Dept. of Pharmacology, 8683
School of Medicine
Tulane University
1430 Tulane Ave
New Orleans, LA 70112
504-988-5444 or 800-347-5935

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Inflammation Block Session Objectives

Antihistamines & Histamine (Mondal)

  1. Explain how histamine is formed and describe the locations of its synthesis, storage and catabolism.
  2. Explain the difference between H1 and H2 receptors.
  3. Describe the "triple response of Lewis" and the mechanism(s) underlying each response.
  4. Describe the physiologic/pathophysiologic functions of histamine in: a) the cardiovascular system; b) the pulmonary system; c) non-vascular smooth muscle; d) sensory nerve endings; e) gastric glands.
  5. Explain the applications of H1 antihistamines in allergy, common cold, local anesthetics, motion sickness, migraine headache, and as antiemetics.
  6. Describe the applications of H2 antihistamines in duodenal ulcers, gastric ulcers, reflux esophagitis & as antacids.
  7. Describe the pharmacokinetic properties, and side effects of H1 and H2 antagonists.

Drug List:
H1 antagonists: bromopheniramine, chlorpheniramine, diphenydramine, fexofenadine, loratidine, hydroxyzine.
H2 blockers
: cimetidine, famotidine, nizatidine, ranitidine.
Antidegranulating drugs: cromolyn sodium, nedocromil sodium**
Histamine, betazole.

**no longer sold in the US (will not be tested on)

Eicosanoids (Kadowitz)

  1. Explain what eicosanoids are, which are the key enzymes in the overall eiccosanoid pathway, what drugs affect each enzyme and the rate-limiting step.
  2. Explain the termination of action of eicosanoids.
  3. Explain what COX1 and COX2 are; explain their physiologic and pathophysiologic significance.
  4. Explain what lipoxygenase products are & how they are formed.
  5. Describe the role of eicosanoids in: a) inflammation, b) pain & c) fever.
  6. Explain the meaning of “aspirin trials” and the theory supporting these trails.
  7. Describe the lipoxygenase pathway of arachidonic acid metabolism & explain how the biologic actions of these products differ from each other.
  8. Explain what PAF is.
  9. Explain what roles are played by PAF.
  10. Describe the role of omega-3 (fish oil) and omega-6 polyunsaturated fatty acids (arachidonic acid) in the formation of lipid mediators.

Drug list:

Selective COX 2 Inhibitors: celecoxib (Celebrex ®), rofecoxib (Vioxx ®)**
Nonselective COX inhibitor: aspirin
Leukotriene Inhibitors: montelukast, zafirlukast, zileuton

**Vioxx is not commercially available. It is mentioned for historical context only.

 NSAIDs & Acetaminophen (Kadowitz)

  1. Describe the common pharmacological effects of NSAIDs.
  2. List the common adverse effects of NSAIDs.
  3. Explain the special properties of aspirin.
  4. Explain the basis for aspirin resistance & aspirin allergy.
  5. Describe the dose-dependent mechanisms for, & symptoms of, aspirin toxicity.
  6. Explain the relationship between Reye's syndrome & aspirin.
  7. Explain the basis for COX-2 inhibitor toxicity.
  8. Explain the therapeutic use of prostaglandins and prostaglandin analogs.
  9. Explain the mechanism of action of acetaminophen and describe the symptoms of acetaminophen toxicity & its treatment.

Drug List:
Selective Cox-2 Inhibitor (NSAID): celecoxib (Celebrex ®)
Nonselective Cox Inhibitors (NSAIDs): aspirin, ibuprofen, naproxen, nabumetone & diclofenac.
Analgesic & Antipyretic: acetaminophen [Rx: N-acetylcysteine]

Glucocorticoids & Pharmacology of the Adrenal Cortex - JiTT Session (Beckman)

  1. Describe the physiologic regulation of the hypothalamic-pituitary adrenal axis.
  2. List the natural and synthetic adrenocortical steroids, their actions, and adverse effects.
  3. Describe the clinical use of glucocorticoids in asthma, Addison’s disease, Cushing’s syndrome.
  4. Explain the major clinical indications of agents that affect the glucocorticoid pathway.
  5. Explain the adverse effects of drugs that affect the glucocorticoid pathway.
  6. Explain what can happen if chronic treatment with glucocorticoids is abruptly ceased. 

Drug List:
prednisone, hydrocortisone, dexamethasone, triamcinolone, fludrocortisone, methylprednisone, mifepristone (RU-486), metyrapone


Treatment of Rheumatoid Arthritis (Clarkson)

  1. What role do different cytokines have on mediating the pathogenesis of rheumatoid arthritis including joint inflammation, destruction of bone & cartilage, and systemic effects?
  2. What are the general principles of management of rheumatoid arthritis?
  3. What role do NSAIDs and corticosteroids have in the treatment of rheumatoid arthritis?
  4. What is methotrexate's mechanism of action as a DMARD?
  5. What are the most commonly used subclasses of biologic DMARDs?
  6. What are the major side effects associated with the use of any DMARD?


Conventional agents: 

  • Antiinflammatory drugs (NSAIDs, corticosteroids)

Nonbiologic DMARDs: 

  • methotrexate, hydrochloroquine, leflunomide, sulfasalazine

Biologic DMARDs: 

  • TNF-alpha inhibitors (adalimumab, certolizumab, etanercept, golimumab, infliximab)
  • IL-6 receptor antagonists (tocilizumab)
  • IL-1 receptor antagonists (anakinra)
  • Biologic response modifiers (abatacept, rituximab)
  • Janus Kinase inhibitor (tofacitinib)

Treatment of Gout (Clarkson)

  1. How common is gout?
  2. What is the relationship between serum urate levels and foot pain (podagra)?
  3. What dietary factors may be contributing to TJ's condition?
  4. Could some of TJ's current medications be contributing to his symptoms?
  5. What drugs of first choice would you recommend TJ take to relieve his pain?
  6. What common anti-inflammatory drug should TJ avoid taking?
  7. What is the relationship between hyperuricemia and other common medical conditions?
  8. What treatment options are available to reduce the incidence of recurrent attacks of gout?


Antiinflammatory Drugs: 

  • ibuprofen
  • naproxen
  • indomethacin
  • keterolac
  • corticosteroids
  • colchicine

Urate lowering: 

  • allopurinol
  • febuxostat
  • probenecid
  • pegloticase

Immunosuppression Following Organ Transplant (Clarkson)

  1. What are the major events involved in the immunology of rejection?
  2. What are the therapeutic goals for the induction & maintenance phases of immunosuppression following an organ transplant?
  3. What is the rational for using multiple drug types to prevent rejection?
  4. What are the mechanisms of action of the major classes of immunosuppressant drugs?
  5. What are the major side effects of each class of immunosuppressant drugs that are commonly used?
  6. What are the two common side effects associated with chronic immunosuppression (independent of the drugs used to produce immunosuppression)?


Conventional agents: 

  • corticosteroids (prednisone)
  • antimetabolites (mycophenolate mofetil & azathioprine
  • calcineurin inhibitors (cyclosporin & tacrolimus)
  • mTor inhibitors (sirolimus & everolimus)

Antibody reagents: 

  • IL-2 receptor antagonist antibody (basiliximab)
  • Polyclonal anti-thymocyte antibodies (anti-thymocyte globulin)
  • Monoclonal anti-thymocyte antibodies (alemtuzumab)







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