COPD Flashcards
** disorder **: Destruction of alveoli and elastin fibres in the lung. May be caused by proteases released during the inflammatory response. Causes respiratory failure. Destruction of alveoli impairs gas transfer
Empyhsema
** Disorder **
* Attacks of winter morning cough
* Progresses to chronic cough with intermittent exacerbations
* Often initiated by an upper respiratory
infection
Bronchitis
main aim in COPD treatment
to reduce the progression of the disease, however does not supress inflammation or prevent the development of Emphysema
1st step in management of COPD
1) Smoking cessation –>Slows the progress of COPD
2) Immunizations –> Superimposed infections are potentially lethal
Drugs used in the treatment of COPD
1) Bronchodilators - β2 Adrenoreceptor agonists
2) Muscarininc receptor anatgonsits
3) Corticosetroids (CS)
short-acting drugs used in the tx of COPD
Short-acting drugs
1) Short-acting anti-muscarinic antagonists (SAMA):
Ipratropium
2) Short-acting beta agonists (SABA): salbutamol
Long-acting drugs used in the tx of COPD
Long-acting drugs
1) Long-acting anti-muscarinic antagonists (LAMA) :
Tiotropium
2) Long-acting beta agonists (LABA): salmeterol or
formoterol (LABA)
Muscarinic receptor antagonists used in the tx of COPD?
1) Ipratropium (Short-Acting Muscarinic Antagonist-SAMA)
2) Tiotropium (Long-Acting Muscarinic Antagonist-LAMA)
Adm of Ipratropim
- Inhalational
- Maximum effect: approximately 30 min after inhalation
- Persists for 3–5 h
Max effect of Ipratropium starts approx. —– after inhalation
30 min
Duration of Action of Ipratropium
3-5 hrs
Adm of Tiotropium
Inhalation
Longer-acting (t1/2=35 hours)
More potent than ipratropium
Which is more potent Ipratropium or Tiotropium?
Tiotropium
Duration of action of Tiotropium
Longer-acting (t1/2=35 hours)
AE of Muscarinic receptor agonists
* Ipratropium, Tiotropium
1) Dry mouth
2) Dry eyes
3) Raised intraocular pressure and blurred vision
(Caution in glaucoma)
4) Metallic taste
5) Constipation
6) Tachycardia (Caution in CV disease)
7) Urinary retention (Caution)
8) Cough/hoarse voice
Contraindications of Muscarinic receptor agonists
1) Glaucoma (raised intraocular pressure and blurred vission)
2) CV disease (Tachycardia)
3) Urinary retention
CU of Tiotropium
1) LAMA added w/ LABA when control insufficient
2) COPD
CU of Ipratropium
1) In Acute sever asthma, SAMA added w/ SABA which aguments (increases) bronchodilation of SABA
2) COPD
treatment approach to reduce inflammation in COPD
ICS (inhaled corticosteroids)
- note: oral corticosteroids should not be given to patients with stable COPD
MoA of inhaled corticosteroids in the management of COPD
1) Aim is to temper inflammation about COPD (tx not monotherpay)
2) Decrease frequency of exacerbation and improve quality of life
* not as effective in asthma
CU of Theophylline in COPD
tx of asthma and COPD esp in patients who tend to reatins CO2
not recommended due to its uncertain benefits!!!
What can you to give patients w/ sever COPD and Hypoxaemia?
Long-term O2 therapy (Adm at home)
Tx approach for Acute COPD exacerbation
1) Inhaled O2
2) Broad-spectrum abx if there is evidence of infection
3) Inhaled bronchodilators for symptomatic
improvement (SABA)
4) Oral prednisolone (CS)
Anti-Histamine 1st generation examples
diphenhydramine,
promethazine,
chlorpheniramine,
meclizine,
dimenhydrinate,
hydroxyzine
MoA of 1st gen Anti-Histamins
Reversible competitive antagonists of H1
receptors
(cross BBB)
AE of Anti-Histamine
1) Sedation caused by CNS histamine receptor blockage
2) Blurred vission, Dry mouth, Urinary retention –> Muscarinic receptor blockade
3) Headache -> α1-Adrenergic receptor blockade
MoA of Hitamine-1 Recptors
1) Bronchoconstriction
2) Increased vascular permeability
3) Itching
4) Nasal irritation/sneezing/ congestion
5) Vasodilation
CU of 1st gen Anti-Histamins
1) Allergic reactions, rhinitis, urticaria
2) Cold medication (tx of symptoms)
3) Sleep aid
4) Pre-op sedation
5) Nausea/vomiting
6) Motion sickness, vertigo
2nd gen Anti-histamines
Loratadine
Desloratadine
Fexofenadine
Cetirizine
-adine
CU of 2nd gen Anti-Histamines
allergy
why are 2nd gen Anti-Histamines preferred over 1st gen?
Because they are less sedative as they have decreased penetrance into CNS
AE of 2nd gen Anti-Histamines
Uncommon
main aim in the treatment of Cough supression
Best to treat underlying cause rather than cough
drugs used to supress cough
weak Opoids
Codeine
Pholcodeine
Morphine
CU of Morphine in respiratory disease
Palliative (soothing) care in lung cancer cough
which opoids are the most to least addictive
Codeine, Morphine, Pholcodeine
least –> most
Phlocodeine < Codeine < Morphine
AE of Opiods
1) Constipation
2) Drowsiness
3) Dry mouth
4) Miosis (“pin point pupil”)
5) Nausea/vomiting
6) Respiratory depression
Opiods are avoided in?
chronic pulmonary infection and asthma
why?
* Thickening of mucus and retention
* Risk of respiratory depression
Morphine Derivative
Dextromethorphan
AE of Dextromethorphan
Uncommon; dizziness, nausea, vomiting,
or GI disturbance
MoA of Dextromethrophan
- Binds σ receptors
- Also binds serotonergic receptors -> inhibits reuptake of serotonin
Contraindications of Dextromethorphan
serotonergic agents –> may cause Seratonin syndrome
Dextromethorphan at high doses can antagonize ——– receptors
Glutamate NMDA
class of N-acetyl cysteine
Mucolytic
CU of N-acetyl cysteine
1) Antidote for patracetamol
2) Cystic Fibrosis
MoA of N-acetyl cysteine (as a mucolytic)
1) Depolymerizes the mucin glycoprotein oligomers
via disulfide bond hydrolysis
2) Decreases mucus viscosity
AE of N-acetyl cysteine
nausea, vomiting, flushing,
rash
peptide Mucolytic
Dornase alfa
MoA of Dornase alfa
depolymerizes DNA
CU of Dornase alfa
Cystic fibrosis
class of Hypertonic Saline
Mucolytic
* i dont think its important
MoA of Hypertonic saline
- Disrupts ionic bonds within the mucus gel
- Dissociates DNA from mucoproteins allowing natural
proteolytic enzymes to digest the mucoprotein
——: a type of cough medicine used to help clear mucus (phlegm) from your airway
Experctorant
Experctorant example
Guaifenesin
CU of Guaifenesin
symptomatic relief of acute
productive cough
MoA of Guanifenesin
- Increases the volume of respiratory secretions
- Decreases the viscosity of bronchial secretions
- Does not suppress the cough reflex
How are Guaifenesin used?
Used alone or in combination with antihistamines,
cough suppressants, and decongestants
Decongestants examples
Pseudoephedrine
Phenylephrine
Moa of Phenylephrine
Selective α1 adrenergic agonist
(Less CNS stimulation than pseudoephedrine)
ΜοΑ of Pseudoephedrine
α1 adrenergic agonist -> release of norepinephrine
ΑΕ of Pseudoephedrine
CNS stimulation, anxiety, hypertension, urinary retention, tachycardia, nausea/vomiting
Pseudoephedrine is a ——– precursor
Methamphetamine
