Patient Profile: 13-month-old girl.
Symptoms:
Altered general status.
Fever.
Headache.
Lethargy.
Diarrhea.
Initial Diagnosis: Viral enterocolitis (COVID-19 negative).
Progression: No significant improvement after one week of hospitalization.
Further Investigation: Re-hospitalization for cardiac investigations due to suspicion of:
Congenital cardiac malformation.
Myocarditis.
Outcome: Sudden death.
Post-mortem: Autopsy required by cardiologist.
Scope:
Lesions of the upper respiratory tract (pp. 545-547).
Pathology of the lung.
Disorders of Pulmonary Air Content:
Atelectasis.
Respiratory distress syndrome (adult and newborn) (pp. 495-497, 278-279).
Obstructive Lung Diseases: (pp. 498-499, 500-506).
Pulmonary Infections: Pneumonias (pp. 519-525).
Injury by Non-Therapeutic Toxic Agents: Drug abuse (pp. 315-317).
Chronic Interstitial Lung Diseases: Smoking-related interstitial diseases (pp. 506-508; 514-515).
Lung Tumors: (pp. 537-544).
Pleural Diseases: (pp. 544-545).
General Terms:
Respiratory system = aparat respirator = appareil respiratoire.
Upper Airway:
Epiglottis = epiglotǎ = épiglotte.
Nasal cavity = cavitate nazală = cavité nasale.
Oral cavity = cavitate bucală = cavité buccale.
Pharynx = faringe = pharynx.
Larynx = laringe = larynx.
Vocal cord = coardă vocală = corde vocale.
Lower Airway:
Trachea = trahee = trachée.
Right lung = plămîn drept = poumon droit.
Upper lobe = lob superior = lobe supérieur.
Middle lobe = lob median = lobe moyen.
Lower lobe = lob inferior = lobe inférieur.
Left lung = plămîn sting = poumon gauche.
Upper lobe = lob superior = lobe supérieur.
Lower lobe = lob inferior = lobe inférieur.
Other Structures:
Esophagus = esofag = desophage.
Heart = inimă = cœur.
Pericardium = pericard = péricarde.
Diaphragm = diafragma = diaphragme.
Aorta = aortă = aorte.
Pulmonary artery = arterǎ pulmonarǎ = artère pulmonaire.
1 pack a day for 20 years.
Etiology:
Common viruses: Rhinoviruses, Coronavirus, Respiratory Syncytial Virus, Adeno-Enteroviruses.
Other identified pathogens: Coxsackievirus A, EBV, Streptococcus β-hemolytic group A.
Unknown causes account for approximately 40% of cases.
Rhinitis:
Acute catarrhal rhinitis (common cold).
Acute necrotizing rhinitis.
Allergic rhinitis: seasonal, perennial.
Chronic rhinitis: hyperplastic polyp, atrophic rhinitis.
Rhinopharyngitis, Pharyngotonsillitis: Primarily in infants.
Otitis: Acute, chronic (cholesteatoma).
Sinusitis: Acute, chronic.
Kartagener Syndrome:
Characterized by the triad of sinusitis, bronchiectasis, and situs inversus.
Associated with defective ciliary function.
Specific Inflammations: Tuberculosis, syphilis, rhinoscleroma, fungal infections (rhinosporidiosis), Wegener’s granulomatosis.
Chronic sinusitis involving the ethmoid and maxillary sinuses.
Caused by Klebsiella rhinoscleromatis.
Histological features: Russell's bodies and Mikulicz cells.
Specific inflammatory condition affecting the respiratory tract and kidneys.
Hyperplasia of sebaceous glands of the nose.
Benign:
Papilloma.
Hemangioma.
Angiofibroma.
Adenoma.
Malignant:
Nasopharyngeal carcinomas.
Squamous cell carcinoma – HPV-related.
Undifferentiated (lymphoepithelial) carcinoma – EBV-related.
Adenocarcinoma, adenoid cystic carcinoma.
Malignant melanoma.
Lymphomas: Burkitt lymphoma (EBV-related) and other non-Hodgkin lymphomas.
Characterized by inward growth pattern.
A benign but locally aggressive tumor, typically occurring in adolescent males.
Tumor located in the nasopharynx region.
Regions:
Supraglottic space.
Glottic space.
Infra-glottic space.
Structures:
Epiglottis.
Ventriculus laryngis.
Vocal cord (Stimmband).
Schildknorpel (Thyroid cartilage).
Luftröhre (Trachea).
Taschenband (Ventricular fold).
Laryngeal Edema:
Causes: Allergies, inflammations, tumors.
Laryngeal Stenosis:
Causes: Obstruction, compression.
Laryngitis:
Acute catarrhal laryngitis: Viruses, allergies.
Acute epiglottitis: Haemophilus influenzae.
Acute pseudomembranous laryngitis (diphtheric croup): Corynebacterium diphtheriae.
Acute necrotizing laryngitis.
Chronic laryngitis with leukoplakia.
Specific Inflammations: Tuberculosis, syphilis, Wegener’s granulomatosis.
Swelling of the larynx, which can compromise the airway.
Obstruction of the larynx, commonly caused by food or foreign objects.
Inflammation of the epiglottis, often caused by bacterial infection.
Inflammation of both the larynx and trachea.
Croup: Viral infection causing inflammation of the larynx and trachea.
Necrotizing tracheitis: Severe inflammation leading to necrosis of the trachea.
Complications:
Intubation-related changes: Spindle-shaped widening, mucosal necrosis.
Post-tracheostomy scar.
Hemorrhagic influenza.
Pseudomembranous formation.
Carcinoma.
Inflammation of the larynx and trachea characterized by hemorrhage and fibrin deposition.
Cyst formation on the epiglottis.
Tuberculosis infection of the larynx, presenting as:
Pseudopolipous tuberculosis.
Ulcerative tuberculosis.
Benign:
Papilloma.
Papillomatosis (HPV 6 and 11).
Singer’s node (laryngeal polyp).
Malignant:
Squamous cell carcinoma:
Supraglottic: Metastasizes to cervical lymph nodes.
Glottic: Best prognosis.
Subglottic: Rare tumor.
Complications: Asphyxia, necrotic pneumonia, hemorrhages.
Sarcomas, malignant lymphomas.
Overview of various laryngeal lesions.
Multiple papillomas in the larynx, caused by HPV infection.
Carcinomas located above the glottis.
Carcinomas originating in the glottis region.
Types: Ulcerated tumors, papillomatous tumors.
Carcinoma located below the glottis.
Presentation of laryngeal cancers in advanced stages.
T1a, pT1a, T1b, pT1b, T2, pT2, T3, pT3, T4, pT4, pT1: Various pTNM staging classifications for laryngeal cancer.
Lung hypoplasia.
Polycystic lung.
Kartagener’s Syndrome:
Situs inversus + bronchiectasis + chronic rhinosinusitis + lack of the frontal sinuses.
Defective ciliary function.
Cystic fibrosis.
α1-Antitrypsin deficiency.
Examples: Lung hypoplasia, polycystic lung (cystic dysplasia).
Genetic disorder affecting the lungs and other organs.
Lung hyperemia.
Lung congestion.
Embolism, DIC (Disseminated Intravascular Coagulation).
Lung infarction.
Lung hemorrhages (Goodpasture syndrome).
Pulmonary hypertension.
Rapid accumulation of fluid in the lungs.
(Brown induration of the lung).
Deep leg vein thrombosis leading to pulmonary embolism.
Types of emboli: Massive coiled embolus, small embolus.
Consequences: Sudden death, pulmonary infarct, pulmonary hypertension.
Bone marrow embolism.
Bone marrow embolism with DIC.
Formation of thrombi in small blood vessels.
Lung hemorrhages associated with autoimmune disease.
Lungenhämosiderose (iron accumulation) in the lungs.
Acute Bronchitis:
Types: Catarrhal, muco-purulent, diphtheric croup, hemorrhagic, necrotizing, ulcerative.
Evolution, complications: Healing, chronic bronchitis, bronchopneumonia, obstruction, lung gangrene, asphyxia.
Comparison of catarrhal, purulent, fibrinous, and necrotizing bronchitis.
Differentiation based on severity of inflammation and necrosis.
Inflammation of the bronchi with mucus and pus production.
Inflammation of the bronchi and bronchioles.
Types: Purulent bronchiolitis, bronchiolitis obliterans.
Causes of bronchiolitis obliterans: Viruses, toxins, collagen diseases, lung transplantation.
Consequences: Bronchopneumonia, asphyxia, luminal obstruction, atelectasis, death.
Obliteration of bronchioles due to inflammation and fibrosis.
Obstructive Lesions:
Lesions of the airways causing improper airflow.
Examples: COPD (chronic bronchitis, asthma, bronchiectasis, emphysema).
Restrictive Lesions:
Decreasing of the lung parenchyma expansion, reducing total pulmonary capacity.
Examples: ARDS, pneumoconioses, interstitial fibrosis, smoking/drug-induced lesions, sarcoidosis, TB, thoracic wall disorders.
Chronic bronchitis.
Bronchial asthma.
Bronchiectasis.
Chronic emphysema.
Chronic cor pulmonale.
Total surface area of the lung (alveolar space): 80 m^2. Daily air volume: 15,000-20,000 liters.
Right ventricular enlargement and heart failure secondary to pulmonary hypertension.
Clinical Definition: Cough and sputum for 3 months in two consecutive years.
Etiology: Smoking, air pollution.
Classification: Simple chronic bronchitis, chronic asthmatic bronchitis (intrinsic asthma).
Consequences: Pneumonia, lung emphysema, lung fibrosis, bronchiectasis, chronic cor pulmonale.
Inflammation of the bronchi.
Comparison of hypertrophic and atrophic types of chronic bronchitis with squamous metaplasia.
Episodic, reversible small airways obstruction: Bronchospasm, inflammation, mucus hypersecretion, edema.
Asthmatic attacks: Acute emphysema, status asthmaticus.
Etiology:
Atopic asthma (seasonal, familial, extrinsic).
Non-atopic asthma (intrinsic).
Drug-related asthma (aspirin).
Occupational asthma.
Allergic bronchopulmonary aspergillosis (mould fungus).
Consequences: Pneumothorax, bronchiectasis, lung emphysema, CCP, prolonged status asthmaticus, death.
Antigen binds to IgE on mast cells, leading to mediator release.
Acute emphysema and mucus hypersecretion in asthma.
Types: Cylindrical, ampullary, saccular.
Congenital and acquired forms.
Causes include bronchial wall weakness, increased bronchial pressure, fibrosis.
Morphology: Dilatation of bronchi, mucus and pus in lumen, inflammatory infiltrate, squamous metaplasia.
Consequences: Pneumonia, lung abscesses, necrotizing bronchitis, lung fibrosis, chronic cor pulmonale, systemic metastatic abscesses, systemic amyloidosis.
Association with polycystic lung and mucoviscidosis.
Localized and diffuse forms of bronchiectasis.
Advanced stage: "bronchiectasis cavernae".
78-year-old man with chronic lung fibrosis and cor pulmonale.
Complications: Bronchopneumonia, pleuritis, right ventricle failure, death.
Emphysema of the air spaces: Acute, vicariant, senile, chronic obstructive.
Interstitial emphysema.
Acute and reversible overdistension of the lung without tissue destruction.
Causes: Disorders of respiration, asphyxia, bronchial asthma.
Macroscopy: Pale and overdistended lungs.
Microscopy: Dilated alveolar spaces.
Evolution: Reversible process.
Dilated spaces around atelectatic areas.
Senile lung atrophy; spongy-like small lungs, emphysematous thorax without chronic cor pulmonale.
Permanent dilatation of air spaces distal to the terminal bronchiole, with alveolar wall destruction.
Pathogenesis: Dilatation, progressive atrophy, decreased vascular network.
Macroscopy: Overdistended lungs, spongy-like aspect, associated with chronic bronchitis.
Microscopy: Large alveolar spaces, thin and broken alveolar septa, stretched capillaries.
Comparison of lung structure in normal and emphysematous lungs.
Methods used for diagnosing lung emphysema.
Exogenous agents (chronic bronchitis, proteolysis) lead to difficulty in expiration, dilatation, destruction, and fusion of air spaces.
Endogenous factors: \alpha-1 antitrypsin deficiency, lack of antiproteases, immune mechanisms.
Role of tobacco, nicotine, and inflammatory mediators in causing alveolar damage.
Types: Centriacinar (centrilobular) and panacinar (panlobular) emphysema.
Formation of large bullae in the lungs.
Chronic hypoxia → pulmonary hypertension → chronic cor pulmonale.
Atrophy of the lung parenchyma → respiratory failure.
Rupture of bullae → pneumothorax.
Arteriolar sclerosis and chronic cor pulmonale.
Penetration of air into the lung interstitium.
Causes: Cough, trauma, artificial respiration (high pressure).
Consequences: Mediastinal emphysema, subcutaneous emphysema, pneumothorax.
Air in interstitial spaces, leading to subcutaneous emphysema, pneumothorax, mediastinal emphysema, and air embolism.
Neonatal atelectasis: Primary (lung anectasis) and secondary (dystelectasis).
Causes of secondary atelectasis: Lack of surfactant, preterm babies, aspiration of amniotic fluid.
Types: Resorption, compression, scarring (contraction).
Consequences: Reversible process, superinfection (pneumonia, purulent inflammation).
Comparison of a normal lung and a lung with total atelectasis.
Total atelectasis: Collapse of the entire lung.
Focal atelectasis: Localized areas of lung collapse.
Acute restrictive lung disease associated with lung dystelectasis.
The alveoli are lined by hyaline membranes.
Hyaline membrane disease (Infant Respiratory Distress Syndrome):
Preterm babies, caesarian intervention, mother’s diabetes, lack of surfactant.
Dystelectasia, congestion, plasma exudation, hyaline membranes.
Treatment: Surfactant, oxygen therapy (may induce retrolenticular fibrodysplasia and bronchopulmonary dysplasia).
Adult respiratory distress syndrome (ARDS), shock lung:
DIC, destruction of surfactant, dystelectasis, hemorrhages, hyaline membranes. Death rate: 40%.
Exudative and proliferative phases with corresponding changes in lung structure.
Dystelectasis in the context of shock.
Formation of hyaline membranes in the alveoli during ARDS.
Inhaled drugs, water pipe smoking, and injected drugs.
History of cocaine from its isolation to its use in medicine and recreational products.
Effects depend on individual immunity, concentrations, routes of administration, and associated substances.
Heroin overdose: Pulmonary hemorrhagic edema.
Cocaine: Alveolar hemorrhages, cardiac arrhythmia, infarction, seizures, respiratory arrest.
Methylphenidate: Pulmonary emphysema.
Inhaled drugs (marijuana – Cannabis sativa, cocaine, tobacco) → chronic bronchitis, metaplasia.
Nasal inhalation (cocaine) → perforation of nasal septa, aspiration pneumonia, pyothorax, foreign body granulomas, pulmonary hypertension.
Injected drugs (heroin) → foreign body granulomas → pulmonary hypertension, infective endocarditis of the right heart → septic pulmonary emboli.
Other lung lesions: Interstitial pneumonia, lung infarction, asthma exacerbation, chronic obstructive pulmonary diseases.
Vasoconstriction, necrosis/perforation of the nasal septum, acute porphyria, intranasal warts, scleroderma, palpable purpura, Henoch-Schöenlein purpura, Churg-Strauss syndrome.
Pigment-laden macrophages and interstitial lymphocytic infiltrate. Production process: Alkalization of cocaine hydrochloride, heating, crystallization to form ‘rocks’.
Caused by inhalation of adulterated marijuana.
Restrictive lung disease due to silicium, magnesium, carbon, and calcium in aluminium-pipe.
Radiographic findings of irregular nodular areas in the upper lobes with architectural distortion.
Associated with intravenous drug abuse (methylphenidate).
Iatrogenic lung injury; over 400 medications can lead to respiratory diseases.
Drug-induced pulmonary toxicity is about 3% of cases.
Symptoms: Dry cough, low-grade fever, dyspnea, wheezing, hypoxemia, chest pain, fatigue, allergic reaction, rash, arthralgia.
Serum: Increased CD8+ lymphocytes and neutrophils + eosinophils.
Rx: Alveolar/interstitial/mixed opacities, subpleural masses, pleural thickening/effusion.
Function: Decrease in the carbon monoxide diffusing capacity.
Bronchoalveolar lavage fluid: Foamy macrophages ± eosinophils.
Drug-induced interstitial lung disease.
Bronchiolitis obliterans organizing pneumonia (BOOP).
Interstitial edema, pneumocyte necrosis → interstitial pneumonia, lipid-laden macrophages in alveolar spaces, cytoplasmic lipid inclusion in pneumocytes/interstitial cells/endothelial cells, mononuclear cell interstitial infiltrate, interstitial fibrosis, proliferation of type 2 pneumocytes (± atypia, metaplasia).
Desquamative interstitial pneumonia.
Diffuse alveolar damage ± hyaline membranes.
Eosinophilic pneumonia.
Granulomatous lung disease.
Hypersensitivity pneumonia.
Organizing pneumonia.
Alveolar hemorrhage is rare.
Presence of granulomas and mononuclear cell infiltrates.
Marked interstitial fibrosis, most significant in the subpleural region.
Non-Specific Inflammations:
Pneumonia: Bacterial (lobar, bronchopneumonia), viral (interstitial pneumonia).
Pulmonary fibrosis.
Pneumoconioses.
Purulent inflammations.
Specific Inflammations:
Tuberculosis.
Sarcoidosis.
Mycoses, etc.
*Different types of pneumonia
Bacterial infection confined to one pulmonary lobe in adults.
Etiology: Streptococcus pneumoniae, etc.
Evolution: Congestion (prehepatization), red hepatisation, grey hepatisation, yellow hepatisation, resolution.
Comparison of macroscopic view, microscopic type of intraalveolar exudate, and auscultation findings for each stage.
Stages: Congestion, red hepatisation, grey hepatisation, resolution.
*Stages of lobar pneumonia
*Red and grey hepatization
*Red hepatisation
*Grey-Yellow hepatisation
Children, elderly people, or immunosuppressed patients.
Localization: Paravertebral areas, bilateral, inferior lobes.
Classification: Disseminated, confluent.
Macroscopy: “Spotted lung”.
Microscopy: Neutrophils and exudation.
Evolution, complications: Similar to lobar pneumonia.
Patchy infiltrations throughout the lungs.
Evolution and complications include healing, death (5-8% of cases), pulmonary complications, and extra-pulmonary complications.
Lung Abscess:
Etiology: Pneumonia, superinfection, lung infarction, lung tumors, bronchiectasis, bronchial obstruction, aspiration, septic emboli.
Evolution, complications: Healing with fibrosis, vascular erosions, thoracic empyema, septicopyemia, amyloidosis.
Lung Gangrene:
Bronchogenic infection with anaerobes.
Localized cavity with gangrenous tissue within lung parenchyma.
Collection of pus within the lung tissue.
Acute community-acquired pneumonia:
Pneumococcic bronchopneumonia: Streptococcus pneumoniae.
Haemophilus influenzae (+epiglottitis, meningitis).
Moraxella catarrhalis – elderly (in children-otitis).
Staphylococcus aureus (rubeola, flu, intravenous drugs – infectious endocarditis) – abscesses or hemorrhagic pneumonia.
Legionella pneumophila – air conditioning devices.
Enterobacteria: Klebsiella pneumoniae – chronic alcohol abuse, upper lobes.
Pseudomonas spp. – nosocomial infections, immunodepressed patients – severe evolution, associated vasculitis.
Atypical community-acquired pneumonia = Interstitial pneumonia = interstitial inflammatory infiltrate – mononuclear cells (lympho-plasmo-histiocytes)
A. Viral pneumonia: Flue pneumonia – para-finfluenza viruses (chidren), A and B influenza viruses (adult) H1N1, H3N2, H5N1-aviar adenovirus (military), coronavirus pneumonia – chicken pox, rubella pneumonia - CMV, respiratory sincitial virus, human metapneumovirus, etc.
B. Pneumonia with Mycoplasma pneumoniae
C. Pneumonia with chlamidiae: ornitosis, psitacosis
D. Pneumonia with Ricketsii - Coxiella burnetti: Q fever
E. Pneumonia with Pneumocystis carinii: preterm babies, AIDS
F. Chronic interstitial pneumonia
Bronchopneumonia characterized by significant hemorrhage.
Caused by Legionella pneumophila.
52-year-old man with alcoholism and an inoperable lung tumor who developed lobar pneumonia due to Klebsiella.
Interstitial pneumonia with mononuclear cell infiltrate.
Includes viral, mycoplasma, chlamydial, rickettsial, and Pneumocystis pneumonia.
I. Acute interstitial pneumonia = inflammatory infiltrate within alveolar septa (lymphocytes)
Influenza viruses (H1N1), measles, Respiratory Sincitial Virus, Mycoplasma pneumoniae
II. Interstitial pneumonia caused by immunosupression
Pneumocystis carinii, CMV: preterm babies, AIDS
*General Information about Interstitial Pneumonia
*Viruses in Interstitial Pneumonia
Viruses, toxic substances, radiations, drugs, collagen diseases.
Hypersensitivity pneumonitis (Extrinsic allergic alveolitis).
Consequences: Respiratory failure, lung fibrosis, Chronic Cor Pulmonale.
Etiology: Lung inflammations or idiopathic.
*Compared to Pulmonary Fibrotic Tissue
Lung inflammation caused by radiation therapy.
3. Nosocomial pneumonia (in-hospital)
Enterobacteria (Klebsiella pneumoniae, Serratia marcescens, E. coli)
Pseudomonas spp.
Staphylococcus aureus
4. Aspiration pneumonia
Anaerobes and aerobs from oral cavity
5. Chronic pneumonia
Nocardia, Actinomyces, granulomatous pneumonia
6. Necrotizing pneumonia and pulmonary abscess
Anaerobe bacteria
S. Aureus, K. Pneumoniae, Streptococcus pyogenes
7. Pneumonia in patients with immunosupression.
CMV, Pneumocystis carinii/jiroveci, Mycobacterium avium complex
Aspergillosis, Candidoza, othere viruses, bacteria and mycoses
8. Other types:
Hypostatic pneumonia, postoperative pneumonia, lipoidic, eozinophilic pneumonia, etc.