Pharmacology Of Asthma And COPD Flashcards
Characteristics for treatments of asthma
2 treatment catagories
1) relievers:
- bronchodilators that open up bronchoconstricted airways
2) controllers:
- anti-inflammatories that reduce inflated airways which causes swelling
Asthma vs COPD general stats
Asthma
- reversible
- FEV1 will return to baseline after use of SABA
- patients are usually younger and has same symptoms as COPD but symptoms are often worsen at night
- high levels of eosinophils and IgE in blood
- uses spirometers to help confirm diagnosis
COPD
- irreversible
- FEV1 will NOT return to baseline after SABA use
- patients are usually older <40 and often cigarette smokers
- no increases in eosinophil/ IgE levels in blood
- uses spirometers to help confirm diagnosis
- shows persistent cough (especially in chronic bronchitis)
Questions to ask when differentiating between asthma and COPD
1) age of patient and onset of disease
2) history of tobacco use
3) due symptoms get worse at night (asthma) or are they constant (COPD)?
4) fa mainly history of asthma?
Reliever drugs include what?
SABA drugs
- short acting beta agonists
- albuterol/terbutaline
- pirbuterol
- bitolterol
Anti cholinergics of LAMA
- long acting muscarinic antagonists
- tiotropium bromide
- ipratropium bromide
Methylxanthines
- theophylline
- aminophylline
Controller drugs for asthma include what?
Corticosteroids
LABA drugs
- long acting beta agonists
- salmeterol
- formoterol
- Vilanterol
Methylxanthines
- theophylline
- aminophylline
Anti-IgE mabs
Leukotriene Inhibtors
what are the final products that cause bronchoconstriction or bronchodilation in the lungs?
Bronchodilation (sympathetic)
- de-phosphorylated (deP) myosin
- generated by B2 receptors
- goes through sympathetic route which uses NE as its neurotransmitter and activates cAMP pathways to generate deP
- hence why B2 agonists are used
Bronchoconstriction (parasympathetic)
- phosphorylated myosin
- generated by Muscarinic receptors
- goes through parasympathetic route which uses ACh as its neurotransmitter and activates IP3 DAG pathways to generate P-myosin
- hence why M antagonists are used
SABA facts
MOA: binds to B2 receptors and generates increase cAMP levels and deP-myosin which bronchodilator lungs
ADRs:
- throat irritation
- muscle tumors
- heart palpitations
- lower extremities edema
Note: tolerance can develop with overuse and if a patient is using SABA >2days a week, consider anti-inflammatory therapy
SABA vs LABA
SABA:
- rapid onset of action
- go away after 4-6 hrs
- used for acute attacks
LABA:
- rapid onset of action
- go away in 12-24 hrs
- NOT used for acute attacks
Muscarinic antagonists
- Ipratropium bromide
- Tiotropium Bromide
MOA:
- prevents ACh from binding to Muscarinic receptors and inhibits smooth muscle contractions and excess mucus production
- are less effective than SABA/LABA, more so a synergist
ADRs Inhibits: - Salivation - Lacrimation - Urination - Defecation Dry mouth GI upset Pupillary dilation (mydriasis)
Methylxanthines
MOA:
- inhibts phosphodiesterase, causing increased cAMP (similar to B2 agonists)
- inhibits this in both smooth muscle and eosinophils, causing bronchodilation and anti-inflammatory effects
- adenosine receptor antagonist causes increased ventilation during asthma attacks
ADRs:
- MUST monitor plasma levels since they can be toxic*
- cardiac arrthymias
- GI upset
- Poor w/ CYP2A inhibtor drugs
- most commonly used when SABAs or corticosteroids are not working/contraindicated
Difference between hypersensitivity and hyperreactivity
Hypersensitivity:
- low levels of stimuli results in constriction responses
Hyperreactivity response:
- exaggerated/amplified response to normal levels of a stimuli
BOTH are seen in asthma
Corticosteroids
- beclomethasone
- triamcinolone
- fluticasone
- budesonide
- fluisolide
- ciclesonide
- prednisone/ methylprednisolone
MOA: Anti-inflammatory that works to decrease cytokines, inhibit mast cells, reduce vascular permeability
(can be inhaled or oral (inhaled decreases systemic effects and requires small doses to get desired effect so is more often used, especially in asthma)
ADRs: depends on pathway
1) inhaled
- oropharyngeal candidiasis (ask patient to rinse mouth or use spacer)
- hoarseness
- can causes neutrophilic leukocytosis
2) oral
- increased appetite and weight gain
- causes hyperglycemia
- suppresses immune system, and promotes osteoporosis
- cant use long term since it stunts adrenal glands if so
Coromolyns
- chlorofluorocarbons
MOA:
- mast cell stabilizing agents which decrease the overall activity and prevent degranulation
better safety profile, but require 4x daily use so patient adherence sucks
ADRs:
- abnormal taste
- cough
- throat irritation
- GI distress
- Dizziness
Leukotriene antagonists
- zileuton
- montelulkast
- zarfirlukast
MOA: arachidonic acid derivative which blocks leukotriene production which disrupts multiple pathways
- leukotriene B4 helps attract additional leukocytes (disabled w/ antagonist)
- leukotriene C4/D4/E4 help increase bronchi reactivity, bronchoconstriction and secretion of mucus (disabled w/ antagonist)
- very useful in aspirin-exacerbated respiratory disease*
ADRs:
- hepatotoxicity (only Zileuton and rare)
- Chung-Strauss syndrome (montelukast and zafirlukast only and rare)
Anti-IgE antibody
- Omalizumab
MOA:
- binds to IgE receptors and prevents IgE from bidding to mast cells and inducing degranulation
ADRs:
- cough
- URIs
- dizziness
- nausea
