Respiratory tract Flashcards
- Infection of upper respiratory tract:
3 TYPES OF RHINITIS
- 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
- Infection of upper respiratory tract:
SINUSITIS
- Acute sinusitis
- from rhinitis
- agent in oral cavity
- non-specific inflammation
- complication: empyema - Chronic sinusitis
- due to mixed microflora infection (bad-mucormycosis)
- Infection of upper respiratory tract:
ACUTE PHARYNGITIS
- 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
- Infection of upper respiratory tract:
TONSILLITIS
- symptoms: sore throat, fever, enlarged and red tonsils, dotted exudate
- cause: common cold viruses, s.pyogenes
- chronic tonsillitis rare
- Infection of upper respiratory tract:
STREPTOCOCCAL TONSILLITIS COMPLICATIONS
- peritonsillary abscesses (quinsy)
- poststreptococcal glomerulonephritis
- acute rheumatic fever
- Infection of upper respiratory tract:
OTITIS MEDIA
= 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
- Infection of upper respiratory tract:
INFECTIOUS AGENTS
- Croup: Parainfluenza virus ⇒ laryngo-tracheo-bronchitis in children
- Diphteria: Corynebacterium ⇒ pseudomembrane
- Acute epiglottitis ⇒ H.influenzae
- Tonsillitis ⇒ Beta hemolytic strep
- Tuberculosis
- Inflammation of trachea and larynx:
TRACHEITIS
- 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
- Inflammation of trachea and larynx:
LARYNGITIS
= 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
- Diseases of vascular origin of the lung, atelectasis:
PULMONARY EMBOLISM, HEMORRHAGE AND INFARCTION
- > 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
- Diseases of vascular origin of the lung, atelectasis:
RISK FACTORS FOR DEEP VEIN THROMBOSIS
- prolonged bedrest
- surgery
- severe trauma
- congestive heart failure
- partition or oral contraceptive use
- disseminated cancer
- primary disorders of hyper coagulability
- Diseases of vascular origin of the lung, atelectasis:
CONSEQUENCES OF OCCLUSION OF MAJOR VESSEL
- sudden increase in pulmonary pressure
- decreased CO
- right sided heart failure
- hypoxemia
- death
- Diseases of vascular origin of the lung, atelectasis:
PULMONARY HYPERTENSION
- 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
- Diseases of vascular origin of the lung, atelectasis:
DIFFUSE ALVEOLAR HEMORRHAGE SYNDROMES
- primary immune-mediated diseases
- symptoms: hemoptysis, anemia, diffuse pulmonary infiltrates
TYPES: - Goodpasture syndrome
- Idiopathic pulmonary hemosiderosis
- Wegener granulomatosis
- Diseases of vascular origin of the lung, atelectasis:
GOODPASTURE SYNDROME
- 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
- Diseases of vascular origin of the lung, atelectasis:
IDIOPATHIC PULMONARY HEMOSIDEROSIS
- rare; unknown etiology
- occurs in children
SYMPTOMS: - pulmonary same as Goodpasture
- no kidney involvement or anti-basement membrane AB
TREATMENT: - steroid + immunosuppressive therapy
- Diseases of vascular origin of the lung, atelectasis:
WEGENER GRANULOMATOSIS
- 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
- Diseases of vascular origin of the lung, atelectasis:
ATELECTASIS
= 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
- Bronchial asthma, emphysema:
OBSTRUCTIVE AIRWAY DISEASE
= limited airflow due to increased resistance or complete obstruction
- normal FCV and decreased FEV1 ⇒ ratio FEV1:FCV decreased
DISORDERS:
- asthma
- emphysema
- chronic bronchitis
- bronchiectasis
- Bronchial asthma, emphysema:
RESTRICTIVE LUNG DISEASE
= 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
- Bronchial asthma, emphysema:
BRONCHIAL ASTHMA
= 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
- Bronchial asthma, emphysema:
TYPES OF ASTHMA
- 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
- Bronchial asthma, emphysema:
EMPHYSEMA
= 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
- Bronchial asthma, emphysema:
TYPES OF EMPHYSEMA
- 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
- 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
- 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
- Chronic bronchitis, bronchiectasis, cystic fibrosis:
PREDISPOSING CONDITIONS TO BRONCHIECTASIS
- Broncial obstruction
- tumors, foreign bodies, mucus plug
- Congenital condition
- cystic fibrosis
- immunodeficiency states
- Kartagener syndrome (AR disorder, bronchiectasis + male sterility) - Necrotizing pneumonia
- associated with virulent organisms
- posttuberculosis
- 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
