Disorders of Gas Exchange and Drugs for Asthma Flashcards
explain the term obstructive airway disease
Obstructive airway diseases exhibit diminished expiratory airflow and involve airways distal to the carina.
what is the role of inflammation in the development of asthma?
the immunologic aspects of asthma include the release of neutrophils, eosinophils, lymphocytes, and mast cells.
these cells cause airway inflammation, which further increases hyperresponsiveness and obstructs airflow.
list the steps following sensitization of an allergen
allergen—>T Cell (Th2)—>IL4, IL5, IL3—>B cell—>IgE—>mast cells—>HISTAMINE, HISTAMINE, HISTAMINE
define status asthmaticus
a severe condition in which asthma attacks follow one another without pause.
explain the difference between extrinsic and intrinsic asthma
Extrinsic asthma is simply asthma caused by an allergic reaction, especially a chronic one. If your asthma is allergic, you will have higher levels of IgE (Immunoglobulin E) present in your blood test.
On the other hand, intrinsic asthma, as you might’ve guessed already, is triggered by various non-allergic factors like stress, cold or dry air, smoke, anxiety, viruses or infections, and more.
relate the pathologic changes that occur in asthma to the clinical manifestations.
wheezing/chest tightness, SOB—>d/t bronchoconstriction
fatigue, moist skin, anxiety—> prolonged attack and bronchospasm, airway obstruction
list diagnostic findings for asthma, including FEV 1
asthma is diagnosed by physical exam, spirometry, and FEV 1 of less than 70%–sometimes it will be reduced by 5% or more, depending on the severity.
describe the symptoms that result from bronchoconstriction in asthma
a patient may be short of breath, have wheezing, tightness or pain in the chest, and finally extreme tiredness during exercise
explain patient teaching for patients living with asthma.
Clinicians should teach patients asthma self-management based on basic asthma facts, self-monitoring techniques, the role of medications, inhaler use, and environmental control measures. Treatment goals should be developed for the patient and family.
nursing implications for beta-adrenergic antagonists and glucocorticoids
glucocorticoids
glucocorticoids: inform patients that glucocorticoids are intended for prevention of asthma-not for aborting an ongoing attack, so administer on a regular schedule, not PRN. teach patients how to use inhaled glucocorticoids. Oral: instruct patients to take one dose every other day in the morning.
teach patients with chronic asthma to monitor and record PEF, symptom frequency/intensity, nighttime awakenings, effect on normal activity and SABA use.
inhaled: advise patients to rinse their mouth and gargle after dosing to minimize dysphoria and oropharyngeal candidiasis.
with patients who have switched from long term oral glucocorticoids to inhaled ones, have them take supplemental systemic glucocorticoids at times of stress (trauma, surgery, infection, because failure to do so can be fatal).
advise patients to ensure adequate intake of calcium and vitamin D and to perform weight bearing-exercise.
nursing implications for beta-adrenergic antagonists.
routes: oral or inhalation
inhalation: teach patients how to use inhalers. inform patients who are using MDIs or DPIs that when do inhalations are needed, there must be a one minute interval between inhalations.
warn patients against exceeding recommended dosages.
inform patients that labeled LABAs (formoterol, arformetoerol, and salmeterol) should be taken on a fixed schedule, not PRN, and ALWAYS in combination with a glucocorticoid, perferably in the same inhalation device.
Oral: instruct patients to take them on a fixed schedule, not PRN. swallow sustained release capsules whole.
- *teach patients with chronic asthma to monitor and record their PEF, symptom frequency and intensity, nighttime awakenings, and SABA use.
- *oral beta 2 antagonists: instruct patients to report any chest pain or changes in heart rate or rhythm.
characterize the early and late phases responses in the the pathogenesis of asthma
early phase
The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. These antibodies respond to certain triggers in the environment, such as the risk factors listed above. IgE antibodies then bind to high-affinity mast cells and basophils. When a pollutant or risk factor gets inhaled, the mast cells release cytokines and eventually de-granulate. Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening
characterize the early and late phase responses in the pathogenesis of asthma
The results of several studies suggest that the early phase response (EPR) usually involves cells which are normal residents of the respiratory epithelium (mast cells) and pre-formed substances (histamine). These produce the initial inflammation and wheezing.
Within the next several hours, the late phase occurs, which eosinophils, basophils, neutrophils, and helper and memory T-cells all localize to the lungs as well, which perform bronchoconstriction and cause inflammation. Mast cells also play an essential role in bringing the late phase reactants to the inflamed sites.
It is critical to recognize both of these two mechanisms to target therapy and relieve both bronchoconstriction and inflammation, depending on the severity of the disease.
for glucocorticoids, list use in asthma, adverse effects, and interaction with adrenal insufficiency.
glucocorticoids are used for prophylaxis of chronic asthma. Dosing must be done on a fixed schedule, NOT PRN. Cannot be used to abort and ongoing attack. First line use for the management of the inflammatory component of asthma. oral ones are prescribed only when symptoms cannot be controlled with safer medications as they can be toxic.
Their interaction with adrenal insufficiency is that when they have been on artificial (that is, ones their body doesn’t make) glucocorticoids, then if they stop treatment cold turkey (even just by switching the route of therapy), the patients can die. Also if not increased during times of physical stress to meet the body’s needs, people can die too.
ae’s inhaled: candidiasis, adrenal insufficiency, bone loss
ae’s oral: adrenal suppression, osteoporosis, hyperglycemia, peptic ulcer disease, growth suppression
contrast short versus long acting beta 2 agonists and list adverse effects
short acting beta agonists are those that have effects beginning almost immediately, peak for 30-60 minutes, and then persist for 3-5 hours. Can be used to abort an ongoing attack, but cannot be used to sustain prophylaxis.
long acting beta antagonists are those where the onset of effects depends on the drug. LABAs are not a first line therapy, and must be combined with a glucocorticoid for best results. Their use alone in asthma therapy is contraindicated.
ae’s: inhaled short acting: tachycardia, tremor, angina–usually minor.
ae’s inhaled long acting: may increase the risk for severe asthma, and asthma related death when used as a monotherapy
ae’s: oral: can cause angina pectoris and tachdysrhythmias. patients should be instructed to report chest pain or changes in heart rate or rhythm, can cause tremor and a lower dosage helps combat this.
