Pulmonary Disease & Dermatology Flashcards
Differential diagnosis of cough based on its character?
DIFFERENTIAL DIAGNOSIS OF COUGH BASED ON ITS DURATION:
- 6 Acute?
- 9 Chronic?
Give 2 differentials for a cough of recent origin, particularly if associated with fever and other symptoms of respiratory tract infection?
- acute bronchitis
- pneumonia
What are the features of a cough in asthma?
A chronic cough (of more than 8 weeks duration) associated with wheezing may be due to asthma; sometimes asthma can present with just cough alone.
What is the single most common cause of chronic cough?
A cough associated with a postnasal drip or sinus congestion or headaches may be due to the upper airway cough syndrome, which is the single most common cause of chronic cough.
Give 2 differentials for a dry cough?
A dry cough may be a feature of:
1. Late interstitial lung disease
2. Associated with the use of the angiotensin-converting enzyme (ACE) inhibitors—drugs used in the treatment of hypertension and cardiac failure.
2 Differentials for a cough that wakes a person at night?
Cough that wakes a patient from sleep may be a symptom of cardiac failure or of the reflux of acid from the oesophagus into the upper airway that can occur when a person lies down.
What would a chronic cough that is productive of large volumes of sputum suggest?
A chronic cough that is productive of large volumes of purulent sputum may be due to bronchiectasis
Differentials for a ‘barking’ cough in children and adults?
In children, a cough associated with inflammation of the epiglottis may have a muffled quality and cough related to viral croup is often described as ‘barking’. In adults a barking cough may indicate a condition of flaccid trachea and large bronchi, known as tracheomalacia.
Differentials for haemoptysis?
- Respiratory? (10)
- Cardiovascular? (3)
9 Common Differentials for a chronic cough?
10 Uncommon Differentials for a chronic cough?
What is Upper airway cough syndrome?
10 lifethreatening causes of cough?
What is Bronchiolitis?
Bronchiolitis:
- Epidemiology?
- Aetiology?
- 6 Risk factors for severe bronchiolitis?
Bronchiolitis:
- Clinical Features?
- Diagnostics - General Principles?
- Diagnostics - Lab Studies?
- Diagnostics - CXR?
- 5 Symptoms of moderate to severe acute bronchiolitis requiring admission to hospital?
- When should you consider early hospital admission in infants with mild symptoms?
Management of Acute Bronchiolitis - What is and isn’t recommended?
Which medication can be used for Bronchiolitis prevention/prophylaxis?
- Indications?
What is Croup?
- Peak incidence?
- Aetiology?
Peak incidence: 6 months to 3 years
Most common pathogen:
1. parainfluenza viruses (75% of cases)
2. Other pathogens: respiratory syncytial virus (RSV), adenovirus, influenza virus, SARS-CoV-2 (COVID-19)
Pathophysiology of Croup?
Clinical Features of Croup?
Diagnostics for Croup
- General principles?
- Imaging?
- Lab studies?
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.
What is the approach to the management of a patient with croup?
- Which severity rating score should be calculated?
What is the Westley Croup Severity Score? Interpretation of results?
Immediate stabilisation measures in Croup?
Non-drug management of Croup?
Treatment for Mild-Moderate Croup?
- 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.
Treatment for Moderate/Severe Croup?
- 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.
What is Nonasthmatic eosinophilic bronchitis (NAEB)?
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.
What is Pertussis?
Pertussis:
- Epidemiology
- Aetiology?
Pertussis:
- Pathophysiology?
What are the 3 Stages of Pertussis?
- 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
How is Pertussis diagnosed?
Treatment for Pertussis
- General approach?
- Medical therapy?
- Which antibiotics in infants <1 month?
Discuss the Immunization available for Pertussis?
- Schedule - Children?
- Adults?
Discuss the post-exposure prophylaxis for pertussis?
- Indication?
- Regimen?
- Isolation?
- Notifiable?
What is Bronchiectasis?
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).
What is the definition of Bronchiectasis?
What is the definition of Acute exacerbation of Bronchiectasis?
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)
Aetiology of Bronchiectasis
- 4 Common causes?
- 8 Less common causes?
- 3 Rare causes?
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.
Clinical Features of Bronchiectasis?
Investigations for and diagnosis of Bronchiectasis?
What are the management goals in bronchiectasis?
What are 5 Key components of bronchiectasis management in adults?
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.
What is COPD?
- Chronic Bronchitis?
- Emphysema?
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.
Epidemiology of COPD?
- Sex?
- Prevalence?
Aetiology of COPD?
- 2 Exogenous factors?
- 5 Endogenous factors?
Sex: 3:2 male/female ratio
Prevalence: 6%
What are the 2 Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifications?
What is Emyphysema?
4 Clinical Subtypes?
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
What are the 2 main types of Emphysema? How do they compare?
What is the Pathophysiology of COPD?
- Chronic inflammation?
- Tissue destruction?
Clinical features of COPD
- Presenting findings?
- Features of advanced COPD?
How is COPD diagnosed?
What test needs to be performed to rule out asthma?
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.
Other than pulmonary function tests, which routine studies would you perform to support a diagnosis of COPD?
List 4 Supportive measures for the management of COPD patients?
What is the stepwise drug management of stable COPD?
Multidisciplinary care for COPD?
TGA Guidelines - Short-acting bronchodilator therapy for COPD?
TGA Guidelines - Long-acting bronchodilator (LABA or LAMA) monotherapy for COPD?
TGA Guidelines - Long-acting bronchodilator (LABA plus LAMA) dual therapy for COPD?
What is Hypercapnia?
List 5 causes?
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).
8 Clinical Features of hypercapnia?
5 Clinical features of hypoxemia?
What is Hypoxemia?
What is Hypoxia?
Causes of each?
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%.
Workup for hypoxemia?
List 5 causes of hypoxemia?
What is the definition of:
- Respiratory failure?
- Hypoxemic respiratory failure?
- Hypercapnic respiratory failure?
What are 7 rapidly reversible causes of respiratory failure and their treatments?
What is Acute respiratory distress syndrome?
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.
Aetiology of ARDS
- 8 Systemic Causes?
- 7 Primary damage to the lungs?
What are the 4 Berlin criteria for ARDS?
Clinical Features of ARDS?
Describe an approach to the management of ARDS?
- Consult ICU early, i.e., as soon as respiratory failure due to ARDS is suspected.
- Address hypoxemia
- Apply lung-protective ventilation strategies.
- 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).
Management checklist for all patients with ARDS?
What is Asthma?
Asthma is a chronic inflammatory disease of the respiratory system characterized by bronchial hyperresponsiveness, episodic acute asthma exacerbations, and reversible airflow obstruction.
Epidemiology of Asthma?
What is Atopic/Allergic/Extrinsic Asthma?
- List 3 triggers?
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)
What is non-atopic/non-allergic/intrinsic asthma?
- List 8 triggers?
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)
7 Clinical features of Asthma?
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)
Pathophysiology of Asthma?
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.
Compare the pathophysiology of asthma in the early and late phases?
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.
How is asthma diagnosed?
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.
What are the characteristic findings of asthma in PFTs?
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
What are the Clinical features that increase and decrease the probability of asthma in children 6 years and older, adolescents and adults?
Which spirometry findings support a diagnosis of asthma?
How can asthma severity be classified?
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
Describe a stepped approach to starting and adjusting asthma therapy in adults and adolescents?
- 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
What are the general principles of antiasthma medications?
List 7 types.
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)
4 Standard tests of airway function and gas exchange?
5 Pulmonary Function Tests performed in specialist respiratory laboratories?
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.
List 4 Uses of PFTs?
Diagnostic pathway for PFTs?
What is Spirometry? Which parameters does it measure?
- 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)
Compare spirometry findings in Obstructive and Restrictive Lung Disease?
Normal
Acute asthma
Emphysema
Fixed upper airway obstruction
Unilateral main stem obstruction
Obesity
Neuromuscular weakness
Fibrosis
What are 8 Relative contraindications to performing spirometry?
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.
What are 2 Specialized lung function tests (spirometry) that can be done to diagnose obstructive lung disease?
Specialized tests (i.e., bronchial challenge tests and/or bronchodilator responsiveness testing) may help distinguish bronchial asthma from other causes of obstructive lung disease.
What is Full-body plethysmography?
- List 3 indications?
- Which parameters can be measured in Plethysmography?
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
What are the Plethysmograph findings in Obstructive vs. Restrictive lung disease?
What are Single-breath diffusing capacity test?
- Indications?
- Procedure?
- Parameters measured?
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.
What is malignant pleural mesothelioma?
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.
Malignant Mesothelioma
- Definition?
- Epidemiology - Sex? Age?
- Aetiology? (2)
- Clinical findings? (3)
- Diagnosis?
- Treatment?
- Prognosis?
What is Restrictive Lung Disease?
- 2 Intrinsic causes? Examples?
- 3 Extrinsic causes? Examples?
What is Interstitial Lung Disease?
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.
Aetiology of Interstitial Lung Disease
- 3 Idiopathic interstitial pneumonias?
- 3 Multisystem disorders?
- 5 Environmental or lifestyle exposures?
- 2 Genetic?
- 3 Other?
Clinical features of ILD?
- 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).
What information from a clinical history should you obtain when you suspect ILD? (10)
What physical exam findings might you expect? (5)
Clinical Features of ILD?
What is the shared pathophysiology in all types of ILD?
Describe an approach to diagnosing ILD?
Describe the role of Pulmonary function tests in the diagnosis of ILD?
Which blood tests would you order to assist in the diagnosis of ILD?
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.
Which imaging modalities would you use in the diagnosis of ILD?
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.
What are the different patterns of ILD seen on HRCT chest?
What imaging modality is this? What does it show?
What imaging modality is this? What does it show?
What imaging modality is this? What does it show?
What is Idiopathic pulmonary fibrosis (IPF)?
- Definition?
- Epidemiology?
- Diagnsosis?
- Prognosis?
Diagnosis and Treatment of idiopathic pulmonary fibrosis?
What are Acute exacerbations of idiopathic pulmonary fibrosis and how are they managed?
What are 5 essential components of a diagnosis of cutaneous drug eruption?
Can we specifically test for a drug reaction?
- When is this not advised?
- Give 3 examples of tests
List 9 Important Factors associated with cutaneous drug eruptions?
What are the 2 main pathological mechnanisms underlying cutaneous adverse drug reactions?
- Give 4 examples of each.
What are the 4 classifications of immunomediated reactions as classified by Coombs and Gell?
What are the 3 categories of genetic basis of adverse drug reactions?
Cutaneous drug reaction in paediatrics
- How do they present?
Cutaneous drug reaction in paediatrics
- Why are they at increased risk?
List some of the pitfalls in ADRs Management = 7
Cutaneous ADRs to Immune modulators/Biologics
- Which 2 drugs are most commonly reported?
- What kind of cutaneous ADRs do each of these drugs cause?
Cutaneous ADRs to Antimicrobials
- Which clinical sign is common?
- What is the usual severity?
- 3 risk factors?
- Which antibiotic showed SJS more commonly?
Cutaneous ADRs in Chemotherapy Regimens
- Why do they occur so often?
- Which type of reactions tend to occur?
List 5 dermatoses which are known to have drug-induced variants?
List 10 Morphological clinical patterns of ADR?
Which 9 clinical features signal development of a serious cutaneous ADR like Stevens-Johnson Syndrome (SJS) or Toxic Epidermal necrolysis (TEN)?
What is DRESS?
- Incidence?
- Generalised eruption?
- Constitutional Sx?
- Is it dose dependent?
- Risk factors?
- Mortality?
- Pathogenesis? (4)
List the 6 drugs most commonly implicated in DRESS?
What is Toxic Epidermal necrolysis (TEN)?
- Commonly implicated drugs? (6)
- Clinical features?
- Onset?
List 7 Differential Diagnoses of SJS/TENS?
What is our current understanding regarding the difference between SJS and TEN? Pathogenesis of these?
What are 6 poor prognostic factors in SJS/TEN?
Describe the management of ADR?
Types of Cutaneous ADRs - Exanthematous
- Incidence?
- Clinical presentation?
- Onset?
- Commonest causing drug?
Types of Cutaneous ADRs - Urticarial
- Onset?
- Clinical presentation?
- Mechanism?
- Which drugs?
Types of Cutaneous ADRs - Erythema Multiforme
- 5 drugs?
Types of Cutaneous ADRs - Vasculitis
- Clinical presentation?
- Mechanism?
- Onset?
Types of Cutaneous ADRs - Vesiculobullous
- 5 drugs?
Types of Cutaneous ADRs - Erythroderma
- Also known as?
- Clinical presentation?
Types of Cutaneous ADRs - Lupus Erythematosus
- Incidence?
- Immunological marker?
- Implicated drugs?
Types of Cutaneous ADRs - Erythema Nodosa
- Clinical features?
- Typical site?
Types of Cutaneous ADRs - Psoriasiform
- Implicated drugs?
Types of Cutaneous ADRs - High potency topical steroids
- What can inappropriate use of fluorinated potent topical steroids cause? (6)
Types of Cutaneous ADRs - Acneiform lesions
- 4 implicated drugs?
