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29 Cards in this Set

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a. Asthma

-glucocorticoid, cromolyn 사용

b. DMARD (disease modifying anti rheumatic drugs)

-NSAIDs, TNFa blocker, Anti IL6, Anti CD20

c. NSAIDS = aspirin.

d. Gout 치료 = colchicine, probenecid, allopurinol.


-chronic bronchiole or lung hyperreactivity that obstructs airflow; the obstruction is reversible.

Asthma treatment

Omalizumab: humanized, monoclonal anti-IgE antibody

Mepolizumab (Anti-IL5 mAbs): shown to reduce bronchila mucosa eosinophilia


-rheumatoid arthritis is an immunological disease that causes significant systemic effects.

Nonbiologicals: MTX (methotrexate), azathioprine

Biologicals: Abatacept, Rituximab, Tocilizumab, TNFa blocking agents

Abatacept (CTLA4-Ig)

-Inhibits the activation of T cells.

-Binds to CD80 & CD86, thus inhibiting the binding to CD28 and preventing the activation of T cell.

-TNFa 와 사용하면 serious infection 생길 수도 잇다.


-targets CD20 B lymphocytes --> leads to depletion of B cells

-used in combination with MTX.

-may develop rash


-Humanized Ab, binds to soluble and membrane bound IL6 receptors

-Indication: Moderate to severe rheumatoid arthritis resistant to TNF antagonists.

TNF a blocking agents

1. Down regulates macrophages and T cell function

2. RA, CNS 관절 질환, crohn's disease 등에 사용

3. Effective both as monotherapy and in combination with MTXs and other DMARDs.

4. Increased risk of tuberculosis.

eg) Adalimumab, Etanerecept, Infliximab


-Inhibition of AICAR transformylase.

-Accumulation of AICAR leads to the accumulation of AMP.

-AMP converted to adenosine, which is a potent inhibitor of inflammation


-inhibits prostaglandin biosynthesis

-downregulates IL1 production

-blocks platelet cycloxygenase.

Cyclooxygenase (COX)

COX1: constitutive

-physiologic production of PG in gastric mucosa, endothelium, platelet, kdiney

COX2: inducible

-catalyzes the synthesis of proinflammatory PG.

참고: phospholipid -> AA -> Prostaglandin (마지막 step 에 COX가 작용)

Selectivity for COX1 vs. COX2

-aspirin, ibuprofen, indomethacin, piroxicam: more effective in inhibiting COX1

COX2 selective

Celecoxib, Meloxicam

NSAIDs adverse effect

1. Nonselective: inhibits platelet aggregation

2. All NSAIDS are associated with GI ulcer and bleeding (COX2 selective 가 덜 그렇다)

3. Edema & Cardiovascular adverse effects should be considered in using COX2 selective agents. COX2 selective Inhibitor can cause renal toxicities.


-Irreversibly inhibits platelet COX so that aspirin's antiplatelet effect lasts 8-10 days

-Adverse effect: contraindication in childhood viral infection due to reye's syndrome

Reye's Syndrome

-Liver: fatty deposit

-Brain: edema

-Risk factor: youth, viral infection + Aspirin (involves mit. dysfunction by mitochondrial toxins)

COX 2 inhibitor

Celecoxib: may cause rashes; interacts with warfarin.

Meloxiam: Not as selective celecoxib; fewer GI symptom.

Diclofenac (Non-selective)

-elevation of serum ALT occurs more commonly than any other NSAIDs

-ophthalmic prep, topical gel 로 사용.

Ibuprofen (Non-selective)

-Has anaglgesic but low anti-inflammatory efficacy

-primary knee osteoarthritis & postsurgical dental pain 에 사용

-May antagonize the irreversible platelet inhibition induced by aspirin (장기 aspirin 복용자 금기약물)

Indomethacin (Non-selective)

-clinical indications: ophthalmic prep, oral cream (for gingival inflammation)

-drug interaction: probenecid prolongs indomethacin's half-life by inhibiting renal & biliary clearance.

Ketorolac (Non-selective)

-Promoted for systemic use mainly as an analgesic.

-used to replace morphine in postsurgical pain.


-nonselective COX inhibitor that inhibits PMN migration, decrease ROS production, inhibits lymphocyte function.

-다른 COX inhibitor 보다 peptic ulcer 가 심하다.


-analgesic effect

-Weak Cox inhibitor but possesses no significant anti-inflammatory effects (different from aspirin)


a. analgesic choice in patients allergic to aspirin, with hemophilia, a history of peptic ulcer or bronchospasm by aspirin.

b. children with viral infections


a. mild increase in hepatic enz

b. severe hepatotoxicity

c. renal dmg

Aspirin vs. Acetaminophen:


1. Gout is a metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate in joints and cartilage

2. Usually associated with a high serum uric acid level (hyperuricemia), a major end product of purine metabolism

Anti-Gout drug

1. Anti-inflammatory gout drug: colchicine (PMN억제함); NSAIDs 를 사용하면 증상 호전됨.

2. Uric acid inhibitor: allopurinol.

3. Uricosurics: probenecid. Uric acid 를 신장에서 배출시킨다.

4. NSAIDs: indomethacin.


-prevents polymerization into microtubule

-adverse effect: diarrhea


-inhibits xanthine oxidase

-azathipurine도 같이 주는 경우, 용량을 줄여야 한다.

-inhibits the metabolism of probenecid.

Uricosuric agents

eg) probenecid

-Dec tot body ppool of urate

-In a patient who excretes large amounts of uric acid, the uriosuric agents should not be used (due to the possible uric acid kidney stone formation)