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IMM Exam 2 > Immunosuppressants and Immunomodulators > Flashcards

Immunosuppressants and Immunomodulators Flashcards

1
Q

immunosuppressant definition

A
  • drugs that increase risk of infection
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2
Q

immunosuppressants target - broad/narrow

A
  • broad targets/effects
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3
Q

age of immunosuppressant drugs

A
  • old drugs
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4
Q

immunomodulators definition

A
  • drugs that DO NOT increase risk of infection
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5
Q

Immunomodulators target - broad/narrow

A
  • narrow targets/effects
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6
Q

age of immunomodulator drug

A
  • new drugs
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7
Q

four characteristics of an inflammatory immune response

A
  • pain (dolor)
  • heat (calor)
  • erythema (rumor)
  • swelling (tumor)
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8
Q

eicanosanoids synthesized by

A
  • most cells
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9
Q

eicanosanoids role in inflammation

A
  • act as local vasodilators
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10
Q

what molecules do drugs affect in eicosanoid production/activity?

A
  • prostaglandins

- leukotrienes

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11
Q

what molecules do drugs affect in inflammatory cytokine production/activity

A
  • TNFa
  • IL-2
  • IL-5
  • IL-6
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12
Q

what molecules do drugs affect in leukocyte activation/proliferation?

A
  • Th-cells
  • B-cells
  • eosinophils
  • mast cells
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13
Q

what are eicosanoids derived from?

A

plasma membrane lipids

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14
Q

what creates arachidonic acid

A
  • from plasma membrane lipids

- by phospholipase A2

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15
Q

what are the three eicosanoids derived from arachidonic acid?

A
  • prostaglandin E2
  • Thromboxane A2
  • Leukotriene E4
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16
Q

prostaglandins E2 produced by

A
  • most cells
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17
Q

thromboxane A2 produced by

A
  • platelets
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18
Q

leukotriene E4 produced by

A
  • leukocytes
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19
Q

cyclooxygenase inhibitors inhibit what process

A
  • synthesis of prostanoids
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20
Q

big class of COX inhibitors

A
  • NSAIDs
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21
Q

COX1 constitutive/inducible

A
  • constitutive
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22
Q

COX1 responsible for

A
  • homeostatic functions
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23
Q

COX2 constitutive/inducible

A
  • inducible
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24
Q

COX2 responsible for

A
  • inflammatory response
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25
Q

homeostatic effects of prostaglandins

A
  • renal homeostasis
  • gastric mucosal production
  • platelet function
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26
Q

inflammatory effects of prostaglandins

A
  • pain
  • inflammation
  • fever
  • limited homeostatic effects
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27
Q

toxic effects of prostaglandin inhibitors target

A
  • renal homeostasis
  • gastric mucosal production
  • platelet function
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28
Q

therapeutic effects of prostaglandin inhibitors target

A
  • pain
  • inflammation
  • fever
  • limited homeostatic effects
  • platelet function
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29
Q

selectivity of NSAIDS for COX

A
  • vary in their selectivity
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30
Q

more toxicities associated with which COX inhibitors

A
  • COX1

- due to inhibition of homeostatic function

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31
Q

fewer toxicities associated with which COX inhibitors

A
  • COX2
  • but not no toxicities
  • due to inhibition of inflammatory effects
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32
Q

prostaglandin E2 (PGE2) role

A
  • responsible for producing and maintaining gastric mucosal protection lining the inside of the stomach
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33
Q

prostaglandin E2 target toxicities of NSAID use

A
  • long term use can lead to deterioration of mucous layer

- can lead to gastric bleeding or ulcers

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34
Q

thromboxane A2 (TXA2) role

A
  • promotes platelet activation for clotting
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35
Q

thromboxane A2 toxicities of NSAID use

A
  • long term use will increase risk of bleeding disorders
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36
Q

thrombaxane A2 target therapeutic of NSAID use

A
  • inhibition of clotting may be therapeutic when treating patients to prevent MI or thrombotic/embolic stroke
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37
Q

aspirin MOA

A
  • irreversibly inhibits COX1/2 through covalent modification

- of acetyl group

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38
Q

aspirin irreversible activation of COX-1 effect

A
  • leads to inhibition of TXA2

- avoiding vasoconstriction and platelet aggregation induced by this prostanoid

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39
Q

aspirin acetylation of COX-2 effect

A
  • inhibition of prostaglandin production

- production of eicosatetraenoic acid as a substrate for new biologically active mediators aspirin triggered lipotoxins

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40
Q

aspirin approved uses

A
  • pain
  • inflammation - RA, OA
  • fever - rheumatic fever
  • ischemic conditions
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41
Q

Off label uses of aspirin

A
  • Kawasaki disease
  • prevention of pre-eclampsia
  • prevention of colorectal cancer
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42
Q

symptoms of Kawasaki disease

A
  • conjunctivitis
  • swollen lymph nodes
  • swollen hands and feet
  • changes in oral mucosa
  • rash
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43
Q

diagnosis Kawasaki

A
  • 4 out of 5 criteria

- + high fever

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44
Q

treatment for Kawasaki

A
  • aspirin + intravenous immunoglobulin
45
Q

definition of pre-eclampsia

A
  • hypertension associated with pregnancy affect 2-8% of pregnancies worldwide
46
Q

how aspirin helps prevent colorectal cancer

A
  • inhibits production of PGE2

- PGE2 associated with colon cancer

47
Q

Aspirin toxicities

A
  • Reye’s syndrome
  • aspirin-sensitive asthma
  • acute/chronic aspirin poisoning
48
Q

Reye’s syndrome affects

A
  • children treated with aspirin during viral infections

- treat with acetaminophen or ibuprofen instead

49
Q

Reye’s syndrome mortality

A
  • 20-40% mortality

- long-term neurologic effects for many survivors

50
Q

aspirin sensitive asthma mechanism

A
  • shut down COX
  • increase rate at which arachidonic acid is converted to lipooxygenases into leukotrienes
  • leukotrienes cause bronchoconstriction
51
Q

pediatric OD numbers

A

> 150mg/kg

52
Q

OTC tablets of aspirin doses

A
  • 81 mg
  • 100 mg
  • 300 mg
53
Q

OTC drugs and aspirin

A
  • many OTC drugs contain aspirin.

- read the label!

54
Q

ibuprofen (Advil, Motrin, Nuprin) inhibits

A
  • eicosanoids
  • its an NSAID
  • COX1/2 inhibitor
55
Q

naproxen (Aleve) inhibits

A
  • eicosanoids
  • its an NSAID
  • COX1/2 inhibitor
56
Q

ibuprofen vs naproxen

A
  • four dose/day vs two dose/day

- naproxen has a long biological half life

57
Q

Vds of ibuprofen and naproxen

A
  • low Vds due to plasma protein binding
58
Q

COX2 selective inhibitors

A
  • Celebrex (Celecoxib)

- Vioxx (Rofecoxib)

59
Q

advantages of COX2 inhibitors

A
  • fewer GI toxicities than COX1 inhibitors
60
Q

disadvantages of COX2 inhibitors

A
  • more CV toxicities (heart attack)
61
Q

why Rofecoxib inhibitors can lead to more heart attacs

A
  • inhibits synthesis of anti-clotting factor prostaclyin (PGI12)
  • increases risk of clotting
62
Q

leukotriene inhibitors MOA

A
  • inhibit synthesis or activity of leukotrienes
63
Q

leukotriene inhibitors examples

A
  • Zileuton

- Montelukast

64
Q

Zileuton MOA

A
  • inhibits lipoxygenase

- blocks SYNTHESIS of leukotrienes

65
Q

Montelukast MOA

A
  • leukotriene antagonist (inhibits receptors)

- blocks FUNCTION of leukotrienes

66
Q

leukotriene inhibitor indications

A
  • good for use in asthma
67
Q

cortisol-derived synthetic drugs

A
  • hydrocortisone
  • prednisone
  • methylprednisolone
  • dexamethasone
68
Q

corticosteroids functions

A
  • inhibitors of eicosanoid production
69
Q

corticosteroids MOA

A
  • alter transcription of cytokines genes in target cells
70
Q

steroid hormones hydrophoblic/philic

A
  • hydrophoblic

- pass through PM to reach their target receptors in the cytoplasm

71
Q

corticosteroids and pro-inflammatory cytokines

A
  • inhibit expression of pro-inflammatory cytokines
72
Q

corticosteroids and anti-inflammatory cytokines

A
  • induce expression of anti-inflammatory cytokines
73
Q

examples of anti-inflammatory cytokines

A
  • lipocortin/annexin 1
74
Q

role of lipocortin

A
  • inhibits phospholipase A2
75
Q

specificity of corticosteroids?

A
  • broad spectrum
76
Q

corticosteroid toxicities

A
  • immunosuppression

- hypercortisolism/cushing syndrome

77
Q

corticosteroid oral inhalation effects

A
  • thrush

- pneumonia

78
Q

symptoms of hypercorticolism/cushing?

A
  • weight gain
  • moon face
  • buffalo hump
  • thinning and fragility of skin
  • new or worsened high blood pressure
  • increased risk of fractures
79
Q

moon face and buffalo hump caused by

A
  • redistribution of fat by high corticosteroid levels
80
Q

two proteins down regulated by corticosteroid use

A
  • osteocalcin - weakens bone

- keratin - weakens skin

81
Q

calcinuerin inhibitors MOA

A
  • inhibit T-cell activation

- block TCR signaling through calcineurin

82
Q

calcineurin inhibitor drug examples

A
  • cyclosporin
  • tacrolimus

Cows (Cal) Cycle Ta Cro (To Grow)

83
Q

calcineurin role

A
  • activates NFAT which is a transcription factor for IL-2
84
Q

calcineurin inhibitor important toxicities

A
  • malignancies (black box warning)

- non-hogkin’s lymphoma

85
Q

more important pro-inflammatory cytokines

A
  • IL-1
  • IL-2
  • IL-3
  • IL-6
  • IL-8
  • IL-11
  • IL-12
  • TNFa
86
Q

JAK/Stat inhibitor drug example

A
  • Tofacitinib

JAK/STAT sitting together - citing

87
Q

JAK/Stat inhibitor MOA

A
  • inhibiting signaling through IL-2 receptor
88
Q

process in JAK/Stat that Tofacitinib inhibits?

A
  • when IL-2 binds to CD25 on T cells, JAK binds with STAT to trigger synthesis of new cytokines
  • Tofacitinib blocks this
89
Q

cytokine antibody drug examples

A
  • Adalimumab, Infiximab, Etaneracept (anti-TNFa)
  • Mepolizumab (anti-IL-5)
  • Tocilizumab (anti-IL-6)

Cyto - signal
AIN(En)TM - America’s Intellectual Next Top Model

90
Q

cytokine antibody MOA

A
  • antibody molecules that bind to cytokines to render them inactive
91
Q

Etaneracept

A
  • antibody-like or non-antibody protein
92
Q

administration of Anti-TNFa antibodies

A
  • large proteins (GI will digest/too large to be absorbed)
  • must be administered IV or IM
  • expensive!!
93
Q

Mepolizumab useful in treating

A
  • eosinophilic asthma
94
Q

DNA synthesis inhibitors MOA

A
  • inhibits proliferation of T cells

- inhibits synthesis of purine nucleotides

95
Q

DNA synthesis inhibitor drug examples

A
  • Azathioprine
  • Mycophenolate
  • Methotrexate

DAMM

96
Q

Azathioprine MOA

A
  • converted to MeTIMP and TGTP

AZA don’t know what ya heard about me but I’m a mutha fuckin’ TIMP

97
Q

MeTIMP role

A
  • inhibits purine synthesis

- primary therapeutic effect

98
Q

TGTP role

A
  • aberrant nucleotide that incorporates into DNA instead of GTP
  • destroys daughter cells once they are produced
99
Q

importance of administration of Azathioprine

A
  • administered as a pro-drug first
100
Q

Azathioprine toxicites

A
  • mutagenicity if daughter T cell survives
  • acute myeloid leukemia
  • lung adenocarcinoma
101
Q

Mycophenolate MOA

A
  • inhibits inosine monophosphate dehydrogenase which catalyzes a step in GTP production
102
Q

Methotrexate MOA

A
  • inhibits dihydrofolatic acid reductase, which synthesizes a folate precursor
  • folate necessary for purine synthesis
103
Q

methotrexate versus folate precursor

A
  • competitive antagonist of folate precursor molecule for binding to the DHFR molecule
  • you must take supplemental folate
104
Q

toxicities of DNA synthesis inhibitors

A
  • embryotoxic/fetal toxic
105
Q

Category D toxicity drugs

A
  • Azathioprine

- Mycophenolate

106
Q

Category X toxicity drugs

A
  • Methotrexate
107
Q

mTOR inhibitor drug example

A
  • Sirolimus (Rapamycin)

(immature) mTOR (serious) Sirolomus (rapping) rapamycin

108
Q

mTOR inhibitor MOA

A
  • inhibits mTOR which carries the signal to the nucleus when IL2 binds T cells
109
Q

Cytokine receptor antibodies drug examples

A
  • Anakinra (IL-1R, various) (Ana Kendrick is Number 1)
  • Basilixumab (IL-2R, T cells) (Drop that Base at 2 AM)
  • Benralizumab (IL-5R, eosinophils) (Ben Folds Five)
  • Omalizumab (IgE, B cells) (OMG except it’s E)
  • Rituximab (CD20, B cells) (Wear at Tux at age 20 people FRIENDS ARE GETTING MARRIED AND IT’S FUCKING TERRIFYING)

IMM Exam 2 (15 decks)

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