Gout, Migraine Flashcards

1
Q

Rheumatoid arthritis

  • disease
  • treatment
A
  • auto-immune disease = + immune cells active = + cytokines needed to communicate with them
  • count number of inflamed joints before and after treatment to see if it was effective
  • treatment: act on immune cells directly
  • Traditional DMARs - monotherapy (leflunomide) or combination therapy
  • Glucocorticoids combined with DMARDs
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2
Q

Anti-rheumatic drugs

A
  • NSAIDs
  • Non-biologic disease modifying anti-rheumatic drugs (DMARDs) – methotrexate, leflunomide, sulfasalazine, gold salts
  • Biologic disease modifying anti-rheumatic drugs (DMARDs) - abatacept, rituximab, tocilizumab, anakinra, adalimumab, etanercept, infliximab
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3
Q

Methotrexate

-mechanism of action (4)

A
  • inhibits enzymes involved in the purine metabolism, leading to accumulation of Adenosine, which is a inhibitor of inflammation
  • DNA and RNA synthesis is inhibited
  • Anti-folic agents –> use folic acid to decrease side effects
  • inhibit dihydrofolate reductase = affect lymphocytes and macrophages function
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4
Q

Methotrexate

  • pharmacokinetics (4)
  • indications (6)
  • adverse effects (3)
A
  • Non-biologic disease modifying anti-rheumatic drug
  • 70% is absorbed after oral administration
  • 1/2 life is 6-9 hours
  • Excreted principally in the urine

-rheumatoid arthritis, psoriasis, Wegener’s granulomatosis, giant cell arteritis, lupus, vasculitis

  • nausea, mucosal ulcers
  • leukopenia, anemia, stomatitis, GI ulcerations, alopecia
  • contraindicated in pregnancy
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5
Q

TNF inhibitors

  • names (3)
  • adverse effects
A

-adalimumab, etanercept, infliximab

  • injection site reactions (adalimumab, etanercept)
  • infusion reactions (infliximab)
  • infectious complications (tuberculosis)
  • development of blocking antibodies
  • other –> lymphomas, vasculitis, congestive heart failure
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6
Q

Gout

  • disease
  • treatment
A

-too much uric acid = some drugs decrease uric acid production and some increase uric acid elimination

  • acute gout attacks - NSAID, corticosteroids, Colchine
  • Prevent episodes - allopurinol, febuxostat
  • urate lithiasis - probenecid, pegloticase
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7
Q

Colchine

-mechanism of action

A
  • used to treat acute between gout attacks
  • relieves the pain and inflammation in 12-24h without other analgesic effects
  1. bind to intracellular protein tubulin
  2. prevents its polymerization into microtubules
  3. leads to inhibition of leukocyte migration and phagocytosis

-it also inhibits the formation of some leukotrienes

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8
Q

Colchine

-adverse effects (4)

A
  • diarrhea, nausea, vomiting, abdominal pain
  • hepatic necrosis
  • acute renal failure
  • hair loss, bone marrow depression, peripheral neuritis
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9
Q

Allopurinol

  • pharmacokinetics
  • mechanism of action
A
  • used between gout attacks
  • 80% absorbed (oral)
  • long duration of action - given only once a day

-uric acid is produced from xanthine –> allopuriol inhibits xanthine oxidase = decrease uric acid production

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10
Q

Allopurinol

  • indications (2)
  • adverse effects (5)
A
  • chronic gout in period between attacks
  • when starting, colchine or NSAID should be used until steady state of uric acid is normalized and they should be co-administered for 6 months or longer
  • GI intolerance
  • bone marrow depression
  • aplastic anemia
  • hepato-toxicitiy
  • cataracts
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11
Q

Febuxostat

A

we dont need to know

huhuhuhu

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12
Q

Uricosuric drugs

  • name
  • mechanism of action
  • contraindication
A
  • Probenecid
  • inhibit active transport site for re-absorption and secretion in proximal renal tubule = net reabsorption of uric acid in the proximal tubule is decreased = high amount will be eliminated in the urine
  • patients with renal failure
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13
Q

Why shouldn’t aspirin be used for the analgesia of gout?

A

Because it causes the net retention of uric acid by inhibiting the secretory transporter

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14
Q

Uricosuric drugs

  • name
  • indications
  • adverse effects
A
  • Probenecid
  • in gouty patients with under excretion of uric acid when other drugs are contraindicated. Should not be started until 2-3 weeks after an acute attack
  • GI irritation, rash, nephrotic syndrome, aplastic anemia
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15
Q

Pathogenesis of migraine

A
  1. initiating event may be abnormal neuronal discharge
  2. Localized spreading depression - aura
  3. Sensitization of central pain pathways
  4. aura = constriction of blood vessels - partial ischemia
  5. acute migraine attack
  6. vessels are dilated (by serotonin), Trigeminal nerve endings are activated
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16
Q

Pathogenesis of migraine

-Cortical spreading depression (CSD) and Neurogenic theory

A
  1. propagating wave of depolarization of neurons and glial cells
  2. this wave activates trigeminal nerve
  3. causing a neurogenic inflammation via the release of neuropeptides
  4. creating migraine
17
Q

Clinical presentation of migraine

A
  • symptoms may vary between patients
  • headache pain, aura + combination of other symptoms
  • nausea, phonophobia (aversion to sound), photophobia (aversion to light)
  • aura - visual disturbances (most of times)
  • neck pain, nasal congestion, fatigue…
18
Q

Migraine treatment

-Acute attacks

A
  • 5-HT1D partial agonists - Ergotamine

- Triptans - Sumatriptan, Naratriptan

19
Q

Triptans

-mechanism of action

A
  • induce vasoconstriction in cranial blood vessels
  • inhibit the release of neuropeptides
  • direct inhibition of neuronal activation, reducing central pain transmission via activation of 5-HT1D and 5-HT1F receptors
20
Q

Triptans

  • names
  • indications
  • contraindication
  • adverse effects
A
  • sumatriptan, naratriptan
  • acute migraine attacks
  • coronary heart disease, not controlled hypertension
  • coronary vasoconstriction, arrhythmias