This document discusses asthma, including its pathophysiology, triggers, symptoms, diagnosis and treatment. It notes that asthma involves inflammation, bronchospasm and excess mucus production. Common triggers include viruses, irritants, allergens and air pollution. Treatment involves bronchodilators, anti-inflammatories like corticosteroids, leukotriene modifiers and mast cell stabilizers. Medications are prescribed based on asthma severity and control.

1. By Linda Self

2. Key Terms
1. Ventilation
2. Perfusion
3. Diffusion
4. Pulmonary Circulation
5. Surfactant
6. pneumocytes

3. Asthma—inflammation, hyperreactivity,
and bronchoconstriction
GERD may cause
microaspiration/resultant nighttime cough
Antiasthma medications can also
exacerbate GERD

4. May be triggered by viruses
Irritants
Allergens
Can develop at any age
Seen more often in children who are
exposed to airway irritants during infancy

5. Bronchoconstriction
Inflammation
Mucosal edema
Excessive mucous

6. Mast cells
Chemical mediators such as histamine,
prostaglandins, acetylcholine, cGMP,
interleukins, leukotrienes are released
when triggered. Mobilization of
eosinophils. All cause movement of fluid
and proteins into tissues.
Bronchoconstrictive substances
antagonized by cAMP

7. Combination of chronic bronchitis and
emphysema
Bronchoconstriction and inflammation are
more constant, less reversibility
Anatomic and physiologic changes occur
over years
Leads to increasing dyspnea and activity
intolerance

8. Bronchodilators and anti-inflammatories

9. Step 1-Mild Intermittent—symptoms 2
days/week or less or 2 nights/month or
less. No daily medication needed; treat
with inhaled beta2 agonist
Step 2-Mild persistent—symptoms
>2/week but <1x/day or >2 nights/month.
In those >5 years old, use inhaled
corticosteroid, leukotriene modifier, Intal
(cromolyn), or sustained release
theophylline

10.  Step 2—Mild persistent
 Children 5 years and younger—inhaled
corticosteroid by nebulizer of MDI with a
holding chamber. Can also use leukotriene
modifier or Intal by nebulizer
 Step 3—Moderate persistent. Symptoms daily
and > one night per week.
 Older than 5yo—low to med. Dose
corticosteroid and long acting beta 2 agonist.
Alternatives p. 714

11.  Step 3—
 Children < 5 yo: low dose inhaled
corticosteroid and a long acting beta 2
agonist or medium dose inhaled
corticosteroid
 Step 4—Severe persistent—symptoms
continual during daytime and frequently at
night.
 >5yo—high dose inhaled corticosteroid, long
acting beta 2 agonist; intermittent admin. of
oral corticosteroids

12. Step 4—
Children less than 5 yo—same as for
adults and older children

13. Adrenergics—stimulate beta 2 receptors in
smooth muscle of bronchi and bronchioles
Receptors stimulate cAMP
=bronchodilation
Cardiac stimulation is an adverse effect of
these medications

14. Cautious use in hypertension and cardiac
disease
Selective beta 2 agonists by inhalation are
drugs of choice
Epinephrine sc in acute
bronchoconstriction

15. Proventil (albuterol)
Xopenex (levalbuterol)

16. Treatment of first choice to relieve acute
asthma
Aerosol or nebulization
May be given by MDI
Overuse will diminish their bronchodilating
effects>>>>tolerance

17. Foradil (formoterol) and Serevent
(salmeterol) are long acting beta 2
adrenergic agonists used only for
prophylaxis. Black box warning on
Serevent—use in deteriorating asthma can
be life-threatening
Alupent (metaproterenol)—intermediate
acting. Useful in exercise induced asthma,
tx acute bronchospasm.

18. Brethine (terbutaline)—selective beta 2
adrenergic agonist that is a long-acting
bronchodilator
When given subq, loses selectivity
Also used to decrease premature uterine
contractions during pregnancy

19. Block the action of acetylcholine in
bronchial smooth muscle when given by
inhalation
Action reduces intracellular guanosine
monophosphate (GMP) which is a
bronchoconstrictive substance
Atrovent (ipratropium)—caution in BPH,
narrow-angle glaucoma
Spiriva (tiotropium)

20. Theophylline
Mechanism of action unclear
Bronchodilate, inhibit pulmonary edema,
increase action of cilia, strengthen
diaphragmatic contractions, over-all anti-
inflammatory action
Increases CO, causes peripheral
vasodilation, mild diuresis, stimulates CNS

21. Contraindicated in acute gastritis and PUD
Second line
Narrow therapeutic window—therapeutic
range is 5-15 mcg/mLh
Multiple drug interactions

22. Suppress inflammation by inhibiting
movement of fluid and protein into tissues;
migration and function of neutrophils and
eosinophils, synthesis of histamine in mast
cells, and production of proinflammatory
substances
Benefits: decreased mucous secretion,
decreased edema and reduced reactivity

23. Second action is to increase the number
and sensitivity of beta 2 adrenergic
receptors
Can be given PO or IV
Pulmonary function usually improves
within 6-8 hours
Continue drugs for 7-10 days

24. Fewer long term side effects if inhaled
End-stage COPD may become steroid
dependent
In asthma, systemic steroids generally are
used only temporarily
Taper high dose oral steroids to avoid
hypothalamic-pituitary axis suppression

25. For inhalation:
Beclovent—beclomethasone
Pulmicor—budesonide
Aerobid—flunisolide
Flovent—fluticasone
Azmacort—triamcinolone
Most inhaled steroids are being
reformulated with HFA

26. Systemic use: prednisone,
methylprednisolone, and hydrocortisone
In acute, severe asthma—a systemic
corticosteroid may be indicated when
inhaled beta 2 agonists are ineffective

27. Leukotrienes are strong chemical
mediators of bronchoconstriction and
inflammation
Increase mucous secretion and mucosal
edema
Formed by the lipoxygenase pathway of
arachidonic acid metabolism in response
to cellular injury
Are release more slowly than histamine

28. Developed to counteract the effects of
leukotrienes
Indicated for long term treatment of
asthma in adults and children
Prevent attacks induced by some
allergens, exercise, cold air,
hyperventilation, irritants and ASA/NSAIDs
Not useful in acute attacks

29.  Injured cell
 Arachidonic acid
 XXXX
 Lipooxygenase
 Leukotrienes
 XXXX
 Bronchi, WBCs
 Bronchoconstriction

30. Singulair (montelukast) and Accolate
(zafirlukast) are leukotriene receptor
antagonists
Can be used in combination with
bronchodilators and corticosteroids
Less effective than low doses of inhaled
steroids
Should not be used during lactation
Can cause HA, nausea, diarrhea, other

31. Intal (cromolyn)
Tilade (nedocromil)
Prevent release of bronchoconstrictive and
inflammatory substances when mast cells
are confronted with allergens and other
stimuli
Prophylaxis only
Inhalation, nebulizer or MDI, nasal spray
as well

32. Xolair (omalizumab) works by binding to
IgE, blocking receptors on surfaces of
mast cells and basophils
Prevents release of chemical mediators of
allergic reactions
Adjunctive therapy
Can cause life-threatening anaphylaxis

33. Histamine is the first chemical mediator
released in immune and inflammatory
responses
Concentrated in skin, mucosal surfaces of
eyes, nose, lungs, CNS and GI tract
Located in mast cells and basophils
Interacts with histamine receptors on
target organs called H1 and H2

34. H1 receptors are located mainly on smooth
muscle cells in blood vessels and the
respiratory and GI tracts
H1 binding causes: pruritus, flushing,
increased mucous production, increased
permeability of veins—edema, contraction
of smooth muscle in
bronchi>>bronchoconstriction and cough

35. With H2 receptor stimulation, main effects
are increased secretion of gastric acid and
pepsin, decreased immunologic and
proinflammatory reactions, increased rate
and force of myocardial contraction

36. Are exaggerated responses by the
immune sysem that produce tissue injury
and possible serious disease
Allergic reactions may result from specific
antibodies, sensitized T lymphocytes, or
both, formed durng exposure to an
antigen.

37. Type I—immediate hypersensitivity, IgE
induced response triggered by the
interaction of antigen with antigen-specific
IgE bound on mast cells
Anaphylaxis is an example
Does not occur on first exposure to an
antigen
Can develop profound vasodilation
resulting in hypotension, laryngeal edema,
bronchoconstriction

38. Type II—IgG or IgM mediated which
generate direct damage to cell surfaces.
Examples include: blood transfusion
reactions, hemolytic disease of newborns,
hypersensitivity reactions to drugs such as
heparin or penicillin

39. Type III is an IgG or IgM mediated reaction
characterized by formation of antigen-
antibody complexes that induce
inflammatory reaction in tissues. Prototype
is Serum Sickness.
Immune response can occur following
antitoxin administration, pcn or sulfa drugs

40. Delayed hypersensitivity
Cell mediated response where sensitized T
lymphocytes react with an antigen to
cause inflammation, release of
lymphokines , direct cytotoxicity or both
Classic examples are tuberculin test,
contact dermatitis and some graft
rejections

41. IgE mediated
Inflammation of nasal mucosa caused by a
hypersensitivity reaction to inhaled
allergens
Presents with itching of throat, eyes and
ears
Seasonal and perennial
Can lead to chronic fatigue, difficulty
sleeping, sinus infections, postnasal drip,
cough and headache

42. Atrovent nasal spray
Beconase (beclomethasone)
Rhinocort (budesonide)
Flonase (fluticasone)
Nasonex (mometasone)
Nasalcrom (a mast cell stabilizer)

43. Type IV hypersensitivity reaction
Poison ivy an example
Usually occurs >24h after re-exposure

44. Allergic food reactions—result from
ingestion of a protein
Most common food allergy is shellfish,
others include milk, eggs, peanuts
Allergic drug reactions—unpredictable,
may occur 7-10 days after initial exposure
Pseudoallergic drug reactions—resemble
immune responses but do not produce
antibodies, i.e. anaphylactoid

45. Inhibit smooth muscle constriction in blood
vessels and the respiratory and GI tracts
Decrease capillary permeability
Decrease salivation and tear formation
Act by binding with the histamine receptor

46. Allergic rhinitis
Anaphylaxis
Allergic conjunctivitis
Drug allergies
Transfusions of blood products
Dermatologic conditions
Nonallergic such as motion sickness,
nausea and vomiting, sleep

47. Caution in pregnancy
BPH
Bladder neck obstruction
Narrow angle glaucoma

48. Bind to central and peripheral receptors
Can cause CNS depression or stimulation
Have substantial anticholinergic effects
Examples:
Chlor-Trimeton (chlorpheniramine)
Benadryl (diphenhydramine)
Vistaril (hydroxyzine)
Phenergan (promethazine)

49. Selective or nonsedating
Do not cross blood brain barrier
Examples:
 Astelin (azelastine)
Allegra (fexofenadine)
Claritin (loratadine)
Clarinex (desloratadine)
Zyrtec
Xyzal

50. Relieve nasal obstruction and discharge
Adrenergic
Rebound nasal swelling called “rhinitis
medicamentosa”
Afrin
Sudafed (pseudoephedrine)
Contraindicated in severe hypertension,
CAD, narrow angle glaucoma, TCAs or
MAOIs

51. Suppress cough by depressing cough
center in medulla or by increasing flow of
saliva
For dry, hacking, non-productive cough
Not recommended in children and
adolescents
Codeine, hydrocodone
dextromethorphan

52. Liquefy respiratory secretions
Guiafenesin

53. By inhalation to liquefy mucous
Mucomyst (acetylcysteine)
May be used in treating acetaminophen
overdose

54. Contain antihistamine, decongestant and
an analgesic
Chlorpheniramine, pseudoephedrine,
acetaminophen, dextromethorphan and
guiafenesin
Decongestants can cause stasis of
secretions
PM contains antihistamine
Tamiflu can be used to limit spread of virus
in respiratory tract

55. 1. Name two beta adrenergic bronchodilators
2. Name an inhaled steroid
3. Give an example of a leukotriene modifier
4. Name a mast cell stabilizer
5. Name a common infection after frequent use
of an inhaled steroid
6. Name a first generation H1 receptor
antagonist
7. Name a second generation H1 receptor
antagonist.
8. Name an H2 receptor antagonist.