Medications for Respiratory Diseases Flashcards

1
Q

Drugs given by inhalation

A

=Bronchodilators (open up airways!)

a. beta2-agonist
- short-acting (SABA)
- long-acting (LABA)
b. muscarinic antagonists
- short-acting (SAMA)
- long-acting (LAMA)

c. inhaled corticosteroids (ICS)
d. various combos of the above

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2
Q

Aerosol

A

mixture of particles suspended in a gas

  • inhalation devices produce medication aerosol with particle size in ‘respirable range’
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3
Q

Advantages and Disadvantages of Inhalers

A

Advantages:

  • drug delivered directly to site of action
  • minimal systemic effects
  • rapid relief of acute attacks
  • portable, durable devices

Disadvantages:

  • technique may be difficult for some
  • poor technique causes reduced efficacy and increased side effects
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4
Q

Metered Dose Inhalers (MDIs)

A

= pressurized canisters of drug and propellant
~ 10% of dose reaches lungs, (~20% with spacer)

a. ‘press and breathe’, requires hand-lung coordination
b. shake prior to use
c. reduced efficacy if canister is cold

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5
Q

MDI Technique

A
  1. sit/stand with back straight
  2. shake inhaler, breathe out normally
  3. wrap lips around mouthpiece, take a slow deep breath in, press on inhaler while breathing in slowly
  4. hold breath between 5-10 seconds
  5. breathe out normally
    * wait one minute if need second puff
  6. rinse mouth to cut down on side effects: thrush (yeast infection causing white coating) or sore throat (from ICS)
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6
Q

Dry Powder Inhalers (DPIs)

A

= breath-activated, easier to use (less hand-lung coordination), multi-dose device
~20%..better drug delivery than MDI

powder may be pre-loaded in device or may require loading of separate dry powder capsule

**biggest problem: inadequate inspiratory flow rate
additives may cause cough and irritation

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7
Q

Turbuhaler (DPI) Technique

A
  1. holding Turbuhaler upright, turn coloured wheel one way and back until it clicks to load a new dose
  2. breathe out normally
  3. put mouthpiece between lips and tilt head back slightly
  4. breathe in deeply and forcefully
  5. hold breath for 10 seconds
  6. remove Turbuhaler and breathe out
    * repeat if need another dose
  7. if contains corticosteroid, rinse with water and spit out
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8
Q

Respimats

A

= ‘press and breathe’ multi-dose, no propellant (works like handheld nebulizer), requires less hand-lung coordination and little inspiratory effort
up to 50% drug delivery to lungs

generates smaller particle size to increase lung delivery and reduce deposition in mouth and throat

**drawback: expensive, not many drugs available in this format, device must be assembled and primed

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9
Q

Nebulization

A

= nebulizer converts drug solution into a mists which is inhaled via face mask or mouthpiece
~10% of dose delivered to lower airways
takes longer to deliver compared to MDI or DPI

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10
Q

Advantages and Disadvantages of Nebulization

A

Advantages:
- requires less coordination, good for acute attacks, anxious patients

Disadvantages:

  • higher dose than MDI or DPI&raquo_space; more side effects
  • more expensive
  • care/maintenance required
  • not portable
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11
Q

Nurse’s Role in proper inhaler use

A

a. assess for potential barriers
- patient impairment
- side effect
- device issue
- coordination (especially in elderly)
b. assess patient technique and provide detailed instruction

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12
Q

Relievers (bronchodilators for intermittent symptoms)

for PRN use only

A

a. short-acting beta2 agonists

b. anticholinergic (less often)

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13
Q

Controllers (maintenance therapy)

for prevention on a fixed schedule

A

a. anti-inflammatory medications
- inhaled and oral corticosteroids (reduce inflammation and immune system activity)
- LTRAs, anti-allergic agents

b. bronchodialtors
- long-acting beta2 agonist
- theophylline
- anticholinergics (rarely)

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14
Q

Adrenocortical Steroid Hormones

“corticosteroids”

A
  1. Glucocorticoids
    - regulate carbohydrate metabolism (blood sugar), regulate body’s response to stress
    * cortisol is most important
  2. Mineralocortcoids
    - regulate electrolyte, salt wand water balance (blood pressure)
    * aldosterone is most important
  3. Androgens
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15
Q

Effects of Corticosteroids

A

Low dose/levels produce physiologic effect
High dose/levels produce pharmacologic effects - treat asthma

a. carbohydrate, fat and protein metabolism, glucose production and storage
b. cardiovascular
- increase blood pressure from Na+/H2O retention, increase RNB, Hgb, WBC
c. CNS
- excitation, insomnia, euphoria, psychosis
d. increase gastric acid production
e. decrease calcium absorption and increase excretion
f. immunosuppression
g. anti-inflammatory

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16
Q

Corticosteroids

A

= anti-inflammatory actions in asthma

a. decrease synthesis and release of mediators
b. decrease inflammatory cell infiltration, reduce airway edema
c. reduce bronchial hyper-reactivity, reduce mucus
d. increase b2-receptors and responsiveness to b agonists&raquo_space; dilation

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17
Q

Corticosteriods in respiratory disorders

A

SLOW ONSET, do not relieve acute symptoms

Asthma
- prophylaxis on a fixed schedule to reduce incidence and severity of acute attacks

COPD
- acute exacerbations, chronic stable disease

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18
Q

Using corticosteroids in asthma

A

Inhaled (ICS)
- first-line therapy except for very mild cases
Onset: days, max effect in 3 months
Prototype: FLUTICASONE

Oral (OCS)
- reserved for severe asthma when symptoms cannot be controlled with other meds
- limit dose/duration of use as much as possible
Protoype: PREDNISONE

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19
Q

Side effects of ICS

A

very little systemic exposure and toxicity

Due to local deposition:

  • dysphonia (difficulty speaking)
  • oropharyngeal candidiasis (“thrush”, yeast infection)
  • *gargle or use spacer

Long term high doses:

  • bone loss in women
  • adrenal insufficiency
    • exacerbation of glaucoma
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20
Q

Side effects of OCS

A

notable with pharmacologic doses

Short term:

  • GI intolerance, n/v, diarrhea, cramps
  • glucose intolerance
  • hypertension
  • edema
  • psychologic disturbances
  • insomnia

Long term: Cushingoid features - too much cortisol

  • adrenal insufficiency
  • osteoporosis, avascular necrosis
  • glaucoma, cataracts
  • body fat redistribution (moon face, buffalo hump, truncal obesity)
  • dermatologic effects (skin atrophy, purpura, telangectiasis, poor wound healing)
  • stunted growth
  • increased risk of infection
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21
Q

Adrenal insufficiency

A

= prolonged OCS use inhibits production of endogenous cortisol (adrenals atrophy)

  • adrenal recover takes time after OCS d/c
  • supplemental steroid dose in times of stress
  • **patient must wear medic alert bracelet and carry emergency supply of corticosteroid

inadequate corticosteroid levels cause hypotension and hypoglycemia
unable to regulate bp, blood glucose during physiologic stress

22
Q

Corticosteroids: drug interactions

A

ICS - few concerns
OCS
a. contraindicated in patients with certain infections
b. do not give live virus vaccine (immunosuppression)
c. caution in pregnancy, lactation
d. hypertension, diabetes, peptic ulcer disease, gastritis, osteoporosis, renal failure, infections
e. NSAIDs increase risk of GI effects

23
Q

Corticosteroids: dosing and administration

A

ICS

a. twice daily
b. use of spacer with MDI improves delivery
c. rinse mouth after use

OCS
a. once daily in AM (to decrease insomnia)
b. with food (to decrease GI effects)
c. physiologic dose < 5mg per day
pharmacologic dose > 5mg per day
24
Q

OCS withdrawal

A

a. TAPER SLOWLY
b. determined by degree of adrenal suppression
c. taper not required for acute dosing of less than 14 days

withdrawal symptoms if tapered too quickly
- hypotension, hypoglycemia, myalgia, arthralgia, fatigue

25
Q

Beta2-agonist

A

= activate b2-adrenergic receptors in lung smooth muscle causing #bronchodilation
Route: inhalation, oral or parenteral

Indications:

  • asthma reliever and controller medication
  • prevention of asthma exercise-induced bronchospasm
  • chronic stable COPD and acute COPD exacerbation
26
Q

Inhaled Short-Acting Beta2 Agonist (SABA)

A

= relief of acute asthma attacks, prevention of exercise-induced symptoms
Onset: QUICK, within 1 minute
Dose: PRN basis, not for regular use

Prototype: SALBUTAMOL (blue coloured MDI)

27
Q

Inhaled Long-Acting Beta2 Agonist (LABA)

A

= sustained relaxation of airways and prolonged symptom relief (good for nocturnal symptoms)
= asthma controller medication, chronic stable COPD
Onset: delayed, 10-30mins
Dose: q12hr

Prototype: SALMETEROL

28
Q

Oral Beta2 Agonists

A

Prototype: SALBUTAMOL

  • slow and erratic absorption
  • will not relieve acute asthma attacks
  • more side effects (in circulatory)
  • longer acting than inhalation
  • regular use, not PRN
  • not commonly used
29
Q

Parenteral Beta2 Agonists

A
  • *asthmatic emergencies
  • unable to use inhaled therapy, coughing excessively, poor response to nebulization/MDI, life-threatening cases

a. Salbutamol
b. epineprhine (non-selective beta agonist)
- SC most often (also IM or IV)
- increased side effects

30
Q

Beta2 Agonist: side effects

A

a. can stimulate beta 1 receptors in heart
- increase HR, contractility, angina, arrhythmias
b. stimulate beta2 in skeletal muscles
- tremor, anxiety, restlessness
c. increase blood glucose (glycogenolysis in liver)
d. hypokalemia

*side effects decreases with continued use

31
Q

Salbutamol Dosing and Route of Administration

A

MDI inhalation: 100-200 mcg
Nebulization solution: 2.5mg
Oral tablet: 2mg
Injection: 4-8mcg/kg

32
Q

Beta2 Agonist Warning (Overuse)

A
  • frequency of use is a marker for asthma control
  • SABA > 3x per week need anti-inflammatory medication
  • SABA several times daily require urgent re-assessment

increased morbidity and mortality with over use

  • masking of serious underlying inflammation
  • increased airway responsiveness to triggers
33
Q

Combination ICS and LABA

A

Advair (FLUTICASONE + SALMETEROL)
- maintenance controller therapy for moderate to severe asthma
Frequency: use regularly, q12h
Route: MDI or DPI

Symbicort (BUDESONIDE + FORMOTEROL)
‘Single inhaler therapy’
- reliever and controller
- or controller alone (formoterol is both SABA and LABA)
- only approved for patients 12 years or older

34
Q

Leukotriene Receptor Antagonists (LTRAs)

A

= block leukotriene receptors
(leukotriene normally causes bronchoconstriction, eosinophil infiltration, mucous production and airway edema)
Onset: days
Dose: once daily, PO only; 2 hours before exercise

asthma controller medication

  • add on ICS+LABA or if unable to use ICS
  • exercise-induced bronchospasm

Prototype: MONTELUKAST (Singulair)

35
Q

LTRAs side effects

A

well tolerated, but may cause headache or nausea

*phenytoin may decrease montelukast levels

36
Q

Theophylline (Uniphyl)

A

= bronchodilation via inhibition of phosphodiesterase and increase cAMP
- good for patients with nocturnal symptoms
- third line agent due to safety and toxicity
NARROW THERAPEUTIC INDEX&raquo_space; TDM to titre

Dose: once or twice daily with food

  • PO or IV, no inhalation
  • sustained release product more stable

Indications:

  • asthma controller medication
  • chronic stable COPD
37
Q

Theophylline: side effects and drug interactions

A
a. GI effects
n/v, diarrhea
b. CNS
insomnia, restlessness, convulsions
c. cardiac effects 
increase HR, arrhythmias

Drug Interactions:

  • caffeine increases theophylline levels which causes addictive CNS and cardiac effects
  • CYP450 inducers reduce levels
  • CYP450 inhibitors increase levels
38
Q

Muscarinic Antagonists (Anti-cholinergics)

A

= bronchodilation due to blockade of muscarinic cholinergic receptors
- SAMA (reliever) or LAMA (controller)
Route: inhalation only

Indications

  • first line therapy in COPD
  • asthma, less common off label use
39
Q

Short-Acting Muscarinic Antagonists (SAMA)

A

= reliever medication for allergen or exercised-induced asthma, acute asthma attacks (emergency management)
- second line, less effect than SABA but can be combined with SABA
Onset: within 1 minute
Dose: q6h, PRN
Route: MDI, nebulizer

***Main use: bronchodilation in COPD

Prototype: IPRATROPIUM BROMIDE (Atrovent)

40
Q

Combination SABA and SAMA

A

Combivent Respimat

IPRATROPIUM + SALBUTAMOL)

41
Q

Long-Acting Muscarinic Antagonists (LAMA)

A
= mostly for bronchodilation in COPD
- role in asthma unclear, may add on as controller if other agents ineffective
Onset: 30 mins
Dose: once daily
Route: DPI using HandiHaler'

Prototype: TIOTROPIUM BROMIDE (Spiriva)

42
Q

Muscarinic Antagonists: side effects

A

a. dry mouth
b. oropharyngeal irritation
c. metallic taste

  • no systemic absorption with inhalation
  • avoid getting spray in eyes: exacerbates glaucoma and dilates pupils
43
Q

Key Principles for Asthma Management

A

a. ICS is first-line therapy for all ages
b. additional therapy added to ICS if control not achieved
c. avoid precipitating factors (allergens) and triggering medications (ASA, NSAIDs)
d. smoking cessation
e. penumococcal and annual flu vaccines
f. patient education**

44
Q

Emergency Management of Asthma

A

Goals: relieve airway obstruction, hypoxemia, normalize lung function

a. O2 for hypoxemia
b. primary therapy: repetitive inhalation of high dose SABA via MDI/nebulizer
c. systemic corticosteroids (PO or IV) in ER
d. discontinue OCS for 5-10 days
e. increase dose ICS maintenance

45
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

= chronic bronchitis and emphysema

  • important clinical difference from asthma!!
  • disease course..progressive worsening

Major features:

a. chronic airway limitation
b. chronic cough, increased sputum, dyspnea, impaired gas exchange

Biggest risk factor: smoking

46
Q

Acute exacerbation of COPD (AECOPD)

A

a. increased respiratory symptoms
- dyspnea, sputum volume, purulence
b. non-specific symptoms
- malaise, sleep disturbance, fatigue, depression, confusion
c. triggers
- inhaled irritants, allergens, GERD, CHF, drug reactions
d. 50% due to viral or bacterial infection
e. most patients get 2-3 AE per year

47
Q

Goals of COPD therapy

A

COPD

a. slow progression
b. control symptoms
c. improve exercise tolerance
d. improve exacerbation
e. improve QoL
f. reduce mortality

AECOD

a. relief of acute symptoms
b. treat infection
c. prevent mortality

48
Q

Management of COPD

A

a. SMOKING CESSATION
b. avoid occupational and air pollutant
c. pulmonary rehab exercise
d. immunization to respiratory infection (influenza, pneumococcal)
e. pharmacotherapy

49
Q

Pharmacotherapy of Chronic Stable COPD

A
  1. SAMA and/or SABA PRN
  2. LAMA and/or LABA
  3. Theophylline
  4. ICS
  5. Phosphodiesterase-4 inhibitors may reduce AE

*add on drugs for more symptom control as disease severity increases

50
Q

Role of ICS in COPD

A
  • severe airflow limitation
  • symptomatic despite max bronchodilators and theophylline
  • more than 2 AE per year or needing hospitalization
  • few patients benefit from maintenance corticosteroid
  • ICS monotherapy not recommended
51
Q

Pharmacotherapy of AECOPD

A
  1. Inhaled bronchodilators for dyspnea
    SABA with or without SAMA
  2. Oral corticosteroids (prednisone, 40mg daily x 5 days)
  3. antibiotics (selected cases)
  4. O2 (target sat 88-92%)
  5. No role for LABA, ICS, theophylline, PDE-4
    *** don’t start but don’t stop
52
Q

Antibiotics for AECOPD

A

= use if increased dyspnea, sputum volume and purulence, or mechanical ventilation

Most common pathogens:
H. influenza, Haemophilus species, M. catarrhalis, Strep. pneumoniae

Common antibiotic choices:

a. amoxicillin
b. 2nd or 3rd generation cephalosporin
c. respiratory fluoroquinolone
d. macrolide