By Linda Self

 Key Terms
1. Ventilation
2. Perfusion
3. Diffusion
4. Pulmonary Circulation
5. Surfactant
6. pneumocytes
 Asthma—inflammation, hyperreactivity,
 and bronchoconstriction
 GERD may cause
microaspiration/resultant nighttime
cough
 Antiasthma medications can also
exacerbate GERD
 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
 Bronchoconstriction
 Inflammation
 Mucosal edema
 Excessive mucous
 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
 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
 Bronchodilators and anti-inflammatories
 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
 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
 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
 Step 4—
 Children less than 5 yo—same as for
adults and older children
 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
 Cautious use in hypertension and cardiac
disease
 Selective beta 2 agonists by inhalation
are drugs of choice
 Epinephrine sc in acute
bronchoconstriction
 Proventil
(albuterol)
 Xopenex (levalbuterol)
 Treatment of first choice to relieve acute
asthma
 Aerosol or nebulization
 May be given by MDI
 Overuse will diminish their
bronchodilating effects>>>>tolerance
 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.
 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
 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)
 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
 Contraindicated in acute gastritis and
PUD
 Second line
 Narrow therapeutic window—therapeutic
range is 5-15 mcg/mLh
 Multiple drug interactions
 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
 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
 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
 For inhalation:
 Beclovent—beclomethasone
 Pulmicor—budesonide
 Aerobid—flunisolide
 Flovent—fluticasone
 Azmacort—triamcinolone
 Most inhaled steroids are being
reformulated with HFA
 Systemic use: prednisone,
methylprednisolone, and hydrocortisone
 In acute, severe asthma—a systemic
corticosteroid may be indicated when
inhaled beta 2 agonists are ineffective
 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
 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
 Injured cell
 Arachidonic acid
 XXXX
 Lipooxygenase

 Leukotrienes
 XXXX
 Bronchi, WBCs

 Bronchoconstriction
 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
 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
 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
 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
 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
 WithH2 receptor stimulation, main
effects are increased secretion of gastric
acid and pepsin, decreased immunologic
and proinflammatory reactions,
increased rate and force of myocardial
contraction
 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.
 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
 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
 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
 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
 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
 Atrovent nasal spray
 Beconase (beclomethasone)
 Rhinocort (budesonide)
 Flonase (fluticasone)
 Nasonex (mometasone)
 Nasalcrom (a mast cell stabilizer)
 Type IV hypersensitivity reaction
 Poison ivy an example
 Usually occurs >24h after re-exposure
 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
 Inhibitsmooth 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
 Allergic rhinitis
 Anaphylaxis
 Allergic conjunctivitis
 Drug allergies
 Transfusions of blood products
 Dermatologic conditions
 Nonallergic such as motion sickness,
nausea and vomiting, sleep
 Caution in pregnancy
 BPH
 Bladder neck obstruction
 Narrow angle glaucoma
 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)
 Selective or nonsedating
 Do not cross blood brain barrier
Examples:
 Astelin (azelastine)
 Allegra (fexofenadine)
 Claritin (loratadine)
 Clarinex (desloratadine)
 Zyrtec
 Xyzal
 Relievenasal obstruction and discharge
 Adrenergic
 Rebound nasal swelling called “rhinitis
medicamentosa”
 Afrin
 Sudafed (pseudoephedrine)
 Contraindicated in severe hypertension,
CAD, narrow angle glaucoma, TCAs or
MAOIs
 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
 Liquefyrespiratory secretions
 Guiafenesin
 By inhalation to liquefy mucous
 Mucomyst (acetylcysteine)
 May be used in treating acetaminophen
overdose
 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
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.