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pharmacology year 3.1 > anti-inflammatory drugs > Flashcards

anti-inflammatory drugs Flashcards

1
Q

examples of inflammatory drugs

A
  • NSAIDs
  • SAIDs
  • disease modifying anti-rheumatoid drugs (DMARD) but now biological response modifiers (BRMs)
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2
Q

what are the pathways for arachidonic acid?

A
  • cyclo-oxygenase producing prostaglandins
  • lipo-oxygenase producing leukotrienes
  • CYP450 producing EET
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3
Q

what is eicosanoids?

A

antacids

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4
Q

what is COX 1?

A
  • control homeostasis production of prostaglandins
  • housekeeping genes
  • expressed in most tissues
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5
Q

what is COX 2?

A
  • increased production of prostaglandin in certain conditions eg: inflammation and cancer
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6
Q

what is COX 3?

A

predominantly found in CNS

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7
Q

where is PGE2 (prostanoids) located and its effect?

A
  • in many cell types as inflammatory cells
  • contraction and relaxation of smooth muscle
  • immunosuppressive and anti-inflammatory
  • fever
  • gastric secretion and inhibition
  • form cancer and promotes metastasize
  • promotes angiogenesis
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8
Q

where is PGI2 (prostanoids) located and its effect?

A
  • in vascular endothelium
  • cause vasodilation
  • inhibit platelets aggregation
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9
Q

where is PGD2 (prostanoids) located and its effect?

A
  • in mast cells
  • cause vasodilation
  • inhibit platelets aggregation
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10
Q

where is TXA2 (prostanoids) located and its effect?

A
  • in platelets
  • cause vasoconstriction
  • promotes platelets aggregation
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11
Q

what are the main aims for anti-inflammatory drugs?

A
  • relieve pain

- arrest tissue damage

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12
Q

what are the 5 major actions in NSAIDs?

A
  1. anti-inflammatory action
  2. analgesic effect
  3. antipyretic effect
  4. anti-platelet effect
  5. anti- cancer effect
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13
Q

what NSAIDs do in anti-inflammatory action?

A

decrease in PGE2 and PGI2, reduce vasodilation

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14
Q

what NSAIDs do in analgesic action?

A

decrease PG production results in decrease sensitivity of nerves to inflammatory mediators

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15
Q

what NSAIDs do in antipyretic action?

A

largely inhibition of PG production in hypothalamus

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16
Q

what NSAIDs do in anti-platelets action?

A
  • reduction in TXA2
  • preventing platelets aggregation
  • prolong bleeding time
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17
Q

what NSAIDs do in anti-cancer action?

A
  • reduce PGE2 formation
  • inhibition of tumour cell proliferation
  • enhance tumour cell apoptosis
  • inhibition of angiogenesis
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18
Q

side effects of NSAIDs in GI (most common)

A
  • GI bleeding
  • ulcer disease
  • perforation in GI tract
  • due to inhibition of PG that protect the mucosa from acidic
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19
Q

side effects of NSAIDs in renal

A
  • cause renal insufficiently due to inhibition of PGE and PGI
  • neuropathy if chronic use
20
Q

side effects of NSAIDs in blood

A
  • disturbance in platelets function

- increase bleeding time

21
Q

side effects of NSAIDs in liver

A

failure to excrete drugs

22
Q

side effects of NSAIDs (coxibs) in heart

A
  • MI
  • angina
  • stroke
  • TIA
23
Q

examples of NSAIDs in cox 1 selective

A
  • aspirin
  • sulindac
  • indomethacin
24
Q

examples of NSAIDs in non-selective cox 1

A
  • ibuprofen

- paracetamol

25
Q

examples of NSAIDs in both selective and non cox 1

A
  • flurbiprofen

- diclofenac

26
Q

examples of NSAIDs in cox 2 selective

A
  • celecoxib

- rofecoxib

27
Q

aspirin?

A
  • oldest NSAIDs

- irreversibly inhibit cox 1 and cox 2

28
Q

side effects of aspirin

A
  • gastric ulcer
  • asthma
  • diabetes
  • gout
  • hypocoagulation state
  • reye’s syndrome in children
29
Q

drugs interactions with aspirin

A
  • increase warfarin
  • heparin
  • increase insulin
  • increase phenytoin
  • increase methotrexate
30
Q

ibuprofen?

A
  • competitive inhibitor of cox 1 and cox 2
  • better tolerated than aspirin and indomethacin
  • fewer GI problems
31
Q

indomethacin and sulindac?

A
  1. not normally used as analgesic/ anti-pyretic
  2. potent anti-inflammatory agents
  3. indomethacin:
    - less tolerated than aspirin and ibuprofen
    - high GI problems
  4. sulindac:
    - better tolerated than indomethacin
    - fewer GI reactions
32
Q

paracetamol?

A
  • suitable for children
  • effective analgesic and anti-pyretic
  • weak anti-inflammatory agents
  • well tolerated
  • overdose cause hepatotoxicity
  • max daily dose 4 g
33
Q

what are celecoxib and rofecoxib?

A
  • cox 2 selective inhibitors
  • competition inhibition of cox 1
  • less serious GI reactions
34
Q

side effects of cox 2 inhibitor

A
  • small GI disturbances
  • dizziness
  • bronchitis
  • coughing
  • pharyngitis
  • rhinitis
  • somnolence
  • insomnia
  • cardiac problems
35
Q

5-lipoxygenase inhibitors?

A
  • blocks antigen and exercise induced asthma
  • reduce underlying inflammation
  • low potency, short half life
  • eg: zileutin
36
Q

cysteinyl leukotriene antagonists?

A
  • competitive antagonist at LT receptor
  • prevents aspirin-induced bronchoconstriction
  • eg: zafirlukast, montelukast, pranlukast
37
Q

dual cox 5-LO inhibitors?

A
  • competitive inhibitor of 5LO and cox 2
  • improved tolerability
  • eg: licofelone
38
Q

indirect inhibitor?

A
  • still under development
39
Q

examples of DMARD

A
  • methotrexate (common use)
  • leflunomide
  • chloroquine (treatment of malaria)
  • sulfasalazine
  • azathioprine
40
Q

DMARD?

A
  • slow onset of action
  • mechanism unclear
  • variable efficacy
  • many side effects
41
Q

biological response modifiers (BRM)?

A
  • quick onset of action
  • target specific receptor
  • fewer side effects
42
Q

examples of TNF inhibitors (BRM)

A
  • etanercept
  • infliximab (mouse gene)
  • adalimumab (100% human genes)
43
Q

examples of anti-interleukin therapy (BRM)

A
  • IL-1 anakinra

- IL-6 tocilizumab

44
Q

examples of B-cell depleting theraphy (BRM)

A

rituximab

45
Q

examples of blocking cell adhesion and migration

A
  • teplizumab

- daclizumab

46
Q

examples of blocking T cell coreceptors

A

abatacept

47
Q

side effects of TNF inhibitor

A
  • fungal infection
  • reactivation of myco tuberculosis
  • malignancy/lymphoma
  • congestive heart failure
  • demyelination
  • autoantibodies
  • congenital abnormalities

pharmacology year 3.1 (8 decks)

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