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Pharmacology Test 1 Material > Inflammation and Immunomodulators > Flashcards

Inflammation and Immunomodulators Flashcards

1
Q

What are the two parts to the immune system?

A

Adaptive immune system: derived from T cell activation in response to foreign antigens and secrete cytokines
Innate immune system: inflammation without adaptive responses initiated by macrophage. This leads mast cell, eosinophil, neutrophil activation causing inflammatory mediators and phagocytosis.

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2
Q

How are antibodies used therapeutically?

A
  1. Passive immunity (vaccines)
  2. Target disease-specific antigens (Cancer drugs)
    * *Parenterally administered
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3
Q

How are immunostimulants used therapeutically?

A

Goal is to enhance developing immune responses or antagonize inhibitors of immune activity (immune check points)

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4
Q

What are two adjuvants that are used to enhance adaptive immune response?

A

Aluminum salts: Used in vaccines that support prolonged exposure for developing immune reactions
BCG: bacillus calmette guerin: surface antigen that interacts with pattern recognition receptors to increase activity

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5
Q

Interleukin-2

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Metastatic melanoma and renal cell carcinoma
  2. Increases proliferation of activated T-cells, produce IFNy, and cytotoxic killer cell activity
  3. **Capillary leak syndrome (systemic immune response), hypotension
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6
Q

Interferon: IFN y

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Severe recurrent infections
  2. Stimulates cell mediated cytotoxic immune response
  3. flu-like symptoms
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7
Q

Interferon: IFN B

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Reduce frequency of MS exacerbations
  2. Maybe reduces pro-inflammatory cytokines…unknown
  3. flu-like symptoms
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8
Q

Ipilimumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Promotes regression of tumors: Metastatic melanoma
  2. Fully human antibody to CTLA-4 which leads to increased T-Cell response
  3. SE: enterocolitis, TENS, neuropathy
    * *often used with nivolumab
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9
Q

Nivolumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Promotes regression of tumors: Metastatic melanoma or non-small cell lung cancer
  2. Fully human antibody to PD-1, it is expressed in some cancer cells
  3. SE: enterocolitis, hepatitis, nephritis
    * *often used with ipilimumab
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10
Q

What are the common adverse effects of all immunosuppressants?

A

Increased risk of infection, increased risk of cancer, metabolic effects, myelosuppression
**Use multiple drugs at lower doses to lessen severity of side effects

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11
Q

Azathioprine

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Renal transplant, Crohn’s, RA
  2. Antimetabolite: Inhibits synthesis of purine nucleotides needed to replicate DN–> cannot be replicated for cellular proliferation
  3. SE: myelosuppression, N/V
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12
Q

Prednisone

  1. Use
  2. Mechanism of action
A
  1. Long term immunosuppression with transplant OR immune mediated inflammatory disease/autoimmune diseases
  2. Prevents expression of genes for cytokines that control immune response
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13
Q

Cyclosporine

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Long term immunosuppression for transplant, psoriasis, RA
  2. Calcineurin inhibitors: inhibit TCR signaling by inhibiting calcineurin by interacting with immunophilin proteins
  3. **Nephrotoxicity, HTN, hyperglycemia
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14
Q

Tacrolimus

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Long term immunosuppression for transplant, psoriasis, RA
  2. Calcineurin inhibitors: inhibit TCR signaling by inhibiting calcineurin by interacting with immunophilin proteins
  3. **Nephrotoxicity, HTN, hyperglycemia
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15
Q

Sirolimus

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Organ transplant
  2. Inhibits IL-2 receptor signaling by mTor to prevent T cell proliferation
  3. **Increased risk of post-surgical bleeding due to bone marrow suppression
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16
Q

Belatacept

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Organ transplant
  2. Fusion protein for CTLA4: No proliferation and no cytokine production
  3. Increased infection, strong association with PTLD **DONT give to patient that’s not immune to EBV
17
Q

Natalizumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. MS and Crohns
  2. Blocks VLA4 and VCAM interaction preventing adhesion of lymphocytes to the vascular endothelial cells
  3. Increased infection, increased risk of PML (demyelinating disorder) **DONT give if + for JCV
18
Q

Basiliximab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. 1-2 dose at time of organ transplant
  2. Antibody binding IL-2 receptor, preventing T cell proliferation
  3. Increased infection risk
19
Q

ATG (anti-T cell globulin)

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Blocks T cell surface receptors and depletes ALL T-cells

3. SE: infection, cytokine release syndrome

20
Q

Ocrelizumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. MS
  2. Depletes and reduces circulating B cells
  3. increased infection, association with PML so don’t give to patients with latent JCV
21
Q

Ustekinumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Psoriasis and Crohn’s
  2. Binds to IL 12 and Il23 that decrease Th1 and Th17 responses
  3. increased infection, reversible posterior leukoencephalopathy syndrome (RPLS) –> swelling in the brain
22
Q

Guselkumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Psoriasis
  2. Antibody for IL23, interferes with Th17 response
  3. increased risk of infection
23
Q

Ixekizumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. Psoriasis
  2. Antibody binds IL17, inhibits Th17 response
  3. Increased risk of infection
24
Q

What are DMARDs?

A

Disease modifying anti rheumatic drugs: target cytokines that promote inflammatory activity

25
Q

Adalimumab

  1. Use
  2. Mechanism of action
  3. SE
A
  1. RA and Crohn’s disease
  2. Antibody to TNFa so that reduces circulating and localized levels of TNFa
  3. increased infections and malignancies
26
Q

Tofacitinib

  1. Use
  2. Mechanism of action
  3. SE
A
  1. RA, ulcerative colitis
  2. Jak inhibitor: suppresses adaptive immunity inflammation from IL23 and IL6 by decreasing signaling from cytokines that depend on tyrosine kinase called Jax
  3. Anemia, neutropenia, myelosuppresion, increased infection, PTLD, lymphoma, increased risk of blood clots**

Pharmacology Test 1 Material (9 decks)

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