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Therapeutics > Immunology > Flashcards

Immunology Flashcards

1
Q

agents that have capacity for both positive and negative actions

A

immunomodulator

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2
Q

stimulate the immune response

A

immunostimulant

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3
Q

most effective when used in combination with antigen administration

A

immunoadjuvants

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4
Q

substances which have the ability to attenuate the immune response

A

immunosuppressants

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5
Q

CSFs, interleukins, interferons, MDP, potent immunopharmacology

A

biological response modifiers

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6
Q

boosts a failing immune system

A

immunopotentiator

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7
Q

mediators of the immune response with pro-inflammatory, regulator, CSF/hematopoietic growth factors, or interferon activity

A

cytokines

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8
Q

make up 50-60% of WBC, first to respond

A

neutrophils

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9
Q

two leukocytes that act as an antigen presenting cell

A

macrophages, monocytes

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10
Q

first line of defense that is nonspecific, has no memory, and it an immediate defense

A

innate immunity

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11
Q

delayed but amplified immune reaction with specific memory

A

adaptive immunity

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12
Q

lymphocytes make up what % if WBC

A

25-35%

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13
Q

cells responsible for humoral immunity

A

B-lymphocytes

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14
Q

B-lymphocyte role

A

Ab production

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15
Q

what can Ab do?

A

activate complement
facilitate opsonization
neutralize viruses
cytotoxicity of cells
direct antimicrobial action
reduce damage of inflammation

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16
Q

cells responsible for cell mediated immunity

A

T-lymphocytes
CD8+ killer, CD4+ helper

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17
Q

active naturally acquired

A

Ag enters body, body induces Ab
ex) infection

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18
Q

passive naturally acquired

A

IgG Ab pass from mother to fetus

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19
Q

active artificially acquired

A

Ag introduced in vaccines, body produces Ab

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20
Q

passive artificially acquired

A

pre-formed Ab in immune serum introduced by injection (immunoglobulins)

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21
Q

genetic defects resulting in impaired function of the immune system

A

primary immunodeficiency

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22
Q

non-genetic and acquired over lifetime (ex. transplant patient)

A

secondary immunodeficiency

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23
Q

diseases caused by the bod’s immune system initiating an immune reaction against self antigens or auto antigens

A

autoimmune disease

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24
Q

human GM-CSF that exhibits a dose dependent increase in production of neutrophils and monocytes and may improve their function

A

Sargramostim (Leukine)

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25
Q

Leukine uses

A

myelosuppressive chemotherapy, bone marrow transplant, myelodysplastic syndromes, HIV, chemotherapy induced neutropenia

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26
Q

AEs of Leukine

A

fever, diarrhea, NV, malaise, weakness, chills, headache, rash

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27
Q

exogenous G-CSF that increases nadir neutrophil counts

A

FIlgrastim (Neupogen), Pegfilgrastim (Neulasta)

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28
Q

uses for neupogen/neulasta

A

bone marrow transplant, myelodysplastic syndromes, HIV, chemotherapy induced neutropenia

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29
Q

AEs of neupogen/neulasta

A

bone pain, NV, marked leukocytosis, increased uric acid, hypersensitivity reactions

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30
Q

exogenous CSF that acts like endogenous EPO and stimulates erythroid progenitors in bone marrow to differentiate and mature into RBCs

A

Epoetin-Alfa (Procrit), Darbepoetin Alfa (Aranesp)

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31
Q

AEs of epo-A

A

HTN, fever, NV, headache, rash, itching, joint aches, cough

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32
Q

recombinant human interferon that induces the innate antiviral immune response and inhibits viral replication of virus infection cells, suppresses cell cycle progression, and induces apoptosis

A

peginterferon alfa-2a (Pegasys), Peginterferon Alfa-2b (Pegintron)

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33
Q

uses for pegasys/pegintron

A

hepatitis C

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34
Q

AEs of pegasys/pegintron

A

bone pain, myalgia, HA, fatigue, fever, neutropenia

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35
Q

IVIG containing pooled IgG Ab used for primary immunodeficiency or idiopathic thrombocytopenia purpura

A

Gammagard S/D, Gamunex, Ocagam

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36
Q

AEs of gammagard

A

myalgia, arthralgia, NV

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37
Q

what is human anti-mouse antibodies (HAMA) reaction?

A

hypersensitivity to the source of Ab in a MoAb

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38
Q

agents that modify activity of TNF-a to reduce inflammation

A

etanercept (enbrel), infliximab (remicade), adalimumab

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39
Q

rapidly developing reaction mediated by IgE Ab release following Ag exposure

40
Q

cells involved in type 1

A

IgE Ab, macrophage, T helper, B lymphocytes, plasma cells, mast cells, basophils, histamines

41
Q

agents used for anaphylaxis (immediate vs late phase)

A

immediate: epinephrine
late: diphenhydramine, IV glucocorticoid (dose taper), anti H2 receptor blocker

42
Q

gradual increased doses of a drug over time to develop tolerance

A

desensitization

43
Q

IgG mediated tissue specific reaction where the Ag on the target cell bind directly with the Ab resulting in cellular function reduction or destruction

44
Q

agent used to prevent sensitization of a negative mother with a RH0(D) positive fetus

45
Q

induced by formation of Ab-Ag complexes that form in circulation and deposit into organs or blood vessels, causing tissue damage (IgG) (complement is activated)

46
Q

examples of type 3 reactions

A

serum sickness, arthus reaction, drug induced lupus

47
Q

type 3 reaction that occurs 5-10 days after exposure to an Ag (common causes bee venom, insulin, vaccines, penicillins, animal serums)

A

serum sickness

48
Q

serum sickness symptoms

A

fever, swollen lymph nodes, arthralgias, dermatitis, vasculitis

49
Q

symptoms of drug induced lupus

A

arthralgia, fever, malaise, minimal organ involvement

50
Q

cell mediated reaction classified into types A-D based on T cell effector mechanism
reexposure to an Ag leads to cell death

51
Q

examples of type 4 reactions

A

contact dermatitis, TB test, SJS, TEN, AGEP

52
Q

contact dermatitis treatments

A

topical steroids
oral antihistamines
topical immunomodulators
systemic steroids

53
Q

absence of a cell mediated immune response

54
Q

drugs commonly cause which type 4 reactions

A

SJS, TEN, sometimes AGEP

55
Q

some drugs that may cause SJS/TEN

A

sulfa drugs, other antibiotics (cephalosporins, fluoroquinolones), anti-epileptics, etc.

56
Q

early and more intense immunosuppression initiated just prior to and during the acute transplant period to prevent the organ rejection process

57
Q

long term or chronic immunosuppressive used to achieve less intense suppression on the immune system over a longer duration for prophylaxis against rejection

A

maintenance immunosuppression

58
Q

what combination of agents are used for maintenance immunosuppression>

A

TAC/CYA + MMF/MPS + PRED

-note tacrolimus is most common, low dose prednisone is used

59
Q

what time interval should maintenance doses be given at, which is best for trough measurement?

A

BID every 12 hours

60
Q

depleting induction agent, polyclonal Ab that opsonize the hosts T cells which are then destroyed by the complement system

A

anti-thymocyte globulin (ATG)

61
Q

side effects of anti-thymocyte globulin

A

flu-like symptoms (cytokine release syndrome), leukopenia, lymphopenia, thrombocytopenia, pruritis, erythema, serum sickness

62
Q

depleting induction agent, MoAb that acts against CD52 surface Ag on mature lymphocytes, leading to B and T cell death

A

alemtuzumab (campath)

63
Q

what additional medications need to be given with campath?

A

-premedicate with IV methylprednisolone
-anti-infective prophylaxis should be given for 2 months or until CD4 counts rise

64
Q

side effects of campath

A

NV, diarrhea, HAMA, fever, rigors, lymphopenia, thrombocytopenia, neutropenia, increased risk of malignancy/infection/autoimmune reactions

65
Q

non-depleting induction agents (2), MoAb IL-2 receptor blockers that act against CD25 to prevent T lymphocyte proliferation since the IL-2 receptor will be resistant to stimulation

best for low risk patients

A

basiliximab (simulect), daclizumab (zenapax)

66
Q

block calcineurin from being released and recognized by the nucleus (signal 1)

A

calcineurin inhibitors
tacrolimus and cyclosporine

67
Q

brand names for cyclosporine

A

neoral, gengraf, sandimmune

68
Q

side effects of cyclosporine

A

hyperlipidemia, nephrotoxicity, tremor, headache, hypertension, hyperglycemia, gingival hyperplasia, hirsutism, diarrhea, vomiting

69
Q

brand names for tacrolimus (IR and ER)

A

IR: prograf
ER: astagraf XL, envarsus, IV prograf

70
Q

drug interactions with CNIs (inhibit 3A4 and P-gp, so higher trough and AUC)

A

 CCBs: diltiazem, verapamil, nicardipine.
 Antifungals: itraconazole, posaconazole, ketoconazole, fluconazole.
 Antibiotics: clarithromycin, erythromycin, quinupristin.
 Protease inhibitors: indinavir, ritonavir, nelfinavir, boceprevir.
 Gastric acid suppressors: lansoprazole, omeprazole, cimetidine, anatacids.
 GFJ (naringin in high amounts).

71
Q

drug interactions with CNIs (induce 3A4 and P-gp, so lower trough and AUC)

A

 Antibiotics: nafcillin, rifampin, rifabutin.
 Antifungals: caspofungin, terbinafine.
 Anticonvulsants: carbamazepine, oxcarbazepine, phenobarbital, phenytoin.
 Herbals: St. John’s Wort, echinacea.

72
Q

what info is important to obtain from a patient when measuring trough concentrations?

A

-timing of prior 24-48 hours of dosages
-exact time concentration was collected relative to patient’s dosing
-exact dosing regimen
-is the dosing of the drug at steady state?

73
Q

side effects of tacrolimus

A

diarrhea, nausea, nephrotoxicity, tremor, headache, insomnia, hyperglycemia, hyperlipidemia, hypertension

74
Q

dosing conversion between Prograf and Astagraf XL

**NOT INTERCHANGEABLE

A

1 mg ER = 1 mg IR

75
Q

ester prodrug, regular release MPA

A

mycophenolate mofetil/CellCept (MMF)

76
Q

sodium salt, delayed release MPA

A

mycophenolic acid sodium/Myfortic (MPS)

77
Q

drug interactions with MPA

A

acyclovir, ganciclovir, co-trimoxazole, COCs, phenytoin, aspirin, glucocorticoids, cholestyramine/bile acid resins, some antibiotics

78
Q

side effects of MPA

A

-GI- NV, diarrhea, dyspepsia- all more with TAC
-Hematologic- leukopenia, neutropenia, anemia, thrombocytopenia
-Opportunistic infections
-CNS- dizziness, insomnia, HA
-CV

79
Q

dose conversion between CellCept (MMF) and Myfortic (MPS)

A

1000 mg CellCept = 720 mg Myfortic

80
Q

drug interactions with glucocorticoids

A

o Metabolic inhibition of GCs (more effect): OCs, CEs, macrolide antibiotics, ketoconazole, isoniazid, naproxen, cyclosporine.
o Metabolic induction of GCs (less effect): phenytoin, phenobarbital, rifampin, carbamazepine, ephedrine.
o Induction by GCs: tacrolimus, cyclosporine, mycophenolic acid.
o Decrease absorption: cholestyramine, antibiotics.
o Enhanced hypokalemia: diuretics, amphotericin B.

81
Q

side effects of glucocorticoids

A

axillary and lower abdominal striae, steroid induced avascular necrosis, ecchymoses
-also note tissue specific AEs

82
Q

what is best for dosing and discontinuing glucocorticoids?

A

single AM dose (circadian rhythm)
dose taper needed to D/C

83
Q

short acting glucocorticoids

A

cortisone, hydrocortisone

84
Q

intermediate acting glucocorticoids

A

prednisone, prednisolone, triamcinolone, methylprednisolone

85
Q

long acting glucocorticoids

A

dexamethasone, betamethasone

86
Q

rank of anti-inflammatory effects of glucocorticoids (high to low)

A

long acting agents > intermediate&raquo_space; short acting (0 effect)

87
Q

rank of mineralocorticoid effects of glucocorticoids (high to low)

A

short acting > prednisone + prednisolone&raquo_space; triamcinolone, methylprednisolone, long acting agents (0 effect)

88
Q

equivalent doses of short acting glucocorticoids

A

cortisone- 25
hydrocortisone- 20

89
Q

equivalent doses of intermediate acting glucocorticoids

A

prednisone- 5
prednisolone- 5
triamcinolone- 4
methylprednisolone- 4

90
Q

equivalent doses of long acting glucocorticoids

A

dexamethasone- 0.75
betamethasone- 0.6

91
Q

drugs for prophylaxis- oral candidiasis

A

fluconazole, clotrimazole, nystatin suspension

92
Q

drugs for prophylaxis- pneumonia

A

trimethoprim/sulfamethoxazole (bactrim, cotrimoxazole), dapsone, pentamidine, atovaquone

93
Q

drugs for prophylaxis- cytomegalovirus (gastroenteritis, colitis, pneumonitis, retinitis, viremia)

A

ganciclovir/valganciclovir, acyclovir/valacyclovir

94
Q

drugs for prophylaxis- UTI

A

bactrim, ciprofloxacin

95
Q

signs of acute graft rejection

A

normal or low CNI trough
fever, HTN, weight gain, rapid rise in SCr, graft swelling
kidney biopsy for diagnosis

96
Q

signs of CNI nephrotoxicity

A

increased CNI trough
increased K, uric acid, decreased Mg
HTN, no temperature rise, normal urine production
CNS toxicities (flushing, tingling extremities, tremor, confusion)

Therapeutics (31 decks)

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