Respiratory Flashcards
Vital capacity
Maximum volume of air that can be expired after maximal inspiration
Pneumothorax algorithm
Even
Indications for corticosteroids treatment for sarcoidosis
Parenchymal lung disease
Uveitis
Hypercalceamia
Neurological or cardiac involvement
HAPE treatment
Nipedefine
Acetozolamide
Phosphordiestarase 4 inhibitors
ABPA
Non responsive asthma
Blood test - eosinophilia
CXR - proximal bronchiactasis
Treatment - oral/ weaning course of prednisolone
Cavitating lung elisions
Staph aureus,klebsiella,pseudomonas,squamous cell cancer,tb,wegeners,or,ra,aspergillosis,histoplasmosis,coccidiomycosis
EGPA Cannot give drug
Monte lucas
Severe obesity in transfer factor
FEV1 reduces
FVC Reduces
FEV1/FVC normal
KCO normal
COPD Staging
Mild stage 1 ~ 80
Stage 2 ~50-80
Stage 3~ 30-50
Stage 4 ~ 30
Asothioprin
1. low TPMT
2. intract
3. pregnancy
- Low TPMT(inhibit purin synthesis) - pansytophenia
- Alo
- safe
ARDS
The symptoms described are consistent with chronic aspiration occurring in the elderly. The CT findings are radiological bronchiectasis, a sequela of recurrent episodes of aspiration pneumonia. This does not, however, equate to a clinical diagnosis of bronchiectasis. The absence of honeycombing and ground-glass opacities counts against the diagnosis of radiation pneumonitis and idiopathic pulmonary fibrosis.
Chronic Pulmonary Aspergillosis (CPA)
Causes and Risk Factors:
Underlying Lung Conditions:
CPA is more common in individuals with pre-existing lung problems, such as: Tuberculosis, COPD, Sarcoidosis , Bronchiectasis Cystic fibrosis, previous lung disease or surgery
Symptoms:
Chronic Cough: A persistent cough, may hemoptysis
Shortness of Breath: Difficulty breathing, especially with exertion -significant symptom.
Weight Loss, Fatigue, Wheezing, chest pain, and fever
Diagnosis - CT - cavities, fungal balls (aspergillomas), and nodules., sputum, bronchoalveolar lavage
Treatment - oral agents like itraconazole or voriconazole, Aspergillus-specific IgG antibody test
primarily caused by Aspergillus fumigatus, that affects the lungs and often occurs in individuals with pre-existing lung conditions. The pathophysiology involves fungal growth and inflammation within the lungs, leading to lung damage and potentially forming cavities or a fungal ball
aspergilloma
a fungus ball formed by the fungus Aspergillus within a pre-existing lung cavity. It’s a non-invasive form of chronic pulmonary aspergillosis. Aspergillomas often develop in areas of the lung previously damaged by conditions like tuberculosis.
spergillomas may be asymptomatic, others can cause symptoms like hemoptysis (coughing up blood), wheezing, shortness of breath, and fatigue.
Diagnosis:
Chest X-rays or CT scans can reveal the characteristic appearance of an aspergilloma, often described as a mobile mass within a cavity.
aspergilloma is a manifestation of CPA, specifically a fungal ball within a lung cavity. CPA is a broader term encompassing various forms of Aspergillus infection, some of which can lead to aspergilloma formation.
invasive aspergillosis
a serious, potentially life-threatening fungal infection that typically affects individuals with weakened immune systems
Invasive aspergillosis is a serious, potentially life-threatening infection that occurs in immunocompromised individuals, while aspergilloma is a fungal ball that typically develops in pre-existing lung cavities and is usually less severe.
fever, cough, chest pain, and hemoptysis (coughing up blood).
It involves the fungus invading tissues and blood vessels, causing inflammation, tissue damage, and the spread of infection to other organs.
Immunocompromised individuals, including those undergoing cancer treatment, bone marrow transplantation, or with certain immune system diseases, are at high risk.
Type I hypersensitivity to Aspergillus fumigatus
an immediate, IgE-mediated allergic reaction to the fungus. It’s a key component of Allergic Bronchopulmonary Aspergillosis (ABPA), a condition primarily affecting individuals with asthma or cystic fibrosis, and is typically diagnosed through skin testing or elevated IgE levels.
IgE-mediated reaction:
Type I hypersensitivity involves IgE antibodies binding to allergens like A. fumigatus antigens
leading to symptoms like asthma exacerbations, mucus production, and even bronchiectasis. symptoms similar to asthma, including wheezing, cough, shortness of breath, and potentially coughing up blood or brown flecks.
Diagnosis:
Aspergillus skin tests (AST) and measuring A. fumigatus-specific IgE levels in the blood are commonly used to diagnose ABPA and confirm the presence of type I hypersensitivity to A. fumigatus.
Allergic Bronchopulmonary Aspergillosis (ABPA)
Type I Hypersensitivity:
The most common type of hypersensitivity in ABPA is the IgE-mediated reaction (Type I). When individuals are exposed to A. fumigatus spores, their immune systems produce IgE antibodies that bind to specific antigens on the fungal spores.
Type III Hypersensitivity:
Type III reactions involve the formation of IgG-mediated immune complexes. These complexes can deposit in the airways and cause inflammation and tissue damage.
Type IV Hypersensitivity:
Type IV reactions are mediated by T cells and can contribute to chronic inflammation and tissue damage in ABPA.
Hypersensitivity Pneumonitis:
Inhalation of A. fumigatus can also trigger hypersensitivity pneumonitis, a type IV reaction characterized by inflammation of the lung tissue.
Severe Asthma with Fungal Sensitization (SAFS):
Fungal sensitization, including A. fumigatus, has been linked to exacerbations of allergic asthma.
Q fever
a disease caused by the bacteria Coxiella burnetii
Acute Q fever often presents with flu-like symptoms like fever, headache, and fatigue, and may include atypical pneumonia or hepatitis. Chronic Q fever, if it develops, is more likely to manifest as endocarditis or other long-term complications.
linical Manifestations:
Acute Q Fever:
Flu-like illness: High fever, headache, fatigue, myalgias (muscle aches) are common.
Atypical pneumonia: May be mild or more severe, with symptoms like cough, chest pain, and shortness of breath.
Hepatitis: Liver inflammation can lead to elevated liver enzymes and, in some cases, jaundice.
Other manifestations: Less common complications include rash, gastrointestinal symptoms, and neurological involvement.
Chronic Q Fever:
Endocarditis: The most common and severe complication, affecting the heart valves.
Other complications: May include myocarditis, pericarditis, and less frequently, other systemic complications like encephalitis or meningitis.
Diagnosis:
Serological Testing:
Blood tests to detect antibodies against C. burnetii are the primary method for diagnosis.
Other tests:
Culture or PCR testing can be used to isolate the bacteria, especially in severe cases or when serological testing is inconclusive.
Treatment:
Acute Q Fever: Doxycycline is the primary antibiotic used for acute Q fever.
Chronic Q Fever: Doxycycline, often in combination with hydroxychloroquine, is used for long-term treatment of chronic Q fever.
Cystic fibrosis (CF)
affecting the lungs and digestive system due to a defect in the CFTR protein, which regulates chloride and water movement across cell membranes. This defect leads to thick, sticky mucus buildup, obstructing airways and digestive tracts. The most commonly affected organs include the sinuses, lungs, pancreas, biliary and hepatic systems, intestines, and sweat glands.
espiratory issues (wheezing, cough, thick mucus), digestive problems (foul-smelling stools, poor weight gain), and other indicators like malabsorption, rectal prolapse, or pancreatitis.
mutations in the CFTR gene
Consequences of Mucus Buildup:
Respiratory: Chronic infections (like Pseudomonas aeruginosa), chronic lung disease, and respiratory failure.
Digestive: Malnutrition, poor growth, and digestive problems.
Other: Skin rashes, sweat-related problems, and potential fertility issues in males.
Diagnosis - A sweat chloride level of 60 mmol/L or greater is strongly indicative of CF. A chloride level of 60 mmol/L or greater strongly suggests CF.
Levels between 30-59 mmol/L require further investigation.
Bronchiectasis
characterized by permanent, abnormal dilation of the bronchi due to inflammation and infection, leading to impaired mucus clearance and recurrent infections. Below is a comprehensive overview of bronchiectasis, including its assessment tools, severity scoring systems, and clinical implications
Pathophysiology: Damage to the bronchial walls causes mucus accumulation, bacterial colonization, and recurrent infections, creating a vicious cycle of inflammation and structural damage
Symptoms: Chronic cough, excessive sputum production, dyspnea, hemoptysis, and recurrent respiratory infections
Etiologies: Post-infectious (most common), cystic fibrosis (CF), immune deficiencies, autoimmune diseases, and idiopathic causes
Diagnostic Tools
Imaging
High-Resolution CT (HRCT): Gold standard for diagnosis, showing bronchial dilation, wall thickening, and mucus plugging
BRICS Score: A radiological scoring system for idiopathic/post-infectious bronchiectasis, assessing bronchial dilatation and emphysema extent.
Microbiological Tests
Sputum cultures to identify pathogens (e.g., Pseudomonas aeruginosa), which worsen prognosis
Pulmonary Function Tests (PFTs)
Reduced FEV1 (forced expiratory volume in 1 second) correlates with disease severity
- Severity Assessment Scores
FACED Score
Components:
FEV1 (<50% = 2 points),
Age (≥70 years = 2 points),
Chronic colonization (Pseudomonas = 1 point),
Extension (>2 lobes = 1 point),
Dyspnea (mMRC 3–4 = 1 point) 1.
Interpretation:
0–2: Mild (5-year mortality <5%).
3–4: Moderate (5-year mortality ~10%).
5–7: Severe (5-year mortality ~30%) 15.
Bronchiectasis Severity Index (BSI)
Components: Age, BMI, FEV1%, exacerbations, hospitalizations, dyspnea, microbial colonization, and radiological involvement
Interpretation:
0–4: Mild (1-year mortality <3%).
5–8: Moderate (1-year mortality ~5%).
≥9: Severe (1-year mortality ~10%) 810.
Comparison of FACED vs. BSI
FACED: Better for predicting mortality (AUC 0.87 vs. 0.75 for BSI) 5.
BSI: More comprehensive, incorporating exacerbations and hospitalizations, and better for predicting hospitalization risk
- Clinical Management
Antibiotics: Chronic macrolides (e.g., azithromycin) for Pseudomonas colonization or frequent exacerbations
Airway Clearance: Physiotherapy (e.g., postural drainage, percussion devices)
Surgery/Lung Transplant: For localized severe disease or respiratory failure - Prognosis
Severe bronchiectasis (FACED ≥5 or BSI ≥9) has high mortality (up to 30% at 5 years) and hospitalization rates (>50%) 18.
COPD
Spirometry: Diagnosis requires a post-bronchodilator FEV1/FVC ratio <0.7 to confirm airflow obstruction. Pre-bronchodilator spirometry may suffice if no obstruction is detected, unless clinical suspicion is high
Clinical Suspicion: Suspect COPD in patients >35 years with risk factors (e.g., smoking, biomass exposure) and symptoms like dyspnea, chronic cough, or sputum production
Exclusions: Differentiate from asthma, bronchiectasis, and heart failure using history, imaging, and additional tests (e.g., CT for structural abnormalities)
Pharmacological Management
First-line: Start with short-acting bronchodilators (SABA or SAMA) for symptom relief.
Maintenance Therapy:
Dual bronchodilators (LABA + LAMA) are preferred over monotherapy for symptomatic patients, regardless of FEV1.
Inhaled corticosteroids (ICS) are added only for patients with asthmatic features (e.g., eosinophilia, prior asthma diagnosis) or frequent exacerbations despite dual therapy.
Avoid ICS in non-asthmatic COPD due to pneumonia risk.
Newer Agents: Consider ensifentrine (PDE3/4 inhibitor) or dupilumab (for eosinophilic COPD) in refractory cases
- Non-Pharmacological Interventions
Smoking cessation: Mandatory, with behavioral support and pharmacotherapy (e.g., varenicline).
Pulmonary rehabilitation: Recommended for symptomatic patients (FEV1 <50%) to improve exercise tolerance and quality of life.
Vaccinations: Annual influenza and pneumococcal vaccines to prevent exacerbations.
Oxygen therapy: For severe hypoxemia (PaO2 ≤55 mmHg or SpO2 ≤88%). - Exacerbation Management
Acute exacerbations: Use oral corticosteroids (e.g., prednisolone) and antibiotics if purulent sputum is present
Prevention: Prophylactic azithromycin (unlicensed) may reduce exacerbations in non-smokers with frequent events, but requires monitoring 9.
Triple therapy (LABA/LAMA/ICS): Reserved for patients with persistent symptoms/exacerbations despite dual therapy and after optimizing non-drug measures.
Pulmonary hypertension: New emphasis on echocardiography for assessment and referral to specialist centers
psittacosis
primarily spread from birds to humans
flu, including fever, headache, muscle aches, and cough. However, in some cases, psittacosis can develop into pneumonia, with symptoms such as shortness of breath and chest pain.
can lead to complications like myocarditis, endocarditis, or even encephalitis
diagnosis - next-generation sequencing (mNGS) are used to identify the bacteria in samples like blood or bronchoalveolar lavage fluid.
Non-small cell lung cancer (NSCLC)
develops in the epithelial cells of the lung, ranging from the central bronchi to the terminal alveoli.
Squamous cell carcinoma: Typically starts near a central bronchus. - 25–30%): Central airways; strongly associated with smoking
Adenocarcinoma: Usually originates in the peripheral lung tissue, often in the mucus-producing cells lining the bronchioles. - (40% of NSCLC): Often found in peripheral lung tissue; linked to both smokers and non-smokers.
Large cell carcinoma: Can occur in various locations within the lung. - (10–15%): Aggressive, can occur anywhere in the lungs
Tobacco smoking is the primary risk factor, with a 90% association - obacco smoke causes DNA damage and mutations
Epigenetic alterations, like DNA methylation, can silence DNA repair genes
Oncogene Activation and Tumor Suppressor Gene Inactivation
Other risks:
Secondhand smoke, radon, asbestos, air pollution.
Genetic mutations (e.g., EGFR, ALK, KRAS) in non-smokers
Family history, HIV infection, and prior radiation therapy
NSCLC progression involves several steps, including hyperplasia, metaplasia, dysplasia, and carcinoma in situ, before becoming invasive cancer.
Persistent cough, hemoptysis, chest pain, dyspnea, weight loss, fatigue, and recurrent infections 36.
Advanced stages may present with hoarseness (vocal nerve involvement) or neurological symptoms (brain metastases)
Treatment by Stage
Stage I–II: Surgery (lobectomy or wedge resection) ± adjuvant therapy (chemotherapy/targeted drugs for high-risk cases).
Stage III: Multimodal approach—chemoradiation ± immunotherapy (e.g., durvalumab) or surgery if resectable.
Stage IV:
Targeted therapy: For driver mutations (e.g., osimertinib for EGFR, alectinib for ALK)
Immunotherapy: PD-1/PD-L1 inhibitors (pembrolizumab, nivolumab) for tumors with high PD-L1 expression
Chemotherapy: Used if no actionable mutations or immunotherapy fails.
