Respiratory pathology Non-neoplastic Flashcards
The respiratory system
Upper airways: nose, accessory air sinuses, nasopharynx, larynx
Lower airways: trachea, bronchi, bronchioles, terminal bronchioles, alveoli
Pleura
Infection upper airways
acute inflammatory process that affects mucous membranes of the respiratory tract
Includes: rhinitis, laryngitis, tonsilitis sinusitis
Symptoms: malaise, headache, sore throat, discharge
Aetiology
Commonly viral
Can get secondary bacterial infection
Lower airways: infectionPNEUMONIA
Inflammation of the lung parenchyma - Consolidation of the affected part - Exudate with inflammatory cells and fibrin in the alveolar air spaces Causes: infectious agents inhalation of chemicals chest wall trauma Setting: Community acquired Hospital acquired Aspiration pneumonia Chronic pneumonia Necrotizing pneumonia and lung abscesses Pneumonia in the immunocompromised host
Pneumonia clinical features
Fever, rigours, SOB, pleuritic chest pain, purulent sputum, cough
Pneumonia Morphology
Lobar
Multifocal/lobular (bronchopneumonia)
Interstitial (focal diffuse)
Community acquired pneumonia
Relatively common, especially in elderly population
Strep. pnuemoniae most common organism
Haemophilus influenzae
Staph aureus- complicates viral infection and in IVDU
Lobar or bronchopneumonia
Hospital acquired pneumonia
Aka nosocomial pneumonia
Any pneumonia contracted by patient at least 48-72hrs after admission
Usually bacterial- gram negative bacilli and Staph aureus
Severe and can be fatal- most common cause of death in ITU
Fever
Increased white cell count
Cough with purulent sputum
Chest X-ray changes
Aspiration pneumonia
Develops after inhalation of foreign material.
Elderly, Strokes, Dementia, Anaesthetic
Usually right middle and right lower lobe
Oral flora +/- other bacteria
Obstructive disease
Characterised by partial or complete obstruction at any level from the trachea to respiratory bronchioles
PFT: limitation of maximal airflow rate during forced expiration FEV1
Restrictive disease
Characterised by reduced expansion with decreased total lung capacity,
FVC is reduced: amount of air that can be blown out after maximal inspiration
COPD - Emphysema
Irreversible enlargement of the airspaces distal to the terminal bronchiole - destruction of their walls without obvious fibrosis
Types: centriacinar / panacinar / paraseptal / irregular
Pathogenesis:
mild chronic inflammation throughout the airways
protease – antiprotease imbalance hypothesis
+ imbalance of oxidants and antioxidants
role of smoking and genetics
Emphysema- morphology and clinical course
Morphology: voluminous lungs large alveoli, large apical bullae or blebs
Clinical course - symptoms:
dyspnoea, cough, wheezing, weight loss
expiratory airflow limitation – “pink pufferrs”
death due to cor pulmonale,
congestive heart failure, pneumothorax
COPD – chronic bronchitis
persistent cough with sputum production
for at least 3 months in at least 2 consecutive years
without any other identifiable cause
- long-standing irritation by inhaled substances (e.g tobacco smoke, dust from grain, cotton, silica)
- hypertrophy of submucosal glands in trachea and bronchi, increase in goblet cells
- mucus hypersecretion + alterations in the small airways chronic airway obstruction
Chronic bronchitis - Morphology and clinical course
Morphology
mucous membrane hyperaemia, swelling, oedema
excessive mucous/mucopurulent excretions,
narrowing of the bronchioles caused by mucus plugging, inflammation and fibrosis,
may cause obliteration in severe cases
Clinical course
persistent cough productive of sputum
dyspnea on exertion
hypercapnia, hypoxemia, mild cyanosis (“blue bloaters”)
Leads to cor pulmonale, cardiac failure, may cause atypical metaplasia/dysplasia
Asthma
Chronic inflammatory disorder of the airways
recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the early morning.
widespread but variable bronchoconstriction and airflow limitation
At least partly reversible (spontaneously/with treatment).
Hallmarks: increased airway responsiveness episodic bronchoconstriction, inflammation of bronchial walls, increased mucus secretion
Types: extrinsic (response to inhaled antigen – atopic, occupational) intrinsic (non-immune mechanisms – cold, exercise,aspirin). Atopic best understood
Asthma - morphology and clinical course
Morphology
lung overinflation + small areas of atelectasis,
thick mucus plugs in bronchi and bronchioles,
airway remodelling
Clinical course
chest tightness, wheezing, dyspnea, cough +/- sputum
status asthmaticus
increase in airflow obstruction, difficulty with exhalation
Bronchiectasis
Permanent destruction and dilatation of the airways associated with severe infections or obstructions:
Aetiology: CF, kartageners, post infectious: TB, measles, bronchial obstruction eg TB/FB
Morphology: dilated, inflamed airways.
Clinical course: persistent cough, purulent sputum +++, haemoptysis,
Restrictive lung disease
Heterogenous group of diseases
Characterised by inflammation and fibrosis of the pulmonary connective tissue (eg interstitium of the alveolar walls)
most common causes- sarcoidosis and occupational/environmental
Restrictive lung disease - morphology and clinical features
Morphology
Xray: bilateral infiltrative lesions - small nodules, irregular lines, ground-glass shadows
Scarring and gross destruction of the lung - end-stage/honeycomb lung
Clinical features
dyspnea, tachypnea, end-inspiratory crackles,
eventual cyanosis, without wheezing
reductions in gas diffusing capacity, lung volume, and compliance
May lead to secondary pulmonary hypertension and right-sided heart failure with cor pulmonale
Pulmonary Embolism
Blockage of a main or branch pulmonary artery by an embolus –
Usual source of emboli are deep venous thrombi of the leg (95% of cases)
Pathophysiology: respiratory compromise and haemodynamic compromise
Pulmonary embolism - morphology and clinical course
Morphology central/peripheral emboli pulmonary haemorrhage pulmonary infarction Clinical course abrupt onset pleuritic chest pain, shortness of breath hypoxia increased pulmonary vascular resistance – right ventricular failure
Pulmonary oedema
Accumulation of fluid in the air spaces and parenchyma of the lungs - Haemodynamic oedema Increased venous pressure Eg left ventricular failure Decreased oncotic pressure Eg nephrotic syndrome Liver failure - Oedema due to alveolar injury infections Shock/trauma - Oedema of undetermined origin Eg neurogenic/high altitude
Pulmonary oedema - morphology and clinical features
Morphology
initial fluid accumulation in basal regions – dependent oedema
engorged alveolar capillaries, intra-alveolar granular pink precipitate
alveolar microhaemorrhages, hemosiderin-laden macrophages
heavy, wet lungs
Clinical features
SOB, pink frothy sputum, characteristic CXR findings
Pneumothorax
Pneumothorax
Air in the pleural cavity
Associated with ephysema, asthma, TB, trauma, idiopathic
