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NUR370 Pathophysiology and Pharmacology > Medications for Respiratory Diseases > Flashcards

Medications for Respiratory Diseases Flashcards

(52 cards)

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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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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
Beta2-agonist
= 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
Inhaled Short-Acting Beta2 Agonist (SABA)
= 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
Inhaled Long-Acting Beta2 Agonist (LABA)
= 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
Oral Beta2 Agonists
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
Parenteral Beta2 Agonists
* *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
Beta2 Agonist: side effects
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
Salbutamol Dosing and Route of Administration
MDI inhalation: 100-200 mcg Nebulization solution: 2.5mg Oral tablet: 2mg Injection: 4-8mcg/kg
32
Beta2 Agonist Warning (Overuse)
- 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
Combination ICS and LABA
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
Leukotriene Receptor Antagonists (LTRAs)
= 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
LTRAs side effects
well tolerated, but may cause headache or nausea *phenytoin may decrease montelukast levels
36
Theophylline (Uniphyl)
= 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 >> 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
Theophylline: side effects and drug interactions
``` 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
Muscarinic Antagonists (Anti-cholinergics)
= 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
Short-Acting Muscarinic Antagonists (SAMA)
= 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
Combination SABA and SAMA
Combivent Respimat | IPRATROPIUM + SALBUTAMOL)
41
Long-Acting Muscarinic Antagonists (LAMA)
``` = 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
Muscarinic Antagonists: side effects
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
Key Principles for Asthma Management
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
Emergency Management of Asthma
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
Chronic Obstructive Pulmonary Disease (COPD)
= 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
Acute exacerbation of COPD (AECOPD)
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
Goals of COPD therapy
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
Management of COPD
a. SMOKING CESSATION b. avoid occupational and air pollutant c. pulmonary rehab exercise d. immunization to respiratory infection (influenza, pneumococcal) e. pharmacotherapy
49
Pharmacotherapy of Chronic Stable COPD
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
Role of ICS in COPD
- 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
Pharmacotherapy of AECOPD
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
Antibiotics for AECOPD
= 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

NUR370 Pathophysiology and Pharmacology (20 decks)

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