NSG 533 – Exam III Study Guide (Modules
IX–XI)
✅ Module IX: Respiratory Disorders (Asthma, COPD,
Allergic Rhinitis)
✅ Learning Objectives – Asthma (Chapter 15)
1. Understand the pathophysiology of asthma.
2. Asthma is a chronic inflammatory disease of the airways involving airflow obstruction,
bronchial hyperresponsiveness, and inflammation. The major pathophysiological
characteristics include airway inflammation, reversible airflow obstruction, and bronchial
hyperresponsiveness. This pathophysiology drives the use of anti-inflammatory therapy
(e.g., inhaled corticosteroids) and bronchodilators (e.g., beta-agonists).
3. Recognize asthma triggers and risk factors for exacerbation.
Triggers include allergens (dust mites, pollen), infections (viral URIs), exercise, smoke,
pollutants, cold air, and medications (beta-blockers, aspirin/NSAIDs, ACE inhibitors). Risk
factors for exacerbation are shown in Table 15-7 and include poor adherence, comorbidities,
high SABA use, and previous ICU admissions.
4. Differentiate quick-relief and long-term control therapies.
a. Quick relief: SABA (e.g., albuterol) – relax bronchial smooth muscle.
b. Long-term: ICS (first-line), LABA (add-on to ICS), LTRA, theophylline, etc.
5. Use GINA treatment guidelines to initiate and adjust therapy.
Treatment decisions are based on severity and symptom control (Table 15-6, 15-9). Stepwise
therapy allows escalation and de-escalation based on control.
6. Apply nonpharmacologic strategies.
, Avoid triggers, implement smoking cessation, vaccination (influenza, COVID), and use written
asthma action plans.
✅ Study Guide Questions – Asthma
Pathophysiology & Therapy Connection:
Chronic inflammation → bronchial hyperresponsiveness → intermittent obstruction →
symptoms.
ICS are cornerstone due to anti-inflammatory effects.
Precipitating Factors (Table 15-7):
Viral infections, allergens, smoking, exercise, medications (ACEi, NSAIDs, BB).
Severity and Treatment Steps:
Use impairment (symptoms, activity limits, spirometry) and risk (exacerbations) to
classify severity.
Step 1: Low-dose ICS-formoterol PRN. Step 2+: ICS maintenance + LABA.
Quick-Relief Meds:
SABA (albuterol): relax smooth muscle; PRN use. All patients need rescue inhaler.
Long-Term Meds:
ICS (fluticasone): reduce inflammation.
LABA (salmeterol): bronchodilation, only with ICS.
LTRA (montelukast): anti-leukotriene.
Theophylline: rarely used due to narrow therapeutic index, interactions.
Step Therapy (Table 15-9):
Step up if not controlled; Step down after 3 months of good control.
Assess Inhaler technique, Compliance, and Environmental control (I.C.E.).
Exacerbation Management:
Oral steroids, SABA, oxygen, follow written asthma action plan.
,✅ Medication Chart – Asthma
Exa
Clas Adverse Contraindic
mpl MOA Monitoring
s Effects ations
e
SAB Albu Tremor, Use caution HR, symptom
Beta-2 agonist
A terol tachycardia in CV disease relief
Fluti Rinse mouth,
Anti- Oral thrush, Not for acute
ICS caso symptom
inflammatory dysphonia relief
ne control
Sal
Long-acting Headache, Monotherap Always with
LABA met
beta-2 agonist tremor y in asthma ICS
erol
Mood
Mon Leukotriene Headache, Depression,
changes,
LTRA telu receptor behavior neuropsychia
symptom
kast blocker changes tric
relief
Theo N/V, Narrow TI, Serum levels
The PDE inhibition,
phyll seizures, drug (5–15
o-24 bronchodilator
ine arrhythmia interactions mcg/mL)
✅ Learning Objectives – COPD (Chapter 16)
1. Differentiate COPD pathophysiology from asthma.
COPD is irreversible airflow limitation with alveolar destruction (emphysema) and chronic
bronchitis. Pathophysiology involves chronic inflammation and airflow obstruction. Unlike
asthma, changes are less reversible.
2. Understand diagnosis and classification.
Diagnosis: post-bronchodilator FEV1/FVC < 0.70. Severity via GOLD classification, CAT
score, mMRC dyspnea score, and exacerbation risk (Figure 16-2).
3. Review pharmacologic therapies.
Bronchodilators (SABA, LABA, SAMA, LAMA) are central. ICS are reserved for select groups
(exacerbators).
4. Know nonpharmacologic interventions.
, Smoking cessation, pulmonary rehab, vaccination (influenza, pneumococcal, COVID), and
oxygen if needed.
✅ Study Guide Questions – COPD
Pathophysiology:
Irreversible obstruction, destruction of alveoli, mucus hypersecretion. Inhaled irritants
trigger inflammation.
Risk Factors:
Smoking, air pollution, occupational dust, genetic (alpha-1 antitrypsin).
Assessment:
GOLD: A-D based on symptoms (mMRC/CAT) and exacerbation risk.
A: few symptoms, low risk. D: high symptoms, high risk.
Treatment Algorithm (Fig 16-2):
A: SABA or SAMA PRN.
B: LAMA or LABA.
C: LAMA.
D: LAMA or LAMA+LABA. Add ICS if eosinophils >300.
ICS:
Use in Groups C/D if exacerbations persist despite bronchodilators.
Roflumilast:
Add-on for chronic bronchitis with frequent exacerbations.
Methylxanthines:
Rarely used. Narrow therapeutic index, many interactions.
Antibiotics:
Use for 5–7 days if sputum purulence + increased volume/dyspnea.
IX–XI)
✅ Module IX: Respiratory Disorders (Asthma, COPD,
Allergic Rhinitis)
✅ Learning Objectives – Asthma (Chapter 15)
1. Understand the pathophysiology of asthma.
2. Asthma is a chronic inflammatory disease of the airways involving airflow obstruction,
bronchial hyperresponsiveness, and inflammation. The major pathophysiological
characteristics include airway inflammation, reversible airflow obstruction, and bronchial
hyperresponsiveness. This pathophysiology drives the use of anti-inflammatory therapy
(e.g., inhaled corticosteroids) and bronchodilators (e.g., beta-agonists).
3. Recognize asthma triggers and risk factors for exacerbation.
Triggers include allergens (dust mites, pollen), infections (viral URIs), exercise, smoke,
pollutants, cold air, and medications (beta-blockers, aspirin/NSAIDs, ACE inhibitors). Risk
factors for exacerbation are shown in Table 15-7 and include poor adherence, comorbidities,
high SABA use, and previous ICU admissions.
4. Differentiate quick-relief and long-term control therapies.
a. Quick relief: SABA (e.g., albuterol) – relax bronchial smooth muscle.
b. Long-term: ICS (first-line), LABA (add-on to ICS), LTRA, theophylline, etc.
5. Use GINA treatment guidelines to initiate and adjust therapy.
Treatment decisions are based on severity and symptom control (Table 15-6, 15-9). Stepwise
therapy allows escalation and de-escalation based on control.
6. Apply nonpharmacologic strategies.
, Avoid triggers, implement smoking cessation, vaccination (influenza, COVID), and use written
asthma action plans.
✅ Study Guide Questions – Asthma
Pathophysiology & Therapy Connection:
Chronic inflammation → bronchial hyperresponsiveness → intermittent obstruction →
symptoms.
ICS are cornerstone due to anti-inflammatory effects.
Precipitating Factors (Table 15-7):
Viral infections, allergens, smoking, exercise, medications (ACEi, NSAIDs, BB).
Severity and Treatment Steps:
Use impairment (symptoms, activity limits, spirometry) and risk (exacerbations) to
classify severity.
Step 1: Low-dose ICS-formoterol PRN. Step 2+: ICS maintenance + LABA.
Quick-Relief Meds:
SABA (albuterol): relax smooth muscle; PRN use. All patients need rescue inhaler.
Long-Term Meds:
ICS (fluticasone): reduce inflammation.
LABA (salmeterol): bronchodilation, only with ICS.
LTRA (montelukast): anti-leukotriene.
Theophylline: rarely used due to narrow therapeutic index, interactions.
Step Therapy (Table 15-9):
Step up if not controlled; Step down after 3 months of good control.
Assess Inhaler technique, Compliance, and Environmental control (I.C.E.).
Exacerbation Management:
Oral steroids, SABA, oxygen, follow written asthma action plan.
,✅ Medication Chart – Asthma
Exa
Clas Adverse Contraindic
mpl MOA Monitoring
s Effects ations
e
SAB Albu Tremor, Use caution HR, symptom
Beta-2 agonist
A terol tachycardia in CV disease relief
Fluti Rinse mouth,
Anti- Oral thrush, Not for acute
ICS caso symptom
inflammatory dysphonia relief
ne control
Sal
Long-acting Headache, Monotherap Always with
LABA met
beta-2 agonist tremor y in asthma ICS
erol
Mood
Mon Leukotriene Headache, Depression,
changes,
LTRA telu receptor behavior neuropsychia
symptom
kast blocker changes tric
relief
Theo N/V, Narrow TI, Serum levels
The PDE inhibition,
phyll seizures, drug (5–15
o-24 bronchodilator
ine arrhythmia interactions mcg/mL)
✅ Learning Objectives – COPD (Chapter 16)
1. Differentiate COPD pathophysiology from asthma.
COPD is irreversible airflow limitation with alveolar destruction (emphysema) and chronic
bronchitis. Pathophysiology involves chronic inflammation and airflow obstruction. Unlike
asthma, changes are less reversible.
2. Understand diagnosis and classification.
Diagnosis: post-bronchodilator FEV1/FVC < 0.70. Severity via GOLD classification, CAT
score, mMRC dyspnea score, and exacerbation risk (Figure 16-2).
3. Review pharmacologic therapies.
Bronchodilators (SABA, LABA, SAMA, LAMA) are central. ICS are reserved for select groups
(exacerbators).
4. Know nonpharmacologic interventions.
, Smoking cessation, pulmonary rehab, vaccination (influenza, pneumococcal, COVID), and
oxygen if needed.
✅ Study Guide Questions – COPD
Pathophysiology:
Irreversible obstruction, destruction of alveoli, mucus hypersecretion. Inhaled irritants
trigger inflammation.
Risk Factors:
Smoking, air pollution, occupational dust, genetic (alpha-1 antitrypsin).
Assessment:
GOLD: A-D based on symptoms (mMRC/CAT) and exacerbation risk.
A: few symptoms, low risk. D: high symptoms, high risk.
Treatment Algorithm (Fig 16-2):
A: SABA or SAMA PRN.
B: LAMA or LABA.
C: LAMA.
D: LAMA or LAMA+LABA. Add ICS if eosinophils >300.
ICS:
Use in Groups C/D if exacerbations persist despite bronchodilators.
Roflumilast:
Add-on for chronic bronchitis with frequent exacerbations.
Methylxanthines:
Rarely used. Narrow therapeutic index, many interactions.
Antibiotics:
Use for 5–7 days if sputum purulence + increased volume/dyspnea.
