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Immunology > immunology - drugs > Flashcards

immunology - drugs Flashcards

1
Q

immunosuppressants - mechanism of action

A

agents that block lymphocyte activation and proliferation

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2
Q

immunosuppressants reduce acute transplant immunity by suppressing

A

cellular immunity

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3
Q

immunosuppressants - frequently combined to …

A

achieve greater efficacy with decreased toxicity

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4
Q

immunosuppressants - chronic suppression –>

A

high risk of: 1. infection 2. malignancy

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5
Q

immunosuppressants - drugs

A
  1. cyclosporine
  2. tacrolimus
  3. Sirolimus (Rapamycin)
  4. Daclizumab
  5. Basiliximab
  6. Azathioprine
  7. Mycophenolate mofetil
  8. Corticosteroids
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6
Q

Cyclosporine - mechanism of action

A

binds cyclophilin –> the complex inhibits Calcineurin (a TCR downstream protein that activates NFAT, a TF, through de-phosphorylation) –> prevent IL-2 transcription
–> blocks T cell activation

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7
Q

Cyclosporine - clinical use

A
  1. transplant rejection prophylaxis
  2. psoriasis
  3. RA
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8
Q

Cyclosporine - toxicity

A
  1. Nephrotoxity
  2. hypertension
  3. hyperlipidemia
  4. neurotoxicity
  5. gingival hyperplasia
  6. hirsutism
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9
Q

Tacrolimus - mechanism of action

A

binds FK506 –> the complex inhibits Calcineurin (a TCR downstream protein that activates NFAT, a TF, through de-phosphorylation) –> prevent IL-2 transcription
–> blocks T cell activation

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10
Q

Tacrolimus - clinical use

A

transplant rejection prophylaxis

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11
Q

Tacrolimus - side effects

A
  1. diabetes
  2. neuphrotoxic
  3. neuroticity
  4. hypertension
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12
Q

Tacrolimus and cyclosporine are both highly …. (side effect)

A

nephrotoxic

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13
Q

Sirolimus (Rapamycin) - mechanism of action

A

binds FKB –> the complex inhibits mTOR (IL-2R downstream) –> blocks T-cell activation and B-cell differentiation by preventing RESPONSE TO IL-2

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14
Q

Sirolimus (Rapamycin) - clinical use

A
  1. kidney transplant rejection prophylaxis

2. also used in drug-eluting stents

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15
Q

A drug-eluting stent (DES) is a

A

peripheral or coronary stent placed into narrowed peripheral or coronary arteries –> slowly releases a drug to block cell proliferation –> prevents fibrosis + clots –> prevent restenosis

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16
Q

Sirolimus (Rapamycin) - side effects

A
  1. pancytopenia
  2. insulin resistance
  3. Hyperlipidemia
    NOT NEPHROTOXIC
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17
Q

Sirolimus (Rapamycin) is NOT (toxicity)

A

nephrotoxic

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18
Q

Sirolimus (Rapamycin) act synergic with

A

cyclosporine

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19
Q

Daclizumab - mechanism of action

A

monoclonal antibody that blocks IL-2R

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20
Q

Basiliximab - mechanism of action

A

monoclonal antibody that blocks IL-2R

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21
Q

Daclizumab, Basiliximab - clinical use

A

kidney transplant rejection prophylaxis

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22
Q

Daclizumab, Basiliximab - side effects

A
  1. edema
  2. hypertension
  3. tremor
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23
Q

Azathioprine - mechanism of action

A

Antmetaboite precursor of 6-MP –> inhibit PRPP amidotransferase –> decrease de novo purine synthesis
–> inhibits lymphocyte proliferation

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24
Q

Azathioprine - toxicity

A
  1. Myelosuppresion
  2. GI. toxicity
  3. Liver toxicity
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25
Q

Azathioprine and MP-6 are metabolized by

A

Xantine oxidase

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26
Q

Azathioprine - clinical use

A
  1. Transplant rejection prophylaxis
  2. RA
  3. IBD
  4. Glomerulonephritis
  5. other autoimmune conditions
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27
Q

Mycophenolate mofetil - mechanism of action

A

Reversibly inhibits IMP dehydrogenase preventing purine synthesis of B and T cells

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28
Q

Mycophenolate mofetil - clinical use

A
  1. Transplant rejection

2. lupus nephritis

29
Q

Mycophenolate mofetil - toxicity

A
  1. GI upset
  2. pancytopenia
  3. hypertension
  4. hyperglycemia
  5. Associated with invasive CMV infecion
    LESS NEPHROTOXIC AND NEUROTOXIC
30
Q

Corticosteroids as immunosuppressants - mechanism of action

A
  1. Inhibit NF-kB –> suppress both B and T-cell function by decreased transcriptio nof many cytokines
  2. induce apotptosis of T-lymphocytes
31
Q

Corticosteroids as immunosuppressants - clinical use

A
  1. Transplant rejection prophylaxis
  2. many autoimmune disorders
  3. many inflammatory disorders
32
Q

Corticosteroids as immunosuppressants - toxicity

A
  1. iatrogenic cushing
  2. cataracts
  3. avascular necrosis of femoral head
33
Q

monoclanal antibodies against IL-2R

A
  1. Daclizumab

2. Basiliximab

34
Q

recombinant cytokines - agents

A
  1. Aldesleukin (IL-2)
  2. erythropietin (epoetin alfa)
  3. Filgrastim (G-CSF)
  4. Sargramostim (GM-CSF)
  5. IFN-α
  6. IFN-β
  7. IFN-γ
  8. Oprelvekin (IL-11)
  9. Romiplostim, eltrombopag (thrombopoietin receptor agonists)
35
Q

erythropoietin (epoetin alfa) - clinical use

A

anemias (esp in renal failure)

36
Q

Granulocyte-colony stimuating factor (G-CSF) - drug and clinical use

A

Filgrastim

Recovery of bone marrow

37
Q

IL-2 - drug and clinical use

A

Aldesleukin –> 1. Renal cell carcinoma

2. metastatic melanoma

38
Q

Granulocyte/macrophage-colony stimuating factor(GM-CSF) - drug and clinical use

A

Sargramostin –> Recovery of bone marrow

39
Q

interferons as drugs - clinical use

A

Interferons - α: 1. chronic hepatitis B, C 2. Kaposi sarcoma 3. hairy cell leukemia 4. condyloma acuminatum 5. renal cell carcinoma 6. malignant melanoma
Interferons - β: multiple sclerosis
Interferons - γ: chronic granulomatous disease

40
Q

IL-11 - drug and clinical use

A

Oprelvekin –> thrombocytopenia

41
Q

thrombopoietin receptor agonists - drugs and clinical use

A

Romiplostim, eltrombopag –> thrombocytopenia

42
Q

immunosuppressants - drugs

A
  1. cyclosporine
  2. tacrolimus
  3. Sirolimus (Rapamycin)
  4. Daclizumab
  5. Basiliximab
  6. Azathioprine
  7. Mycophenolate mofetil
  8. Corticosteroids
43
Q

Therapeutic antibodies for cancer (drug and target)

A
  1. alemtuzumab –> CD52
  2. bevacizumab –> VEGF
  3. Cetuximab –> EGFR
  4. Rituximab –> CD20
  5. Trastuzumab (Herceptic) –> HER2/neu
44
Q

Trastuzumab (Herceptic) - target and clinical use / toxicity

A

target: HER2/neu
1. HER-2 (+) breast cancer 2. Gastric cancer
SE: cardiotoxicity

45
Q

Bevacizumab - target and clinical use

A

target: VEGF (inhibits angiogenesis)
1. Colorectal cancer
2. renal cell carcinoma
3. Neovascular age-related macular degeneration (Ranibizumab, Bevacizumab)

46
Q

Bevacizumab - side effects

A
  1. hemorrhage
  2. blood clots
  3. impaired wound healing
47
Q

Cetuximab - target and clinical use

A

target: EGFR
1. Stage IV colorectal camcer (Wild type KRAS)
2. head and neck cancer

48
Q

Cetuximab - side effects

A
  1. Rash
  2. elevated LFTs
  3. diarrhea
49
Q

Rituximab - target / clinical use

A

target: CD20
1. B cel non-Hodgkin 2. CLL 3. RA
4. Idiopathic thrombocytopenic purpura (ITP)
SE: increased risk for progressive multifocal leukoencephalopathy

50
Q

alemtuzumab - target and clinical use

A

CD52

1. CLL 2. MC

51
Q

Therapeutic antibodies for cancer (drug and target)

A
  1. alemtuzumab –> CD52
  2. bevacizumab –> VEGF
  3. Cetuximab –> EGFR
  4. Rituximab –> CD20
  5. Trastuzumab (Herceptic) –> HER2/neu
52
Q

Therapeutic antibodies for autoimmune disease therapy (drug and target)

A
  1. Adalimumab –> Soluble TNF-α
  2. Certolizumab –> Soluble TNF-α
  3. Infliximab –> Soluble TNF-α
  4. Eculizumab –> Complement protein C5
  5. Natalizumab –> a4 integrin
53
Q

monoclonal antibodies against TNF-α

A
  1. Adalimumab
  2. Certolizumab
  3. Infliximab
54
Q

monoclonal antibodies against TNF-α clinical use / SE

A
  1. IBD
  2. RA
  3. Psoriasis
  4. Ankylosing spondylitis
    SE: predispose to: infection, including reactivation of latent TB
55
Q

Etanercept - mechanism of action

A

fusion protein (receptor for TNF-A+IgG1 FC) produced by recombinant DNA (A DECOY) –> not antibody

56
Q

eculizumab - target and clinical use

A

target: C5 protein

paroxysmal noctural hemogloinuria

57
Q

Natalizumab - mechanism of action

A

target α4-integrin -WBC adhesion

58
Q

Natalizumab - clinical use

A
  1. MS

2. Crohn disease

59
Q

Natalizumab - side effect

A

risk for PML in patients with JC virus

60
Q

Abciximab - mechanism of action

A

monoclonal antibody against platelet glycoproteins IIb/IIIa

61
Q

Abciximab - clinical use

A

antiplatelet agent for preventon of ischemic complications in patients undergoing percutaneous coronary intervention

62
Q

Denosumab - mechanism of action / clinical use

A

monoclonal antibody against RANKL –> inhibits osteoclast maturation (mimics osteoprotegerin)
clinical use: osteoporosis

63
Q

Digoxin immun Fab - mechanism of action and clinical use

A

monoclonal antibody against Digoxin

Antidote for digoxin toxicity

64
Q

Omalizumab - mechanism of action and clinical use

A

monoclonal antibody against IgE –> prevent IgE bidning to FCεRI
allergic asthma

65
Q

Palivizumab - mechanism of action / clinical use

A

monoclona antibody against RSV F protein

clinical use: RSV prophylaxis for high risk infants

66
Q

monoclonal antibodies against VEGF

A
  1. Ranibizumab

2. Bevacizumab

67
Q

monoclonal antibodies against VEGF - clinical use

A
  1. Neovascular age-related macular degeneration (Ranibizumab, Bevacizumab)
  2. Colorectal cancer (Bevacizumab)
  3. renal cell carcinoma (Bevacizumab)
68
Q

monoclona antibody against CD52 - drugs and clinical use

A

Alemtuzumab

1. CLL 2. MS

Immunology (10 decks)

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