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Pharmacology > Immunosuppressives > Flashcards

Immunosuppressives Flashcards

1
Q

Define autograft

A

a graft of tissue from one point to another of the same person’s body

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2
Q

Define allograft

A

one donating to another within same species

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3
Q

Define xenograft

A

getting donation from another species

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4
Q

What are 3 types of graft rejection?

A

1) hyperacute: in minutes
2) acute: 7-21 days
3) chronic: > 3 months

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5
Q

What are 2 types of drugs that act on immune response induction phase?

A

1) Interleukin-2 production inhibitors: cyclosporine, tacrolimus
2) Cytokine gene expression inhibitor: glucocorticoids

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6
Q

Cyclosporine (CsA) indication:

A
  • Organ transplant tx

- Autoimmune disease tx (e.g.: RA) at low doses

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7
Q

Cyclosporine administration:

A

PO (slow and incomplete absorption), IV

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8
Q

Cyclosporine metabolism:

A

occurs in GI, liver

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9
Q

Where is cyclosporine concentrated?

A

In peripheral tissue (lymphomyeloid, adipose)

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10
Q

Name 4 AEs of cyclosporine:

A

1) Nephrotoxicity
2) HTN
3) Increased risk of infection
4) Liver dysfunction (management: regular blood level monitoring to avoid kidney and liver toxicity)

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11
Q

Name 4 classes that inhibit CsA metabolism:

A

1) Ca channel blockers
2) Antifungal agents (azoles)
3) Antibacterial agents (erythro/clarithromycin)
4) Grapefruit juice

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12
Q

Name 2 classes that induce CsA metabolism:

A

1) Anticonvulsants (Phenytoin)

2) AntiTB agents (Isoniazid)

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13
Q

Tacrolimus administration:

A

PO, IV

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14
Q

Tacrolimus metabolism:

A

liver (99%)

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15
Q

Tacrolimus indication:

A

To prevent organ transplant rejection

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16
Q

Tacrolimus AEs:

A

Similar to cyclosporine

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17
Q

Name 5 classes of anti-rejection drugs

A

1) Interleukin 2 inhibitor: sirolimus
2) Purine synthesis inhibitor:
3) Alkylating cytotoxic agents
4) Immune response suppressor
5) Immunosuppressive antibodies

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18
Q

What is sirolimus?

A

New macrolide antibiotic

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19
Q

What do anti-rejection drugs work on?

A

Effector phase of immune response

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20
Q

Mycophenolate Mofetil administration:

A

PO (well absorbed)

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21
Q

What impairs mycophenolate absorption?

A

Al, Mg

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22
Q

Name the metabolites of mycophenolate (2) and their fate.

A

Metabolites: mycophenolic acid, glucuronide conjugate
Fate: undergoes enterohepatic circulation

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23
Q

Mycophenolate elimination:

A

via kidneys as inactive glucuronide

24
Q

Mycophenolate indication:

A

transplant recipients (+ cyclosporine, steroids)

25
Q

Name 3 indications for Azathioprine:

A

1) IV loading dose on transplant day
2) PO dosing for maintenance
3) Used in combo with other immunosuppressant drugs for kidney/liver transplants + RA

26
Q

Name a major SE of azathioprine:

A

bone marrow depression

27
Q

What is cyclophosphamide?

A

Nitrogen mustard, alkylating agent

28
Q

Cyclophosphamide indication:

A

Lupus, RA tx

29
Q

Cyclophosphamide administration:

A

PO, inactive until metabolized by liver into active phosphoramide mustard

30
Q

Cyclophosphamide AE (2):

A

1) bone marrow depression (leukocytes > platelets)
2) GI
3) hemorrhagic cystitis

31
Q

Name 3 glucocorticoids

A

Prednisone
Methylprednisolone
Dexamethasone

32
Q

Name 3 clinical uses of glucocorticoids:

A

1) Anti-inflammatory and immunosuppressive tx: asthma, AR, RA, organ transplant
2) Neoplastic disease: Hodgkin’s disease, acute lymphatic leukaemia
3) Replacement tx: Addison’s syndrome

33
Q

Name 4 AEs of glucocorticoids:

A

1) Insomnia, mood changes (take in AM)
2) Increased appetite, weight gain
3) Suppress response to injury or infection
4) Metabolic effects: fluid retention, osteoporosis, hyperglycemia, GI bleeding

34
Q

What are immunosuppressive antibodies?

A

Antibodies against human lymphocytes or their surface receptors have significant immunosuppressant actions

35
Q

What are polyclonal antibodies?

A

Binds to proteins on lymphocyte surface –> lymphocyte lysis (affects all T cells)

36
Q

What are monoclonal antibodies?

A

Affects induction and effector phases of immune response to allograft - works against specific surface component of T cells

37
Q

Polyclonal ABs AEs:

A

Newly synthesized ABs can produce anaphylactic reactions

38
Q

Name a monoclonal AB drug:

A

Infliximab (directed to TNF-alpha)

39
Q

What happens in central tolerance?

A

Immature lymphocytes are deleted in bone marrow and thymus that recognize self-antigens with high affinity

40
Q

What is peripheral tolerance?

A

Mature autoreactive lymphocytes are inactivated by various mechanisms

41
Q

What are the 3 stages associated with rheumatoid arthritis (RA)?

A

1) Initiation phase: inflammation within joint
2) Amplification phase: T cell activation
3) Chronic inflammatory phase: tissue injury due to bone destruction and joint remodelling

42
Q

Anti-TNF alpha and anti-IL therapies are considered what?

A

Disease-modifyig anti rheumatic drugs (DMARDs)

43
Q

Why are anti-TNF alpha and anti-IL therapies effective DMARDs?

A

Bc they are released within the joint during the chronic inflammatory phase

44
Q

Name 5 drugs that are anti-TNF based?

A

1) Entanercept
2) Infliximab
3) Adalimumab
4) Certolizumab
5) Golimumab

45
Q

Thiopurine derivatives MOA:

A

DNA synthesis inhibitors (may take weeks to months to work)

46
Q

Thiopurines indication:

A
  • Steroid-resistant or dependent pts

- Remission and reduction of UC/CD relapse (NOT acute attacks)

47
Q

What is a risk with thiopurines?

A

Infection (esp when co-tx with steroids)

48
Q

Methotrexate MOA:

A

Dihydrofolate reductase inhibitor (blocks DNA synthesis)

49
Q

Methotrexate indication:

A

Steroid resistant or dependent pts

50
Q

Cyclosporine MOA:

A

calcineurin inhibitor

51
Q

Cyclosporine indication:

A
  • Tissue transplantation
  • MOST serious cases of UC/CD
  • Before surgery
52
Q

What is a SE of cyclosporine?

A

SEVERE IMMUNE SUPRESSION

53
Q

TNF-a inhibitors MOA:

A

Inhibits pro-inflammatory ligand (tnf-a)

54
Q

Infliximab (Remicade) TNF-a inhibitor MOA:

A

Engineered antibody that may kill cell to which it attaches

55
Q

Why does infliximab have a prolonged effect?

A

Bc

  • it has a long half-life (8-10 days)
  • MOA (kills immune cells so they have to repopulate)
56
Q

Entanercept also reduces TNF-a

A

but NOT effective as an UC tx

57
Q

What is a SE of tnf-a inhibitors?

A

Increases changes of serious lung infection (esp TB)

Pharmacology (9 decks)

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