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1. Anti-Inflammatory and Anti-asthmatic Agents MODULE F
2. Objectives List two mast cell stabilizers.
Describe and diagram the antigen/antibody reaction on mast cells
Explain which antibody is elevated in allergic asthma.
List three mediators that are released with inflammation.
Explain the effects of chemical mediators such as histamine and leukotrienes on airway epithelium.
3. Objectives Given signs and symptoms, differentiate between the early and late phase of an inflammatory response.
Describe how cromolyn sodium and nedocromil are anti-inflammatory agents.
State the generic and trade names, modes of action, adverse reactions, routes of administration, dosages, and adverse reactions for cromolyn sodium and nedocromil sodium.
State the origin of corticosteroid secretion.
Describe why corticosteroids are now considered first line drugs in the treatment of asthma.
Describe the pathway for the release and control of corticosteroids in the body.
4. Objectives Define HPA insufficiency.
Differentiate between systemic and inhaled corticosteroids.
List three actions of steroids on inflammation.
Describe the process of weaning a patient from steroids.
List four side effects or adverse reactions of steroid administration.
State the trade and generic names of the inhaled steroids discussed in class.
5. Objectives Describe how a RCP can decrease the incidence of oral fungal infections when administering aerosolized steroids.
List three leukotrienes inhibitors discussed in class.
State two side effects of leukotrienes.
State how leukotrienes are administered.
Describe the cellular mechanism for leukotriene production.
State three medication types that are used for upper-airway congestion.
State the IgE inhibitor used to treat asthma.
6. Anti-Inflammatory Drugs Non-Steroidal Anti-inflammatory
Mast Cell Stabilizers or anti-asthmatics
Leukotriene Antagonists (anti-leukotrienes)
Corticosteroids or Steroids
8. Mechanism of Inflammation Mast Cells, eosinophils, macrophages, basophils are found in submucosa.
The cells contain granules that are storehouses of the chemical mediators of lung inflammation.
Antigen-Antibody reactions causes the influx of Ca+2 into the cells and release of mediators.
IgE primary antibody
9. Mechanism of Inflammation Mediator Release
Vasodilation resulting in mucosal edema
Increased vascular permeability
Increased mucus gland secretion
10. Mediators of Inflammation Histamine
Platelet Activating Factor
Eosinophil Chemotactic Factor of Anaphylaxis (ECF-A)
Neutrophil Chemotactic Factor of Anaphylaxis (NCF-A)
Leukotrienes (formerly known as slow-reacting substance of anaphylaxis ? SRS-A)
11. Explanation of Mast Cell rupture (Degranulation)
Figure 7-1, p. 132
Mast cells are found throughout the body and their sensitization explains the watery eyes, runny nose, etc. that accompanies an allergic reaction.
12. Phases of Inflammatory Response in Asthma Early phase - Immediate
Late phase ? 6 to 8 hours after exposure
13. Early Phase Local vasodilation
Increased vascular permeability
14. Late Phase Effect of WBC (lymphocyte) and other mediators
Hypersecretion of mucus and mucosal swelling
Breakdown of Mast Cell releases Arachidonic Acid
Production of leukotrienes
16. Goal of Therapy Stop Mast Cell from degranulating
Stop specific inflammatory processes
Broad spectrum response
17. Mast Cell Stabilizers Prevent Ca+2 influx into the cell, thereby preventing mediator release.
These medications do not operate through the C?AMP system and do not stimulate b or a receptor sites
Best used in limited populations and mild asthma
18. Indications for Mast Cell Stabilizers
Prophylactic management of Asthma.
Pre-treatment for expected exposure.
Prevention of exercise induced asthma
Do not use to treat an asthmatic attack
19. cromolyn sodium (1973) Small Volume Nebulizer
Supplied in a 2 mL ampule (unit dose) containing 20 mg (20 mg/2 mL).
Give one ampule QID; may need to add additional diluent (2 mL may nebulize too quickly).
2 inhalations QID
Ophthalmic and Nasal solutions available
20. Hazards/Adverse Reactions Generally well tolerated
Feeling of chest tightness
Give b2 agonist prior to administering Cromolyn
21. nedocromil sodium (1992) Tilade
2 inhalations QID
Side Effects similar to cromolyn
22. Adrenocorticosteroids Secreted from the adrenal cortex.
Epinephrine secreted from adrenal medulla.
Multiple functions of medication.
Orally, parenterally, aerosol.
First line drugs in the management of asthma.
Reliever and controller medication.
Given to control allergies.
23. Adrenal Gland
24. HPA Axis Hypothalamic Pituitary Adrenal Axis
Low blood levels of steroids.
Hypothalamus is stimulated.
Sends impulse to Anterior Pituitary Gland which stimulates Corticotropin Releasing Factor (CRF).
This stimulates the formation of Adrenocorticotropin hormone (ACTH ).
ACTH in bloodstream stimulates Adrenal Cortex to produce and release Corticosteroids.
Increases blood levels of corticosteroids.
26. HPA Axis Diurnal or Circadian Rhythm
Levels are highest around 8:00 a.m.
Giving a patient steroids can suppress the body?s HPA axis (Body stops producing steroids).
If you stop the added steroids abruptly, the patient will experience HPA insufficiency and death can occur.
27. HPA Insufficiency Once adrenal suppression has occurred, the patient must be weaned slowly from systemic steroids.
This will allow for recovery of the body?s own secretion.
HPA insufficiency begins 1 day after use of systemic steroid administration.
28. Prevention of HPA Insufficiency Low dose steroid for 5 days or less.
Take steroids in the morning when natural levels are high.
High dose tapered regimen lasting 5-6 days.
Alternate day therapy.
30. Cushing's Syndrome Increased secretion of corticosteroids caused by a tumor of the adrenal glands
31. Aerosolized Steroids Advantage is that aerosolized steroids do not increase the blood levels of steroids
Does not cause HPA insufficiency
Less side effects
Goal is to try to gain control of asthma with the aerosolized steroids
May take 4-8 weeks for maximum improvement
32. Oral vs. Aerosol Corticosteroids
33. Common Inhaled Steroids
34. Adverse Reactions of Aerosolized Steroids Fungal Infections may occur after aerosol
Rinse mouth and use spacer
Throat irritation, hoarseness, dry mouth and coughing have occurred
HPA insufficiency may occur during transfer from systemic to aerosol steroids
Severe asthma may occur following withdrawal of oral/IV steroids
35. Adverse Reactions/Precautions Aerosolized steroids may not be adequate to control asthma during periods of stress and systemic administration may be necessary
36. Leukotriene ModifiersAnti-LeukotrienesLeukotriene AntagonistsLeukotriene Inhibitors
37. Leukotriene Inhibitors Indications
Prophylactic treatment of asthma
Not to be used to treat an asthma attack
39. Leukotriene Inhibitors zileuton (Zyflo)
12 years of age or older
Works well in aspirin-sensitive asthmatics
600 mg orally QID
Elevate liver enzymes
5 - Lipoxygenase inhibitor
40. Leukotriene Inhibitors zafirlukast (Accolate)
12 years of age or older
10 or 20 mg orally BID
Elevates liver enzymes
Blocks the leukotriene receptor site (leukotriene receptor antagonist)
41. Leukotriene Inhibitors montelukast (Singular)
4 mg packet of granules (6 to 23 months )
4 mg chewable tablet or 4 mg packet of granules (2 to 5 years of age)
5 mg chewable tablet (child)
10 mg tablet (adult)
Side effects: headache, influenza, abdominal pain
Blocks the leukotriene receptor site (Leukotriene receptor antagonist)
42. Disadvantage of Anti-leukotrienes Inhibit one mediator pathway
Asthma involves multiple mediators
50 ? 70% of patients respond to the medication
Trial & Error
43. Upper Airway Congestion Allergic Rhinitis
Prevents release of histamine.
Significant side effects
Newer generation are more ?forgiving?
Mast Cell Stabilizers (Nasalcrom)
Table 7-14 (page 140)
45. IGE Inhibitors omalizumab (Xolair)
46. Dosing http://www.xolair.com/hcp/dosing_calculator2.jsp