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22 Cards in this Set

  • Front
  • Back
Gout- biochem
due to elevated concentration of uric acid (UA) in blood and tissues due to overproduction or undersecretion- problems in the purine catabolism (AG)

Important enzymes- Adenine deaminase, guanine deaminase, and xanthine oxidase
Gout- pathophys
elevated UA levels cause the formation of sodium urate crystals (tophi)- joints become inflamed, painful, and arthritic

(can be deposited in kidney tubules and lead to a damaged kidney and decreased excretion of UA)
NSAIDs- for Gout
Acute Gout (esp Indomethacin)

relieve acute inflammation

*Indomethacin has severe CNS side effects

Aspirin is contraidicated at low dose
Acute Gout

block the mobilization of the granulocytes leading to inhibition of inflammation- disrupts cellular microtubules

*used prophylactically when initiating therapy with probenecid or allopurinol

Side effects (due to microtuble effect)- GI distress, bone marrow depression, and alopecia
Chronic Gout

Xanthine oxidase inhibitor- allopurinol and its metabolite alloxanthine are able to inhibit xanthine oxidase- blocks overproduction of UA

Side Effects: Initiation of therapy can increase frequency and severity of acute attacks
Chronic Gout

uricosuric agent- targets the anion exchanger needed for UA reabsorption- promotes excretion of UA based on blocking reabsorption

Side Effects:increase in frequency and severity of acute attacks or kidney stones
Non-Pharmacological Tx in Gout
Avoid purine-rich foods (liver)
Avoid excessive alcohol
Increase fluid intake
Alkalinize urine
Rheumatoid Arthritis (RA)
systemic inflammatory disorder- autoimmune mechanism that results in joint inflammation and bone destruction

symptoms: pain, stiffness, and swelling of peripheral joints
for analgesic and anti-inflammatory effects

block PG production by blocking cyclooxygenase (COX)

* no effect on the disease process
Selective COX-2 inhibitors
Celecoxib and Rofecoxib

Not constituatively on like COX1- COX2 expression is inducible in response to inflammation

Side effects: dyspepsia, diarrhea, nausea, vomiting, skin reactions, CNS, etc.
Disease-modifying antirheumatic drugs-
1. Immunosuppressant agents: Methotrexate (MTX), Leflunomide, Azathioprine
2. Gold compound such as auranofin
3. Other secondary agents such as Hydroxychloroquine
4. Glucocorticoids such as prednisone
5. Cytokine antagonists: etanercept, infliximab, anakinra
Methotrexate (MTX)
most widely used DMARD for RA

MTX inhibits dihydrofolate reductase, lymphocyte proliferation and cytokine production, and interferes with migration of leukocytes

*anchor agent in combination therapies.
-rapid onset of action (2-3 wks)
DMARD for RA patients- immuno-suppressant- alternative to MTX

Inhibits dihydroorotate dehydrogenase in pyrimidine synthesis, thus preventing DNA replication and the synthesis of RNA and proteins in immune cells
DMARD for RA- Gold compounds

aren’t used much anymore mechanism is unclear

high incidence of adverse reactions
DMARD for RA- Other secondary agents

anti-malarial drug with anti-RA activity
often used with an NSAID for mild RA.

Side Effects: retinopathy (blurred vision and night blindness)
DMARD for RA- Glucocorticoids

use is infrequent because of side effects
Cytokine antagonists
DMARD for RA- newest generation ($$$)
TNF antagonists: etanercept, infliximab, adalimumab
IL-1 antagonists: anakinra

*The 2 major cytokines in RA are TNF ( inflammatory reaction) and IL-1 (cartilage destruction)
Etanercept (Enbrel)
DMARD for RA- cytokine antagonist

soluble TNF-alpha receptor fused with the Fc portion of an antibody- binds to and clears TNF-_ to prevent its action with endogenous receptors.

*used in combination with MTX- injected subcutaneously twice a week
Infliximab (Remicad)
DMARD for RA- cytokine antagonist

a chimeric humanized anti-TNF-_ monoclonal antibody that binds to and clears TNF-_
Adalimumab (Humira)
DMARD for RA- cytokine antagonist

HUMAN IgG1 monoclonal antibody against TNF-_
Anakinra (Kineret)
DMARD for RA- cytokine antagonist

recombinant IL-1 receptor antagonist (IL-1Ra) which competitively inhibits the binding of IL-1 to IL-1R1

subcutaneously injection, and a response is seen within 4-13 wks
Combination therapy for RA
MTX is the anchor drug:

MTX + etanercept
MTX + infliximab
MTX + leflunomide
MTX + sulfasalazine and hydroxychloroquine