respiratory Flashcards
what does ABPA stand for?
what is it?
allergic bronchopulmonary aspergillosis
asthma triggered by exposure to aspergillus fungus
what are the 4 types of hypersensitivity reactions?
incl. time before clinical signs, molecular characteristics + examples
type 1 - Anaphylaxis/Allergy/Atopy
- <30mins
- IgE, degranulation of mast cells
- hay fever/asthma/allergy/etc
type 2 - antiBodies
- 5-12hrs
- antigen -> formation of IgM + IgG antiBodies which destroy target cells which have antigen
- transfusion reactions/Rh incompatability
type 3 - immune Complex
- 3-8hrs
- antibodies + antigens form complexes that cause damaging inflammation
- SLE/RA/serum sickness
type 4 - Delayed cell-mediated reaction
- 24-48hrs
- antigens activate T cells (all others are B cell related)
- transplant rejection/contact dermatitis (eg poison ivy)
what are 3 changes seen in chronic asthma?
- bronchiolar wall smooth muscle hypertrophy
- mucus gland hyperplasia
- resp bronchiolitis -> centrilobular emphysema
bronchiectasis:
- what is it?
- causes? 5
- signs/symptoms? 3
PERMANENT dilation of bronchi + bronchioles dt destruction of the muscle + elastic tissue
- infections (TB, fungal, without Abx)
- CF
- kartagener syndrome (aka primary ciliary dyskinesia)
- bronchial obstruction (tumour, foreign body)
- autoimmune conditions (lupus, RA, IBD, GVHD)
- long-standing cough
- intermittent fever
- copious amounts of foul-smelling sputum
what is the technical definition of chronic bronchitis?
cough + sputum for 3 months in each of 2 consecutive years
what is the pathology of chronic bronchitis?
- mucus gland hyperplasia + hypersecretion
- secondary infection by low virulence bacteria
- chronic inflammation
chronic inflammation of small airways -> wall weakness + destruction -> centrilobular emphysema
what are the types of emphysema seen in:
- smokers?
- people with a1-antitrypsin deficiency?
smokers:
- centrilobular (aka centiacinar)
a1-antitrypsin deficiency
- panlobular (aka panacinar)
what are the differences between COPD which is predominantely bronchitis and that which is predominant emphysema:
- age?
- dyspnoea?
- cough?
- infections?
- CXR findings?
- stereotype?
predominantely bronchitis:
- age 40-45
- dyspnoea: mild
- cough: lots, copius sputum
- infections: common
- CXR findings: prominent vessels, large heart
- stereotype: ‘blue bloater’
predominant emphysema
- age 50-75
- dyspnoea: severe
- cough: not as much, scanty sputum
- infections: rare
- CXR findings: small heart, hyperinflated lungs
- stereotype: ‘pink puffer’
chronic bronchitis + emphysema in coal miners
- what is it? (legally)
- how many years of work qualify?
- what does degree of compensation depend on? 2
UK prescribed occupational disease in coal miners
- chronic bronchitis +/or emphysema
> 20 years underground work
- degree of disability
- smoking history
nb no CXR or history of dust exposure needed
what features are common to all interstitial lung diseases? 3
- increased tissue in alveolar-capillary wall (-> increased gas diffusion distance)
- inflammation -> fibrosis
- decreased lung compliance
acute interstitial pneumonia/pneumonitis:
- what is it?
- cause?
- treatment?
- similar to?
acute diffuse damage to interstitium of lungs
- short period between beginning of symptoms to resp failure
idiopathic
mechanical ventilation + corticosteroids
- but prognosis poor, only cure is transplant
acute/adult respiratory distress syndrome (ARDS) - aka ‘shock lung’
chronic interstitial lung diseases:
- symptoms? 2
- signs? 2
- end-stage sign?
- examples? 3
symptoms:
- increasing dyspnoea (for years)
- dry cough
signs:
- clubbing
- fine crackles
end-stage sign = ‘honeycomb lung’
examples:
- idiopathic pulmonary fibrosis
- many pneumoconioses
- sarcoidosis
- collagen vascular diseases-associated lung diseases
idiopathic pulmonary fibrosis:
- which lobes first + worst affected?
- histology?
- histology same as? 2
lower lobes affected first + most severely
interstitial chronicinflammation + variably mature fibrous tissue
- adjacent normal alveolar walls
- collagen vascular disease-associated interstitial lungdisease
- asbestosis
sarcoidosis in lungs:
- pathology?
- other organs that can be affected?
- what else affected?
- often mistaken for?
- blood test results? 2
- normally seen in?
non-caseating pulmonary granulomas
- skin
- heart
- brain
- liver
- hilar lymph nodes
mistaken for TB
- granulomas are necrotic in TB, not in sarcoidosis
- hypercalcaemia
- high serum ACE
young adult women
definition of pneumoconioses?
non-neoplastic lung diseases due to inhalation of mineraldusts, organic dusts, fumes + vapours
- often occupational
aka ‘the dust diseases’
what is cor pulmonale?
the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance (such as from pulmonic stenosis) or high blood pressure in the lungs
silicosis:
- cause?
- people affected? 2
- pathology?
- increased risk of?
exposure to silica - sand + stone dust
- stone masons
- building site workers
fibrosis + very discrete fibrous silicotic nodules (also found in adjacent lymph nodes)
- lung cancer
hypersensitivity pneumonitis:
- aka?
- type of hypersensitivity reaction?
- two examples of types?
- pathology?
- can lead to?
extrinsic allergic alveolitis
type 3 (immune Complex)
- ‘farmer’s lung’ - antigens in hay
- ‘pigeon fancier’s lung’ - bird antigens
inflammation around bronchioles, with poorly formed non-caseating granulomas extends alveolar walls
repeated episodes -> interstitial fibrosis
nb reversible in early stages
4 major types of primary malignant lung tumours?
- small cell carcinoma
non-small cell:
- adenocarcinoma
- squamous cell carcinoma
- large cell undifferentiated carcinoma
what is the difference between a sarcoma and a carcinoma?
carcinoma: epithelial tissue tumour
sarcoma connective/non-epithelial tissue tumour
causes of lung cancer? 5
- tobacco smoking
- occupationa/industrial hazards (eg asbestos, uranium, nickel)
- radiation (eg radon mining, post atom bomb)
- lung fibrosis
- genetic mutations
lung cancer:
- symptoms? 7
- signs? 3
symptoms:
- haemoptysis
- cough
- breathlessness
- fatigue
- weight loss
- hoarse voice (if recurrent laryngeal nerve)
- horner’s syndrome (symp chain)
signs:
- clubbing
- pleural effusion (if spreads to pleura)
- raised ACTH, ADH + PTH
where does lung cancer commonly metastasise to? 6
how might these present?
- lymph nodes (swollen in neck)
- pleura (pleural effusion)
- liver
- bone (fractures)
- adrenal
- brain (seizures)
what electrolyte disturbances are seen in small cell carcinomas? 3
- hyponatraemia
- hypokalemia
- hypercalcaemia
what is lymphangitis carcinomatosa?
lymphatics within lung are diffusely involved by tumour
what % of lung cancer patients are elligable for surgery?
about 10%
- either cancer not resectable of physically not fit enough (as it’s major surgery), often both as present late
what is the normal lung pleura made up of?
single layer of mesothelial cells (with connective tissue on non-pleural-cavity side)
- on both layers of pleura
secrete hyaluronic acid rich mucinous pleural fluid
what are 7 causes of pleural inflammation?
primary inflammatory diseases
- eg SLE, RA
infections
- norm secondary to pneumonias or TB
- primary coxackie B infection
pulmonary infarction
- secondary to pulm arterial thromboembolism
emphysema
- secondary to ruptured bullae
cancer
therapeutic
- pleurodesis, usually with talc, to treat recurrent pleural effusions or recurrent pneumothoraxes
iatrogenic
- radiotherapy to thorax
- immune reactions to drugs
pleural inflammation:
- names? 2
- symptom?
- sign?
- associated condition?
- can develop into?
pleurisy or pleuritis
pleuritic chest pain
- sharp localised pain exacerbated by breathing
auscultation of a PLEURAL RUB during breathing
often associated pleural effusion
- weak breath sounds on auscultation
- dull on percussion
pleural fibrosis
what are the 2 types of asbestos associated pleural fibrosis?
- level of asbestos exposure?
- symptoms?
- is it elligable for industrial injuries disablement benefit?
parietal pleural fibrous plaques
- low-level exposure
- asymptomatic
- not elligIble
diffuse pleural fibrosis
- high-level exposure
- breathlessness
- elligible
what are the effects of pleural fibrosis?
what procedure can be done to reduce these?
- prevent normal expansion + commpression of lung -> breathessness
pleural decortication
- removal of the fibrous tissue
what is is called when these fluid are in the pleural cavity:
- serous fluid?
- pus?
- blood?
- lymph?
- air?
serous fluid = pleural effusion
pus = empyema/pyothorax (norm secondary to pneumonia)
blood = haemothorax (norm traumatic or secondary to ruptured thoracic aortic aneurysm)
Lymph = chylothorax (norm trauma to thoracic duct)
air = pneumothorax
2 types of pleural effusions = transudates + exudates, what is the difference between them:
- pathology?
- protein content?
- lactate dehydrogenase content?
- causes? (trans = 4, exu = 2)
transudates:
- low capillary osmotic pressure +/or high capillary hydrostatic pressure
- low protein
- low lactate dehydrogenase
- high vascular hydrostatic pressure (LV failure, renal failure)
- low capillary osmotic pressure (hypoalbuminaemia - hepatic cirrhosis, nephrotic syndrome)
exudates:
- pathological capillaries loose semi-permeability
- high protein
- high lactate dehydrogenase
- inflammation (with or without infection)
- cancer
“stuff to do with osmosis forms a transudate, it is just TRAvelling through, so doesn’t leave lots of proteins etc, EXudate can develop into Empyema, everything EXits the capillaries”
treatments for pleural effusions? 4
- aspiration of fluid with needle + syringe (ultrasound guided)
- treat underlying cause (if possible)
- pleural drain (for recurrent effusions)
- pleurodesis (for recurrent effusions)
what are the 2 different types of pneumothorax?
pathologies?
what can both cause?
open pneumothorax:
- chest wall perforation
- normally traumatic
- connects body surface to pleural cavity
- external air -> pleural cavity during inspiration, reducing potential lung expansion
closed pneumothorax
- lung perforation
- usually not traumatic
- connects lung air spaces to the pleural cavity
- lung air -> pleural cavity during inspiration, reducing potential lung expansion
both can cause: tension pneumothorax
- air in during inspiration but not out during expiration
causes of closed pneumothoraxes? 4
ruptured emphysematous bullae
common inflammatory lung diseases
- asthma
- pneumonia
- TB
- CF
traumatic
- lung tears from fractured ribs
iatrogenic
- mechanical ventilation at high pressures
- lung + pleural biopsies
pneumothorax:
- symptoms? 2
- signs? 5
symptoms: (small ones may be asymptomatic)
- breathlessness
- pleuritic chest pain
signs:
- cyanosis
- tachycardia
- tracheal deviation (in tension pneumothorax)
- hyperressonant percussion
- reduced breath sounds on auscultation
what is the most common type of primary pleural neoplasm?
what 2 cancers often metastasise to the pleura?
malignant mesothelioma
- breast
- lung
malignant mesothelioma:
- cause?
- cells/tissues it affects?
- metastasise?
if pleural, 80-90% caused by asbestos
(- thoracic radiation)
(- BRAC1 gene)
mesothelial cells that line serous cavities:
- pleura (92%)
- peritoneum (8%)
- pericardium
- tunica vaginalis
tend not to metastasise widely
- but if they do then go to other lung pleuraor peritoneum etc
how do you diagnose a malignant mesothelioma?
- can use imaging but difficult to identify and thus target biopsies at
if the is an accompanying pleural effusion, malignant cells may be shed into this
- therefore effusion cytology may allow an early tissue diagnosis to be made
nb a small tumour can produce a large pleural effusion
then use dyes to work out cell type tumour has grown from to differentiate between mesothelioma + lung tumours
what does desmoplasia mean?
the growth of fibrous or connective tissue
so if something is desmoplastic (eg a tumour) then it has low cellular component and is largely connective tissue
what is asbestosis?
is it elligible for industrial injuries disablement benefit?
a usual pneumonia-like proggressive pulmonary interstitial fibrosis caused by high level exposure to asbestos dust
- fibrosis of the alveolar walls impairs both gas exchange + lung expansion + contraction during breathing
yes