

Tacrolimus
Cyclosporine
MPA

50
Q

What two classes of drugs that decrease steroid absorption?

A

Cholestyramine
Antacids

51
Q

What are some long term adverse effects of glucocorticoids? (Many!)

A

Adrenal Gland: Adrenal Atrophy, **Cushing’s Syndrome
Cardiovascular System: Dyslipidemia, HTN, Thrombosis, Vasculitis
Central Nervous System: Changes in behavior, cognition, memory, and mood
Gastrointestinal System: GI Bleeding, Pancreatitis, Peptic Ulcer
Immune System: Broad Immunosuppression, Activation of Latent Viruses
Integument: delayed wound healing, striae, echimoses/easy bruising
Skeletal: Bone thinning, osteoporosis
Eyes: cataracts, glaucoma

52
Q

What are 6 post-transplant complications?

A

HTN
Opportunistic infections
Diabetes
Hyperlipidemia
Osteoporosis
Lymphoproliferative disorder

53
Q

What are the four goals of immunosuppressive Rx treatment?

A
  1. Suppress immune response
  2. Use a multiple drug regimen approach
  3. Use different MoA drugs
  4. Minimize long term drug related AEs
54
Q

What are the two depleting induction agents?

A

Anti-thymocyte globulin
Alemtuzumab

55
Q

How should anti-thymocyte globulin be administered?

A

IV infusion over 4-6 hours for 2-4 daily doses

56
Q

What are the two types of anti-thymocye globulin and what are the source animals?

A

ATGAM = horse Ab
Thymoglobulin = rabbit Ab

57
Q

What is an adverse effect from anti-thymocyte globulin treatment?

A

Flu-like symptoms (CYTOKINE RELEASE SYNDROME)

58
Q

Patients to receive anti-thymocyte globulin should be pre-medicated with…?

A

Diphenhydramine
APAP

59
Q

High risk patients should receive _________ induction therapy and low risk patients should receive ________ induction therapy post op.

A

High risk = depleting
Low risk = non-depleting

60
Q

What is the MoA for anti-thymocyte globulins?

A

Ab coat host T cells and destroy them

61
Q

Alemtuzumab is not FDA approved as a depleting inducing agent. What is it actually approved for?

A

Multiple sclerosis

62
Q

What cluster differentiation (CD) is targeted by Alemtuzumab Abs?

A

CD52

63
Q

What are the two dosing regimen options for Alemtuzumab?

A
  1. TWO doses x 0.3 mg/kg/dose
  2. 20-30 mg IV single dose over 2-3 hours
64
Q

What are some adverse effects of Alemtuzumab? (3)

A

Infusion-related reactions (HAMA)
GI disorders
Profound lymphopenia/neutropenia/thrombocytopenia

65
Q

What NON-DEPLETING induction agent drugs are there? What is it’s class + MoA?

A

IL-2 receptor blockers
Basiliximab = mAb binds to CD25 which prevents activation of T cell proliferation
[no depletion, only stopping proliferation]

Daclizumab (off-market)

66
Q

If a patient taking a CNI is above the target range (ie. CYA trough is 350 ng/mL when goal is 150<x<250) what should you do?

A
  1. Hold one dose
  2. Reduce the dosing regimen by 25-30%
  3. Repeat trough in ~24 hrs
67
Q

What is a Granulocyte-Monocyte CSF (GM-CSF)? What is one example of an Rx?

A

Causes a dose-dependent increase in the production of neutrophils and monocytes

Sargramostism

68
Q

What is a Granulocyte CSF (G-CSF)? What is one example of an Rx?

A

Increases neutrophil counts only

Filgrastim (Neupogen)
Pegfilgrastim (Neulasta)

69
Q

How do erythropoesis-stimulating agents (ESAs) like Epoetin-Alfa work?

A

Stimulates erythropoietin formation, which responds to low oxygen levels by increasing RBC production in bone marrow, thereby increasing the oxygen carrying capacity.

70
Q

Interferons are antiviral and growth inhibitors of malignant cells. What is Peginterferon Alfa-2a/b indicated for and why are pegylated interferons better?

A

Indicated for Hep C virus (HCV)

Pegylation improves PK and reduces dosing frequency. Also reduces adverse effects & increased sustained viral response.

71
Q

Is Alemtuzumab monoclonal or polyclonal?

A

Monoclonal!

Immunology And Infectious Diseases (7 decks)

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