Chapter 37 Respiratory Drugs Flashcards
The LRT is located almost entirely within the thorax and is composed of the?
trachea, all segments of the bronchial tree, and the lungs.
Diseases that affect the URT include colds, rhinitis, and hay fever. The major diseases that impair the function of the LRT include?
asthma, emphysema, and chronic bronchitis. All of these diseases have one feature in common, they all involve the obstruction of airflow through the airways.
Bronchial asthma is defined as a recurrent and reversible shortness of breath and occurs when the?
airways of the lung become narrow as a result of bronchospasm, inflammation and edema of the bronchial mucosa, and the production of viscous mucus.
Allergic asthma, or extrinsic asthma, is caused by a hypersensitivity to an allergen or allergens in the environment.
• Intrinsic, or idiopathic, asthma does not have a specific cause but certain factors have been noted to precipitate asthma attacks including?
respiratory infections, stress, and cold weather.
Chronic bronchitis is a continuous inflammation and low-grade infection of the bronchi. The inflammation in the bronchioles is responsible for?
most of the airflow obstruction.
Emphysema is a condition in which the air spaces enlarge as a result of the destruction of the alveolar walls, caused by the effect of proteolytic enzymes released from leukocytes in response to?
alveolar inflammation.
In the past, the treatment of asthma and other chronic obstructive pulmonary diseases (COPDs) was focused primarily on the use of drugs that cause the airways to dilate; now the focus has shifted from the bronchoconstriction component of the disease to the?
inflammatory component.
Bronchodilators relax bronchial smooth muscle, which causes dilation of the bronchi and bronchioles that are narrowed as a result of the disease process. There are three classes of such drugs:
(1) beta-adrenergic agonists
(2) anticholinergics
(3) xanthine derivatives
The beta-adrenergic agonists are commonly used during?
acute phase of an asthmatic attack to quickly reduce airway constriction and restore airflow to normal. They are agonists, or stimulators, of the adrenergic receptors in the sympathetic nervous system.
Short-acting beta agonist (SABA) inhalers include albuterol (e.g., Ventolin), levalbuterol (Xopenex), pirbuterol (Maxair), terbutaline (Brethine), and metaproterenol (Alupent).
.
Long-acting beta agonist (LABA) inhalers include arformoterol (Brovana), formoterol (Foradil, Perforomist), and salmeterol (Serevent). Because the LABAs have a longer onset of action, they must never be used for acute treatment.
.
The newest LABA are indacterol (Arcapta Neohaler); vilanterol in conjunction with fluticasone (Breo Ellipta); and vilanterol in conjunction with the anticholingeric, umeclidinium (Anoro Ellipta). The term Ellipta refers to a new delivery system. Because the LABAs have a longer onset of action, they must never be used for acute treatment.
.
Nonselective adrenergic drugs, such as?
epinephrine, stimulate the beta, beta1 (cardiac), and beta2 (respiratory) receptors.
Nonselective beta-adrenergic drugs, such as?
metaproterenol, stimulate both beta1 and beta2 receptors
Selective beta2 drugs, such as?
albuterol, primarily stimulate the beta2 receptors.
The primary therapeutic effect of the beta agonists is the?
prevention or relief of bronchospasm related to bronchial asthma, bronchitis, and other pulmonary diseases. However, they are also used for effects outside the respiratory system.
The broncchioles are surrounded by smooth muscle. When the smooth muscle contracts, the airways are narrowed and the amount of oxygen and carbon dioxide exchanged is reduced. The action of beta agonist bronchodilators begins at the?
Specific receptor stimulated and ends with the relaxation and dilation of the airways. Many reactions must take place at the cellular level for bronchodilation to occur. When a beta 2 adregnergic receptor is stimulated by a beta agonist, adenylate cyclase is activated and produces cyclic adenosine monophosphate (cAMP). Adenylate cyclase is an enzyme needed to make cAMP. the increased levels of cAMP cause bronchial smooth muscles to relax, which results in bronchial dilation and increased airflow into and out of the lungs.
Non-selective adrenergic agonist drugs such as epinephrine also stimulate?
Alpha-adrenergic receptors, causing constriction w/in blood vessels. This vasoconstriction reduces the amount of edema or swelling in the mucous membranes & limits the quantity of secretions produced by these membranes.
-in addition these drugs stimulate beta 1 receptors resulting in cardiovascular effect such as Increase in HR, force of contraction, and BP, as well as CNS effects such as nervousness and tremor
Drugs such as albuterol that predominantly stimulate the?
beta 2 receptors have more specific drug effects and cause less AEs. By primarily stimulating the beta 2-adrenergic receptors of the bronchial and vascular smooth muscles, they cause bronchodilation & may also have dilating effect on the peripheral vasculature
Beta-Adrenergic agonists indications
Prevention or relief of bronchospasm related to bronchial asthma, bronchitis, and other pulmonary diseases. Also used for effects outside the respiratory system. Because some of these drugs have the ability to stimulate both beta 1 and alpha adrenergic receptors, they may be used to treat hypotension and shock
Beta-Adrenergic agonists Contraindications
known drug allergy, uncontrolled hypertension or cardiac dysrhythmias, and high risk of stroke (because of the vasoconstrictive drug action)
Beta-Adrenergic agonists adverse effects
Mixed alpha/beta agonists produce the most adverse effects, including insomnia, restlessness, anorexia, cardiac stimulation, hyperglycemia, tremor, and vascular headache.
The adverse effects of the nonselective beta agonists are
limited to?
beta-adrenergic effects, including cardiac stimulation,
tremor, anginal pain, and vascular headache.
The beta2 drugs can cause?
hypertension and hypotension, vascular headaches, and tremor.
Overdose management of Beta-adrenergic agonist drugs
Careful administration of beta blocker while patient under close observation due to risk for bronchospasm.
Beta-Adrenergic agonists interactions
- when nonselective beta blockers used w/beta agonist the bronchodilation from the agonist is diminished
- MAOIs and other sympathomimetics should be avoided because the enhanced risk for HTN
- diabetics may require adjustment in dosage of their hypoglycemic drugs, especially pt’s receiving epinephrine, because of the increase in blood glucose levels can occur
Beta Adrenergic Agonist Drug: Albuterol (Proventil)
- short-acting, beta 2-specific, bronchodilating, beta agonist
- If used too frequently, dose-related AEs may be seen, because it loses its beta 2 specific actions, especially at larger doses. As a consequence, the beta 1 receptors are stimulated, which causes nausea, increased anxiety, palpitations, tremors, and an increased HR
- oral & inhalation (metered dose inhaler MDI, solutions)
- levorotatory isomeric form of albuteral sometimes used as alternative for pt’s w/certain risk factors (tachycardia, including tachycardia associated with albuterol Tx)
Anticholinergic drugs are used for?
maintenance and not for relief of acute bronchospasm and work by blocking the bronchoconstrictive effects of acetylcholine ACh.
Mechanism of action for anticholinergic drugs: On the surface of the bronchial tree are receptors for acetylcholine (ACh), the neurotransmitter for the PNS. When PNS releases ACh from its nerve endings, it binds to ACh receptors on the surface of the bronchial tree, resulting in bronchial constriction and narrowing of the airways. Anticholinergic drugs?
block these ACh receptors to prevent bronchoconstriction. This indirectly causes airway relaxation and dilation. Anticholinergic agents also help reduce secretions in COPD pt’s