Pulmonary drugs Flashcards
Decongestants MOA
alpha 1 adrenergic agonists, increase SNS
Cause vasoconstriction
Decongestants AE
HA, CV irregularities (increased BP, palpations)
*can mimic the effects of increased sympathetic NS activity
Who shouldn’t use Decongestants
Hypertensive people and people who take a beta blocker b/c cancel each other and alpha agonist drugs
Antitussives uses and MOA
Cough suppression
decrease afferent nerve activity or decrease cough center sensitivity (Codeine)
Antitussives are helpful in treating in what kind of cough?
Dry cough but their use may not be justified in treating an active, productive cough
How codeine MOA and what kind of cough should avoid?
Act to suppress cough reflex centrally
Also thicken sputum, reduce clearance- don’t take if you have wet cough
Antihistamines (Benadryl) MOA
Block histamine receptors reducing:
Mucosal irritation
Decreases sneezing caused by histamine-associated sensory neural stimulation
Decrease nasal congestion due to vascular engorgement associated with vasodilation and increased capillary permeability
acts as a local anesthetic on the respiratory epithelium
Antihistamines AE
Sedation (most common AE) and Dizziness- especially with antihistamines
GI upset (especially with opioidsconstipation)
Histamines normally work on what receptor and normal response
H1 receptor
Cause vasodilation, increased vascular permeability, sneezing, nasal congestion
1st generation Antihistamines vs 2nd generation Antihistamines AE
1st generation cross blood brain barrier so you get sedation and fatigue feeling (Benadryl) while 2nd generation do not easily cross BBB
What kind of pathology can use Antihistamines
Asthma
Mucolytics MOA
MOA: split disulfide bonds
Drugs which decrease the viscosity of respiratory secretions (mucus)
In doing so, they loosen and clear mucus from the airways (makes mucous thinner)
Reduce the energy costs of coughing
Expectorants
Facilitate the production and ejection of mucus
Causes a thinning of the mucus
Lubricates the irritated respiratory tract
Promote a productive cough
Prevent the accumulation of thick, viscous secretions
What do you look out for when taking cold remedies and High Blood Decongestants can mimic effects of increased sympathetic activity
Vasoconstriction can increase blood pressure
Individuals with HTN should avoid OTC products that contain: endings with
-rine
Decongestants can mimic effects of increased sympathetic activity
Vasoconstriction can increase blood pressure
Individuals with HTN should avoid OTC products that contain: endings with
-rine
What drug class to treat COPD?
Inhaled beta agonists
Inhaled antimuscarinics
Inhaled corticosteroids
Inhaled Beta Agonists MOA
MOA: agonize β2 receptors = bronchodilation
Inhaled Beta Agonists drug endings?
-terol
Inhaled Beta Agonists AE
generally well tolerated; although fairly selective can cause tachycardia, tremor, hypokalemia
Inhaled Antimuscarinics (AKA: anticholinergics) MOA
primarily bind M3 in airway smooth muscle; antagonizes ACh actions at these sites = bronchodilation
Molecule structure ↓ systemic absorption = ↓ anticholinergic effects
Inhaled Antimuscarinics (AKA: anticholinergics) AE
dry mouth
Inhaled Corticosteroids uses
COPD: typically used for exacerbations or more severe disease
Unclear safety if used >3 years
If inhaled steroid is stopped, monitor for worsening sx- increase SOB
Inhaled Corticosteroids AE
oral candidiasis- rinse out mouth, hoarse voice, skin bruising; elderly on high doses: osteoporosis, cataracts
Why take combination bronchodilators?
Combining bronchodilators may increase effect with lower AE as compared to increasing the dose of a single product
Ex of SABA/SAMA drug
albuterol/ipratropium (Combivent)
Ex LABA/ICS drugs (2)
formoterol/budesonide (Symbicort), salmeterol/fluticasone (Advair)
What if inhalers aren’t working?
Disease progression
Incorrect inhaler or nebulizer use
Nonadherence- need education on PRN vs maintenance meds, cost concerns
What if patient can produce enough inhalation force
Refer to the provider to discuss if a spacing device is needed or if a change from dry powder inhaler is needed
When do use antibiotics?
Used in acute exacerbations
Extended treatment only in patients prone to exacerbations
Azithromycin 250 mg daily or 500 mg three times per week x 1 year
Erythromycin 500 mg twice daily x 1 year
Asthma short-term and long-term treatment
short-term: SABS
long-term: ICS and LABA
When would you use a LABA?
Only in combo with ICS for prn relief or long-term control
Helps lower ICS dose to prevent ICS AE
Do NOT use alone for acute symptoms
What are Leukotrines?
released from mast cells and eosinophils to play a role in airway edema, smooth muscle contraction, inflammatory process
Leukotriene receptor antagonist (LTRA) PO drugs and MOA
montelukast (Singulair), zafirlukast (Accolate)
MOA: competitively antagonize leukotriene receptors
Montelukast when do you take it for allergies and when do you take it for asthma?
Alllergies: AM
Asthma: PM
Immunomodulators: Anti-IgE drugs and MOA
omalizumab (Xolair)
prevents IgE binding to receptors on mast cells and basophils limits activation and release of allergic response mediators
what to look out for when taking Immunomodulators: Anti-IgE
Very rare but anaphylactic allergic reaction may occur- must administer in provider’s office
How often can you use SABA?
up to 3 treatments at 20 minute intervals no relief go see medical treatment
Drug class to treat CF?
LABA, SABA, CFTR Modulators, Mucolytics, Inhaled/PO Antibiotics
CF transmembrane regulator role?
is a membrane protein, and chloride channel regulates sodium and water which helps keep mucous thin
Genetic mutation of CF transmembrane regulator causes?
Genetic mutations cause closing and/or narrowing CFTR or stop CFTR from getting to the cell surface
CFTR Modulator drugs
tezacaftor/ivacaftor (Symdeco), lumacaftor/ivacaftor (Orkambi)
MOA Ivacaftor and Tezacaftor/ lumacaftor
facilitate trafficking of CFTR to the cell membrane surface = improved chloride transport.
Improved regulation of sodium and water = mucous thinning
CFTR modulators must be taken with?
with high fat meal to ↑ absorption
AE for CFTR Modulators
dizziness, hypertension (Orkambi only)
Mucolytics Drug classes
Hypertonic saline and Donase alfa (Pulmozyme)
Hypertonic saline MOA
↑ hydration of airway mucus secretions, ↑ mucociliary function
Dornase alfa (Pulmozyme) MOA
MOA: cleaves DNA = ↓ mucous viscosity = improved airflow
mucous has high levels of extracellular DNA that inhibit mucociliary function and may ↑ infection risk (“sticky” mucous
Inhaled Antibiotics dosage
Nebulized twice or three times daily x28 days on then 28 days off
Nutritional Support
Supplement vitamins A, D, E, and K (fat soluble vitamins have poor absorption)
Digestive enzymes
with H2-blocker or proton pump inhibitor (PPI) to maintain an alkaline environment
What additional complications with CF?
Cystic fibrosis related diabetes, bone disease, liver disease, lung transplant
How do you treat additional complications?
Cystic fibrosis related diabetes (CFRD)- scars pancreas, requires insulin
Bone disease- vit D, vit K, calcium, bisphosphonates (ie: alendronate)
Liver disease- Manage complications, may require liver transplant
Lung transplant- Require antirejection meds and chronic steroids
Therapeutic Concerns with pulmonary drugs
Individuals with respiratory conditions typically have reduced exercise capacity
muscle weakness, cardiac involvement, hypoxemia, etc
Coordinate PT sessions with timing of respiratory medications
Therapeutic concerns with Anticholinergic Drug, Steroids, β2-agonists
Anticholinergic Drug (ABCDs)
Tachycardia
HTN
Dry mouth- have water for them to avoid dry mouth
Steroids
Inhaled drugs: Oral candidiasis and thrush
Increased infection risk
HTN
Hyperglycemia- if the person is already dibetic
Osteoporosis (more long-term effect)
Muscle weakness, skin atrophy
β2-agonists Tremor Tachycardia Hypokalemia Hyperglycemia
