Respiratory Flashcards
Sympathetic nervous system review (alpha and beta receptors)
Sympathetic nervous system – epinephrine and noradrenaline bind to adrenergic receptors
Adrenergic receptors alpha and beta (split into a1 a2, b1 b2)
A1 – causes vasoconstriction
A2 – don’t worry
B1 – heart muscle cells, act on SA node leads to increase heart rate. Act on muscle cells you get increase in the force of contraction
B2 – lungs, bronchodilators
Parasympathetic nervous system
Acetylcholine receptors are muscarinic and nicotinic
Nicotinic is on skeletal muscles, causes muscles to contract
Muscarinic is on heart muscle cells, causes increase in heart rate
Asthma
Narrowing of airways due to:
Recurrent and reversible
an allergen. causes release of histamines and leads to:
bronchospasms due to triggers
and inflammation (of mucosa)
COPD
Chronic obstructive pulmonary disease
- chronic bronchitis (hypersecretion of mucous, inflammation) and emphysema (destruction of alveoli)
Respiratory Drugs, especially for asthma (3)
Bronchodilators (B2-adrenergic agonists)
- salbutamol
Anticholinergics
- ipratropium bromide
Xanthine derivatives
- theophylline/aminophylline
Respiratory Drugs, for both asthma and COPD (2)
Anti-inflammatory Drugs/Glucocorticoids
- budesonide
Leukotriene Modifiers
- montelukast
Bronchodilators: β-Agonists
Name one
Mechanism:
Salbutamol (short-acting rescue drug)
Mechanism: Sympathomimetic bronchodilators - mimic the sympathetic nervous system to relax smooth muscles of the airway and dilate the bronchioles
Stimulate bronchial smooth muscle B2-adrenergic receptors
β-Agonists
Indications:
Adverse Effects:
Care Implications:
Indications: Relief of bronchospasm related to asthma, bronchitis. Acute attacks and for prevention (like before exercise)
Adverse Effects: tachycardia, tremors, restlessness, insomnia
Salbutamol causes tremors, anxiety, increased HR, palpitations, angina
Care Implications: Stop smoking, Adequate fluid intake
Monitor for therapeutic effects
Bronchodilators: Anticholinergics
Name one
Mechanism:
Adverse Effects:
ipratropium bromide
Mechanism: Anticholinergics block acetylcholine receptors to reduce constriction (since acetylcholine causes constriction)
competitive inhibition
Prevents bronchoconstriction, but is NOT used alone for acute exacerbations!
Adverse Effects: dry mouth (Ach blocks salivation), very minimal systemic effects
Bronchodilators: Methylxanthines (not the preferred choice)
Name two
Routes:
Mechanism:
Theophylline and Aminophylline
Routes: Oral and IV respectively
Mechanism: bronchodilation (maybe cAMP, maybe anti-inflammatory. not sure how)
Methylxanthines
Adverse Effects: (think caffeine)
Interactions:
Adverse Effects: CNS stimulation
anxiety, insomnia, seizures
Cardiovascular stimulation
Palpitations (increased force of contraction/fast HR)
Sinus tachycardia (increased HR)
Ventricular dysrhythmias
GI distress
nausea, vomiting
Interactions: so many! it has one of the longest lists. remember Ciprofloxacin which inhibits liver CYP metabolism and causes increased effects of theophylline
Anti-inflammatory drugs: Glucocorticoids
What are they?
Prescribed frequency:
Why inhaled?
They’re steroids, made with a base of cholesterol. Similar action to cortisol. Anti-inflammatory action
Frequency: Prescribed to be taken once or twice a day, every day. They keep the symptoms under control.
Inhaled for chronic asthma and COPD control
Inhaled forms reduce systemic effects
Glucocorticoids
Name two: Mechanisms: Combination Preparations: Advair disks: Indication: Adverse Effects:
Budesonide and fluticasone
Mechanisms: reduces prostaglandins, cytokines, activity of leukocytes, reduces edema
Combined: Add in a long-acting B2-agonist (LABA) bronchodilator like formoterol
Disks use fluticasone and are combined with salmeterol (LABA)
Indications: Prophylactic treatment of bronchospastic disorders asthma and COPD
Adverse Effects: oral fungal infections (candida)
What is taken first: bronchodilator or glucocorticoid?
Bronchodilator should be used several minutes before the glucocorticoid
to provide bronchodilation before administration of the glucocorticoid
Anti-inflammatory Drugs: Leukotriene Modulators
Name one
Review physiology
Indications:
Montelukast
Arachidonic acid is converted into leukotrienes through the action of lipoxygenases
Review: released in immune responses in asthma
Leukotrienes cause
inflammation
bronchoconstriction (smooth muscle constricts)
mucus production
can lead to shortness of breath
Indications: Prophylaxis and chronic treatment of asthma. Continuous schedule
What do Leukotriene Modulators do?
Reduce inflammation in lungs to reduce asthma symptoms
Prevent smooth muscle contraction of the bronchial airways
Decrease mucus secretion
Prevent vascular permeability
Decrease neutrophil and other leukocyte infiltration to the lungs, preventing inflammation
