16. Pulmonary Pathology Flashcards
What is an acinus/terminal respiratory unit?
Briefly describe the trachea, bronchi, bronchioles, alveolar ducts and alveolar sacs (in terms of cartilage, mucous, glands, cilia etc).
Functional unit of respiratory tract distal to terminal bronchioles. Many lobed sacs containing groupings of alveoli.
Trachea: C-shaped cartilage rings (allows trachea to collapse slightly to allow food to pass down oesophagus), mucous glands
Bronchi: discontinuous cartilage plates, mucous glands
Bronchioles: NO cartilage or mucous glands, terminal bronchioles <2mm diameter, respiratory bronchioles where GE begins.
Alveolar ducts: flat epithelium, no glands or cilia
Alveolar sacs: no glands or cilia.
Breifly describe the following diseases of vascular origin:
a) Pulmonary oedema
b) Diffuse alveolar damage (ARDS (adult resp distress syndrome); shock lung)
c) Emboli and infarction
d) Pulmonary hypertension
a) Haemodynamic, usually cardiogenic (blockage in pulmonary vasculature/IHD). Heavy wet lungs. Alveolar pink granular fluid, may contain haemosiderin - laden macrophages (‘heart failure cells’). Resolution or ‘brown induration’ if long-standing.
b) Oedema caused by injury to alveolar capillary endothelium. Triggered by shock, trauma, sepsis, viral infections, noxious gases, radiation and others. Rapidly developing life-threating respiratory insufficiency. Oedema fluid and fibrinous membranes lining alveoli. Does not resolve -> severe scarring. (pic - thick fibrin layer - too thick for GE)
c) Pulmonary artery occlusion by circulating clots usually from the lower limb veins in bedridden. Large saddle emboli are immediately fatal - lodge at bifurcation of pulmonary trunk. Smaller emboli lodge peripherally and result in characteristic wedge-shaped infarcts - only a problem if many.
d) Pulmonary circulation is low resistance. Increase in pressure can be 2o to COPD, L heart valvular disease or recurrent thromboemboli. This causes R ventricular hypertrophy and failure - ‘chronic cor pulmonale’.
Distinguish between obstructive and restrictive pulmonary disease (incl. FEV1).
What are COPDs? List the main 4.
Obstructive aka airway disease: increased resistance to airflow at any level, no decrease in lung capacity, reduced FEV1. Airway narrowing/loss of recoil.
Restrictive: reduced expansion of lung parenchyma, decreased TLC with proportionate reduction in FEV1. Chest wall disorders or interstitial/infiltrative diseases.
A group of diseases characterised by obstruction to air flow - intermittent, reversible or irreversible; at any level of the respiratory tract. COPDs include: chronic bronchitis, emphysema, bronchial asthma, bronchiectasis (permanent enlargement of parts of the airways of the lung).
Chronic bronchitis and emphysema are almost always co-existant and entirely due to smoking. Explain:
a) chronic bronchitis incl. clinical definition and symptoms
b) emphysema inc. pathological definition and symptoms
Describe the 4 different types of emphysema.
a) Clinical definition: ‘productive cough >3 months in 2 consec yrs’. Mucous gland hypertrophy, mucus hypersecretion +/- infection. Progressive. Hypoxia, hypercapnia and cyanosis-prone. “Blue bloater”.
b) Pathological definition: ‘permanent dilation of airways distal to terminal bronchiole’. Centriacinar/paracinar/irregular. Elastin destruction leading to loss of recoil -> protein replaced with collagen. Tend to hyperventilate; normal blood gases. “Pink puffer” - have to actively expire.
1) Centriacinar: central/proximal parts of resp bronchioles affected; distal spread; seen in smokers.
2) Panacinar: uniform dilation of acini from resp bronchiole to alveoli, seen in A1AT deficiency.
3) Paraseptal (distal acinar): peripheral, along lung margins; occurs adjacent to scarring, collapse or fibrosis; predisposes to spontaneous pneumothorax in young adults.
4) Irregular: irregular involvement of acini; seen with scarring.
What is the protease (e.g. elastase)-antiprotease (e.g. alpha-antitrypsin) hypothesis for emphysema pathogenesis?
What does the picture on the L, and the 2 on the R show?
What is brochial asthma?
Imbalance between these results in destruction of elastin. Both smoking (via O2 free radicals) and congenital A1AT deficiency can result in this imbalance -> elastic damage -> emphysema. (pic)
L: peripheral emphysema, subpleural bullae - can burst -> tension pneumothorax!
R: centrilobular emphysema (bottom - massively dilated alveoli in middle, smaller normal one to the left)
Increased irritability of bronchial tree. Paroxysms of reversible bronchospasm. Commonest: ‘Atopic’ caused by type 1 hypersensitivity to common allergens e.g. pollon, house dust. Others: aspirin-induced, occupational, infection (allergic bronchopulmonary aspergillosis).
What is bronchiectasis? What are the symptoms/signs, and complications?
Restrictive lung diseases are a heterogenous group. What are they characterised by? What are some physiological changes? What might you see on a CXR?
Permanent dilation of bronchi and bronchioles with necrosis of their walls. Usually follows obstruction or childhood viral pneumonia. Airways become saclike, filled with foul smelling pus. Chronic paroxysmal cough, typically brought on by posture change. Copious foul smelling sputum. Complications: abscess, fibrosis, amyloid, clubbing, cor pulmonale. (pic - L = dilated segment, pus filled)
Diffuse and chronic damage to delicate pulmonary interstitium: basement membranes, collagen fibres, elastic tissue fibroblasts, few leucocytes. Physiological changes: reduced O2 diffusing capacity, lung volume and compliance. 15% of non-infectious resp illness. CXR: diffuse infiltration by small nodules, irregular lines or ground glass shadows.
List some causes of restrictive lung diseases.
What is occupational lung disease? What are the 2 broad mechanisms of lung injury?
Give 4 examples of occupational lung diseases.
Environmental diseases incl. occupational (25%). Sarcoidosis (20%). Collagen vascular diseases (10%). Idiopathic pulmonary fibrosis (15%). Over 100 other.
Diseases caused by inhalation of dust particles, mineral or organic substances over many yrs due to occupational exposure. Diffuse, interstitial, restrictive. Legal implications. 2 mechanisms:
1) Scarring from chronic irritation: inert substances eg. coal workers’ pneumoconiosis
2) Hypersensitivity: organic dusts
1) Coal workers’ pneumoconiosis: anthracosis, macules, progressive massive fibrosis
2) Silicon (foundry work, sandblasting): silicosis, Caplan’s syndrome
3) Asbestos (mining, building, insulation): asbestosis, pleural plaques, Caplan synd, mesothelioma, Ca lung, lx, stomach, colon
4) Farmers’ lung, bagassosis, byssinosis, bird breeders’ lung etc. due to organic dusts
What is sarcoidosis?
What can cause lung (bronchogenic) cancer?
Describe how lung cancer develops (cell-wise).
Systemic disease of unknown cause characterised by non-caseating granulomatous reaction in many tissues, lungs involved 99%. Varying severity; may be found incidentally/present with resp or constitutional symptoms. Course with steroid therapy = unpredictable. (L pic)
Direct cause = smoking (>1200 potential carcinogens in smoke, can cause lip, tongue, mouth floor, larynx, oesophagus, bladder, pancreas and kidney cancer). Others: asbestos, mineral dusts, radiation, pollution, scarring (?). Commonst site of 2o. Commonest malignancy of West.
(R pic - response to any tissue constantly being injured = metaplasia: cells replace cells with more hardy ones. When smoke and damage -> metaplasia -> susceptible to oncogenic activity.)
What are the 4 main different histological classifications of lung cancer (bronchogenic carcinoma)?
How are small cell carcinomas (SCLC) and non-small cell carcinomas (NSCLC) treated?
What are some local and general clinical features of LC?
1) Squamous cell carcinoma (25-40%)
2) Adenocarcinoma (25-40%) (gland cells) (top pic)
3) Small cell (oat cell) carcinoma (20-25%) (bottom pic)
4) Large cell carcinoma (10-15%)
And others.
SCLC: not treatable surgically; usually widely disseminated at time of dx; rx chemotherapy. V. agressive
NSCLC: surgically treatable. Targeted tx now
Local: cough, haemoptysis, pain
General: wt loss, clubbing, hypertrophic pulmonary osteoarthropathy
Paraneoplastic syndrome: due to extopic hormone production by tumour cells e.g. hypercalcaemia, SIADH
What is the prognosis for lung cancer?
What does this image show?
Staging most important determinant of outcome. Overall 5yr survival < 10%.
Honeycomb lung - seen with widespread fibrosis, defined by presence of small cystic spaces with irregularly thickened walls composed of fibrous tissue. Dilated and thickened terminal and respiratory bronchioles produce cystic airspaces = honeycomb appearance on CXR.
