Respiratory tract Flashcards
(71 cards)
1
Q
- Infection of upper respiratory tract:
3 TYPES OF RHINITIS
A
- Allergic rhinitis
- hay fever
- allergic response, T1HR - Infectious rhinitis
- common cold
- symptoms: catarrhal discharge, sneezing, sore throat, increased temperature
- pathogens: rhino-, adeno-, echovirus etc
- self limiting
- complication: otitis media, sinusitis - Chronic rhinitis
- repeated acute rhinitis
- serous exudate
- more with a deviated septum or nasal polyps
2
Q
- Infection of upper respiratory tract:
SINUSITIS
A
- Acute sinusitis
- from rhinitis
- agent in oral cavity
- non-specific inflammation
- complication: empyema - Chronic sinusitis
- due to mixed microflora infection (bad-mucormycosis)
3
Q
- Infection of upper respiratory tract:
ACUTE PHARYNGITIS
A
- symptoms: sore throat, red and edema of nasopharyngeal mucosa
- cause: rhino-, echo- and adenovirus
- more severe:
- tonsillitis - s.pyogenes, s.aureus, adenovirus
- herpangina - coxsackievirus A
- mononucleosis - EBV
4
Q
- Infection of upper respiratory tract:
TONSILLITIS
A
- symptoms: sore throat, fever, enlarged and red tonsils, dotted exudate
- cause: common cold viruses, s.pyogenes
- chronic tonsillitis rare
5
Q
- Infection of upper respiratory tract:
STREPTOCOCCAL TONSILLITIS COMPLICATIONS
A
- peritonsillary abscesses (quinsy)
- poststreptococcal glomerulonephritis
- acute rheumatic fever
6
Q
- Infection of upper respiratory tract:
OTITIS MEDIA
A
= inflammation of middle ear due to dysfunction of Eustachian tube due to inflam. of nasopharynx
- can lead to hearing loss
- mostly young children
TYPES:
1. Acute otitis media
- blockage of Eustachian tube ⇒ buildup of air in middle ear
- cause: s.pneumonia, h.influenzae, moraxella catarrhalis
- diagnosis: non-infectious fluid in middle ear for more than 3 months
2. Otitis media with effusion
- generally no symptoms
- collection of fluid in middle ear
- cause: bacteria, virus
7
Q
- Infection of upper respiratory tract:
INFECTIOUS AGENTS
A
- Croup: Parainfluenza virus ⇒ laryngo-tracheo-bronchitis in children
- Diphteria: Corynebacterium ⇒ pseudomembrane
- Acute epiglottitis ⇒ H.influenzae
- Tonsillitis ⇒ Beta hemolytic strep
- Tuberculosis
8
Q
- Inflammation of trachea and larynx:
TRACHEITIS
A
- Bacterial tracheitis
- cause: s.aureus, s.pneumonia, h.influenzae, m.catarrhalis
- young children
- can lead to airway obstruction
- symptoms: coughing, insp. stridor, chest pain, fever, ear ache, headache, dizziness - Decubitus
- cause: long-term incubation
- superficial, circumscribed, inflammatory and traumatic injury of mucosa + fibrin coverage
9
Q
- Inflammation of trachea and larynx:
LARYNGITIS
A
= inflammation of larynx ⇒ hoarse voice, complete loss of focal function
- part of upper airway infection or exposure to toxins
1. Acute Bacterial Epiglottitis - young children
- h. influenzae
- symptoms: pain + obstruction
2. Acute Laryngitis - cause: inhalation of irritants, allergic reaction, common cold agents
- Forms:
- Tuberculosis laryngitis
- Diphteritic laryngitis
3. Laryngotracheobronchitis = croup
- cause: parainfluenza virus
- children
- self-limited
- symptoms: stridor, cough, airway narrowing
10
Q
- Diseases of vascular origin of the lung, atelectasis:
PULMONARY EMBOLISM, HEMORRHAGE AND INFARCTION
A
- > 95% from deep vein thrombi
CONSEQUENCES: - increase in pulmonary artery pressure
- ischemia of downstream parenchyma
MORPHOLOGY: - infarct: wedge shaped, apex towards hilum, hemorrhagic
- early: raised, red-blue + fibrinous exudate
- late: pale ⇒ red-brown with hemosiderin
- histo: coagulative necrosis
CLINICAL FEATURES: - 60-80% silent
- 10-15% pulmonary infarction ⇒ dyspnea
- 5% sudden death, acute cor pulmonale, cardiovascular collapse
- 3% recurrent multiple emboli ⇒ pulmonary hypertension, chronic cor pulmonale, vascular sclerosis
11
Q
- Diseases of vascular origin of the lung, atelectasis:
RISK FACTORS FOR DEEP VEIN THROMBOSIS
A
- prolonged bedrest
- surgery
- severe trauma
- congestive heart failure
- partition or oral contraceptive use
- disseminated cancer
- primary disorders of hyper coagulability
12
Q
- Diseases of vascular origin of the lung, atelectasis:
CONSEQUENCES OF OCCLUSION OF MAJOR VESSEL
A
- sudden increase in pulmonary pressure
- decreased CO
- right sided heart failure
- hypoxemia
- death
13
Q
- Diseases of vascular origin of the lung, atelectasis:
PULMONARY HYPERTENSION
A
- pressure: 1/4th or more of systemic pressure (normally 1/8)
- secondary to decreased cross-sectional area or increased blood flow
CAUSES: - chronic obstructive/interstitial lung disease
- recurrent pulmonary emboli
- antecedent heart disease
PATHOGENESIS: - primary HT: BMPR-2 mutation⇒ abnormal monoclonal vascular endothelial and SM prolif., 5HTT mutation ⇒ proliferation due to serotonin
- secondary HT: underlying disorder⇒ less vasodilatory agents
- p. a. HT: VSCM dysfunction ⇒ fibrosis⇒ cor pulmonale
- p. v. HT: left heart failure ⇒ pooling ⇒ pulmonary edema + effusions
MORPHOLOGY: - intimal thickening and narrowing of the lumen
- plexiform lesions
CLINICAL FEATURES: - young adult, women
- fatigue, syncope, dyspnea, chest pain
- resp. insuff + cyanosis
- needs lung transplant
14
Q
- Diseases of vascular origin of the lung, atelectasis:
DIFFUSE ALVEOLAR HEMORRHAGE SYNDROMES
A
- primary immune-mediated diseases
- symptoms: hemoptysis, anemia, diffuse pulmonary infiltrates
TYPES: - Goodpasture syndrome
- Idiopathic pulmonary hemosiderosis
- Wegener granulomatosis
15
Q
- Diseases of vascular origin of the lung, atelectasis:
GOODPASTURE SYNDROME
A
- proliferative, rapidly progressing glomarulonephritis + hemorrhagic interstitial pneumonitis
- Type 2 HR ⇒ Antibodies against collagen 4
RISK FACTORS: - HLA- DR15 gene
- infections
- smoking
- oxidative stress
- hydrocarbon-based solvents
MORPHOLOGY: - heavy lungs, red-brown consolidations
- focal necrosis, intra-alveolar hemorrhage, fibrous septal thickening, hypertrophic type 2 pneumocytes, hemosiderin
- Ig deposits in glomerulus
SYMPTOMS: - hematuria, proteinuria
- nephritic syndrome
- cough, hemoptysis
- restrictive lung disease
TREATMENT: - plasmaphoresis + immunosuppressive therapy
- kidney transplant
DIAGNOSIS: - kidney biopsy
16
Q
- Diseases of vascular origin of the lung, atelectasis:
IDIOPATHIC PULMONARY HEMOSIDEROSIS
A
- rare; unknown etiology
- occurs in children
SYMPTOMS: - pulmonary same as Goodpasture
- no kidney involvement or anti-basement membrane AB
TREATMENT: - steroid + immunosuppressive therapy
17
Q
- Diseases of vascular origin of the lung, atelectasis:
WEGENER GRANULOMATOSIS
A
- pulmonary angiitis + granulomatosis
- rare
- immune vasculitis
- PR3-ANCAs
SYMPTOMS: - pulmonary: patchy moving necrotizing vasculitis + parenchymal necrotizing granulomatous inflammation
- cough, hemoptysis, chest pain
- upper airway: sinusitis, epistaxis, nasal perforation
18
Q
- Diseases of vascular origin of the lung, atelectasis:
ATELECTASIS
A
= incomplete expansion of lungs, or collapse of inflated lung
- prevent oxygenation + increases risk for infection
- reversible
TYPES:
1. Neonatal atelectasis
2. Aquired atelectasis
a. Resorption atelectasis:
- obstruction ⇒ oxygen trapped reabsorbed ⇒ alveolar collaps
- asthma, chronic bronchitis, bronchiectasis, postoperative state, foreign body aspiration, neoplasm
b. Compression atelectasis:
- congestive heart failure ⇒ pleural effusion
- pneumothorax
- ascites ⇒ elevated diaphragm ⇒ basal atelectasis
- mediastinum shifts away from atelectatic lung
c. Contraction atelectasis
- fibrotic changes in pleura/lung
19
Q
- Bronchial asthma, emphysema:
OBSTRUCTIVE AIRWAY DISEASE
A
= limited airflow due to increased resistance or complete obstruction
- normal FCV and decreased FEV1 ⇒ ratio FEV1:FCV decreased
DISORDERS:
- asthma
- emphysema
- chronic bronchitis
- bronchiectasis
20
Q
- Bronchial asthma, emphysema:
RESTRICTIVE LUNG DISEASE
A
= decreased lung parenchyma expansion with decreased total lung capacity
- FCV decreased, FEV1 normal ⇒ FEV1:FCV normal
DISORDERS:
1. Chest wall disorders with normal lungs
- severe obesity
- pleural disease
- neuromuscular disorders
- respiratory muscle disease
2. Interstital lung disease
- ARDS
- pneumoconiosis, interstitial fibrosis, sarcoidosis
21
Q
- Bronchial asthma, emphysema:
BRONCHIAL ASTHMA
A
= chronic inflammatory disorder of airways. Obstructive lung disease
CAUSE:
- hygiene hypothesis
- respiratory infections, irritant exposure, cold air, stress, exercise
PATHOGENESIS:
- TH2 reaction ⇒ cytokines ⇒ inflammation
- recurrent inflam ⇒ hypertrophy of SM and mucus glands + increased vascularity + deposition of collagen
MORPHOLOGY:
- overinflation + atelectasis in lungs
- mucus plugs + Curschmann spirals + Charcot Leyden crystals
- thick wall + fibrosis + hypertrophy
CLINICAL FEATURES:
- asthma attack: dyspnea + wheezing + difficult expiration
TREATMENT:
- bronchodilators + corticosteroids
22
Q
- Bronchial asthma, emphysema:
TYPES OF ASTHMA
A
- Atopic asthma
- begins in childhood
- Type 1 HR
- allergic rhinitis, urticaria, eczema
- triggers: environmental Ag, infections
- diagnosis: Allergic skin test, serum radioallergosorbent tests - Non-atopic asthma
- no allergen sensitization
- triggers: viral resp. infection, inhaled air pollutants - Drug-induced asthma
- aspirin!
- rhinitis, nasal polyps, urticaria, bronchospasm - Occupational asthma
- triggers: fumes, organic dusts, gases
23
Q
- Bronchial asthma, emphysema:
EMPHYSEMA
A
= abnormal, permanent enlargement of airspace after terminal bronchioles with wall destruction
- obstructive lung disease
PATHOGENESIS:
- toxin exposure ⇒ inflammation with neutrophil, macrophage + lymphocytes ⇒ elastase, cytokines, oxidants ⇒ epithelial injury + proteolysis of ECM ⇒ loss of septa
- TGFB gene: regulate response to mesenchymal injury
- MMPs
MORPHOLOGY:
- Panacinar: pale, voluminous lungs, obscure the heart
- Centriacinar: deeper pink, less volume, deformed bronchioles
CLINICAL FEATURES:
- dyspnea (coughing + wheezing)
- weigth loss
- decreased FEV1:FCV ratio
- barrel chest
- death due to pulmonary failure or cor pulmonale
24
Q
- Bronchial asthma, emphysema:
TYPES OF EMPHYSEMA
A
- Centriacinar emphysema
- respiratory bronchiole
- both emphysematous + normal air spaces in same acinus
- upper lobes
- associated with tobacco - Panacinar emphysema
- acini uniformly enlarged, resp bronchioles to terminal alveoli
- lower lung areas
- associated with alpha1-antitrypsin deficiency - Distal acinal emphysema
- worse next to pleura, along lobular CT septa + margins of lobules
- next to fibrosis, scarring + atelectasis
- upper lobes
- unknown cause - Irregular emphysema
- acinus irregularly involved
- associated with scarring
- asymptomatic
25
36. Chronic bronchitis, bronchiectasis, cystic fibrosis:
| CHRONIC BRONCHITIS
- obstructive lung disease
- associated with smoking or pollution
- persistent cough for 3 months in 2 years
PATHOGENESIS:
- hyper secretion of mucus
- toxins ⇒ hypertrophy of mucus glands ⇒ increased goblet cells
- airway obstruction: goblet cell metaplasia + mucus plug + inflammation + wall fibrosis, coexistent emphysema
TYPES:
- simple
- asthmatic
- obstructive
MORPHOLOGY:
- hyperemic and swollen mucosal lining + mucopurulent secretion
- goblet cell metaplasia, mucus plugging, inflammation, fibrosis
- REID index: gland layer to wall ratio, normal 0,4
CLINICAL FEATURES:
- hypercapnia, hypoxemia, cyanosis
- often also emphysema
- complications: pulmonary HT, cardiac failure
26
36. Chronic bronchitis, bronchiectasis, cystic fibrosis:
| BRONCHIECTASIS
= permanent dilation of bronchi due to destruction of muscle and elastic tissue
- obstructive lung disease
PATHOGENESIS:
- obstruction ⇒ blocks normal clearance ⇒ infection
- chronic infection ⇒ weakening + dilation of walls
MORPHOLOGY:
- lower lobes on both sides
- dilated up to 4x
- active: inflammatory exudate in walls, ulceration
- chronic: peribronchiolar fibrosis, wall fibrosis
- abscess cavity ⇒ aspergilloma formation
CLINICAL FEATURES:
- cough, mucopurulent sputum, hemoptysis
- symptoms are episodic
- clubbing of fingers
- hypoxemia, hypercapnia, HT, cor pulmonale, metastatic brain abscess, reactive amyloidosis
27
36. Chronic bronchitis, bronchiectasis, cystic fibrosis:
| PREDISPOSING CONDITIONS TO BRONCHIECTASIS
1. Broncial obstruction
- tumors, foreign bodies, mucus plug
2. Congenital condition
- cystic fibrosis
- immunodeficiency states
- Kartagener syndrome (AR disorder, bronchiectasis + male sterility)
3. Necrotizing pneumonia
- associated with virulent organisms
- posttuberculosis
28
37. Diffuse alveolar damage, pneumoconiosis:
| DIFFUSE ALVEOLAR DAMAGE DAD
```
- restrictive lung disease
= histological patterns of ARDS
PATHOGENESIS:
- Alveolar capillary membrane injury ⇒ direct (pneumonia or aspiration of gastric content) or indirect (sepsis, severe trauma) ⇒ hyaline membrane + loss of diffusion capacity + surfactant abnormalities
MORPHOLOGY:
1. Acute phase
- dark red, firm, airless, heavy
- congestion, necrosis, edema, hemorrhage
- hyaline membrane
2. Organized phase
- profile of type 2 pneumocytes
- organization of fibrin exudate⇒ thick alveolar septa
CLINICAL FEATURES:
- 40% mortality with treatment
```
29
37. Diffuse alveolar damage, pneumoconiosis:
| PNEUMOCONIOSIS
- restricitve lung disease
- occupational disease, inhalation of dust
PATHOGENESIS:
- reaction to dust depend on: size, shape, solubility, reactivity of the particles
- particles trapped in alveolar bifurcations ⇒ macrophage accumulation + endocytosis ⇒ release inflammatory mediators ⇒ fibroblast proliferation and collagen deposition
MINERAL DUSTS:
- coal dust
- silica
- asbestos
30
37. Diffuse alveolar damage, pneumoconiosis:
| COAL WORKER PNEUMOCONIOSIS
```
- coal= carbon + trace metals + inorganic minerals + crystalline silica
MORPHOLOGY:
1. Pulmonary antracosis
- inhaled carbon pigment engulfed by macrophages ⇒ accumulates in CT along lymphatics or in LN
- benign + no change in lung function
2. Simple CWP
- coal macules + coal nodules
- upper zones of lungs
- centrilobular emphysema
3. Complicated CWP
- melding of coal nodules
- black scars >2cm
- histo: dense collagen + pigment
- pulmonary dysfunction, HT and cor pulmonale
```
31
37. Diffuse alveolar damage, pneumoconiosis:
| SILICOSIS
CAUSE:
- inhalation of crystalline silica (toxic + fibrinogenic)
PATHOGENESIS:
- silica + macrophage ⇒ activation + release of mediators⇒ fibrinogenesis
- silicotic nodule: concentrally arranged hyalinized collagen fibers with amorphous center
MORPHOLOGY:
- fibrotic nodules + massive fibrosis alveolar proteinosis
- detect via chest radiograph
- susceptibility to tuberculosis
32
37. Diffuse alveolar damage, pneumoconiosis:
| ASBESTOSIS
```
CAUSE:
- asbestos: crystalline hydrate silicates with fibrous geometry
PATHOGENESIS:
- inhalation ⇒ macrophage ⇒ fibrosis
- tumor initiator and promoter
MORPHOLOGY:
- parenchymal interstitial fibrosis
- localized fibrous plaques
- pleural effusions
- bronchogenic carcinoma
- pleural and peritoneal mesothelioma
- laryngeal carcinoma
- Asbestos bodies: gold brown beaded rods with translucent center
- begin in lower lobes and move upward
- honeycomb appearance
```
33
38. Pulmonary infections:
| CLASSIFICATION OF PNEUMONIA
1. Clinical data: acute / chronic
2. Histological spectrum
- fibrinopurulent alveolar exudate
- mononuclear interstitial infiltrates
- granulomas and cavitations
3. Patterns
- bronchopneumonia
- lobar pneumonia
4. Clinical feature: atypical / hypostatic
5. Type of infection: community / nosocomial / opportunistic
6. Based on agents: bacterial / viral / fungal
7. Based on host: normal / immunocompromised
34
38. Pulmonary infections:
| COMMUNITY-ACQUIRED PNEUMONIA
```
SYMPTOMS:
- high fever, shaking chills, chest pains, productive mucopurulent cough, hemoptysis
CAUSE:
- S.pneumoniae
⇒ people with chronic diseases
⇒ people with immunoglobulin defect
⇒ people with decreased/absent splenic function
MORPHOLOGY:
- lobar or broncho pneumonia
- lower or right middle lobe
COMPLICATIONS:
- abscess formation
- empyema
- scarring
- dissemination ⇒ meningitis, arthritis, infective endocarditis
DIAGNOSIS:
- sputum + gram staining
```
35
38. Pulmonary infections:
| LOBAR PNEUMONIA STAGES
1. Congestion
- heavy, red and boggy lobes
- vascular congestion, proteinaceous fluid, neutrophils + bacteria in alveoli
2. Red Hepatization
- within few days
- liver like consistency
- alveolar spaces packed with neutrophils, RBCs and fibrin
3. Grey Hepatization
- dry, grey and firm
- fibrinosuppurative exudate in alveoli
4. Resolution
- exudates enzymatically digested ⇒ granular, semi-fluid debris ⇒ macrophages
- pleural reaction ⇒ fibrous thickening
36
38. Pulmonary infections:
| BRONCHOPNEUMONIA morphology
- 3-4cm wide, grey-yellow elevated lesions
| - focal suppurative exudate that fills bronchi, bronchioles and alveoli
37
38. Pulmonary infections:
| LEGIONELLA PNEUMONIA
- causes: Legionnaire's disease + Pontiac fever
- source: water cooling tower, air-conditioning system, water pipes
- transmission: inhalation or aspiration of contaminated water
- risk factors: smoking, renal failure, obstructive pulmonary disease, diabetes
38
38. Pulmonary infections:
| ORGANISMS CAUSING COMMUNITY-ACQUIRED PNEUMONIA
1. H. influenza ⇒ pneumonia in children
2. M. catarrhalis ⇒ elderly, otitis media in children
3. S.aureus ⇒ secondary bacterial pneumonia
4. K.pneumoniae ⇒ debilitated and malnourished people
5. P. aeruginosa ⇒ nosocomial
39
38. Pulmonary infections:
| COMMUNITY ACQUIRED ATYPICAL PNEUMONIA
```
CAUSATIVE AGENTS:
- Mycoplasma pneumoniae
- Chlamydia pneumoniae
- Coxiella burnetti
- viruses
PATHOGENESIS:
- attachment of organism to resp. epith. ⇒ necrosis of cells ⇒ inflammatory response ⇒ damage to mucociliary clearance ⇒ secondary bacterial infection risk
MORPHOLOGY:
- affected areas red-blue + congested
- inflammatory reaction inside alveoli
- alveolar spaces are free of cellular exudates
CLINICAL FEATURES:
- fever, headache, malaise
- cough + little sputum
```
40
38. Pulmonary infections:
| NOSOCOMIAL PNEUMONIA
- hospital aquired
- in patients with underlying disease, immune suppression or prolonged antibiotic therapy
CAUSATIVE AGENTS:
- enterobacteriaceae
- pseudomonas spp
- s.aureus
41
38. Pulmonary infections:
| ASPIRATION PNEUMONIA
- occurs in debilitated patients or those who aspirate gastric content
- partially chemical, partially bacterial
- abcess formation common
CAUSATIVE AGENTS:
- anaerobic oral flora
- s.pneumonia
- s.aureus
- h.influenzae
- p.aerginosa
42
38. Pulmonary infections:
| LUNG ABCESS
```
= collection of pus in a cavity. Result of body's defense reaction to foreign material or pathogen
TRANSMISSION:
- aspiration of infective material
- aspiration of gastric content
- complication of necrotizing bacterial pneumonia
MORPHOLOGY:
- 1mm-6cm
- more common on right side
- tend to rupture into airways ⇒ bronchopleural fistula ⇒ pneumothorax or empyema
CLINICAL FEATURES:
- prominent cough
- smelly, purulent or bloody sputum
- malaise, spiking fevers
```
43
38. Pulmonary infections:
| CHRONIC PNEUMONIA
- localized lesions in immunocompetent person. LN involvement
- granulomatous inflammation
CAUSATIVE AGENTS:
- nocardia
- actinomyces
- mycobacterium tuberculosis
- histoplasma capsulatum, coccidioides immitis, blastomyces dermatitidis
44
38. Pulmonary infections:
| OPPORTUNISTIC INFECTIONS
1. Candida albicans
- part of normal flora in oral cavity, GI, vagina
- Candidasis ⇒ mucus membrane, skin, deep organs
2. Aspergillus
- invasive aspergillosis ⇒ pneumonia
- aspergilloma= fungal balls with micro abscesses
3. Cytomegalovirus
4. Pneumocystis jiroveci
5. Mycobacterium avium
45
39. Pulmonary hypertension, pleural lesions:
| PLEURAL EFFUSION AND PLEURITIS
1. Transudate ⇒ hydrothorax
- increased fluid pressure or decreased colloid oncotic pressure
- cause: CHF
⇒ resorbed
2. Exudate
- cause: suppurative pleuritis, cancer, pulmonary infarction, viral pleuritis
⇒ fibrinous organization
TREATMENT:
- drainage
46
39. Pulmonary hypertension, pleural lesions:
| PNEUMOTHORAX
```
TYPES:
1. Spontaneous pneumothorax
2. Secondary pneumothorax (lung ot thoracic disorder)
3. Traumatic pneumothorax (injury)
COMPLICATIONS:
1. Tension pneumothorax
2. Infection
3. Empyema (pyopneumothorax)
```
47
39. Pulmonary hypertension, pleural lesions:
| HEMOTHORAX
= accumulation of whole blood in the pleural cavity
| - usually complication of ruptured intrathroacic aortic aneurysm
48
39. Pulmonary hypertension, pleural lesions:
| CHYLOTHORAX
= pleural collection of milky lymphatic fluid containing micro globules of lipid
- implies obstruction of major lymph duct, usually intrathoracic cancer
49
39. Pulmonary hypertension, pleural lesions:
| MALIGNANT MESOTHELIOMA
- rare cancer of mesothelial cells
- in parietal or visceral pleura, also peritoneum and pericardium
- cause: asbestos
- latent period: 25-40 years
MORPHOLOGY:
- pleural fibrosis and plaque formation
- begin in localized area ⇒ spread widely
- yellow-white firm gelatinous layer of tumor on top of lung
- rarely metastasize
50
40. Tumors of nasal passages, nasopharynx and larynx:
| NASOPHARYNGEAL CARCINOMA
```
ETIOLOGY:
- strong links to EBV
- Africa ⇒ common childhood cancer
- China ⇒ common adult cancer, 70% male
PATHOGENESIS:
- EBV replicate in mucosal nasopharyngeal epithelium ⇒ infect B cells of tonsils
MORPHOLOGY:
- 3 histological subtypes:
1. well differentiated keratinizing squamous carcinoma
2. moderately differentiated non-keratinizing squamous c
3. undifferentiated type
- spread to cervical LN, metastasize to distant sites
TREATMENT:
- immunotherapy
- radiotherapy
- chemotherapy
- 5 year survival 50%
```
51
40. Tumors of nasal passages, nasopharynx and larynx:
| VOCAL CORD POLYPS
- smooth, hemispherical protruding mass of tissue
- location: true vocal cords
- nodules composed of fibrous tissue and covered by strat. squamous mucosa
- cause: smoking, singing
52
40. Tumors of nasal passages, nasopharynx and larynx:
| LARYNGEAL PAPILLOMA
- benign neoplasm
- location: true vocal cords
- do not become malignant ⇒ often spontaneously regress
- complication: trauma ⇒ ulceration + hemoptysis
- children: recurrent respiratory papillomatosis (HPV 6 and 11, vertical transmission)
- adults: solitary papillomas, usually in men
- Differential diagnosis: verrucous carcinoma
53
40. Tumors of nasal passages, nasopharynx and larynx:
| CARCINOMA OF THE LARYNX
```
- after age 40, more in men 7:1
CAUSE:
- smoking
- alcohol
- asbestos
- HPV
-95% squamous cell carcinoma
LOCATION:
- 60-75% glottic tumors
- 25-40% supraglottic
- <5% subglottic
GROWTH PATTERN:
- in situ lesion ⇒ pearly grey, wrinkled plaque ⇒ ulcerated and necrotized
TREATMENT:
- surgery, radiation, combined therapy
```
54
40. Tumors of nasal passages, nasopharynx and larynx:
| TUMORS OF THE NASAL PASSAGES
- squamous cell carcinoma
- adenocarcinoma
- malignant melanoma
- inverting papilloma
- esthesioneuroblastoma
- midline granuloma
- lymphoma
- sarcoma
55
41. Benign and metastatic tumors of lung:
| HAMARTOMA
- excessive focal overgrowth of cells and tissues native to the organ ⇒ completely benign
- grows in a disorganized mass within normal tissue
- arise from CT
- can compress surrounding tissue
56
41. Benign and metastatic tumors of lung:
| ADENOMAS
- adenomas in the bronchi
- arise from mucous glands and ducts of the trachea or bronchi
- types: alveolar, bronchial gland, papillary, pleomorphic
57
41. Benign and metastatic tumors of lung:
| SOLITARY FIBROUS TUMOR
- rare mesenchymal tumor in pleura
- can be very large
- usually asymptomatic
- Treatment: surgical resection
58
41. Benign and metastatic tumors of lung:
| DESMOID TUMOR
- benign slow growing soft tissue tumor
| - infiltrative, well-differentiated, firm overgrowth of fibrous tissue
59
41. Benign and metastatic tumors of lung:
| CARCINOID TUMOR
- slow growing neuroendocrine tumor
- bronchial carcinoids arise fron Kichitsky cells
- contain dense-core neurosecretory granules
60
41. Benign and metastatic tumors of lung:
| SCLEROSING HEMANGIOMA
- arise from incompletely differentiated resp. epith.
- asymptomatic, peripheral, solitary, well circumscribed
- women around 50 years
- metastasis: regional LN
- histo: surface + round cells
⇒ papillary, sclerotic, solid or hemorrhagic
- treatment: surgical excision
61
41. Benign and metastatic tumors of lung:
| METASTATIC TUMORS
1. breast carcinoma
2. colorectal carcinoma
3. renal cell carcinoma
4. uterine leiomyosarcoma
5. head and neck squamous cell carcinoma
6. malignant melanoma
7. sarcoma
8. lymphoma + leukemia
9. germ cell tumors
62
41. Benign and metastatic tumors of lung:
| METASTASIS FROM LUNGS
1. LN
2. hematogen
3. brain
4. bone
5. liver
6. adrenal gland
7. skin
8. serous membrane
9. other lung
63
42. Malignant lung tumors:
| LUNG CARCINOMAS
```
RISK FACTORS
- smoking
- carcinogens
- radiation therapy
- recurrent inflammation
- talc + talcpowder
SYMPTOMS:
- dyspnea, coughing, weight loss
- age: 50-60
- 5 year survival ⇒ 15%
CLASSIFICATION:
2 therapeutic types:
- small cell lung cancer SCLC
- non-small cell lung cancer NSCLC
4 histological types:
- squamous cell carcinoma
- adenocarcinoma
- small-cell carcinoma
- large-cell carcinoma
- combined patterns
MORPHOLOGY:
- firm and grey-white small lesions
- intraluminal masses, invade bronchial mucosa or bulky masses pushing adjacent lung parenchyma
- central necrosis + hemorrhage
- virchow node involvement
```
64
42. Malignant lung tumors:
| SCLC vs. NSCLC
SCLC:
- neuroendocrine cells, anaplastic cells
- risk factor: smoking
- origin: Kulschitzky cells, stem cells
- therapy: chemo - + radiation therapy
- RB mutation
NSCLC:
- squamous epith cell, adenocarcinoma, large cell carcinoma
- risk factor: smoking
- origin: scc- metaplasia, adc- pneumocyte 2, stem cells
- therapy: surgery
- inactive p16/CDKN2A
65
42. Malignant lung tumors:
| SQUAMOUS CELL CARCINOMA
- more common i men, age 40
- related to smoking
- arise centrally in major bronchi ⇒ spread to local lymph nodes
- preneoplastic lesion ⇒ carcinoma in situ
- histo: well differentiated squamous neoplasm with keratin pearls and intracellular bridges - poor differentiated with minimal residual features of squamous cell
66
42. Malignant lung tumors:
| ADENOCARCINOMA
- malignant form originating from glandular tissue or produced a glandular pattern
- some have mutation in EGFR
- can be central lesions or in the periphery
- grow slowly and form smaller masses
- metastasize a lot in early stage
- forms: acinar, papillary and solid
- precursor lesion: adenomatous hyperplasia AAH
67
42. Malignant lung tumors:
| SMALL CELL CARCINOMA
- pale grey, centrally located masses, send extensions into lung parenchyma
- early involvement of hilar and mediastinal LN
- cells: round-fusiform, little cytoplasm, finely granular chromatin, mitotic figures
- precursor lesions: neuroendocrine cells (Kulschitzky cells)
- cause paraneoplastic syndromes
68
42. Malignant lung tumors:
| LARGE-CELL CARCINOMA
- undifferentiated malignant epithelial tumors
- no cytological features like small cell carcinoma, no glandular or squamous diff.
- cells: large nuclei, prominent nucleoli, moderate amount of cytoplasm
69
42. Malignant lung tumors:
| PANCOAST TUMORS
- location: pulmonary apex
- type: non-small cell lung cancer
- clinical relevance: compress cervical sympathetic ganglion ⇒ Horner syndrome:
⇒ ptosis: drooping of eyelid
⇒ miosis: constriction of pupil
⇒ enophthalmus: sunken in eyes
⇒ anhidrosis: no sweating
+ pain in distribution of ulnar nerve
+ destruction of 1st and 2nd ribs
70
42. Malignant lung tumors:
| CARCINOID TUMORS
= malignant tumors made of cells containing neurosecretory granules
CLASSIFICATION:
1. typical low grade:
- uniform cells with regular round nuclei + salt and pepper chromatin
2. atypical intermediate grade:
- higher mitotic rate + focal necrosis
- more LN and distal metastases
- p53 mutations
ETIOLOGY:
- men around 40 years
MORPHOLOGY:
- originate in main bronchi
- growth patterns:
1. obstructing, polyploid, spherical, intraluminal masses
2. mucosal plaque, penetrates bronchial wall⇒ collar-button lesion
- metastasize to hilar LN
- result in small cell carcinoma
CLINICAL FEATURES:
- asymptomatic
- cough, hemoptysis, infection
- carcinoid syndrome: diarrhea, flushing, cyanosis
71
42. Malignant lung tumors:
| PARANEOPLASTIC SYNDROMES
3-10%
1. PTH related peptide ⇒ hypercalcemia
2. ACTH ⇒ Cushing syndrome
3. inappropriate ADH secretion
4. neuromuscular syndromes
5. clubbing of fingers + hypertrophic pulmonary osteoarthropathy
6. hematological manifestations: DIC, migratory thrombophlebitis
