objective 2.3 (2) Flashcards

1
Q

 A sudden and dramatic onset is referred to as an asthma attack.
 Prolonged asthma attack that does not respond to typical drug therapy is
known as status asthmaticus

A

asthma

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2
Q

 Recurrent and reversible shortness of breath
 The airways of the lungs become narrow as a result of:
 Bronchospasms, Inflammation and edema of the bronchial mucosa,Production of viscous
mucus
 The alveolar ducts and alveoli remain open, but airflow to them is obstructed

A

bronchial asthma

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3
Q

Progressive respiratory disorder
Characterized by chronic airflow limitation, systematic
manifestations, and significant comorbidities

A

chronic obstructive pulmonary disease

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4
Q

Presence of cough and sputum for at least 3 months in each of 2
consecutive years
Separate disease from chronic obstructive pulmonary disease

A

chronic bronchitis

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5
Q

Relax bronchial smooth muscle, which causes dilation of the
bronchi and bronchioles that are narrowed as a result of the
disease process

A

bronchodilators

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6
Q

what three classes of bronchodilators?

A

 β-adrenergic agonists,
 anticholinergics, and
 xanthine derivatives

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7
Q

what are short acting B agonist inhalers?

A

salbutamol (Ventolin®)
Terbutaline sulphate (Bricanyl®)

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8
Q

what are long acting B agonist inhalers?

A

formoterol (Foradil®, Oxeze®)
salmeterol (Serevent®)

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9
Q

what are the long acting B agonist and glucocorticoid steroid combo inhaler?

A

budesonide/formoterol fumarate dihydrate (Symbicort®)
Use as a reliever or rescue treatment for moderate to severe asthma when
symptoms worsen

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10
Q

what are the 3 subtypes of B-adrenergic agonists?

A

nonselective adrenergic
nonselective B-adrenergic
selective B2 drugs

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11
Q

Stimulate ß-, ß1- (cardiac), and ß2- (respiratory) receptors
Example: epinephrine (EpiPen®)

A

nonselective adrenergic

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12
Q

Stimulate both ß1- and ß2-receptors
Example: isoproterenol hydrochloride

A

nonselective B-adrenergic

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13
Q

Stimulate only ß2-receptors
Example: salbutamol (Ventolin®)

A

selective B2 drugs

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14
Q

what is the MOA of B-adrenergic agonists?

A

 Used during acute phase of asthmatic attacks
 Quickly reduce airway constriction and restore normal airflow
 Agonists, or stimulators, of the adrenergic receptors in the sympathetic
nervous system
 Sympathomimetics bronchodilators– relax smooth muscle and inhibit inflammatory
response.

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15
Q

what are the indications of B-adrenergic agonists

A

 Relief of bronchospasm (asthma, chronic obstructive pulmonary disease
(COPD), and other pulmonary diseases)
 Treatment and prevention of acute attacks

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16
Q

what are the contraindications of B-adrenergic agonists?

A

Known drug allergy
Uncontrolled cardiac dysrhythmias
High risk of hypertension/ stroke

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17
Q

what are the AE of B-adrenergic agonists?

A

α and ß (epinephrine): Insomnia, Restlessness, Anorexia, Vascular headache,
Hyperglycemia, Tremor, Cardiac stimulation
 ß1 and ß2 : Cardiac stimulation, tachycardia, Tremor, Anginal pain, Vascular headache
 ß2 (salbutamol): Hypotension or hypertension, Vascular headache, Tremor

18
Q

what are the interactions of B-adrenergic agonists?

A

Diminished bronchodilation when nonselective ß-blockers are used
with the ß-agonist bronchodilators
Monoamine oxidase inhibitors
Sympathomimetics
Monitor patients with diabetes; an increase in blood glucose levels
can occur.

19
Q

 Short-acting ß2-specific bronchodilating ß-agonist
 Most commonly used drug in this class
 Don’t exceed max. daily dosage.
 Oral, parenteral, and inhalational use
 Inhalational dosage forms include metered-dose inhalers as well as solutions for
inhalation (aerosol nebulizers)

A

salbutamol sulphate

20
Q

 Long-acting ß2-agonist bronchodilator
 Never to be used alone but in combination with an inhaled glucocorticoid steroid
 Used for the maintenance treatment of asthma and COPD; salmeterol maximum daily
dose (one puff twice daily) should not be exceeded.

A

salmeterol

21
Q

what is the MOA of anticholinergics?

A

Acetylcholine (ACh) causes bronchial constriction and narrowing of the
airways.
Anticholinergics bind to the ACh receptors, preventing ACh from binding.
Result: bronchoconstriction is prevented, airways dilate

22
Q

what are the AE of anticholinergics?

A

Dry mouth or throat, Nasal congestion, Heart palpitations, Gastrointestinal
distress, Urinary retention, Increased intraocular pressure, Headache,
Coughing, Anxiety

23
Q

 Oldest and most commonly used anticholinergic bronchodilator
 Available both as a liquid aerosol for inhalation and as a multidose inhaler
 Usually dose 2 puffs tid-qid
 Child (5-12 years)125-250mcg /puff
 Adult: 250-500mcg/ puff

A

ipratropium bromide

24
Q

 Indirectly cause airway relaxation and dilation
 Help reduce secretions in COPD patients
 Indications: prevention of the bronchospasm associated with COPD; not for the
management of acute symptoms

A

ipratropium, tiotropium bromide monohydrate

25
Q

theophylline and caffeine are currently used clinically

A

plant alkaloids

26
Q

what is action of xanthine derivatives?

A

smooth muscle relaxation, bronchodilation, and increased
airflow

27
Q

what are the indications of xanthine derivatives?

A

Dilation of airways in asthmas and COPD
Mild to moderate cases of acute asthma
Not for management of acute asthma attack
Adjunct drug in the management of COPD
Not used as frequently because of potential for drug interactions and
variables related to drug levels in the blood

28
Q

what are the contraindications of xanthine derivatives?

A

Known drug allergy, Uncontrolled cardiac dysthymias, Seizure
disorders, Hyperthyroidism, Peptic ulcers

29
Q

what are the AE of xanthine derivatives?

A

Nausea, vomiting, anorexia
Gastroesophageal reflux during sleep
Sinus tachycardia, extrasystole, palpitations, ventricular dysrhythmias
Transient increased urination
Hyperglycemia

30
Q

 Most commonly used xanthine derivative
 Oral and injectable (as aminophylline) dosage forms
 Aminophylline: intravenous (IV) treatment of patients with status asthmaticus
who have not responded to fast-acting ß-agonists such as epinephrine
Body weight is used to calculate dosage

A

theophylline

31
Q

 Used without prescription as a central nervous system stimulant or analeptic to
promote alertness (e.g., for long-duration driving or studying)
 Cardiac stimulant in infants with bradycardia
 Enhancement of respiratory drive in infants in NICUs

A

caffeine

32
Q

 Newer class of asthma medications
 Nonbronchodilating
 Currently available drugs: montelukast (Singulair®), zafirlukast (Accolate®)

A

leukotriene receptor antagonists

33
Q

what is the MOA of leukotriene receptor antagonists?

A

 Leukotrienes are substances released when a trigger, such as cat hair or
dust, starts a series of chemical reactions in the body and cause
inflammation, bronchoconstriction, and mucus production.
 Result: coughing, wheezing, shortness of breath
 Leukotriene receptor antagonists prevent leukotrienes from attaching to
receptors on cells in the lungs and in circulation.
 Inflammation in the lungs is blocked, and asthma symptoms are relieved.

34
Q

what are the indications of leukotriene receptor antagonists?

A

 Prophylaxis and long-term treatment and prevention of asthma in adults and children
 Montelukast safe in children 2 years of age and older; Zafirlukast safe in children 12 years of age and
older
 Not meant for management of acute asthmatic attacks
 Montelukast is also approved for treatment of allergic rhinitis
 Improvement with their use is typically seen in about 1 week

35
Q

what are the contraindications of leukotriene receptor antagonists?

A

 Known drug allergy, Previous adverse drug reaction
 Allergy to povidone, lactose, titanium dioxide, or cellulose derivatives—important to note
because these are inactive ingredients in these drugs
 Usage may lead to liver dysfunction.

36
Q

 Anti-inflammatory properties, Used in treatment of pulmonary diseases
 Oral or inhaled forms, may be administered intravenously
 Inhaled forms reduce systemic effects.
 May take several weeks before full effects are seen

A

corticosteroids

37
Q

what is the MOA of corticosteroids?

A

 Stabilize membranes of cells that release harmful broncho constricting
substances
 These cells are called leukocytes (white blood cells).
 Increase responsiveness of bronchial smooth muscle to ß-adrenergic
stimulation
 Dual effect of both reducing inflammation and enhancing the activity of ß-
agonists

38
Q

what are the indications of inhaled corticosteroids?

A

Primary treatment of bronchospastic disorders to control the
inflammatory responses that are believed to be the cause of these
disorders
Persistent asthma
Often used concurrently with the ß-adrenergic agonists
Systemic corticosteroids are generally used only to treat acute
exacerbations or severe asthma.
IV corticosteroids: acute exacerbation of asthma or other COPD

39
Q

what are the contraindications of inhaled corticosteroids?

A

Drug allergy, Not intended as sole therapy for acute asthma attacks, Hypersensitivity to
glucocorticoids, Patients whose sputum tests are positive for Candida organisms ,
Patients with systemic fungal infection

40
Q

what are the AE of inhaled corticosteroids?

A

 Pharyngeal irritation, Coughing, Dry mouth, Oral fungal infections
 Systemic effects are rare because low doses are used for inhalation therapy

41
Q

what are the interactions of inhaled corticosteroids?

A

 Drug interactions are more likely to occur with systemic (versus inhaled) corticosteroids.
 May increase serum glucose levels, possibly requiring adjustments in dosages of antidiabetic drugs
 May raise the blood levels of the immunosuppressants cyclosporine and tacrolimus; itraconazole may
reduce clearance of the steroids
 phenytoin, phenobarbital, and rifampin
 Greater risk of hypokalemia with concurrent diuretic use (e.g., furosemide, hydrochlorothiazide)