Respiratory Flashcards
Anticholinergic Drugs- For COPD and asthma: improves lung function by blocking muscarinic receptors in the bronchi, decreases bronchoconstriction. For allergic rhinitis: blocks nasal cholinergic receptors to decrease secretions from serous and seromucous glands lining the nasal mucosa to decrease rhinorrhea
SE: dry mouth and irritation of pharynx (COPD/Asthma use), may raise IOP of pts with glaucoma, nasal drying and irritation (allergic rhinitis use).
Albuterol(Bronchodilator): The mechanism of action of bronchodilators includes targeting the beta-2 receptor, which is a G-protein coupled receptor, in the lung airways. When the beta-2 receptor is activated, the smooth muscle of the airway relaxes.
Side effects: increased heart rate, tremors, nervousness, cough, dry mouth
Leukotriene Receptor Antagonists-compounds that supress the effects of leuoktrienes. Leukotrienes promote smooth muscle constriction, inflammatory responses, and increase blood vessel permiability. They encourage the inflammatory response by direct effects as well as via recruitment of inflammatory cells such as eosinophils. In asthma patients, these drugs decrease inflammatory responses like edema and mucus secretion and decrease bronchoconstriction through their antagonistic effects.
Side effects: Zileuton can cause liver injury, neuropsychotic effects such as depression, anxiety, agitation, hallucinations, dream alterations, insomnia, suicidal thoughts or actions. Zafirlukast should not be taken with food as food decreases absorption. It can cause GI disturbances, arthralgias/myalgias, as well as the same neuropsychotic effects noted above. It may also be related to development of Churg-Strauss Syndrome. Montelukast has also been associated with Churg-Strauss Syndrome and mood changes and suicidal ideations
Anti-inflammatory Agents: Glucocorticoids. MOA: Reduce respiratory symptoms by suppressing inflammation. Specific anti-inflammatory effects include: decreased synthesis and release of inflammatory mediators (e.g., leukotrienes, histamine, prostaglandins); decreased infiltration and activity of inflammatory cells (e.g., eosinophils, leukocytes); decreased edema of the airway mucosa (secondary to a decrease in vascular permeability). By suppressing inflammation, glucocorticoids reduce bronchial hyperreactivity and decrease airway mucus production.
Side effects: oropharyngeal candidiasis and dysphonia (hoarseness, difficulty speaking) both result from local deposition of inhaled glucocorticoids. Adrenal suppression/insufficiency may develop (hypoglycemia, hypotension, mental status alterations) children are at increased risk. Growth is slowed in children and adolescents. Long-term use of inhaled glucocorticoids may promote bone loss. Prolonged therapy may increase the risk for cataracts and glaucoma. Potential adverse effects with prolonged therapy of oral glucocorticoids include adrenal suppression, osteoporosis, hyperglycemia, peptic ulcer disease, and growth suppression.
Phosphodiesterase Inhibitors: Exert their effects on their targeted phosphodiesterase enzymes (PDE-3, PDE-4,PD-5), preventing cGMP or cAMP degradation furthering increasing their levels in smooth muscle cells, causing relaxation and vasodilatory effect in target cells.
Side effects include diarrhea, weight loss, reduced appetite, nausea, headache,back pain and insomnia.
Beta adrenegic agonist/anticholinergic drugs promotes bronchodliation by stimulating adrenergic recepors whiles cholinergic antagonist promote bronchodilation by blocking cholinergic receptors. This in the end relaxes smooth muscle tone by preventing stimulation of cholinergic receptors. There is an affect on the bronchi and broncholes which further enhances bronchodilation
“Side effects are dry mouth, constipation, cough, nausea and also systemic effects such tachycardia, angina , palpitations and tremors but usually are minimal
Monoclonal antibodies: forms complexes with free IgE in the blood and thereby reduces the amount of IgE available to bind with its receptors on mast cells. This greatly reduces the number of IgE molecules on the mast cell surface and therefore limits the ability of allergens to trigger release of mediators that cause bronchospasm and airway inflammation
Adverse effects are injection-site reactions, viral infections, upper respiratory infections, sinusitis, headache, and pharyngitis
Bronchodilators: MOA for inhaled Beta-2-adrenergic agonists (albuterol) relaxes smooth muscles in the lungs. They relieve bronchospasms by promoting bronchodilation in activating Beta-2 receptors and partly by suppressing histamine release (mast cells).
SE: minimal bc albuterol is highly selective drug, includes hyperglycemia (especially patients with diabetes), skeletal muscles tremors, and if too much is administered, Beta-1 receptors also get activated causing tachycardia.
Glucocorticoid/long-acting beta 2 agonist combinations (fluticasone/salmeterol, fluticasone/vilanterol, budesonide/formoterol, mometasone/fomoterol) are combination drugs. The glucocorticoid part of the medication works to suppress inflammation by decreasing synthesis and release of inflammatory mediators (leukotrienes, histamine, prostaglandins), decreasing infiltration and activity of inflammatory cells (eosinophils, leukocytes), and decreasing edema of the airway mucosa (due to a decrease in vascular permeability). The long-acting beta 2 agonst part of the medication works by activating beta 2- adrenergic receptors in the smooth muscle of the lungs, leading to bronchodilation and decreased bronchospasm. Beta 2 agonists also can help suppress histamine release in the lungs and increased ciliary motility.
All products have a black box warning because of long acting beta agonist (LABA) component. All LABAs have a risk for asthma-related deaths when prescribed as monotherapy. When prescribed in combination with a glucocorticoid (preferably in the same inhaler), the risk is minimal. The most commonly reported adverse effects are oral candidal infections, hoarseness, and pharyngolaryngeal pain.
Ipratropium is an anticholinergic drug, that improves lung function by blocking muscarinic receptors in the bronchi, reducing bronchoconstriction. By blocking muscarinic cholinergic receptors in the bronchi, ipratropium prevents bronchoconstriction. Therapeutic effects begin within 30 seconds, reach 50% of their maximum in 3 minutes, and persist approximately 6 hours. Ipratropium is effective against allergen induced asthma and EIB but is less effective than the beta agonists. However, because ipratropium and the beta two adrenegic agonists promote bronchodilation by different mechanisms, their beneficial effects are additive.
Adverse effects- Systemic effects are minimal because ipratropium is a quaternary ammonium compound and therefore always carries a positive charge. As a result the drug is not readily absorbed from the lungs or from the digestive tract. Most common adverse reactions are dry mouth and irriation of the pharynx. If systemic absorption does occur, the drug may rais IOP in patients with glaucoma. Adverse cardiovascular events, heart attack, stroke, death, have occurred in people taking ipratropium, however absorption is minimal, it seems unlikely that ipratropium is the cause.
Antiinflamatory Agent (Inhaled glucocorticoids such as budesonide or fluticasone). These medications provide long-term inflammation suppression by decreasing inflammatory mediators, decreasing the activity of inflammatory cells, and decreasing airway edema. Through reduced inflammation, the mucus production in the airway is also reduced and the brochials are less reactive.
The adverse effects of inhaled glucocorticoids are oropharyngeal candidiasis and dysphonia, which can present as speaking difficulty or hoarseness. If patients rinse and gargle their mouth after use of these medications, side effects are less likely to occur. The use of a spacer with the inhaler will reduce the risk of candidiasis. Long term use of this medication can result in adrenal suppression, this is more likely to occur in young children using this medication for over 6 months. This type of medication can also slow growth, though it does not reduce a person’s final height. Bone loss may also occur with long term use, but it is less common with inhaled glucocorticoids than with oral glucocorticoids. Long term use of high-dose inhaled glucocorticoids can increase the risk for cataracts and glaucoma, but this is not a concern for low or medium dose inhaled glucocorticoids.
Phosphodiesterase inhibitors are a class of medications that promote blood vessel dilation (vasodilation) and smooth muscle relaxation in certain parts of the body, such as the heart, lungs, and genitals. Phosphodiesterases are a diverse family of enzymes that play a key role in regulating cell functions by indirectly increasing the intracellular levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), both of which are “second messengers” that regulate the primary effects of hormones and neurotransmitters.
Roflumilast reduces inflammation in the lungs that leads to COPD (chronic obstructive pulmonary disease). Roflumilast is used to prevent worsening of symptoms in people with severe COPD.Roflumilast sude effects include diarrhea, headache, nausea, weight loss, and psychiatric signs and symptoms.
