Resp Flashcards
dilatation of the airway and excess mucus production. caused by tobacco smoke, air pollution.
Histology shows goblet cell hyperplasia and hypertrophy of mucous glands.
Chronic bronchitis
airway dilatation and scarring often occuring in children secondary to respiratory infections. present with cough, sputum, fever. histology shows permanent dilatation of the bronchi.
bronchiectasis
complications of bronchiectasis
recurrent infections, haemoptysis, hypoxia, amyloidosis
smooth muscle hyperplasia of the bronchus with excess mucus production and inflammation. histology shows eosinophils, Curshcmann spirals and Charcot leyden crystals.
Asthma
acinar airspace enlargement and wall destruction. Histology shows loss of alveolar parenchyma distal to the terminal bronchiole.
Emphysema
centrilobular pattern of alveolar parnechyma destruction
smoking
Pan-acinar pattern of alveolar parenchymal destruction
a1-AT
congenital causes of bronchiectasis
PCD, CF, hypogamaglobulinaemia, yellow nail syndrome, young syndrome (rhinosinusitis azoospermia and bronch)
a group of >200 different lung pathologies characterised by inflammation and fibrosis of pulmonary connective tissue, particularly the peripheral and delicate alveolar wall tissue.
shows a RESTRICTIVE pattern on spirometry
Interstitial lung disease
diffuse interstitial fibrosis/pneumonia with some cystic changes, leads to loss of normal lung architecture with honeycomb appearance. begins at the peripheries. Affects older patients, present with exertional SOB and non-productive cough.
Cryptogenic Fibrosing alveolitis (idiopathic pulm fibrosis)
presents with exertional SOB, cough, cyanosis, pulm HTN and clubbing.
may be associated with inflammatory disease i.e RA SLE
Progressive disease - over 50% die within 2-3years
Rx of cryptogenic fibrosing alveolitis (IPF)
steroids
azathioprine
cyclophosphamide
(SAC - cus it forms little cyst sacs)
an occupational lung disease that typically affects the upper lobe. often called dusty lung as its caused by inhalaation of mineral dusts or inorganic particles. Coal workers typically affected. leads to permanent alteration to the lungs structure.
Pneumoconioses
can cause benign lesions such as plaques and fibrosis, or malignant lesions such as mesothelioma, adenocarcinoma. tends to affect the lower lobe.
Asbestosis
Macrophages, pigment and fibrosis seen on lungs. fibrotic nodules. history of working in coal industry.
Coal workers pneumoconiosis
a group of immune mediated lung disorders caused by prolonged or intense exposure to inhaled organic antigens, leading to widespread alveolar damage
Eosinophilic interstitial lung diseases (EAA)
an occupational lung disease that can have a chronic or acute form.
histologically there is presence of polypoid plugs, loose connective tissue within alveoli and bronchioles, leading to granuoloma formation and organising pneumonia.
Extrinsic allergic alveolitis
inhaled antigenic dust in a sensitised indivudial leading to systemic symptoms such as fever, chills, chest pain, sob and cough) within hours of exposure. usually settles by the following day.
Acute EEA - can progress to chronic
early recognition is vital in prevention of progression to fibrosis by removal of antigenic trigger
Persistent productive cough, SOB, loss of weight and finger clubbing. symptomatic whenever they are at work.
Chronic EEA.
EEA caused by mouldy grain, hay, silage - saccharopolyspora rectiv
Farmers lung
pigeon exposure, protein in excreta/feathers
pigeon fanciers lung
heated water reservoirs
humidfiers lung
germinating barley - aspergillus clavatus/fumigatus
malt-workers lung
mouldy cheese - aspergillus clavatus
cheese washers lung
risk factors for lung cancer
asbestos, heavy metals, genetics, susceptibility genes, smoking
makes up the majority of lung cancers, M>F, closely correlated with smoking.
p53 and c-myc mutations often present
usually found in the central/proximal bronchi with local spread and late mets.
squamous cell carcinoma
associated with p53, cmyc, p63 and CK5/6
histology shows keratinisation and intercellular prickles
most common lung ca in women and nonsmokers. glandualr differentiation, mucus production. often occurs peripherally and mets early. EGFR mutations.
Adenocarcinoma —- e(G)fr - Glandular
mets early to the alveolar walls, leads to breakdown of elastin wall –> desmoplasia, ANGULAR glands
Rx - TARCEVA - anti-EGFR
80% present with advanced disease. occurs centrally in the proximal bronchi. arises from neuroendocrine cells. associated with paraneoplastic syndromes.
highly malignaant, mets early - bone brain adrenal liver
strong association with smoking. p53 and RB1 mutations.
Small cell carcinoma
poor prognosis despite being very chemosensitive due to rapid mets.
poorly differentiated
poorly differentiated malignant epithelial tumour. large cells with large nuclei and prominent nucleoli.
large cell carcinoma
poor prognosis
EGFR mutations, non-smokers. Histology shows cells containing mucin vacuoles. poor prognosis.
adenocarcinoma
lung cancer associated with ectopic ACTH secretion. Lambert Eaten and cerebellar degeneration. poor prognosis.
Small cell carcinoma
assocaited with p53 and cmyc mutations, can secrete ectopic PTH. various subtypes - papillary, basaloid.
Squamous cell carcinoma
paraneoplastic serotonin secretions leads to
Carcinoid syndrome - flushing, diarrhoea, bronchoconstriction
ERCC1 mutation
poor response ot cisplation
EGFR
adenocarcinoma. good target for TKI therapy - young patients non smokers
K Ras
assocaited with adeno and squamous cell carcinoma. usually poor prognosis
parietal or visceral pluera, spreads wiudely within the pleural space. associated with extensive pleural effusion, chest pain, and dyspnoea. Long latent period (25-45 years)
Mesothelioma.
<1% of lung ca, poor prognosis.
asbestos related. epitheloid or sarcomatoid.
peripheral wedge infarctions
small pulmonary emboli
causes pleuritic chest pain
acute cor pulmonale and cardiogenic shock
large emboli in the main pulm arteries
mean pulmonary artery pressure at rest
25mmHg
complications of pulmonary hypertension
right sided heart ailure, venous congestion of organs, nutmeg liver, plueral effusions, decreased lung perfusion
intra-alveolar fluid accumulation leading to poor gas exchange. histology shows iron laden macrophages and intraalveolar fluid
pulmonary oedema
main aetiology LHF
diffuse alveolar and endothelial damage. result in rapid onset resp failure. congested, expanded, firm plum coloured lungs on histology, airless, weigh >1kg. High mortality and morbidity.
ARDS
