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123 Cards in this Set

  • Front
  • Back
Which 3 sicknesses are common for upper respiratory infections?
Upper respiratory:

1. common cold
2. rhinitis
3. sinusitis
What 2 sicknesses are common for lower respiratory infections?
Lower respiratory:

1. asthma
2. COPD

*we focus on the lower respiratory system
What is asthma?
A chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus often in response to one or more triggers
What is COPD?
characterized by the presence of progressive airflow obstruction
Is COPD reversible?
no
What are 2 classes of medications for the respiratory system?
1. bronchodilators
2. anti-inflammatory agents
Should you prescribe bronchodilators for acute or chronic respiratory illness?
acute
What do bronchodilators do?
bronchodilators dilate pulmonary vasculature
Why would you prescribe an anti-inflammatory agent?
preventative medical use
What do anti-inflammatory agents do?
they decrease production and release of inflammatory mediators
Give 3 examples of bronchodilators.
1. beta2-adrenergic receptor agonists
2. ethylxanthines
3. anticholinergic Agents
Give 3 examples of anti-inflammatory agents.
1. corticosteroids
2. mast cell stabilizers
3. leukotriene modifiers
Which adrenergic receptor does the lungs have? What is the physiologic response associated with this receptor binding?
beta2

relaxation of smooth muscle
Which adrenergic receptors does the heart have? What is the physiologic response associated with this receptor binding?
beta1 & beta2

increased heart rate
Name 5 beta2-adrenergic receptor agonists. Why are these Xosignificant?
1. Epinephrine (Adrenalin, Primatene)
2. Albuterol (Proventil, Ventolin)
3. Levalbuterol (Xopenex)
4. Salmeterol (Serevent)

*these are the primary bronchodilators used to treat asthma
What are the major effects that beta2 adrenergic agonists have on the heart and lungs?
heart: increase HR

lungs: cause relaxation of smooth muscles (bronchodilation)
Describe the MOA for beta2 adrenergic receptor agonists in the lungs.
*these drugs act on the B2 receptors in the lungs by...

1. binding to b2 receptor induces...
2. cAMP concentration in the bronchial smooth muscle increases so...
3. relaxation of this airway smooth muscle occurs, resulting in...
4. bronchodilation
What is the therapeutic effect of beta2-adrenergic receptor agonists?
relaxation of smooth muscle leads to bronchodilation
There are 2 categories of beta2-adrenergic receptor agonists. What are they?
1. Short acting agents
2. Long acting agents
What is the onset of action for short acting beta2 adrenergic receptor agonists?
5 min
What is the duration of action of short acting beta2 adrenergic receptor agonists?
3-8 hours
What is an example of short acting beta2 adrenergic receptor agonists?
Albuterol
What is the onset of action of long acting beta2 adrenergic receptor agonists?
20 min

*you wait longer for the effects, but it lasts longer
What is the duration of action of long acting beta2 adrenergic receptor agonists? How frequent should you administer a dose?
12 hours

2x/day
Give an example of long acting beta2 adrenergic receptor agonists.
Salmeterol (Serevent)
Why would you use a short acting beta2 adrenergic receptor agonists?
to immediately relieve acute symptoms

*they act quickly, but they don't last long
Why would you use long acting beta2 adrenergic receptor agonists?
to maintain symptoms

*they act slowly, but last a long time
What are 2 categories of beta2 adrenergic receptor agonists in terms of selectivity?
1. non-selective agents
2. selective agents
Which receptors do non-selective beta2 adrenergic receptor agonists act on? Give an example.
BOTH beta 1 and beta 2 receptors

Epinephrine
Why does epinephrine have an increased number of side effects?
the agent is more general, so even if it is administered to act on the lungs it may also increase HR
What receptor do selective beta2 adrenergic receptor agonists act on? Give examples.
ONLY beta2

Albuterol, salmeterol
What is the key advantage in choosing selective beta2 adrenergic receptor agonists over the non-selective ones?
they minimizes effects

BUT

if you increase the dose enough, you may get nonselective effects
What are 3 routes of administration for beta2 adrenergic receptor agonists?
1. inhalation
2. oral
3. subcutaneous
What are 3 inhalation methods that can be used to administer a beta2-adrenergic agonist?
1. nebulization
2. metered dose inhaler (MDI)
3. dry powder
What are 2 advantages of administering beta2-adrenergic agonists by the INHALATION route?
1. allows for direct administration at the site of action
2. minimal absorption from the lung into the circulation
-90% of the drug stays in the lung
-10% of the drug gets absorbed systemically
What is a major advantage associated with using the inhalation route?
fewer side effects
Name the 4 parts of a nebulizer.
1. mouthpiece
2. nebulizer cup
3. tubing
4. compressor
Describe the process of using a metered-dose inhaler (MDI).
1. shake well before each use
2. breathe out fully through the mouth
3. while breathing in deeply and slowly through the mouth, fully depress the top of the metal canister
4. hold breath as long as possible (~10 seconds)
How long should you wait before taking an additional puff from an MDI?
1 minute
When should you use a spacer with an MDI?
for patients, such as children, who lack the coordination of breathing and pressing an MDI
Name a medicine that is administered through an MDI.
Albuterol
How do you use a dry powder inhaler to administer a beta2 adrenergic receptor agonist?
1. open DISKUS
2. activate dose
3. exhale fully while holding the DISKUS level and away from your mouth
4. breathe in quickly and deeply through the DISKUS through the mouth
5. hold breath for ~10 seconds, or as long as comfortable
6. breathe out slowly
How do you activate the dose in a dry powder inhaler?
slide the lower level away from you as far as it will go until it clicks
What tells you how many doses are left in your dry powder inhaler?
dose indicator on the top of the DISKUS

the number usually starts at 60, which refers to a 1 month supply at 2 doses/day
What types of agents would you administer via the dry powder inhalation route?
those that are more long-lasting
Give an example of a beta2 adrenergic receptor agonist that is administered orally.
Albuterol

*given in capsule form
What is a disadvantage of administering beta2 adrenergic receptor agonists via the oral route?
increased risks of adverse effects

*this drug becomes nonselective when given orally, so it can effect the heart
What is a disadvantage of administering beta2 adrenergic receptor agonists via the subcutaneous route?
increased risk of adverse effects
Give an example of a beta2 adrenergic receptor agonist that is given SubQ.
Epinephrine
List 4 adverse effects associated with beta2 adrenergic receptor agonists.
1. tachycardia
2. decreased serum K+ levels
3. tremor
4. tolerance
Why does tachycardia occur as an adverse effect for beta2 adrenergic agonists?
When beta2 receptors are activated in the heart

(you see more in orally administered agents than in inhaled agents)
Why does decreased K+ serum levels occur as an adverse effect for beta2 adrenergic agonists?
K+ is pushed into the cell, so the patient becomes predisposed to the arrhythmias
Why do tremors occur as adverse effects for beta2 adrenergic agonists?
from activated beta2 receptors
Why does tolerance occur as an adverse effect for beta2 adrenergic agonists?
the body downregulates its beta2 receptors

counteract with:
1. withdrawal
2. additional meds
What are significant drug interactions that occur with beta2 adrenergic agonists?
1. adrenergic medications (ie, caffeine has an additive effect)

2. beta2 blockers (may reverse what you're trying to do for the lungs because they may be nonselective; they mostly work in the heart, however)
After using an beta2 adrenergic agonist via the inhalation route, why might the patient be too jittery?
too many puffs
How should you guide a patient who uses an beta2 adrenergic agonist inhaler and wants to exercise?
tell the patient to use it 30 minutes before he/she exercises
Give 2 examples of Methylxanthines.
1. aminophylline (truphylline)
*used more often
2. theophylline (Slo-Bid, Theo-Dur)

*neither used as much anymore
What type of inhibitor is methylxanthine?
Phosphodiesterase inhibitor
Where is phosphodiesterase located?
phosphodiesterase is predominant in airway smooth muscle
What does phosphodiesterase do?
it is an enzyme responsible for the breakdown of cAMP
Describe the MOA of methylxanthines.
Methylxanthine INHIBITS phosphodiesterase, therefore increasing the cAMP concentration in the smooth muscle.

***has nothing to do with beta2 receptors
What therapeutic effect do methylxanthines produce?
by causing an increase in cAMP concentration..

this leads to relaxation of the airway smooth muscle, which causes BRONCHODILATION
How is theophylline administered?
all ORAL
Theophylline has many brand names: Theo-24, TheoCap, Theochron, Uniphyl. Why can't you simply switch from one to another?
they all have different salts and cannot be substituted mg for mg
Why must you monitor theophylline closely?
1. it has a very small therapeutic window
2. many drug interactions occur with theophylline
How is aminophylline administered?
IV
Give 2 examples of methylxanthines.
1. theophylline
2. aminophylline
Where and in what percentage are methylxanthines metabolized?
90% in the liver through CYP1A2
In the setting of a CYP INDUCER, how should you administer methylxanthines? Give examples of CYP inducers.
increase the maintenance dose when CYP inducers are present

smoking, AEDs
In the presence of a CYP INHIBITOR, how should you administer methylxanthines? Give examples of CYP inhibitors.
decrease the maintenance dose

some antimicrobials, antifungals, and antibodies
What adverse effects are observed with methylxanthines?
methylxanthines have a very narrow therapeutic window, these are observed at serum levels above 20mcg/mL

1. N/V
2. tremor
3. headache
4. arrythmias
5. seizures
Why would you administer an oral methylxanthine with food or milk?
to reduce GI effects
Describe the anticholinergic MOA?
Competes with Ach at the muscarinic receptor site...
causing decreased vagal tone to the airway...
leading to bronchodilation
What occurs when Ach is normally allowed to bind to the muscarinic receptor? How is this disturbed by anticholinergic agents?
muscarinic receptor binding to Ach causes an increased calcium influx, which leads to contraction

Anticholinergic agents bind to muscarinic receptors, which prevents calcium influx and therefore prevents contraction
Give 2 examples of anticholinergic agents.
1. Ipratropium (Atrovent)
2. Tiotropium (Spiriva)
How long does Ipratropium act?
Ipratropium has a short acting duration of action (3-4 hr)
What is the Ipratropium dose?
2 puffs 4x daily
What is the duration of action of Triotropium?
Triotropium has a long acting duration of action (24 hr)
what is the Triotropium dose?
1 capsule inhaled 1x daily

The capsule looks like a DISKUS, but is aactually a capsule. The pressure of breathing pops a hole in the capsule and you breathe in the powder.
What is the only route that anticholinergic agents are administered?
INHALATION ONLY
What are the adverse effects associated with anticholinergic agents?
1. blurred vision (mydriasis)

With high doses:
1. headache
2. flushed skin
3. tachycardia
4. urinary retention
*from muscarinic inhibition
Why would you provide a patient who is taking anticholinergic agents with a sugarless lozenge?
to prevent dry mouth side effect
What are 2 routes that corticosteroids can be administered?
1. inhalation
*fewer side effects
2. systemic (oral or parenteral)
Name 2 corticosteroids that are delivered via the inhalation route.
1. Budesonide (Pumicort)
2. Fluticasone (Flovent)
Name 4 corticosteroids that are delivered systemically or parenterally.
1. Hydrocortisone (Solu-Cortef)
2. Methylprednisolone (Solu-Medrol)
3. Prednisone (Deltasone)
4. Dexamethasone (Decadron)
What is the primary MOA of corticosteroids?
corticosteroids inhibit the production or release of inflammatory mediators
What is an additive MOA of corticosteroids?
corticosteroids improve beta2 receptor agonists sensitivity to the beta2 receptor in an acute setting

*they prevent or reverse airway remodeling
Are corticosteroids good as long term agents?
no
What is the corticosteroid dose dependent on?
the severity of disease
What is the therapeutic effect of corticosteroids?
reducing inflammation
What is systemic administration of corticosteroids reserved for?
patients with acute exacerbations or severe disease refractory to other treatments

**not used for acute relief of bronchospasms
Why would one one to administer a corticosteroid via the inhalation route?
for maintnenance,

systemic administration tends to be for acute reasons
What is the adverse effect associated with INHALATION-delivered corticosteroids?
fungal infections of the mouth (instruct the patient to rinse after each use!)
What are the adverse effects associated with SYSTEMICALLY delivered corticosteroids?
1. *osteoporosis (decreased Ca++ in bones)
2. *hypertension
3. *hyperglycemia (glucose intolerance)
4. thinning of the skin
5. myopathy (muscle weakness)
6. CNS effects (euphoria, depression)
7. Impaired wound healing
When should you not administer a corticosteroid?
to treat acute asthmatic attacks
Give an example of a mast cell stabilizer.
Cromolyn (Intal, Nasalcrom)

*not used very often
How is Cromolyn administered?
nebulizer or dry powder
What are mast cell contents? What do they cause?
Mast cell contents:
1. histamine
2. prostaglandins
3. leukotrienes

*cause bronchoconstrictions
Are mast cell stabilizers used for acute relief?
no
Describe the MOA of mast cell stabilizers.
Mast cell stabilizers INHIBIT the breakdown of mast cells (thereby preventing the release of mast cell contents)
What is the therapeutic effect of mast cell stabilizers?
prevention of bronchospasm (bronchoconstriction)
When are mast cell stabilizers most effective?
when they are administered 30 minutes before exposure to an allergen or exercise
What are adverse effects associated with mast cell stabilizers?
1. tracheal irritation
2. cough
3. taste disturbances (patient may say he has an aluminum taste in his mouth)
What must you be sure to tell a patient when he is taking a mast cell stabilizer?
1.continue using it even if he feels better/is symptom-free

2. do not discontinue abruptly
What type of relieve do bronchodilators provide?
acute relief
What type of relieve do anti-inflammatory agents provide?
preventative measures
What are 2 categories of leukotriene modifiers?
1. receptor antagonists
2. inhibitor of 5-lipoxygenase
What are 2 leukotriene modifier receptor antagonists?
1. Montelukast (Singulair)
2. Zafirlukast (Accolate)
What is an example of a 5-lipoxygenase inhibitor?
Zileuton (Zyflo)
What do leukotrienes cause?
bronchoconstriction
Which cascade do leukotrienes come from?
arachidonic acid cascade
What is the MOA of 5-lipoxygenase inhibitors?
they prevent the formation of leukotrienes and therefore reduce bronchoconstriction
What is the MOA of leukotriene modifier receptor antagonists?
prevents binding to leukotriene receptors (see slide)
What are 2 leukotriene modifer MOAs?
1. either inhibit 5-lipoxygenase
2. block the leukotriene receptor site
What is the therapeutic effect of leukotriene modifiers?
reduce inflammation (often used as an alternative to corticosteroids)
What shouldn't you use leukotriene modifiers for?
Do NOT use for the acute relief of bronchoconstriction

*more of a preventative drug
What are 3 drug interactions with leukotriene modifiers?
1. Zafirlukast
2. Zileuton
3. Montelukast
Which of the drugs that interact with leukotriene modifiers are INHIBITORS?
1. Zafirlukast
(inhibits CYP2C9 and CYP3A4)
2. Zileuton
(inhibits CYP1A2 and CYP3A4)
Which of the drugs that interact with leukotriene modifiers are NOT inhibitors?
Montelukast (metabolized by CP3A4 and CYP2C9)

**most commonly used because it doesn't inhibit (less interactions)
What are the adverse effects associated with leukotriene modifiers?
1. hepatotoxicity (#1 side effect)
2. headache
3. GI upset
When one is taking leukotriene modifiers, what safety measures should you take?
1. monitor liver enzymes every 6 months

2. caution the patient to take the drug continuously
Should the patient's stomach be full or empty when he is given a leukotriene modifier?
empty