Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Immunopharmacology > Flashcards

Immunopharmacology Flashcards

1
Q

applications of immunosuppression

A
  • hypersensitivity
  • autoimmunity
  • organ transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

immune tolerance due to

A

antigen-specific

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

application of immunostimulation (biological response modifers)

A

immunodeficiency

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

see diagram and blurb in pdf

A

see diagram and blurb in pdf

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

name 5 immunosuppressive agents

A
  1. glucocorticoids
  2. calcineurin inhibitors
  3. antiproliferative/antimetabolic agents
  4. agents affeting lymphocyte distribution
  5. antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the most common glucocorticoids used

A
  1. prednisone
  2. prednisolone
  3. dexamethasone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how are glucocorticoids administered

A
  • oral
  • IV
  • topical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what bond is required for glucocorticoid but no mineralocorticoid activity

A

11Beta-OH

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

addition — bond selectively increases glucocorticoid activity

A

1,2 double bond

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

— bond increases both glucocrticoid and minteralocorticoid activity

A

9 alpha F

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

substitution at — eliminates mineralocorticoid activity

A

C16

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

the glucocorticoid receptor is a member of

A

the nuclear hormone receptor superfamily

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

the cortisol-receptor complex is translocated to

A

the nucleus where it binds as homodimers to DNA transcripts that contain glucocorticoid response elements (GREs) and regulates gene expression of those genes

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

cortisol-receptor complex binding influences

A

transcription factors that act on other response elements. Therefore glucocorticoids influence the expression of genes

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

what are the anti-inflammatory/Immunosuppressive Effects of Glucocorticoids

A
  • decrease cytokines, other inflammatory mediators
  • redistribution of peripheral leukocytes
  • decrease activity of peripheral leukocyes at site of inflammation
  • impaired macrophage, T-cell, B-cell responses
  • vasoconstriction
  • decrease capillary permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the therapeutic uses for immunosuppression (glucocorticoids)

A
  • prevention and treatment of transplant rejection
  • graft-versus-host disease in bone-marrow transplantation
  • autoimmune disorder (Rheumatoid and other arthritides, systemic lupus erthematosus)
  • systemic dermatomyositis
  • psoriasis and other skin conditions
  • asthma and other allergic disorders
  • inflammatory bowel disease
  • inflammatory opthalmic disease
  • autoimmune hematologic disorders
  • acute exacerbation of MS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

effective doses of glucocrticoids to relieve symptoms are determined

A

empirically

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

short term admin of glucocrticoids (up to 10 days) in the absence of contraindictions does not produce

A

adverse side effects

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

for prolonged use of glucocrticoids , benefits must be weighted against production of

A

iatrogenic Cushing’s

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

high doses of glucocrticoids cause

A

mineralcorticoid effects - concern in pts with heart disease

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

prolonged use of glucocrticoids causes

A
  • increase susceptibility to infection
  • inhibits growth
  • induces myopathy, osteoporosis, cataracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what happens when glucocrticoids are used for more than 2 weeks

A
  • adrenal suppression may be induced by negative feedback
  • reduced ACTH secretion
  • adrenocortical atrophy
  • acute adrenal insufficiency in times of stress or upon withdrawal of the corticosteroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is cyclosporine

A

-lipid soluble peptide antibiotic

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

cyclosporine also known as

A

cyclosporin A

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

how is cyclosporine administered

A
  • oral
  • IV
  • ophthalmic emulsion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cyclosporine binds to

A

cyclophilin C

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

binding of cyclosporine to cyclophilin C causes

A
  • decrease calcineurin (cytoplasmic phosphatase)
  • decrease production of cytokines
  • decrease response of T cells to antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

therapeutic use of cyclosporine

A
  • graft-versus host disease in bone-marrow transplantation
  • aplastic anemia in patients ineligible for transplants
  • kidney, liver, heart and heart-lung transplantation
  • autoimmune diseases
  • dry eye syndrome (opthalmic emulsion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

cyclosporine toxicity can cause

A
  • reversible nephrotoxicity (dose limiting)
  • vascoconstriction that may lead to hypertension
  • neurotoxicity
  • hyperlipidemia
  • transient hepatotxicity
  • stimulates TGF-beta which may lead to an increase risk of cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

cyclosporine is metabolized by

A

cytochrome P450 (especially CYP3A4)

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

what drugs inhibit metabolism and reduces cyclosporine clearance

A
  • erythromycin
  • ketoconazole
  • Amphotericin B
  • grapefruit juice

“A-KEG”

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

what drugs increase cyclosporine clearance

A
  • phenobarbital

- rifampin

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

what is Tacrolimus

A

a macrolide antibiotic

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

Tacrolimus binds to

A

FK506-binding protein-12 (FKBP-12) an immunophilin structurall related to cyclophilin

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

function of Tacrolimus

A
  • inhibits calcineurin
  • decreases production of cytokines
  • decreases response of T cells to antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

administration of Tacrolimus

A
  • oral

- injection

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

therapeutic use of Tacolimus

A

SAME AS CYCLOSPORINE:
Graft-versus-host disease in bone-marrow transplantation
Aplastic anemia in patients ineligible for transplants
Kidney, liver, heart and heart-lung transplantation
Autoimmune diseases

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

Tacrolimus is — times more potent than cyclosporine

A

10 to 100

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

toxicity and drug interactions of Tacrolimus

A

same as for cyclosporine

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

what is Sirolimus

A

macrocyclic lactone

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

Sirolimus binds to

A

FKBP-12

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

does Sirolimus inhibit calcineurin

A

no!

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

function of Sirolimus

A
  • inhibits mTOR (mammalian target of rapamycin, key enzyme in cell cycle progression)
  • inhibit T-cell activation and proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

administration of Sirolimus

A

oral

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

therapeutic use of Sirolimus

A
  • inhibition of transplant rejection (often include combination with a calcineurin inhibitor and glucocorticoid)
  • preservation of graft-versus-host reaction
  • treatment of autoimmune disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

effects of Sirolimus persists for —- after discontinuing therapy

A

several months

47
Q

toxicity accompanying the use of Sirolimus includes

A
  • dose-dependent thrombocyopenia
  • leukopenia
  • hyperlipidemia
48
Q

renal transplant patients on Sirolimus may show

A

a dose-dependent increase in serum cholesterol and triglycerides

49
Q

adverse side effects of Sirolimus toxicity

A
  • anemia
  • hypotension
  • hypokalemia or hyperkalemia
  • fever
  • gastrointestinal effects
  • increase risk of lymphomas
  • increased infections
50
Q

Sirolimus interacts with what substrate

A

CYP3A4 - see cyclosporine for interactions

51
Q

what is Azathioprine a derivative of

A

6 mercaptopurine (6-MP) derivative

52
Q

Azathioprine has a better — than (6-MP)

A

oral absorption

53
Q

Azathioprine inhibits

A

S phase of DNA synthesis

54
Q

Azathioprine is converted to

A

thioinosinic acid

55
Q

thionosinic acid is a competitive inhibitor of

A

purine synthesis

56
Q

Therapeutically thionosinic affects

A

T cells more than B cells

57
Q

administration method of Azathioprine

A

oral

IV

58
Q

Azathioprine is used in combination with corticosteroids to

A

inhibit rejection of organ transplants and for rheumatoid arthritis

59
Q

Azathioprine toxicity can lead to

A
  • bone marrow suppression, gastrointesinal toxicity, mild hepatotoxicity
  • lead to severe infection
  • mutagenic, carcinogenic
60
Q

what happens if Azathioprine is co-administered with allopurional

A

toxicity may increase

61
Q

Mycophenolate Mofetil is a semisynthetic derivative of

A

mycophenolic acid

61
Q

therapeutic use of Fingolimod

A

treatment of patients with relapsing multiple sclerosis to reduce frequency of exacerbations and delay the physical disability

61
Q

function of Mycophenolate Mofetil

A
  • inhibits inosine monophosphate dehydrogenase
  • decreases purine biosynthesis
  • decreases proliferation of T and B lymphocytes
61
Q

administration of Mycophenolate Mofetil

A

oral, IV

61
Q

Mycophenolate Mofetil is used in combination with cyclosporine and corticosteroids to

A

prevent organ rejection in allogenic renal transplant pts and in liver and cardiac transplant patients

61
Q

Mycophenolate Mofetil toxicity causes

A
  • diarrhea
  • leukopenia
  • cytomegalovirus infections and gastrointestinal hemorrhage
62
Q

what happens when Mycophenolate Mofetil is co-administered with antacids (magnesium, aluminim hydroxides)

A

decreases absorption

62
Q

Mechanism of action of Fingolimod

A

-sphingosine 1-phosphate receptor (S1P-R) agonist

63
Q

administration of Fingolimod

A

-oral

64
Q

what type of vaccine should be avoided when taking Fingolimod

A

live attenuated vaccines during and for 2 months after stopping due to risk of infection

65
Q

effects of Fingolimod toxicity

A
  • decrease heart rate and/or AV conduction after first dose
  • infections
  • macular edema
  • decrease in pulmonary function
  • hepatotoxicity
66
Q

why should women of childbearing potential on Fingolimod use contraception during and for 2 months after stopping

A

bc Fingolimod increases fetal risk

67
Q

Fingolimod has a pharmacodynamic interaction meaning

A

Antiarrhythmic drugs and Beta blockers increase risk of additive effects on heart rate

68
Q

Vincristine used to teat

A

idiopathic thrombocytopenic purpura

69
Q

Fingolimod clearance is decreased by

A

ketoconazole (inhibitor of CYP4F)

70
Q

other antimetabolites used for immunisuppression

A
  1. cyclophosphamide
  2. methotrexate
  3. Vincristine
71
Q

Methotrexate used to treat

A

rheumatoid arthritis

72
Q

Vincristine used to teat

A

idiopathic thrombocytopenic purpura

73
Q

therapeutic use of ATG

A

can be used alone or in combination with corticosteroids and azathioprine to prevent renal allograph rejection

74
Q

ATG toxicity can lead to

A

hypersensitivity

nephritis and anaphylaxis (occurs rarely)

75
Q

what is Muromonab-CD3

A

a mouse monoclonal Ab

76
Q

mechanism of action of Muromonab-CD3

A
  • blocking Ab
  • CD3 localized adjacent to antigen recognition complex, which is blocked as well
  • T cells are unable to recognize foreign antigen
77
Q

what is antithymocyte globulin (ATG)

A

is a purified equine immunoglobulin against human thymus lymphocytes

79
Q

name 2 IL-2 Receptor (Anti-CD25) Antibodies

A
  1. Basiliximab

2. Daclizumab

79
Q

both Basiliximab and Daclizumab are

A

mouse/human monoclonal antibodies

80
Q

infliximab toxicity causes

A
  • infusion rxn - fever, urticaria, hypotension, dyspnea within 1-2 hrs after administration
  • upper respiratory and urinary tract infections
  • development of antinuclear Abs, rarely a lupus-like syndrome
81
Q

therapeutic use of Basiliximab and Daclizumab

A
  • prevention of acute renal transplant rejection

- both are given with cyclosporine and corticosteroids

82
Q

Basiliximab and Daclizumab toxicity

A

well tolerated; no significant drug interactions

83
Q

therapeutic use of Muromonab-CD3

A
  • treatment of acute kidney or hepatic transplant rejection
  • prophylaxis in cardiac transplantation
  • depletions of T cells in marrow from donors before bone marrow transplantation
84
Q

name an Anti-TNF reagent

A

infliximab

85
Q

Muromonab-CD3 toxicity causes

A
  • fever
  • pulmonary edema
  • vomiting
  • headache
  • anaphylaxis
  • infection during chronic therapy
86
Q

what is infliximab

A

a chimeric anti-TNF -alpha monoclonal antibody

87
Q

sites of action of immunosuppressive agents of T-cell activation (see slide 26)

A
  1. glucocorticoids
  2. cyclosporine
  3. tacrolimus
  4. sirolimus
  5. Azathioprine
  6. Fingolimod
  7. Mycophenolate
  8. Muromonab- CD3
  9. Daxlizumab, Basiliximab
88
Q

infliximab toxicity causes

A
  • infusion rxn - fever, urticaria, hypotension, dyspnea within 1-2 hrs after administration
  • upper respiratory and urinary tract infections
  • development of antinuclear Abs, rarely a lupus-like syndrome
89
Q

therapeutic use of Rho immune globulin

A

prevention of hemolytic disease of Rh-positive newborns

90
Q

mechanism of action of Etanercept

A

blocks the effects of TNF-alpha

91
Q

therapeutic use of Etanercept

A

rheumatoid arthritis - patients who do not respond to other treatments

92
Q

Etanercept toxicity cause

A
  • injection site rxns

- infections

93
Q

BCG toxicity leads to

A

severe hypersensitivity and shock

94
Q

what are immune globulins

A
  • human plasma from donors in the general population or hyperimmunized individuals (for specific exposures such as hepatitis B, rabies, tetanus, varicella-zoster, cytomegalovirus, botulism, respiratory syncytial virus)
  • replacing missing Abs
95
Q

what are immunostimulants

A

biological response modifiers

96
Q

What is Bacillus Calmette-Guerin (BCG)

A
  • an immunostimulant

- viable attenuated strain of Myobacterium bovis

97
Q

mechanism of action of BCG

A

-has an adjuvant effect to stimulate T cells and natural killer cells

98
Q

therapeutic use of BCG

A

bladder cancers

99
Q

BCG toxicity leads to

A

severe hypersensitivity and shock

100
Q

therapeutic use of immune globulin

A

passive immunization

  • immunodeficiencies
  • prevention of infection in chronic lymphocytic leukemia
  • Kawasake disease (acute multisystem inflammatory disease of children)
101
Q

immune globulin toxicity leads to

A
  • anaphylactoid rxns and severe hypotension

- theoretical risk of infection due to plasma source

102
Q

name 2 recombinant cytokines

A
  1. interleukin-2

2. interferons

109
Q

name 2 Myeloid Colony Stimulating Factors

A

Granulocyte-macrophage colony stimulating factor (GM-CSF)

Granulocyte stimulating factor (G-CSF)

110
Q

what drugs are calcineurin inhibitors

A
  • cyclosporine

- Tacrolimus

111
Q

what drugs are Antiproliferative & Antimetabolic drugs

A
  • Sirolimus
  • Azathioprine
  • Mycophenolate Mofetil
  • Fingolimod
  • Cyclophosphamide
  • Methotrexate
  • Vincristine
112
Q

what drugs are antibodies

A
  • antithymocyte gloulin (ATG)
  • Muromonab -CD3 (Anti-CD3 Monoclonal Ab)
  • Basiliximab (IL-2 Receptor Antibodies)
  • Daclizumab (IL-2 Receptor Antibodies)
  • Infliximab (Anti-TNF Reagents)
  • Rho Immune Globulin
113
Q

what drugs are Anti-TNF reagents

A

-Etanercept

114
Q

what drugs are immunostimulants

A

immune globulin

Pharmacology (23 decks)

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