Upgrade to remove ads
Only $35.99/year

Asthma case

Terms in this set (51)

Is asthma a restrictive or an obstructive airway disease?
obstructive airway disease
what triggers may aggravate asthma
1. allergens: airborn pollens (trees, grass, and weeds), house-dust mites, animal danders, cockroaches, fungal spores
2. Environmental factors-cold air, fog, ozone, surfur dioxide, nitrogen dioxide, tobacco smoke, cannabis smoke
3. Anxiety, stress and laugther
4. Exercise in cold dry climate
how can we modify these in Sara (if present)?
1. quit smoking and donot allow smoking in home, car or around her
2. Dust mites-Encase mattress and pillow in special dust mite-proof cover. Wash sheets and blankets on your bed each week in hot water
3. animal dander-keep animal with fur or hair out your bedroom and keep the bedroom door closed.
Remove carpets and furniture covered with cloth from your room.
4. cockroaches-keep all food out of your bedroom
keep food and garbage in closed containers
If you use spray to kill roaches, stay out of the room until the odor goes away
5. Indoor mold
Clean moldy surfaces, fix leaking faucets, pipes, or other sources of water.
6. Exercise or sports-take your medication before exercise to prevent symptoms
warm up for a period before you exercise
Other: Sulfites in food: do not drink beer or wine or eat processed potatoes
cold air: Cover your nose and mouth with a scarf on cold or windy days.
what are the clinical manifestations of asthma and which symptoms are affecting Sara
wheezing, breathlessness, coughing and chest tightness
How is asthma diagnosed
1. episodic symptoms of obstruction and hyperresponsiveness, inflammation
2. documented spirometry that shows obstruction and reversibility of obstruction
what are PFTs?
A group of tests that measures Volumes and ventilation
Examples:
- Spirometry
- Peak flow meters
What is responsiveness to pharmacotherapy?
Patient with FEV1/FVC < 80% is reversible after inhaled SABA administration. Approximately 12% improvement in FEV1
What is the dose of salbutamol
Inhale 2 puffs every 4-6 hours TID or QID as needed.
Maximum of 8 puffs a day
What are the adverse effects of salbutamol
nervousness, tremor, tachycardia and palpitations
What is salbutamol's mechanism of action?
salbutamol binds to the beta-2-adrenergic receptors in the smooth muscles of the respiratory system and stimulate adenylate cyclase to form cAMP from ATP.
cAMP activates protein kinase which result in dilation of the airway smooth muscles.
What is the structure of salbutamol?
what was the likely lead compound for the development of salbutamol?
epinephrine
Which structural regions were varied?
1. N-alkyl group was increased to obtain beta 2 selectivity
2. hydroxyl group on catecholamine skeleton
What functional groups were incorporated? Why?
hydroxyl methylene on the catecholamine and t-butyl group
The hydroxylmethylene group prevents metabolism to inactive compound by catechol O-methyl transferase (COMT). It is slowly metabolised to to a phenolic sulphate
The tert-butyl group enable selective binding to the beta 2 adrenoceptors which are more express in the lungs than in the heart. it is 2000 times less active in the heart so prevent adverse reaction to the heart.
Increase retention in the lung tissue to to hydrophobic tert butyl broup.
what are the interactions that occur when agonist binds to the adrenoceptor
1. 2 H-bonds (2 ser and OH of catecholamine)
2. 2 van der waal forces between valine and side chain and between phenyl ring of catechol and Phe
3. ionic bond between Asp and the amine group
4. hydrophobic interactions via the amine R group
Are there drugs similar to salbutamol?
samefamol, salmeterol, formoterol, idacaterol, vilanterol, olodaterol and fenoterol
What is their struture activity relationship? how do they differ and why
duration of action increases with increasing hydrophobicity of
What is levalbuterol? What is the rationale for the development of this compound? Which patients may benefit from this agent and is it available in Canada?
It is the R enantiomer of salbutamol also called xopenex
How is levalbuterol different from the other beta2 adrenergic receptor agonist?
It does not have the S-enantiomer which causes adverse effects. Its potency is achieved at one fourth the dose of racemic albuterol along with marked reduction in side effects
Consider the structures of metaproterenol, terbutaline, salbutamol, salbutamol, fenoterol and salmeterol. Generate a table to include information on receptor selectivity, duration of bronchodilation, duration of protection, elimination, dosing regimen, and available dosage forms. Wherever possible, explain these pharmacokinetic and pharmacodynamic data in terms of the structural features of the drugs
1. duration of action increases with substitution of more bulky alkyl group at the amine position
2. Also as bulky groups are added there is increase selectivity for beta 2 receptor
3. elimination halflife also become longer as hydrophobic group increases in size
As hydrophobicity increases, the ligand mind more strongly to the tissue in the vicinity of the adrenoceptor and this makes it available to act for a longer period
Who will benefit from levalbuterol
levalbuterol was developed because it was noticed that the S enantiomer accumulates to a greater extend in the body and produces adverse effects
Patients with cardiovascular problems would benefit from levalbuterol
What is the mechanism of action of inhaled corticosteriods (ICS)?
anti-inflammation, inhibition of cytokines and interleukin 1, and inhibition of mast cell release of autocoids. The corticosteriods bind to their receptor in the cytoplasm and that the glucocorticoid-receptor complex travels into the nucleus, where it binds to DNA and affects gene transcription, which increases and, sometimes, decreases the production
of important biologically active compounds.
Does the mechanism of action of ICS differ from the mechanism of action of topical steroids that you learned about in the first term?
Same mechanism of actio
Day 2-How would you classify Sara's severity of asthma based on the information provided?
...
Day 2 How would you classify Sara's level of control -Is she well-controlled, or very poorly controlled?
...
Educate Sarah on the proper use of her puffer
...
What are the 2 most common adverse-effects of high-dose ICS therapy and what interventions can the pharmacist make to help minimize the risk of Sara experiencing these?
...
what was the mouth rinse that was prescribed to Sara
Nyastatin
What is an acute asthma exacerbation?
...
What are the risk factors for death associated with acute asthma exacerbations
...
Is Sara in the Green, yellow or Red Zone in terms of PEF and how to these zones impact home treatment of asthma exacerbations?
...
What are the goals of therapy for acute asthma exacerbations?
...
Diagram the relationship between particle size and airway penetration.
...
Diagram how long clearance mechanism impact upon the fate of inhaled drug
...
how might the fate of drug then impact upon the effects (pharmacologic and adverse) of drugs administered via the pulmonary route?
...
Identify the major advantages and disadvantages of each aerosol delivery system. Can a major disadvantage (e.g. incorrect use) of a particular device (MDIs) be overcome by simply switching to an alternative (e.g. DPIs)
...
Describe the various mechanism of particle deposition in the lung. What is the purpose of "spacing" devices between the actual delivery system and the oral cavity of the patient? Which mechanisms of particle deposition is this device based on? Would you recommend the use of home-made spacers? Are there clinical differences between home-made and commercially available spacers
...
Following administration by inhalation, how does a drug reach the systemic circulation? How does this compare to oral drug administration? Wish respect to pharmacokinetics and pharmacokinetics and pharmacodynamics why is it beneficial to apply drugs topically to the lung?
...
Based on statistic Canada 2014, what was the % of people greater or equal to 12 years diagnosed with asthma
8.1
asthma is characterized by
1. inflammation of airways
2. airways hyperresponsiveness
3. airways obstruction
Main clinical presentation of asthma
1. wheezing
2. breathlessness
3. chest tightness
4. coughing
Cells involved in the mediation of inflammation in asthma are
1. mast cells
2. eosinophils
3. T lymphocytes
4. macrophages
5. neutrophils
6. epithelial cells
What causes airway obstruction in asthma
1. bronchoconstriction
2. edema
3. mucus hypersecretion
Based on Sara symptoms in day 1 what is her diagnosis
mild persistent asthma
Write a DRP for Sara on day 1
Sara is esperiencing mild persistent asthma and require drug therapy
What are goals and specific outcomes for Sara on
1. Prevent asthma related mortality
2. Prevent complications-exacerbation and hospitalizations
• Minimize impairment
- Achieve symptom relief following SABA
immediately
- Maintain normal activity (exercise, other physical
actvity, & attendance at school)
• Prevent adverse effects
What are the various options for quick relief of asthma symptoms
1. SABA
2. fast acting beta agonist-formeterol
3. Ipratropium bromide
4. systemic corticosteroid
The Expert Panel recommends which drug
of choice for treating acute asthma symptoms and
exacerbations and for preventing exercise induced
bronchoconstriction (Evidence A).
SABAs
The Expert Panel recommends what medicatio for long term therapy control of asthma
ICSs are the most potent for step 2
Diagram the relationship between particle size and airway penetration
The optimum size for particles to settle in the airways is 2-5 μm mass median aerodynamic diameter (MMAD). Larger particles settle out in the upper airways, whereas smaller particles remain suspended and are therefore exhaled. There is increasing interest in delivering drugs to small airways, particularly in COPD and severe asthma (Sturton et al., 2008). This involves delivering drug particles of ∼1 μm MMAD, which is now possible using drugs formulated in hydrofluoroalkane (HFA) propellant.
diagram how lung clearance mechanisms then impact upon the fate of inhaled drug. how might the fate of the drug then impact upon the effects of drugs administered via the pulmonary route
Of the total drug delivered, only 10-20% enters the lower airways with a conventional pressurized metered-dose inhaler (pMDI). The fate of the inhaled drug is poorly understood. Drugs are absorbed from the airway lumen and have direct effects on target cells of the airway. Drugs may also be absorbed into the bronchial circulation and then distributed to more peripheral airways. Whether drugs are metabolized in the airways is often uncertain, and there is little understanding of the factors that may influence local absorption and metabolism of inhaled drugs. Drugs with higher molecular weights tend to be retained to a greater extent in the airways. Nevertheless, several drugs have greater therapeutic efficacy when given by the inhaled route. The inhaled corticosteroid ciclesonide is a prodrug activated by esterases in the respiratory tract to the active principle des-ciclesonide. More extensive pulmonary distribution of a drug with a smaller MMAD increases alveolar deposition and thus is likely to increase absorption from the lungs into the general circulation resulting in more systemic side effects. Thus, although HFA pMDIs deliver more inhaled corticosteroid to smaller airways, there is also increased systemic absorption, so that the therapeutic ratio may not be changed.
Other sets by this creator