Pulmonary Disease & Dermatology Flashcards

Question

**Diagnostics for Croup** - General principles? - Imaging? - Lab studies?

Answer 1

Do not delay treatment of stridor to perform diagnostic studies. The steeple sign is not specific to croup; it may also be present with bacterial tracheitis, epiglottis, and noninfectious etiologies such as thermal injuries and neoplasms.

Answer 2

- Mild to moderate croup (see Severity assessment of croup) can be treated in the community with a single dose of corticosteroid and nondrug management. The use of a single dose of corticosteroids in children with mild to moderate croup reduces hospital admission rates and prevents repeat presentations. - Observe for at least 30 minutes after the dose of corticosteroid. If accessory muscle use, stridor at rest, or distress have not improved, treat as for severe croup. - If the child settles initially after treatment for mild to moderate croup, they can return home; advise parents or carers that if the child develops stridor at rest later the same day, they should go to hospital. Management as for severe croup is required. - Give paracetamol or ibuprofen if the child has pain and is irritable. - Cough suppressants such as codeine have no proven effect on the course or severity of croup, and can cause respiratory depression and increase sedation.

Answer 3

- For a child with severe croup (see Severity assessment of croup), arrange immediate transfer to hospital (if not already in hospital) because severe croup can rapidly progress to life-threatening croup. - Hydrocortisone should not be used because evidence of efficacy is lacking and it has a short duration of action. - Nondrug strategies should be used in the treatment of severe croup. - Observe the child for at least 4 hours after giving initial treatment of severe croup. - If there is no stridor at rest, the child may be safe for discharge. - Follow up all children who have had severe croup within 24 hours of discharge. - If there is no response (eg ongoing stridor at rest) or deterioration occurs, escalate to senior or intensive care team involvement, and arrange hospital admission. - Differential diagnoses include bacterial tracheitis and conditions associated with airway obstruction or deep neck space infection (see here ...); antibiotics may be indicated.

Answer 4

**Nonasthmatic eosinophilic bronchitis (NAEB)** = A respiratory condition characterized by eosinophilic inflammation of the bronchi. Symptoms include cough, wheezing, and dyspnea, and sputum eosinophilia is a characteristic finding. Usually has a good response to corticosteroids. Unlike in asthma and COPD, there is no obstruction or airway hyperresponsiveness in nonasthmatic eosinophilic bronchitis.

Answer 5

- The typical whooping cough manifests mainly in children aged 6 months to 5 years. The individual stages of the disease may be indistinguishable in young infants and adults. - Catarrhal stage manifests with Coryza, while the Paroxysmal stage manifests with Posttussive vomiting and whooPing cough

Answer 6

Bronchiectasis is an irreversible and abnormal dilation in the bronchial tree caused by cycles of bronchial inflammation leading to mucous plugging and progressive airway destruction. Bronchiectasis is classified according to etiology as either cystic fibrosis (CF) bronchiectasis or non-CF bronchiectasis (e.g., secondary to severe or protracted pneumonia, immunodeficiency, or COPD).

Answer 7

**Bronchiectasis**: an irreversible and abnormal dilation of the bronchial tree that produces chronic respiratory symptoms (e.g., chronic productive cough) **Acute exacerbation of bronchiectasis:** a deterioration in the symptoms of bronchiectasis that requires a change in the regular treatment (e.g., adding antibiotics, increasing airway clearance techniques)

Answer 8

Bronchiectasis requires the combination of two important processes taking place in the bronchi: either local infection or inflammation along with either inadequate clearance of secretions, airway obstruction, or impaired host defenses. These processes result in the permanent dilation of airways.

Answer 9

Management goals are to stop or delay disease progression, reduce exacerbation frequency (goal ≤ 2 per year), achieve symptom control, and improve the patient's quality of life.

Answer 10

Chronic obstructive pulmonary disease (COPD) is characterised by persistent airflow limitation resulting from a combination of small airways disease and alveolar destruction (emphysema). It is caused by an abnormal inflammatory response in the lungs to noxious particles or gases, most commonly tobacco smoke. COPD is a progressive disease; however, smoking cessation can slow progression, and treatment can improve the patient’s quality of life.

Answer 11

**Sex**: 3:2 male/female ratio **Prevalence**: 6%

Answer 12

Emphysema is defined by irreversible enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls. Subtle but functionally important small airway fibrosis (distinct from chronic bronchitis) is also present and is a significant contributor to airflow obstruction. Emphysema is classified according to its anatomic distribution within the lobule. Recall that the lobule is a cluster of acini, the terminal respiratory units. Based on the segments of the respiratory units that are involved, emphysema is subdivided into four major types: (1) centriacinar, (2) panacinar, (3) paraseptal, and (4) irregular. Of these, only the first two cause clinically significant airflow obstruction

Answer 13

**Postbronchodilator test** Used to assess the reversibility of bronchoconstriction: - Change in FEV1 < 12%: irreversible bronchoconstriction - Change in FEV1 > 12%: reversible bronchoconstriction The degree of reversibility alone cannot reliably distinguish between the diagnosis of asthma vs. COPD.

Answer 14

**Hypercapnia** = An elevation of CO₂ > 45 mm Hg in arterial blood (normal pCO₂: 33–45 mm Hg). - Can be acute (e.g., respiratory muscle paralysis, asthma, pneumonia) or chronic (e.g., COPD). - Can be caused due to increased ventilation-perfusion mismatch (e.g., pneumonia, pulmonary embolism), decreased respiratory drive (e.g., sedative overdose, brainstem stroke), or decreased respiratory nerve/muscle function (e.g., poliomyelitis, Guillain-Barré syndrome).

Answer 15

**Hypoxemia** = A decreased oxygen content in arterial blood. Typically results in a partial pressure of oxygen (PaO₂) of < 80 mm Hg and/or an oxygen saturation of less than 95%.

Answer 16

ARDS is a clinical syndrome of acute respiratory failure characterized by hypoxemia and bilateral pulmonary infiltrates that cannot be fully accounted for by heart failure or fluid overload.

Answer 17

1. Consult ICU early, i.e., as soon as respiratory failure due to ARDS is suspected. 2. Address hypoxemia 3. Apply lung-protective ventilation strategies. 4. Augment therapy as needed based on severity (see the Berlin criteria for ARDS). - Moderate-severe ARDS: Apply prone positioning, lung recruitment maneuvers; consider neuromuscular blockade. - Severe ARDS refractory to therapy: Consider indications for ECMO based on the Murray score. - Identify and treat the underlying cause (e.g., pneumonia, pancreatitis, sepsis).

Answer 18

Asthma is a chronic inflammatory disease of the respiratory system characterized by bronchial hyperresponsiveness, episodic acute asthma exacerbations, and reversible airflow obstruction.

Answer 19

The exact etiology of asthma remains unknown. Risk factors for asthma include: 1. Family history of asthma 2. Past history of allergies 3. Atopic dermatitis 4. Low socioeconomic status 5. Childhood exposure to second-hand smoke increases the risk of developing asthma.

Answer 20

**Triggers of Atopic Asthma:** 1. Cardinal risk factor: atopy 2. Environmental allergens: pollen (seasonal), dust mites, domestic animals , mold spores 3. Allergic occupational asthma from exposure to allergens in the workplace (e.g., flour dust)

Answer 21

**Triggers of Non-Atopic Asthma** 1. Viral respiratory tract infections (one of the most common stimuli, especially in children) 2. Cold air 3. Physical exertion (laughter, exercise-induced asthma) 4. Gastroesophageal reflux disease (GERD): often exists concurrently with asthma 5. Chronic sinusitis or rhinitis 6. Medication: aspirin/NSAIDS (aspirin-induced asthma), beta blockers 7. Stress 8. Irritant-induced asthma (e.g., from exposure to solvents, ozone, tobacco or wood smoke, cleaning agents, isocyanates)

Answer 22

**Clinical Features of Asthma** Typical features: The following features are usually intermittent and can occur either sporadically or in response to an asthma trigger. 1. Persistent, dry cough that worsens at night, with exercise, or on exposure to triggers/irritants (e.g., cold air, allergens, smoke) 2. End-expiratory wheezes 3. Dyspnea (shortness of breath) 4. Chest tightness 5. Prolonged expiratory phase on auscultation 6. Hyperresonance to lung percussion 7. Features of common comorbid conditions (e.g., atopic conditions like allergic rhinitis, or eczema)

Answer 23

The asthmatic airway is marked by accumulation of mucus in the bronchial lumen secondary to an increase in the number of mucus-secreting goblet cells in the mucosa and hypertrophy of submucosal glands; intense chronic inflammation due to recruitment of eosinophils, macrophages, and other inflammatory cells; thickened basement membrane; and hypertrophy and hyperplasia of smooth muscle cells. (C) Inhaled allergens (antigen) elicit a Th2-dominated response favoring IgE production and eosinophil recruitment. (D) On re-exposure to antigen, the immediate reaction is triggered by antigen-induced cross-linking of IgE bound to Fc receptors on mast cells. These cells release preformed mediators that directly and via neuronal reflexes induce bronchospasm, increased vascular permeability, mucus production, and recruitment of leukocytes. (E) Leukocytes recruited to the site of reaction (neutrophils, eosinophils, and basophils; lymphocytes and monocytes) release additional mediators that initiate the late phase reaction. Several factors released from eosinophils (e.g., major basic protein, eosinophil cationic protein) also cause damage to the epithelium. IL-5, Interleukin-5.

Answer 24

***Pathophysiology of asthma*** **Early phase:** An antigen is taken up by dendritic cells, causing the release of interleukins from T-helper cells and starting a cascade of intracellular events resulting in mast-cell chemoattraction and degranulation. Mast cells release a variety of chemokines resulting in vasoconstriction, increased vascular permeability (edema), and mucus production. **Late phase:** Prolonged activation of initial pathophysiological response (early phase) results in the cellular destruction.

Answer 25

The diagnosis of asthma is based on clinical assessment supported by lung function tests (primarily spirometry) that demonstrate airflow limitation or airway inflammation. Lung function tests have significant false positive and negative results. No single test or symptom can be used to diagnose asthma, and isolated signs or symptoms have poor predictive value.

Answer 26

**Characteristic findings of Asthma in PFTs:** 1. An obstructive pattern of airflow limitation 2. Reversibility of airflow obstruction on bronchodilator administration 3. Excessive variability of lung function parameters (FEV1, PEFR) on repeat testing

Answer 27

The National Asthma Education and Prevention Program (NAEPP) guidelines classify asthma severity as intermittent or persistent in individuals who have not yet been initiated on long-term therapy based on the following: 1. Symptom severity 2. Degree of impairment in lung function 3. Frequency and risk of exacerbations

Answer 28

- Assess response to therapy in 2–6 weeks - Good response for ≥ 3 consecutive months: Consider a gradual decrease in pharmacotherapy (step down). - Inadequate response: Assess treatment adherence, inhaler technique. - Manage comorbidities and environmental factors

Answer 29

**Anti-asthma medications** 1. Short-acting beta-2 agonists (SABA) 2. Long-acting beta-2 agonists (LABA) 3. Inhaled corticosteroids (ICS) 4. Oral corticosteroids 5. Leukotriene receptor antagonists (LTRAs) 6. Long-acting muscarinic antagonists (LAMA) 7. Short-acting muscarinic antagonists (SAMA)

Answer 30

See Yr1 Pharmacology

Answer 31

Standard tests of airway function and gas exchange include: 1. Spirometry 2. Peak expiratory flow monitoring 3. Pulse oximetry 4. Arterial blood gas analysis and venous blood gas analysis. Tests performed in specialist respiratory laboratories include: 1. Diffusing capacity of the lung for carbon monoxide (DLCO) 2. Static lung volumes 3. Bronchial provocation testing 4. Exercise testing 5. Hypoxic challenge testing.

Answer 32

- Spirometry is the best initial test for the evaluation of pulmonary function. - The patient breathes forcefully through their mouth into an external device. - Flow-volume loops (i.e., graphical representation of spirometry results) are generated to demonstrate inspiratory and expiratory airflow (y-axis) against lung volume (x-axis)

Answer 33

Relative contraindications to performing spirometry include: 1. acute myocardial infarction in the previous week 2. history of syncope related to forced expiration or cough 3. recent concussion with continuing symptoms 4. eye, sinus or middle ear surgery in the previous week 5. middle ear infection in the previous week 6. current or recent pneumothorax 7. thoracic or abdominal surgery in the previous 4 weeks 8. current haemoptysis.

Answer 34

Specialized tests (i.e., bronchial challenge tests and/or bronchodilator responsiveness testing) may help distinguish bronchial asthma from other causes of obstructive lung disease.

Answer 35

A type of pulmonary function test that measures volumes that cannot be measured via spirometry (e.g., functional residual capacity, residual volume). Performed with the patient placed in a sealed container and breathing into a mouthpiece. Mainly used to diagnose obstructive and restrictive lung diseases. **Indications** 1. Patients who cannot actively participate in spirometry 2. Obstructive lung disease on spirometry: to evaluate for air trapping (e.g., in emphysema) 3. Restrictive lung disease: to distinguish between extrinsic vs. intrinsic causes

Answer 36

**Transfer factor for carbon monoxide** Abbreviations: DLCO, TLCO A measure of the ability of the lungs to transfer gas from inhaled air to red blood cells in the pulmonary capillaries. The main determinants for diffusing capacity include the area and thickness of the alveolar-capillary barrier and the diffusion constant of the measured gas. Results are used to further characterize obstructive and restrictive lung diseases. Abnormal DLCO despite normal lung volumes may be seen in patients with pulmonary vascular diseases (e.g., pulmonary hypertension), systemic disorders, (e.g., anemia), or early interstitial lung disease.

Answer 37

Malignant mesothelioma is a cancer usually associated with prior asbestos exposure. It most commonly develops in the pleura of the lungs (malignant pleural mesothelioma), but may also develop in the peritoneum, pericardium or reproductive organs. Australia has one of the highest incidences of malignant mesothelioma. Most people diagnosed with malignant mesothelioma have a history of distant exposure to asbestos (eg occupational exposure, contact with contaminated materials, history of home renovation). Patients with a history of exposure to asbestos may be eligible for legal compensation.

Answer 38

The interstitial lung diseases (ILDs) are a diverse group of conditions characterised by varying degrees of inflammation or fibrosis, predominantly affecting the lung interstitium. In many ILDs, the airways, parenchyma and pulmonary vasculature are also involved. The terms ILD and pulmonary fibrosis are often used interchangeably.

Answer 39

- Patients with interstitial lung disease (ILD) usually present with nonspecific symptoms such as dyspnoea and dry cough, often resulting in delayed diagnosis. - There may be crackles on chest auscultation; however, crackles can also occur with pulmonary oedema, bronchiectasis or pneumonia. Clubbing of the fingers or toes may also be present. - Advanced disease presents with tachypnoea, tachycardia and low oxygen saturation as measured by pulse oximetry (SpO2).

Answer 40

**Blood tests** - Blood tests can help determine the cause of ILD. Initial blood tests may include full blood count (FBC) with eosinophil count, antinuclear antibodies (ANA), extractable nuclear antigens (ENA), double-stranded DNA (dsDNA), serum calcium and rheumatoid factor (RF). - Additional tests may be ordered by the specialist depending on the clinical scenario, such as antineutrophil cytoplasmic antibodies (ANCAs) if pulmonary vasculitis is suspected, or precipitins against environmental antigens (eg avian or mould precipitins) if hypersensitivity pneumonitis is suspected.

Answer 41

**X-ray chest** - Normal in approx. 10% of patients - Predominantly basilar increase in reticular opacities (sign of fibrosis) - Patients may have nodular or mixed patterns.

Answer 42

AGEP = Acute generalized exanthematous pustulosis (AGEP) is a severe, usually drug-related reaction, characterized by an acute onset of mainly small non-follicular pustules on an erythematous base and spontaneous resolution usually within two weeks.

Pulmonary Disease & Dermatology Flashcards

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