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
Leukine uses
myelosuppressive chemotherapy, bone marrow transplant, myelodysplastic syndromes, HIV, chemotherapy induced neutropenia
26
AEs of Leukine
fever, diarrhea, NV, malaise, weakness, chills, headache, rash
27
exogenous G-CSF that increases nadir neutrophil counts
FIlgrastim (Neupogen), Pegfilgrastim (Neulasta)
28
uses for neupogen/neulasta
bone marrow transplant, myelodysplastic syndromes, HIV, chemotherapy induced neutropenia
29
AEs of neupogen/neulasta
bone pain, NV, marked leukocytosis, increased uric acid, hypersensitivity reactions
30
exogenous CSF that acts like endogenous EPO and stimulates erythroid progenitors in bone marrow to differentiate and mature into RBCs
Epoetin-Alfa (Procrit), Darbepoetin Alfa (Aranesp)
31
AEs of epo-A
HTN, fever, NV, headache, rash, itching, joint aches, cough
32
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
peginterferon alfa-2a (Pegasys), Peginterferon Alfa-2b (Pegintron)
33
uses for pegasys/pegintron
hepatitis C
34
AEs of pegasys/pegintron
bone pain, myalgia, HA, fatigue, fever, neutropenia
35
IVIG containing pooled IgG Ab used for primary immunodeficiency or idiopathic thrombocytopenia purpura
Gammagard S/D, Gamunex, Ocagam
36
AEs of gammagard
myalgia, arthralgia, NV
37
what is human anti-mouse antibodies (HAMA) reaction?
hypersensitivity to the source of Ab in a MoAb
38
agents that modify activity of TNF-a to reduce inflammation
etanercept (enbrel), infliximab (remicade), adalimumab
39
rapidly developing reaction mediated by IgE Ab release following Ag exposure
type 1
40
cells involved in type 1
IgE Ab, macrophage, T helper, B lymphocytes, plasma cells, mast cells, basophils, histamines
41
agents used for anaphylaxis (immediate vs late phase)
immediate: epinephrine late: diphenhydramine, IV glucocorticoid (dose taper), anti H2 receptor blocker
42
gradual increased doses of a drug over time to develop tolerance
desensitization
43
IgG mediated tissue specific reaction where the Ag on the target cell bind directly with the Ab resulting in cellular function reduction or destruction
type 2
44
agent used to prevent sensitization of a negative mother with a RH0(D) positive fetus
Rho-Gam
45
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)
type 3
46
examples of type 3 reactions
serum sickness, arthus reaction, drug induced lupus
47
type 3 reaction that occurs 5-10 days after exposure to an Ag (common causes bee venom, insulin, vaccines, penicillins, animal serums)
serum sickness
48
serum sickness symptoms
fever, swollen lymph nodes, arthralgias, dermatitis, vasculitis
49
symptoms of drug induced lupus
arthralgia, fever, malaise, minimal organ involvement
50
cell mediated reaction classified into types A-D based on T cell effector mechanism reexposure to an Ag leads to cell death
type 4
51
examples of type 4 reactions
contact dermatitis, TB test, SJS, TEN, AGEP
52
contact dermatitis treatments
topical steroids oral antihistamines topical immunomodulators systemic steroids
53
absence of a cell mediated immune response
anergy
54
drugs commonly cause which type 4 reactions
SJS, TEN, sometimes AGEP
55
some drugs that may cause SJS/TEN
sulfa drugs, other antibiotics (cephalosporins, fluoroquinolones), anti-epileptics, etc.
56
early and more intense immunosuppression initiated just prior to and during the acute transplant period to prevent the organ rejection process
induction
57
long term or chronic immunosuppressive used to achieve less intense suppression on the immune system over a longer duration for prophylaxis against rejection
maintenance immunosuppression
58
what combination of agents are used for maintenance immunosuppression>
TAC/CYA + MMF/MPS + PRED -note tacrolimus is most common, low dose prednisone is used
59
what time interval should maintenance doses be given at, which is best for trough measurement?
BID every 12 hours
60
depleting induction agent, polyclonal Ab that opsonize the hosts T cells which are then destroyed by the complement system
anti-thymocyte globulin (ATG)
61
side effects of anti-thymocyte globulin
flu-like symptoms (cytokine release syndrome), leukopenia, lymphopenia, thrombocytopenia, pruritis, erythema, serum sickness
62
depleting induction agent, MoAb that acts against CD52 surface Ag on mature lymphocytes, leading to B and T cell death
alemtuzumab (campath)
63
what additional medications need to be given with campath?
-premedicate with IV methylprednisolone -anti-infective prophylaxis should be given for 2 months or until CD4 counts rise
64
side effects of campath
NV, diarrhea, HAMA, fever, rigors, lymphopenia, thrombocytopenia, neutropenia, increased risk of malignancy/infection/autoimmune reactions
65
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
basiliximab (simulect), daclizumab (zenapax)
66
block calcineurin from being released and recognized by the nucleus (signal 1)
calcineurin inhibitors tacrolimus and cyclosporine
67
brand names for cyclosporine
neoral, gengraf, sandimmune
68
side effects of cyclosporine
hyperlipidemia, nephrotoxicity, tremor, headache, hypertension, hyperglycemia, gingival hyperplasia, hirsutism, diarrhea, vomiting
69
brand names for tacrolimus (IR and ER)
IR: prograf ER: astagraf XL, envarsus, IV prograf
70
drug interactions with CNIs (inhibit 3A4 and P-gp, so higher trough and AUC)
 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
drug interactions with CNIs (induce 3A4 and P-gp, so lower trough and AUC)
 Antibiotics: nafcillin, rifampin, rifabutin.  Antifungals: caspofungin, terbinafine.  Anticonvulsants: carbamazepine, oxcarbazepine, phenobarbital, phenytoin.  Herbals: St. John’s Wort, echinacea.
72
what info is important to obtain from a patient when measuring trough concentrations?
-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
side effects of tacrolimus
diarrhea, nausea, nephrotoxicity, tremor, headache, insomnia, hyperglycemia, hyperlipidemia, hypertension
74
dosing conversion between Prograf and Astagraf XL **NOT INTERCHANGEABLE
1 mg ER = 1 mg IR
75
ester prodrug, regular release MPA
mycophenolate mofetil/CellCept (MMF)
76
sodium salt, delayed release MPA
mycophenolic acid sodium/Myfortic (MPS)
77
drug interactions with MPA
acyclovir, ganciclovir, co-trimoxazole, COCs, phenytoin, aspirin, glucocorticoids, cholestyramine/bile acid resins, some antibiotics
78
side effects of MPA
-GI- NV, diarrhea, dyspepsia- all more with TAC -Hematologic- leukopenia, neutropenia, anemia, thrombocytopenia -Opportunistic infections -CNS- dizziness, insomnia, HA -CV
79
dose conversion between CellCept (MMF) and Myfortic (MPS)
1000 mg CellCept = 720 mg Myfortic
80
drug interactions with glucocorticoids
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
side effects of glucocorticoids
axillary and lower abdominal striae, steroid induced avascular necrosis, ecchymoses -also note tissue specific AEs
82
what is best for dosing and discontinuing glucocorticoids?
single AM dose (circadian rhythm) dose taper needed to D/C
83
short acting glucocorticoids
cortisone, hydrocortisone
84
intermediate acting glucocorticoids
prednisone, prednisolone, triamcinolone, methylprednisolone
85
long acting glucocorticoids
dexamethasone, betamethasone
86
rank of anti-inflammatory effects of glucocorticoids (high to low)
long acting agents > intermediate >> short acting (0 effect)
87
rank of mineralocorticoid effects of glucocorticoids (high to low)
short acting > prednisone + prednisolone >> triamcinolone, methylprednisolone, long acting agents (0 effect)
88
equivalent doses of short acting glucocorticoids
cortisone- 25 hydrocortisone- 20
89
equivalent doses of intermediate acting glucocorticoids
prednisone- 5 prednisolone- 5 triamcinolone- 4 methylprednisolone- 4
90
equivalent doses of long acting glucocorticoids
dexamethasone- 0.75 betamethasone- 0.6
91
drugs for prophylaxis- oral candidiasis
fluconazole, clotrimazole, nystatin suspension
92
drugs for prophylaxis- pneumonia
trimethoprim/sulfamethoxazole (bactrim, cotrimoxazole), dapsone, pentamidine, atovaquone
93
drugs for prophylaxis- cytomegalovirus (gastroenteritis, colitis, pneumonitis, retinitis, viremia)
ganciclovir/valganciclovir, acyclovir/valacyclovir
94
drugs for prophylaxis- UTI
bactrim, ciprofloxacin
95
signs of acute graft rejection
normal or low CNI trough fever, HTN, weight gain, rapid rise in SCr, graft swelling kidney biopsy for diagnosis
96
signs of CNI nephrotoxicity
increased CNI trough increased K, uric acid, decreased Mg HTN, no temperature rise, normal urine production CNS toxicities (flushing, tingling extremities, tremor, confusion)