It occurs when obstruction prevents air from reaching distal airways, causing alveoli in the affected area to collapse.
Emphysema, Chronic bronchitis, Asthma, Cystic Fibrosis.
A lung condition that causes shortness of breath due to damage to the air sacs in the lungs.
Mucous plugs, tumors, and foreign bodies.
Human papillomavirus (HPV) types 6 and 11 (low-risk).
Lung disorders caused by inhalation of mineral dusts.
Nodules coalesce into hard collagenous scars.
Surgical excision, including laser ablation.
Human papillomavirus (HPV) types 6 and 11 (low-risk).
Reduced compliance and decreased total lung capacity.
Cell-mediated immunity.
Involvement of lymph nodes.
Abnormal function of an epithelial chloride channel protein.
Localized, fibrocalcified nodules.
Unknown, but theories include disordered or exaggerated immune response, genetic predisposition, and exposure to environmental agents.
Inflammation.
Laryngeal Squamous Cell Carcinoma.
Adenocarcinoma is a type of cancer that forms in the glands and can occur in many different parts of the body.
Mucus hypersecretion.
Necrotizing granuloma.
Recruited leukocytes and inflammatory cells damage the epithelium, leading to airway remodeling and thickened/narrowed airways.
Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue as a reparative or reactive process.
CFTR (cystic fibrosis transmembrane conductance regulator) gene.
By a positive tuberculin skin test.
Approximately 5% of cases, mostly due to impaired immunity.
Severity.
No, there is no firm evidence to suggest this.
Diffuse alveolar damage.
Edema fluid and a layer of mucinous or mucopurulent secretions.
Hyaline membranes.
Approximately 95%.
It has a genetic predisposition.
The air sacs, or alveoli, of the lungs fill up with fluid or pus.
Approximately one-sixth.
Immunocompetent individuals.
Carcinoma-in-situ.
African American females aged 20-40 years old.
Idiopathic Pulmonary Fibrosis.
75%.
They become abnormally enlarged.
Smoking, which leads to increased proteolytic agents (e.g. elastase).
It is a TB blood test, also known as Interferon-Gamma Release Assays.
Progressive dyspnea with expiratory airflow limitation (low FEV).
Relatively normal.
No, it does not differentiate latent TB from active disease.
Pseudostratified columnar epithelium.
A chronic inflammatory disorder of the airways.
Hypoxemia, cyanosis, and clubbing.
Location and stage of the cancer.
It shows evidence of allergen sensitization and immune activation.
Spontaneously within a few hours or with treatment.
Keratin pearl formation.
Smoking or singers (singer’s nodes).
“Pink puffers”.
4 to 9 months.
Right-sided heart failure due to lung disease.
Yes, it may progress even after exposure has ceased.
For life (20 - 40 years latency).
Cigarette smoking.
Hematogenous → periapical tissues → bone.
Through clinical signs, lung function tests, and imaging.
Smoking.
IgE triggering mast cell mediators.
Upper airway obstruction, loss of ventilatory drive, loss of normal gas exchange, and mechanical impairment.
It can be a primary cause of respiratory failure.
It can result in respiratory failure.
Expiration.
Coating mast cells and mediating allergic responses.
Only 2 - 4 years.
Community-Acquired Pneumonia, Nosocomial (hospital-acquired) pneumonia, Gram-negative rods, Staph aureus (usually methicillin-resistant).
Transbronchial lung biopsy.
Because other diseases can also produce non-necrotizing granulomas.
A multisystem disease characterized by non-necrotizing granulomas in many organs.
Smoking.
Permanent dilation of the bronchi.
Mycobacterium tuberculosis.
Surgery, radiation, chemotherapy, immunotherapy, and targeted tyrosine kinase inhibitors.
More prevalent in males (M>F).
Approximately 77% overall.
Squamous cell carcinoma.
Streptococcus pneumoniae.
Dysplasia.
Goblet cell hyperplasia.
Symptoms of asbestosis include shortness of breath, a persistent cough, chest tightness, and clubbing of the fingers.
It is reduced, making the lungs stiff and inelastic.
Hard, collagenous scars.
Nonproductive cough and progressive dyspnea.
Pericarditis, tamponade.
It thickens.
Decreased expiratory flow rate.
Productive cough, significant COPD with outflow obstruction, hypoxia, hypercapnia, and cyanosis.
Lung cancer.
Lung collapse due to pressure in the pleural cavity.
Infection.
Due to reduced salivary flow.
15%.
Adenocarcinoma.
Cold air.
Thinning and destruction.
Uranium, asbestos, arsenic, chromium, nickel, vinyl chloride, mustard gas, high dose ionizing radiation.
HPV (Human Papillomavirus).
Aspirin.
Cigarette smoking and other factors.
Chest radiograph.
Close to 100% of tumors have RB loss-of-function aberrations.
Intermittent and reversible airway obstruction, chronic bronchial inflammation, smooth muscle hypertrophy & hyperactivity, and increased mucus secretion.
It has a rapid onset of life-threatening respiratory insufficiency.
Attracts and activates eosinophils.
Lung transplant.
No definitive diagnostic test.
It helps in the removal of foreign particles and microorganisms from the respiratory tract.
Incomplete expansion or collapse of lung parenchyma.
Asbestos fiber core coated with iron-containing protein.
PMF.
It shows no evidence of allergen sensitization.
Squamous metaplasia or dysplasia.
It decreases the risk, but it never returns to baseline levels.
Years.
Less than 5%.
Loss or mutation of suppressor genes TP53, CDKN2A (p16), RB.
Increased goblet cells in the lining epithelium and loss of cilia.
Dyspnea, cough, wheezing.
Tuberculosis.
Occupational exposure.
Bronchoconstriction, increased vascular permeability, increased mucus production, and increased inflammatory cell recruitment.
Sputum/smear.
MYC (oncogene) family.
Treatment for asbestosis focuses on relieving symptoms and preventing further lung damage. This may include oxygen therapy, pulmonary rehabilitation, and in severe cases, lung transplantation.
Central area of whorled collagen fibers with a more peripheral zone of dust-laden macrophages.
Airway obstruction by tumor.
Supplying O2 to and removing CO2 from blood in capillaries of alveoli.
Golden brown, fusiform or beaded rods.
Bacterial and viral infections.
A rare, rapidly fatal cancer of mesothelial cells.
Anti-inflammatory drugs, particularly glucocorticoids, and bronchodilators.
Pulmonary hypertension, cor pulmonale, increased susceptibility to infection, and double the risk of cancer.
20%.
Central caseation - caseous necrosis.
Before the age of 55 years.
Small cell carcinoma.
Unknown (possibly genetic predisposition).
The normal balance between proteolytic agents and their antagonists is disturbed.
In the large airways.
PD-L1 inhibitors.
Enlarged parotid glands.
It is not affected by prior BCG vaccination and is not expected to give a false-positive result.
Irregular linear densities.
Tiny nodules.
It has a very poor prognosis.
Deterioration.
Silicosis.
It may be fatal.
Miners, quarry workers, and workers in the construction industry.
Cigarette smoking.
Cervical lymphadenitis, also known as scrofula.
Heart failure.
Rare, especially in immunocompromised individuals.
A smoking history.
Right-sided heart failure.
Fever, fatigue, weight loss, anorexia, night sweats.
Diagnosing Latent Tuberculosis Infection (LTBI).
Overuse and trauma (preacher’s, singer’s nodules).
Enzyme alpha 1-antitrypsin, found in serum, tissue fluids, and macrophages.
It becomes markedly thickened.
QuantiFERON - TB test.
Abrupt onset, fever, shaking chills, chest pain, cough.
Pneumonia, COVID, sepsis, aspiration, trauma.
Honeycomb pattern.
Massive rib fracture or muscle disease.
Cough, involvement of central airways, hemoptysis, chest pain, pneumonia, abscess, lobar collapse, airway obstruction, lipoid pneumonia, pleural effusion, hoarseness, dysphagia, diaphragm paralysis, rib destruction, SVC syndrome, pericarditis, tamponade.
Reduced Cl- secretion into respiratory tract lumen leading to increased reabsorption of Na+ ions and water.
38.5%.
65 - 70%.
12 - 18 months.
Ghon focus.
Usually as a secondary infection to pulmonary disease via infected sputum.
It increases the risk of cancer by two times.
Cigarette smoking (95% related).
Exercise-induced.
It grows more slowly and forms smaller masses than other subtypes.
Gain-of-function mutations in multiple growth genes encoding receptor tyrosine kinases.
With corticosteroids.
Only about 1%.
Asbestosis is a chronic lung condition caused by inhaling asbestos fibers, leading to scarring of the lung tissue.
Wheezing, breathlessness, chest tightness, and cough, particularly at night or early in the morning.
Squamous metaplasia.
ILs (cytokines).
Metaplasia.
Esophageal invasion.
Exocrine gland epithelium.
Fatigue, weight loss, low-grade fever, night sweats.
It involves abnormal wound healing, leading to excessive scarring of the lung tissue.
Lungs.
Chronic irritation or overuse.
Due to decreased oxygen exchange.
Lobar and Bronchopneumonia.
Spaces or holes are formed when the septum is destroyed.
Hypertrophy of submucosal glands, hypersecretion of mucus, and inflammatory infiltrate.
Structural changes in the airway.
Persistent productive cough for 3 consecutive months in 2 consecutive years.
EGFR (epidermoid growth factor receptor), ALK (anaplastic lymphoma kinase), KRAS (Ras family oncogene).
Radiologic and histologic progressive fibrosis.
Unpredictable, with periods of activity and remissions, sometimes permanent.
It is lung swelling and fluid build-up in alveoli.
Cigarette smoking, genetic predisposition, environmental and occupational pollutants.
Biopsy.
Eosinophils.
50% - 75%.
Via airways, leading to an acute bacterial pneumonia-like disease, and via systemic blood vessels.
They increase life expectancy.
Productive cough, hemoptysis, pleuritic pain.
20%.
More common in men.
Occasionally in members of household of asbestos workers and in the general public.
As effective.
Often insidious lesions that have spread and are unresectable before producing symptoms.
Small cell carcinoma.
Destruction of their walls without obvious fibrosis.
Chronic obstructive pulmonary disease.
20%.
Other diseases.
TP53 (90% of tumors).
Barrel-shaped chest.
T H 2 -dominated response.
Stratified squamous epithelium.
It represents the risk factor associated with smoking and lung diseases.
SVC compression by tumor (face/neck swelling, distended neck veins, cough, dyspnea, orthopnea).
Supplemental oxygen therapy and mechanical ventilator.
Mining, stone cutting, and ceramics production.
Schaumann bodies and Asteroid bodies.
50 or older.
It has risen.
Isoniazid (INH), rifampin (RIF), ethambutol (EMB), pyrazinamide (PZA).
Lymph nodes, spleen, bone marrow, eyes, skin, oral mucosa, heart, CNS, and parotid glands.
Via airborne droplets.
EGFR and ALK mutations.
Trachea, bronchi, bronchioles, alveolar ducts, alveoli.
It is lost, requiring affected persons to forcefully squeeze air out of the lungs.
The extent of associated chronic bronchitis.
Antibiotics.
Pneumonia or respiratory failure.
Neoplastic bronchial change.
It is one of the primary causes of respiratory failure.
Dysplasia.
Hemorrhage from tumor in airway.
Healed lesions (organisms not viable), Latent lesions (dormant organisms), Progressive primary tuberculosis.
Non-necrotizing granulomas.
Tuberculosis in previously unexposed people.
Bronchial carcinoids (neuroendocrine), Mesotheliomas, Spindle cell malignancies, Benign tumors.
Progressive massive fibrosis (PMF) stage.
Bilateral hilar lymphadenopathy.
Alveoli.
Centrally in major bronchi.
Influenza types A and B, respiratory syncytial viruses, human metapneumovirus, adenovirus, rhinoviruses.
Abnormal permanent enlargement of air spaces distal to terminal bronchioles, especially in the upper lobe of the lung.
Women and non-smokers.
Chronic bronchitis and emphysema.
More than 10%.
10 years after first exposure and more common after 20 to 30 years.
Dyspnea and cough.
Inflammatory mediators.
E & F. Carcinoma in situ.
Progressive massive fibrosis.
Antifibrotic agents like Nintedanib and Pirfenidone.
A lung disease caused by inhaling crystalline silica dust.
It makes the mucus more concentrated and viscid, leading to obstruction.
Partial or complete obstruction.
It reduces oxygenation of blood.
Chronic bronchitis, bronchiectasis, lung abscesses.
Pneumothorax.
Adrenal glands, liver, brain, and bone.
Formation of mucus plugs.
Immunocompromised individuals with CD4+ T cell counts below 200 cells/μL.
Nasal cavity, pharynx, larynx.
Up to 20-25%.
Epithelial TGF-β leading to fibroblasts, myofibroblasts, and collagen production.
Quantiferon.
Smoking.
Basal cell hyperplasia.
Asbestosis is diagnosed through a combination of medical history, physical examination, lung function tests, and imaging studies such as chest X-rays and CT scans.
It may be static or progress to respiratory failure, cor pulmonale, and death.
Invasive squamous cell carcinoma.
Recurrent laryngeal nerve invasion.
Tobacco smoke, dust, grain, cotton, and silica.
Idiopathic Pulmonary Fibrosis.
Severe disease can impair oxygenation of blood, leading to respiratory failure.
Recurrent infections and respiratory failure.
Shortness of breath, cough, and chest pain.
Blood tests, Chest X-ray/CT, Pulse oximetry, Sputum test.
In the pleura and rapidly encases the lungs.
Reactivation of bacilli in dormant lesions following reduced host resistance.
Diabetes, alcoholism.
Irregular, indurated, red or ulcerated, often painful.
Insidious onset of respiratory abnormalities such as shortness of breath, cough, chest pain, and hemoptysis.
Approximately 46% overall.
To diagnose tuberculosis.
Aerobic, acid-fast, slender rods.
4th leading cause of death.
Phagocytose silica crystals.
By isolating Mycobacterium tuberculosis complex bacilli from bodily secretions or tissue.
No, there is no known preinvasive phase.
Carcinoma-in-situ.
Extension of tumor into mediastinum, pleura, or chest wall.
