asthma
disorder that causes the airways of the lungs to swell and narrow, leading to wheezing,
shortness of breath, chest tightness, mucus production and coughing.
asthmatic lung
has inflammation, constriction, mucus, airway hyperresponsiveness, and airway
remodeling. Mucus and bronchoconstriction are bad because they create suffocation.
Remodeling due to chronic exposure to allergens.
substances that trigger asthma
include inflammatory factors (respiratory infections, allergens, work), irritants (temp
change, exercise, cold air, strong odors, stress and emotions), and others (tobacco,
meds, food additives, gastric reflux, pollutants)
major characteristics of asthma
include eosinophilia, inflammation, increase in serum IgE (antibodies that target the
allergy), increase in mucus production, airway hyperresponsiveness caused by
bronchoconstriction.
treatment of asthma
include drugs that reduce inflammation (long-term control) and/or drugs that reduce
bronchospasm (quick relief/rescue).
long-term control asthma medications
decrease airway inflammation. Control/prevent asthma symptoms, decrease sensitivity
to "triggers", prevent inflammation, and are taken daily. Include corticosteroids,
cromolyns, leukotriene modifiers, long-acting B2 agonists, sustained-release
methylxanthines, and antagonism of IgE.
quick relief (rescue) asthma medications
decrease bronchospasm. For acute episode relief. Include mainly bronchodilators.
Include specifically corticosteroids given IV (not for rescue but shortens severe
episode), short-acting B2, methylxanthines, and muscarinic cholinergic antagonists.
sympathetic response in lungs
causes dilation of bronchioles
parasympathetic response in lungs
causes constriction of bronchioles and increases secretions
beta 2 adrenergic receptor agonists
act by activating adenylate cyclase, which leads to increaes in cyclic AMP which cause
the bronchioles to relax. The cyclic AMP causes an increase in PKA, which leads to
increase in calcium activated K+ channel activation, decrease in other pathways,
increase in sodium calcium exchange and ATPase, and decrease in myocine light chain
kinase. Also inhibit release of inflammatory mediators/cytokines in mast cells, basophils,
eosinophils, neutrophils, and lymphocytes. Include short acting and long acting
short acting beta agonists (SABAs)
quick relief asthmatic drug; include epinephrine, terbutaline, albuterol, pirbuterol,
bitolterol, and levalbuterol. Onset of 5-10 minutes, peak effect of 30 min, 3-6 hour
duration. Inhaled, oral administration. Side effects include tremor, tachycardia (B1),
hypokalemia. Contraindicated in cardiac ischemia or arrhythmia.
long acting beta agonists (LABAs)
include formoterol and salmeterol. Onset of 15-30 minutes, peak effect of 22 hours and
duration of 22-24 hours. Inhaled administration. Side effects include hypertension,
vascular headaches, tremors, and tolerance. May increase risk of death if used along
(without a corticosteroid) in asthma. So not indicated for use as a single agent in
asthma!!*! Should not be given alone!
corticosteroids
suppress inflammatory gene regulation, therefore suppressing the immune response. 5-
8 hour onset, 6-24 hour duration. Include inhaled, oral, and IV. Short term use leads to
pneumonia, mood disturbances, increased appetite, impaired glucose control in
diabetics, oropharyngeal candidiasis. Long term use leads to bone resorption,
cutaneous thinning, cataracts. Adequate calcium and vitamin D intake and weight
exercise are recommended to avoid bone loss.
inhaled corticosteroids
triamcinolone, flutaicasone, budesonide, flunisolide, mometasone, beclomethasone,
ciclesonide. Should always be paired with a LABA.
oral corticosteroids
prednisone, prednisolone.
IV corticosteroid
include hydrocortisone. Can shorten severe episode.
muscarinic cholinergic antagonists
quick relief asthmatic drug, competitive antagonist of M3 ACh receptors. This prevents
airway smooth muscle contraction. Essentially inhibiting parasympathetics. 5-15 min
onset, 1-2 hour peak effect, duration 6-8 hours for ipratropium and 24 hours for
tiotropium. Side effects include bitter taste, dry mouth and airway, headache,
tachycardia, dry eyes/blurred vision, urinary retention. Typically used in asthmat patients
non-responsive to beta blocker therapy, or when that therapy is contraindicated. This
drug is contraindicated in glaucoma, prostatic hyperplasia, and pyloric stenosis. Inhaled
- ipratropium, tiotropium. Oral - tiotropium. IV - atropine.
methylxanthines
for maintenance and rescue; act as PDE inhibitor, leading to increased cyclic AMP and
smooth muscle relaxation. Also act as adenosine receptor antagonist (adenosine
receptor causes bronchoconstriction, so blocking that). Causes IL-10 release
(immunosuppressive cytokine). Prevents NFkB nuclear translocation. Promotes
apoptosis of eosinophils and neutrophils. Causes histone acetylase activation,
preventing transcription of different inflammatory genes. Includes theophylline and
caffeine (natural forms). Synthetic forms include aminophylline, dyphilline, oxtriphyline.
Admin can be oral, inhaled, rectal, IV. Onset varies, effect 1-2 hours, duration varies.
Use for mild chronic asthma, but not preferred option. Side effects include seizures,
tachycardia, N&V.
mast cell stabilizers (cromolyns)
long term control; block the release of inflammatory mediators from mast cells,
eosinophils, basophils, and lymphocytes. This prevents histamine release along with
other inflammatory responses. Admin is inhaled. Effect for weeks. Side effects include
increased coughing, wheezing. Typically very safe. The basic one for children and
adolescents. Nedocromil for people older than 12. Prophylactic therapy* for mild
moderate allergic asthma. Also used for allergic rhinitis.
leukotriene modifiers
maintenance asthma; inhibit synthesis of leukotrienes (produced in inflammatory cells in
lungs such as eosinophils, mast cells) - Zileuton. OR competitive antagonist of
leuketriene receptors - Montelukast. Two classes of drugs that both lead to decreased
inflammation. Inhaled or oral admin. Onset 3-6 hours, 4 hours effect, 24 hour duration.
Side effects include Churg-Strauss syndrome and hepatic dysfunction. Used for mild
chronic asthma, allergic rhinitis. An alternative - not preferred!
zileuton
leukotriene synthesis inhibitor. Seldom used in US.
montelukast, zafirlukast
these are leukotriene receptor antagonists.
Churg-Strauss syndrome
disorder marked by blood vessel inflammation, that can restrict blood flow to vital
organs and tissues, sometimes permanently damaging them. Can be a side effect of
leukotriene modifiers.
Anti-IgE therapy
blocks IgE from downstream pro-inflammatory signaling. Blocks IgE from binding to
mast cell to cause release of histamines. Include omalizumab. Admin is subcutaneous.
Peak plasma levels after 7-8 days, duration of 26 days. Side effects include injection-
site reactions, infections, anaphylaxis, cancer. Use is for moderate to severe
persistence asthma and for those 12 years and older.
step 1 practical management
SABA PRN is preferred for this.
step 2 practical management
Low-dose ICS is preferred. Alternative - cromolyn, LTRA, nedocromil, or theophylline.
step 3 practical management
preferred low dose ICS and a LABA or a medium dose ICS. Alternative is a low dose
ICS with either a LTRA, theophylline, or zileuton.
step 4 practical management
preferred is medium dose ICS and a LABA. Alternative is a medium dose ICS and either
LTRA, theophylline, or zileuton.
step 5 practical management
preferred is high dose ICS and LABA along with the consideration of omalizumab for
patients who have allergies.
step 6 practical management
preferred is high dose ICS and a LABA and an oral corticosteroid along with the
consideration of omalizumab for patients who have allergies.
mild intermittent asthma
medication includes reliever only PRN
mild persistent asthma
medication includes controller (low dose) and reliever.
moderate persistent asthma
medication include controller (medium dose) plus long-acting bronchodilator and
reliever.
severe persistent asthma
medication includes controller (high dose) plus long acting-bronchodilator and reliever.
order of med admin
if someone is taking both inhaled reliever and inhaled controller at the same time, give
reliever med first before taking the controller and wait a few minutes between
medications. The bronchodilators (often the relievers) open up the airways, allowing
better dispensation of the ICS.
COPD
caused by smoking in 90% of cases, pollution/gas fumes, and sometimes genetics
(alpha 1 anti-trypsin deficiency). Constant limitation of expiratory airflow specially in
small airways due to anatomical lesions, including loss of lung elasticity and fibrosis.
Elastin breakdown with resultant loss of alveolar wall integrity. Inflammation, edema,
and purulent secretions. Neutrophilia. Alveolar wall destruction. Emphysema - damage
to air sacs (alveoli)
management of COPD
non drug includes smoking cessation, exercise, adjunctive therapies (chest
physiotherapy, percussion/vibration). Drugs include SABAs, LABAs, anticholinergics,
corticosteroids, methylxanthines, and combination therapies (steroid + LABA).
asthma main points
usually less than 30 age of onset. Cough is nocturnal or after exercise. Prominent atopy
(hyperallergic). Less prominent airway remodeling. Common bronchodilator reversibility.
Strong steroid responsiveness. Eosinophils are hallmark inflammatory cells. Family
history is common. Intermittent symptoms. Inhaled corticosteroid is first line agent for
control. Sputum unlikely. Smoking is variable.
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