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Clinical Pathology > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

What is Asthma?

A
  • Chronic inflammatory disorder of the airways
  • Paroxysmal bronchospasm
  • Wheeze
  • Cough
  • Variable bronchoconstriction that is at least partially reversible
  • Mucosal inflammation & oedema of airways mucosa
  • Hypertrophic mucous glands & mucus plugs in bronchi
  • Hyperinflated lungs
  • Clinicopathological classification
  • Causes; Atopic , non-atopic, aspirin-induced, allergic bronchopulmonary aspergillosis (ABPA)- from aspergillus fungus
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2
Q

What is Atopic Asthma?

A

• Type I hypersensitivity reaction;
o Allergen- dust, pollen, animal products
o Cold, exercise, resp infecs
o Many diff cell types & inflamm mediators involved
o Degranulation of IgE bearing mast cells;
 Histamine initiated bronchoconstriction & mucus prduc obstructing air flow
 Eosinophil chemotaxis- lots of eosinophils inflamed
• Persistent/ irreversible changes
o Bronchiolar wall smooth muscle hypertrophy
o Mucus gland hyperplasia
o Respiratory bronchiolitis leading to centrilobular emphysema
Atopic Asthma- Clinical
• Children & young adults
• Common; 33.9% UK children 12-14yrs with ‘wheeze’ (2002), 1 in 10 UK kids diagnosed with asthma, 590,000 teens, 9-15% adult onset asthma is occupational (commonest occupational lung disease)
Atopic Asthma- At Autopsy
• Acute asthma- a mucus plugged small bronchus with eosinophils
• Airway occluded by mucus=death
• Cells- eosinophils

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3
Q

What is Obstructive Pulmonary Disease?

A

Localised or diffuse obstruction of air flow
• Localised;
o Tumour or foreign body
o Distal alveolar collapse (total) or over expansion (valvular obstruct
o Distal retention pneumonitis (endogenous lipid pneumonia- rec in alveoli) & bronchopneumonia
o Distal bronchiectasis (bronchial dilation- 1 bit of lung expands, compresses bit next to it)

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4
Q

What is Bronchiectatsis?

A

Bronchiectatsis
• Permanent dilation of bronchi & bronchioles caused by muscle destruct & elastic tissue
• Results from chronic necrotizing infection
• Rare ( for now…..)- due to antibiotics that work
• Site: bronchus/ bronchioles
• Cause: infections, predisposing conditions (so infecs can’t be cleared by antibiotics);
o Cystic fibrosis
o Primary ciliary dyskinesia (inherited- cilia don’t function properly), Kartagener syndrome (cilia affecetd)
o Bronchial obstruction: tumour, foreign body
o Lupus, rheumatoid arthritis, inflammatory bowel disease, GVHD
• Signs/Symptoms: long standing cough, intermittent fever, lots of foul smelling sputum
• May be localised- so can be resectable
• Complications- pneumonia, septicaemia, metastatic infec, amyloid

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5
Q

What is Chronic Obstructive Pulmonary Disease?

A
  • Combination of chronic bronchitis & emphysema
  • Cor pulmonale- R sided heart failure
  • Blue bloater (hypoxic, large patient)
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6
Q

What is Chronic Bronchitis?

A
  • Cough & sputum for 3 months in each of 2 consecutive years
  • Site: bronchus
  • Cause: chronic irritation, smoking & air pollution
  • Middle aged & old
  • 1 in 20 of >65yr consultant g.p. per year
  • Pathology: Mucus gland hyperplasia & hypersecretion, 2ndry infec by low virulence bacteria (don’t kill you but hard to get rid of), chronic inflamm of small airways of lung cuases wall weakness & destrc = centrilobular emphysema
  • Diff to asthma as has no acute component
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7
Q

What is Emphysema?

A

• Loss of elasticity of alveoli & abnormal enlargement of airspace vol in alveoli- caused by proteases (made by immune cells during inflamm) digesting the elastin
• Classification (& causes);
o Centrilobular (centiacinar- upper lung zones; focal enlargement & destruc of resp bronchiole, distal alveoli unaffected)- coal dust, smoking
o Panlobular (panacinar- destruc & enlargement of bronchioles & alveoli) - >80% a1 antitrypsin (an anti-protease) deficiency (rare, autosomal dominant- causes emphysema & liver disease) , severest in lower lobe bases
o Paraseptal (distal acinar- bronchioles unaffected but airspaces enlarged & alveoli destruc)- Upper lobe subpleural bullae adjacent to fibrosis. Pneumothorax if rupture
• Site: acinar (distal lung)
• Symptoms: dyspnoea (progressive & worsening)

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8
Q

What is Interstitial Lung Disease?

A

• Heterogenous group of diseases lumped together- usually diffuse (affect whole lung) & chronic
• Diseases of pulmonary connective tissue- mainly alveolar walls
• Restrictive rather than obstructive lung disease
• Causes: often unknown
• Pathological, radiological & clinically descriptions diff
• Pathology;
o Increased tissue in alveolar-capillary wall- increased gas diffusion distance
o Inflammation & fibrosis- decreased lung compliance
o Limited morphological patterns- differ with site & with time in any individual but with many causes & clinical associations
• Normal alveoli; thin walls
• Interstitial disease- expands interstitial space in alveolar walls (full of inflamm cells), gas exchange would be impaired
• More interstitium than gas- gas exchange effectively not going to occur

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9
Q

What is Acute Interstitial Lung Disease?

A
  • Diffuse alveolar damage – exudate & death of type I pneumocytes form hyaline membs lining alveoli, followed by type II pneumocyte hyperplasia (line alveolar walls)
  • Histologically called acute interstitial pneumonia
  • Adult respiratory distress syndrome (shock lung) - shock, trauma, infecs, smoke, toxic gases, oxygen, paraquat poisonig (weed killer), narcotics, radiation, aspiration, DIC
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10
Q

What is Chronic Interstitial Lung Disease?

A

Presentation (gradual);
• Dyspnoea increasing for months to years
• Clubbing, fine crackles, dry cough
• Interstitial fibrosis & chronic inflamm with varying radiological & histological patterns
• Common end-stage fibrosed “honeycomb lung”
• Examples (diff types);
o idiopathic pulmonary fibrosis,
o many pneumoconioses (dust diseases)
o sarcoidosis,
o collagen vascular diseases-associated lung diseases

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11
Q

What is Idiopathic Pulmonary Fibrosis?

A

Idiopathic Pulmonary Fibrosis (/Cryptogenic Fibrosing Alveolitis)
• Alveoli become increasingly scarred- lungs become stiff & difficult to get oxygen into blood
• Bosselated (“cobblestone”) pleural surface due to contrac of interstitial fibrous tissue accentuates lobular architecture

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12
Q

What is Sarcoidosis?

A
  • Lymph node enlargement & widespread granuloma appearance
  • Non-caseating (non-necrotic) perilymphatic pulmonary granulomas, then fibrosis
  • Hilar nodes usually involved
  • Breathless- have x ray- hilar nodes
  • Other organs may be affected- skin,heart, brain, kidneys
  • Hypercalcaemia & elevated serum ACE
  • Typically young adult females (20-40 yrs), aetiology unknown
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13
Q

What is Pneumoconioses?

A

• Originally- non neoplastic lung diseases due to inhalation of mineral dusts in the workplace
• Now also includes organic dusts, fumes and vapours
• Inhaled dusts;
o Chemically inert
o Fibrogenic reac
o allergenic
o oncogenic- lung carcinoma & pleural mesothelioma
• <3mm diameter to reach alveoli
• Often occupational

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14
Q

What is Coal Workers Pneumonconiosis (CWP)?

A
  • Anthracosis- milder asymptomatic type of pneumoconiosis caused by carbon accumul in lungs due to repeated exposure to air pollution/ inhalation of smoke/ coal dust particles
  • Simple (macular) CWP
  • Can progress to Nodular CWP
  • Progressive massive fibrosis
  • COPD (‘chronic bronchitis & emphysema’) if >20yrs underground mining
  • Don’t have to have COPD to have CWP- just need to have dust in lungs
  • Black in lungs - inhaled coal dust
  • Heterotrophy of R ventricle due to vascular resistance of affected lungs
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15
Q

What is Silicosis?

A
  • Silica - sand & stone dust
  • Kills phagocytosing macrophages (which eat it)
  • Fibrosis & fibrous silicotic nodules, also in nodes
  • Possible TB reactivation
  • Increased risk of lung carcinoma with silicosis- prescribed occupational disease (gov recognises the association)
  • Mixed dust pneumoconiosis – silica with exposure to other dusts
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16
Q

What is Hypersensitivity Pneumonitis?

A

Hypersensitivity Pneumonitis (/Extrinsic Allergic Alveolitis)
• Type III hypersensitivity reaction to organic dusts
• Farmers’ lung – exposed to actinomycetes in hay (develop hypersensitivity pneumonitis)
• Pigeon fanciers’ lung - pigeon antigens
• Peribronchiolar inflammation with poorly formed non-caseating granulomas extends alveolar walls
• Repeated episodes lead to chronic irreversible interstitial fibrosis
• These reversible in early stages

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17
Q

What is Cystic Fibrosis?

A

• Autosomal recessive inherited multi-organ disorder of epithelial cells- affects fluid secretion in exocrine glands & epithelial lining of resp, GI & reproductive organs
• Epidemiology: Incidence 0.4 per 1000 live births, mostly affects Caucasians
• Bronchioles distended with mucus
• Hyperplasia mucus secreting glands, bronchioles distended with mucus, mucus plugged exocrine glands
• Multiple repeated infections
• Severe chronic bronchitis and bronchiectasis
• Atrophy and fibrosis of gland
• Impaired fat absorption, enzyme secretion, vit deficiencies (as can’t absorb fat soluble vits pancreatic insufficiency)
• Small bowel: mucus plugging - meconium ileus
• Liver: plugging of bile cannaliculi = cirrhosis
• Salivary glands: Similar to pancreas: atrophy and fibrosis
• 95% of males are infertile
• Tests; part of newborn screening in UK, sweat test, genetic testing
• Median survival in UK 41 yrs
• Treatments;
o Physiotherapy
o Mucolytics (are inhaled- loosen mucous)
o Heart/lung transplants
o Why hasn’t gene therapy worked?- is a single gene disorder but gene therapy failed
o Orkambi (lumacaftor-ivacaftor) drug- prolong peoples lives (not on NHS as too expensive)
• Further reading- molecular basis of CF & it’s treatment;
o CTFR gene found at 508th position on chromosome- codes for protein ion channel that transports chloride & thiocyanate ions across membs
o Common mutation in CTFR gene- deltaF508 (deletion of 3 nucleotides causing a.a. phenylalanine loss at 508th position)
o Most affects lungs, liver, pancreas, intestine
o Abnormal sodium & chloride transport across epithelium
o Mucus sticky as not humidified enough- hard to remove form airway infecs
o Duct that leads from pancreas to gut blocked no pancreatic enzymes so can’t digest food properly= poor growth & diarrohea
o Treatment;
 Lungs; antibiotics (prvent infecs), ivacaftor (reduce mucus), bronchodilators, steroids (treat nasal polyps)
 Airway clearance techniques: e.g. active cycle of breathing tchniques (ACBT)
 Dietary: digestive enzyme capsules
 Lung capsules
 For associated probs: bisphospahates- brittle bones, insulin- diabetes

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18
Q

What is Malignant Lung Pathology?

A

Definition- tumours in lung that possess potentially lethal abnormal characteristic that enables them to invade & metastasize to other tissues

  • Primary- arise within the lungs (then can spread)
  • 2ndry- originally elsewhere (e.g. kidneys) then metastisise to lungs
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19
Q

What are Primary Malignant Lung Tumours?

A

• Most common (>90%) are carcinomas- arise from epithelium
• The 4 major types of lung carcinomas, classified based on light microscopy (histology) are;
o Adenocarcinoma (30-40%)
o Squamous cell carcinoma (20-30%)
o Small cell carcinoma (15-20%)
o Large cell undifferentiated carcinoma (10-15%)

Other Primary Malignant Lung Tumours
• Carcinoid tumours– low grade malignant tumours, better survival (from neuroendocrine cells in lung)
• Malignant mesenchymal tumours – very rare, most common is synovial sarcoma
• Primary lung lymphomas – originate in lung lymphoid tissue, rare, can be seen in HIV/AIDS patients (treated by chemo so slightly better survival)

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20
Q

What are Secondary Lung Tumours?

A
  • Very common, more common than primary tumours
  • Usually present as multiple discrete nodules, can also be solitary nodule in lung (need to differentiate if it’s primary or come from elsewhere)
  • Most common are carcinomas from various sites eg. Breast, GI tract, Kidney
  • Sarcomas
  • Melanomas e.g. from skin
  • Lymphomas
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21
Q

What is the Epidemiology of Lung Cancer?

A
  • Most common cause of cancer death in UK & worldwide (major public health prob)
  • 45 000 new cases diagnosed each year and >30 000 deaths/year (UK)
  • M > F, only slight
  • Age usually between 40 and 70 yrs, rare in younger individuals
  • Major risk factor- cigarette smoking; lung cancer incidence rise closely paralleled increase in cigarette smoking, incidence & mortality rates been decreasing due to decrease smoking rates.
  • Overall prognosis is poor, 5 year survival is between 5 – 10%.
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22
Q

What is the Aetiology of Lung Cancer?

A
  • Tobacco smoking
  • Occupational/Industrial hazards, eg Asbestos, uranium, arsenic, nickel mines
  • Radiation – mines where radon emitted (Japan- atomic bomb survivors after WWII- high lung cancer incidence)
  • Pulmonary fibrosis patients have an increased lung cancer risk
  • Genetic mutations- EGFR, KRAS, ALK mutations etc (usually in lung cancers of never smokers)
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23
Q

What is the Pathogenesis of Lung Cancer?

A
  • Not very well understood
  • Mutations in key genes regulating; cell prolif, DNA repair & apoptosis
  • Squamous cell carcinoma- cigg smoking is irritant to bronchial epithelial cells (squamous metaplasia= dysplasia= carcinoma in-situ= frank squamous carcinoma)
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24
Q

What is a pack year?

A
  • Major risk factor- tobacco smoke is a carcinogen
  • Almost linear dose relationship between n.o. of ciggs smoked/ day & risk of developing lung cancer e.g. risk x10 higher if smoke 10 per day
  • ‘Pack years’ quantifies; 1 pack year= 20cigarettes per day for 1yr e.g. 40 cigarettes/day for 6 mnths
  • Passive smoking does increase risk for lung cancer
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25
Q

What are the Clinical Features of Lung Cancer?

A
  • Local effects of tumour (symptoms related to tumour in chest)
  • Distant metastases (symptoms related to metastasis)
  • Non-specific features
  • Asymtomatic, discovered incidentally (e.g. from a CT)
  • As tumour grows= ulcerates= bleeds=cough up blood (haemoptysis) — presenting sign
  • Distally develop consolidation

= pneumonia
• Pleural effusion=breathlessness

Non-Specific Features
• Usually metabolic effects- weight loss, lethargy
• Electrolytic disturbances, e.g. small cell carcinoma – hyponatraemia, hypokalaemia, hypercalcaemia
• Finger clubbing
• Can produce hormones e.g. ACTH
• CT saggital section of chest; lung lymphatics stuffed with tumour- Lymphangitis carcinomatosa

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26
Q

What are the Local Effects of Lung Cancer?

A
  • Central tumours in proximal airways can ulcerate and bleed –haemoptysis.
  • Tumour obstructing airways with distal collapse or consolidation – breathlessness or features of pneumonia.
  • Tumour infiltrating into adjacent strucs, eg Pleura – pleural effusion presenting as breathlessness, can invade chest wall/ribs – chest pain
  • Recurrent laryngeal nerve – hoarseness
  • Horner’s syndrome – sympathetic chain, ptosis (eyelids drooping)
  • Oesophagus - dysphagia
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27
Q

What are Distant Metastases of Lung Cancer?

A
  • Can present with disseminated disease.
  • Common sites – lymph nodes, pleura liver, bone, adrenal, brain
  • Depending on site can present with pathological fractures (tumour from lung metastised e.g. to hip causing fracture), seizures, lumps in neck etc
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28
Q

What is Lung Cancer Management?

A

Lung Cancer Management (Primary)
• Small % of patients diagnosed with early stage (disease limited to lung/ extension into local nodes), offered Surgery or radical radiotherapy.
• Majority present with advanced disease – used to be limited to Chem or Palliative Radiotherapy.
• Only about 10% have surgery (early stage of surgery)- not all fit for surgery (e.g. have other conditions) even if have localised disease
• (Don’t operate on people with metastases)
• Recent advances in lung cancer treatment with advanced disease;
o Targeted/tailored therapy
o Based on tumour genomics eg EGFR mutations, ALK re-arrangements
o I.d. Immune checkpoint inhibitors eg PD-L1 receps in tumour (know they’ll respond to anti-PD-L1 drugs; makes their own immune system fight against tumour (isn’t chemo/ radio therapy))
o Send it for genomic studies- see mutations (may have drug against mutation)

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29
Q

What is Normal Mesothelium?

A
  • Single layer of mesothelial cells lines pleural cavity
  • They secrete hyaluronic acid rich mucinous pleural fluid- lubricates visceral & parietal pleural movement against each other during resp
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30
Q

What is Pleural Inflammation?

A

Causes
• Primary inflammatory diseases- collagen vascular diseases e.g. systemic lupus erythematosus & rheumatoid arthritis
• Infecs- usually 2ndry to pneumonias or pulmonary TB. Viral- primary Coxsackie B infec (Bornholm disease)
• Pulmonary infarction- usually 2ndry to pulmonary arterial thromboembolus
• Emphysema- 2ndry to ruptured bullae
• Neoplasms- primary or secondary pleural neoplasms
• Theraputic- pleurodesis usually with talc to treat recurrent pleural effusions/ recurrent pneumothoraxes
• Iatrogenic- radiotherapy to thorax, immune reacs to drugs (eosinophils- markers for this for pleura)
Diagnosis
• If there is no associated pleural effusion;
o Symptomatic- pleuritic chest pain (sharp localised pain exacerbated by breathing)
o Sign- auscultation of a pleural rub during breathing
Usually associated pleural effusion- excess fluid in pleural cavity

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31
Q

What is Pleural Fibrosis?

A

• Usually 2ndry to pleural inflamm;
o Uni or bilateral
o Localised or diffuse
• Asbestos associated pleural fibrosis;
o Parietal pleural fibrous plaques
o Diffuse pleural fibrous
Effects of Pleural Fibrosis
• Widespread thick fibrosis- prevent normal lung expansion during respiration causing breathlessness
• Fibrous adhesions- wholly/ partly obliterate pleural cavity
• Fibrous tissue removal (pleural decortication)- improve lung expansion & compression during resp

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32
Q

What is Parietal Pleural Fibrous Plaques?

A
  • Associated with low level asbestos exposure
  • Asymptomatic
  • May be visibe on chest radiographs
  • Dense poorly cellular collagen
  • Not a UK Gov Prescribed Occupational Disease- doesn’t cause disability
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33
Q

What is Diffuse Pleural Fibrosis?

A
  • Assocaited with high level asbestos exposure
  • Usually bilateral
  • Dense cellular collagen not extending into interlobar fissures
  • Benign fibrosis doesn’t go into fissures (malignant do- how radiologists distinguish the two)
  • Prevents normal expansion and compression of the lung during breathing causing breathlessness
  • IS a UK Gov prescribed Occupational Disease for specified high exposure occupations eligible for Industrial Injuries Disablement Benefit
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34
Q

What are Pathological fluids in Pleural Cavity?

A

LIQUIDS;
• Serous fluid- pleural effusion (compresses lung so vol reduced- breathless)
• Pus- empyema or pyothorax (usually 2ndry to pneumonia)
• Blood- haemothorax (usually traumatic/ ruptured thoracic aortic aneurysm)
• Bile- chylothorax (usually traumatic)
GAS
• Air- pneumothorax

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35
Q

What are the different types of Pleural Effusion?

A

• TRANSUDATES
o Fluid pushed through capill due to high pressure in capill
o Low capill oncotic (colloid osmotic) pressure &/or high capill hydrostatic pressure
o Intact capillaries retain semipermeability
o Low protein (<2.5g/dL) & low lactate dehydrogenase

• EXUDATES
o Fluid leaks around cells of capills caused by inflamm
o Pathological capillaries loose semipermeability
o Normal capillary oncotic pressure and normal vascular hydrostatic pressure
o High protein (>2.9 g/dL) & high lactate dehydrogenase

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36
Q

What are the causes of Pleural Effusions?

A

Causes
• Nephrotic syndrome- protein leaks out, low serum albumin
Transudates
• High vascular hydrostatic pressure- left ventricular failure, renal failure
• Low capillary oncotic (colloid osmotic) pressure- hypoalbumenaemia (hepatic cirrhosis, nephrotic syndrome)
Exudates
• Inflammation with/without infection- an acute inflammatory effusion become an empyema when see lots of neutrophils it’s an empyema
• Neoplasms either primary or secondary

37
Q

What are the signs and symptoms of Pleural Effusions?

A

• Symptoms;
o Breathlessness - effusion compresses the lung
o Little/no pleuritic pain – the visceral and parietal pleura are not in contact

• Signs;
o Percussion- dull (as fluid underneath)
o Auscultation- reduced breath sounds (as fluid)
• Investigations to support diagnosis; imaging (ultrasound, chest radiograph, CT)

38
Q

What is the treatment of Pleural Effusions?

A

• Treat the breathlessness by removing the fluid
o Aspiration with a needle & syringe, ultrasound guided (so don’t cause a pneumothorax)
o Reaspirate if the fluid reaccumulates
o For recurrent effusions consider a temporary or permanent pleural drain
o For recurrent effusions when the lung expands after drainage and the underlying cause remains consider pleurodesis to obliterate the pleural cavity
• Identify and treat the underlying cause
• Local- pleural fluid for cytology, microbiology, & biochemistry, pleural biopsy
• Systemic – investigate the systemic causes of pleural effusions

39
Q

What is a Pneumothorax ?

A
  • Air in pleural cavity

* Common, occasionally fatal

40
Q

What is a open Pneumothorax ?

A

o Chest wall perforation usually traumatic- ‘sucking shest wound’- connects body surface to pleural cavity
o External air drawn into pleural cavity during inspiration, reducing potential lung expansion

41
Q

What is a closed Pneumothorax ?

A

o Not traumatic (e.g. ruptured bullae)
o Lung perforation- connects lung air spaces to pleural cavity
o Lung air drawn into pleural cavity during inspiration, reducing potential lung expansion
o Causes;
 Ruptured emphysematous bullae
 Common inflamm lung diseases; asthma, pneumonia, TB, cystic fibrosis
 Traumatic- lung tears from fractured ribs
 Iatrogenic- mechanical ventilation at high pressures, lung & pleural biopsy procedures
 Some rare cystic lung diseases- Langerhans’ cell histiocytosis, lymphangioleiomyomatosis
 Catamenial due to pleural endometriosis

42
Q

What is a Tension Pneumothorax?

A
  • Rupture forms a valve (closes)- air can’t get out
  • Perforation into pleural cavity, in an open/closed pneumothorax can be valvular- allowing air into cavity during inspiration but not out during expiration
  • Pressure in pneumothorax can rise above atmospheric pressure (think of blowing up a balloon)
  • This can compress mediastinal strucs e.g. vena cavae & heart and move the mediastinum compressing the contralateral lung
  • A tension pneumothorax is potentially fatal and requires urgent treatment
43
Q

What are the signs and symptoms of a Pneumothorax?

A

Symptoms (small ones may be asymptomatic);
• Breathlessness
• Pleuritic chest pain
Signs;
• Cyanosis
• Tachycardia
• Contralateral tracheal deviation in tension pneumothorax
• Percussion – hyperresonant
• Auscultation – reduced breath sounds
Investigations to support diagnosis;
• Imaging – ultrasound, chest radiograph, CT
• Symptomatic pneumothoraces are often initially treated without further investigation

44
Q

What is treatment of a Pneumothorax?

A
  • May resolve spontaneously
  • Tension pneumothorax- can be decompressed as an emergency procedure using a needle inserted via an intercostal space
  • With open pneumothorax the penetrating chest wound causing it can be covered with an occlusive adhesive dressing that may incorporate a valve to allow air out but not in
  • For any pneumothorax a chest drain tube can be inserted incorporating a valve to allow air out but not in while the pneumothorax resolves
  • For recurrent pneumothoraces- pleurodesis considered
45
Q

What are Pleural Neoplasms ?

A

Primary;
• Benign/ low grade malignant- uncommon/ rare e.g. low grade mesothelial tumours (cells lining pleural cavity)
• Malignant- e.g. malignant mesothelioma (common), others (uncommon/ rare)
Secondary Malignant;
• Carcinomas – breast, lung, others- common
• Others – lymphoma, melanoma, others

46
Q

What is a Malignant Mesothelioma?

A

• Neoplasm of mesothelial cells that line serous cavities- pleura, peritoneum, pericardium, tunica vaginalis
• 92% pleural, 8% peritoneal
o Both commoner in men
o Peritoneal mesotheliomas affect a higher proportion of women, have a higher proportion of the low grade type & less strongly associated with asbestos exposure
• Tend not to metastasise widely

Mesothelioma- 17th most common cause of cancer deaths
In older people
Expecting to see a fall in the disease as asbestos banned
Low survival

47
Q

What is a early Malignant Mesothelioma ?

A
  • Breathlessness
  • A small tumour can produce a large pleural effusion
  • Tumour can be difficult to i.d. on imaging & so is difficult to target biopsies at it
  • Can shed malignant cells into effusion so effusion cytology may allow early tissue diagnosis
48
Q

What is an advanced Malignant Mesothelioma?

A
  • If have biopsy- can go along needle tract to chest wall
  • 1st spreads around lung
  • Spreads into fissure
49
Q

What is the Histology of a Malignant Mesothelioma ?

A

Malignant Mesothelioma Histology
• Mixed tubopapillary epithelioid & spindle cell sarcomatoid (soft tissue tumour) morphology
• Can be either type alone
• Can be poorly cellular- ‘desmoplatic’
• Main morphological differential diagnosis is malignant mesothelioma or non-small carcinoma
• In pic; tubules and solid aggregates of malignant mesothelial cells, morphological differential diagnosis is adenocarcinoma or epithelioid malignant mesothelioma
Malignant mesothelioma Immunostaining
• Uses antibodies linked to a dye to identify antigens is cells
• Mesothelial cells & epithelial cells express diff antigens- can be differentiated from each other
• There is some cross reaction therefore a panel of 4 or more antibodies is used
• Mesothelium-associated antigen stains in pics
o Top- cytoplasmic stain cytokeratin 5
o Middle- stained with Wilms tumour antigen
o Bottom- calretinin (stains cytoplasm & nucleus)

50
Q

What are the causes of a Malignant Mesothelioma?

A

• Asbestos (80-90% of cases)
o Strong association with asbestos over general pop leve exposure but exposure can be quite low level
o Risk increases e.g. higher risk after 60 years than 15 years even if have same exposure
o Mesothelioma develops 15 years to over 60 years after exposure
o The risk increases with cumulative exposure level and time from exposure
o Is the background level safe? - Not certain but fairly safe
o Estimated 1 to 2 “spontaneous” cases per million persons per year
• Thoracic irradiation (theraputic)
• BAP1 (oncogene) (BRCA1- associated protein 1) mutations- germline mutations in a familial cancer syndrome with uveal melanomas and mesotheliomas

51
Q

What is Asbestos?

A

• Fibrous metal silicates, 5-100μm x diameter 0.25-0.5μm
o Amphibole - blue asbestos (crocidolite), brown asbestos (amosite)
o Serpentine - white asbestos (chrysotile)
• When inhaled some become coated with mucopolysacharides containing iron- form asbestos bodies
• Can see asbestos bodies in tissue sections by light microscopy, brown when unstained or blue if iron is stained, and quantified – a cheap simple process
• Asbestos fibres can be quantified in lung extracts by electron microscopy – complex & expensive

Asbestos Use
• A fire-proof material in commercial & domestic buildings & in shipbuilding (1940s to the 1990s)
• 5.5 million tons of asbestos imported into the UK (1940-1998)
• Crocidolite & amosite imports banned in 1985 & all asbestos imports banned in 1999
• A lot is still in buildings- risk to those working in/near building maintenance & demolition processes

Asbestos caused about 5000 UK deaths in 2014

52
Q

What is Asbestos Oncogenicity?

A
  • Amphiboles particularly crocidolite- most oncogenic & persist in the lungs
  • Chrysotile is less oncogenic and is more readily cleared from the lungs
  • Erionite (fibrous zeolite mineral)- fibre struc similar to asbestos.
  • Is used as a building material in areas of Cappadocia, Turkey- very high incidence of mesothelioma occurring in young people

Asbestos & Lung Carcinoma
• High level exposure to asbestos dust- independent risk factor for lung carcinomas of all types
• 2000-2500 UK carcinomas/yr mainly in men due to asbestos
• 5% of 46,403 cases diagnosed in 2014
• Lung carcinoma IS high exposure occupation in Gov Prescribed Occupational Disease

53
Q

What is Asbestosis?

A
  • Asbestosis- an usual interstitial pneumonia-like progressive pulmonary interstitial fibrosis caused by high level exposure to asbestos dust
  • Fibrosis of alveolar walls impairs gas exchange & lung expansion & contraction during breathing
  • Asbestosis associated with any occupation working with asbestos is a UK Gov Prescribed Occupational Disease that is eligible for Industrial Injuries Disablement Benefit
  • Increasing in incidence & mortality
  • 431 registered deaths in 2014,
  • 985 new Industrial Injuries Disablement Benefit cases in 2014 & 1175 cases in 2015

Can see Asbestos corns – benign hyperkeratotic wart-like skin lesions

54
Q

What are the Possible Causes of an Acute Sore Throat?

A

• History key points:
o Rapidity of onset of sore throat
o Difficulty breathing/speaking
o Ability to eat/drink/swallow
o Associated neck pain/swellings
o Symptoms of systemic infection e.g. fever, chills, rigors, general malaise
o Travel history
• Pharyngitis: inflamm of back of the throat (pharynx), resulting sore throat & fever (patient will say ‘I.ve got a sore throat’)= most common cause is viral
• Acute tonsillar pharyngitis: symmetrically inflamed tonsils and pharynx (+/- fever +/- headache) (Severe infec: patient has marked systemic symptoms of infec &/or unable to swallow).
• Consider infectious mononucleosis (EBV) (glandular fever): symmetrically inflamed tonsils/ soft palate inflamm & posterior cervical lymphadenopathy (don’t really need antibiotics)
• Suspect epiglottitis: sudden onset of severe sore throat, no inflammation of the tonsils and/or oropharynx & systemic symptoms/signs of infection- watch out for this, can make it worse when do throat exam!

55
Q

What is the most common cause of a Sore Throat?

A

VIRUSES ACCOUNT FOR THE MOST COMMON SORE THROAT- EXAM Q!!! But in 1/3rd of ppl no cause can be found

56
Q

What is are the causes of Pharyngitis & Tonsillar Pharyngitis?

A

VIRUSES ACCOUNT FOR THE MOST COMMON SORE THROAT- EXAM Q!!! But in 1/3rd of ppl no cause can be found

Common infectious causes;
• Viruses: Rhinovirus, Coronovirus, Parainfluenza, Influenza (A & B), Adenovirus etc. Viruses account for ~50% and are the most common cause of sore throat.
• Bacteria: Group A beta-haemolytic Streptococcus (GABHS) is the most common bacterial cause of sore throat. (15–30% of sore throats in children, and 10% in adults).
• Group A strep if in blood stream- life threatening

Rare causes:
• Neisseria gonorrhoeae (Gonococcal pharyngitis)- Gonorrhoae causes sore throat if infected in pharynx
• HIV-1 (can be the first presentation of HIV infection)
• Corynebacterium diphtheriae (Diptheria)

57
Q

What is the Centor Criteria?

A

• Used by GP’s to clinically differentiate if something viral or bacterial
• Gives indication of likelihood sore throat a bacterial infec
• Criteria;
o Tonsillar exudate
o Tender anterior cervical lymphadenopathy
o Fever over 38°C
o Absence of cough
• If 3 or 4 of criteria met +ve predictor value 40-60% likely to have a bacterial infec
• Absence of 3 or 4 of criteria fairly high –ve predictive value of 80%- more likley to be viral

58
Q

What are the investigations & management of a Acute sore throat?

A

• Outpatient/ambulatory investigation- usually clinical assessment no routine investigations unless infectious mononucleosis is suspected
• Inpatient (severe infec) investigation- (assume patient more unwell), Throat swab for culture, blood cultures, (blood tests: FBC, U&Es, liver function tests). If suspected infectious mononucleosis: blood sample for Monospot or EBV serology.
• Management;
o Oral analgesics (paracetamol, ibuprofen)- help bring temp down
o Most sore throats don’t need antibiotics as most NOT caused by bacteria, but if non severe acute tonsillar pharyngitis symptoms present for 1 week & getting worse may give antibiotics (non severe acute tonsillar pharyngitis if symptoms present for 1 week and getting worse)

59
Q

What is Infectious Mononucleosis?

A

Infectious Mononucleosis/ Glandular Fever/ Kissing Disease
• Epstein-Barr virus (EBV)
• Teenagers. Often asymptomatic.
• Characterised by a triad of symptoms: fever, tonsillar pharyngitis, and cervical lymphadenopathy.
• Complications e.g. splenic rupture
• Avoid ampicillin (not an allergy, it reacts with EBV forming mac-pap rash)
• Blood for Monospot +/- EBV serology

60
Q

What is Epiglottitis?

A

• Epiglottitis (supraglottitis): inflamm of strucs above glottis.
• Almost always caused by bacterial infec
• Haemophilus influenzae type b (Hib) was commonest cause in >90% of paediatric cases but Hib vaccine significantly reduced rate of Hib epiglottis. Still do see Hib cases in adults & rarely in children.
• Other causative organisms: Streptococcus pneumoniae & Group A Streptococcus.
• Investigations: Blood cultures & epiglottic swabs (examining throat may cause total airway obstruct- only do so when anaesthetic support present)
• Management: -
o Acute epiglottitis & associated upper airway obstruct- signif morbidity & mortality and may cause resp arrest & death within 24 hrs. Securing airway & oxygenation is a priority!
o IV antibiotics (usually 3rd generation cephalosporin)
o Analgesia
o Hib epiglottitis - Inform public health
o Secure airway & ensure patient has antibiotics

61
Q

What is Otitis Externa?

A

• Ear canal- only skin-lined cul-de-sac in the body
• OE = inflammation of external ear canal presenting with a combination of: otalgia, pruritus and non mucoid ear discharge.
• Split into 2;
o Symptoms < 3/52 (less than 3 wks)= acute OE
o Symptoms >3/52 (over 3 wks)= chronic OE
• Risk factors; swimming (or other water exposure), trauma (e.g. ear scratching, cotton swabs), occlusive ear devices (e.g. hearing aids, ear phones), allergic contact dermatitis (e.g. due to shampoos, cosmetics) & dermatologic conditions (e.g. psoriasis).
• Pain, itchy ear
• Can have eczma & sirrhosis in ear canal- causes OE

62
Q

What is Acute Otitis Externa?

A

• Acute OE range in severity mild/moderate/severe + necrotising (malignant) OE
• Unilateral
• 90% AOE bacterial (most common: Pseudomonas aeruginosa & Staphylococcus aureus), 2% fungal
• Chronic- bilateral
• Diagnosis: history & otoscopic examination
• Investigations: Ear swab or pus sample from ear for culture
• In necrotising otitis externa: CT temporal bone (& bone biopsy), blood cultures if systemically unwell
• Non-Antimicrobial Management;
o Remove/modify precipitating factors
o Remove pus and debris from ear canal (called ‘toileting’)
o Analgesia
• Antimicrobial management:
o Topical agents for mild-moderate
o Topical plus systemic antibiotic such as flucloxacillin for severe AOE

63
Q

What is Malignant (Necrotising) External Otitis?

A
  • Malignant (necrotising) external otitis- when external otitis spreads to skull base (soft tissue, cartilage, & bone of temporal region & skull).
  • Can be life threatening
  • Most commonly develops in elderly diabetic/ other immunocompromised patients
  • Severe pain, otorrhoea, granulation tissue in canal floor, & cranial nerve palsies may be present.
  • These patients should be promptly referred ENT
  • Treat for a minimum of 6 weeks e.g. with iv ceftazidime then po ciprofloxacin
64
Q

What is Chronic Otitis Externa?

A
  • Symptoms over 3 wks
  • Pruritus , mild discomfort, erythematous external canal that is usually devoid of wax.
  • Often bilateral.
  • White keratin debris may fill ear canal- over time canal wall skin thickens &narrows external ear canal
  • A common cause- allergic contact dermatitis (e.g. from chemicals in cosmetics or shampoos)
  • Generalised skin conditions e.g. atopic dermatitis or psoriasis can also predispose to chronic OE
  • More likely to be caused by chemicals
  • Treat underlying cause (often a skin condition)
65
Q

What is Otitis Media?

A
  • Middle ear inflamm (not canal)
  • Pressure build up behind tympanic memb
  • Fluid in middle ear
  • V. common in children
  • Uncomplicated acute OM is defined as: mild pain <72hrs duration & no severe systemic symptoms, with temp less than 39⁰C & no ear discharge
  • Complicated acute OM defined as: severe pain, perforated eardrum &/or purulent discharge, bilateral infec, mastoiditis
  • Organismsa: viruses, bacteria- streptococcus pneumoniae, Haemophilus influenza & Moraxella catarrhails
  • Treatment: depending how severe e.g. if not too severe- GP can wash (but will need to follow up), if not unwell watch & treat symptomatically (analgesia, decongestant etc.) & review early. If unwell - amoxicillin
66
Q

What is Mastoiditis?

A
  • Infec spread to mastoid bone & air cells
  • Most common AOM complication- incidence reduced if use antibiotics for OM
  • Mastoiditis & other severe AOM complications of AOM rare in adults
  • In <1 in 1000 children with untreated AOM
  • Clinical features; fever, posterior ear pain &/or local erythema over mastoid bone, oedema of pinna, or a posteriorly & downward displaced auricle
  • Always need CT scan
  • Treatment: Analgesia, IV antibiotics +/- mastoidectomy
67
Q

What is Pinna Cellulitis ?

A
  • Pinna- bit on outside of ear
  • Associated with trauma (including ear piercing & acupuncture), surgery or burns
  • Perichondritis: complication of high ear piercing (puncture through cartilage of upper third of pinna)
  • Swab area & blood cultures (if in secondary care) should be obtained prior to starting antibiotics
  • Usual infective agent(s) in auricular perichondritis: Pseudomonas aeruginosa &/or Staphylococcus aureus
  • Empirical treatment: ciprofloxacin + flucloxacillin (or vancomycin if penicillin allergy)
  • Remove piercing & treat infec
68
Q

What is Pneumonia? What are its anatomical patterns?

A

• Infec affecting the most distal airways & alveoli
• Formation of inflamm exudate
• 2 anatomical patterns;
o Bronchopneumonia- characteristic patchy distribution centred on inflamed bronchioles & bronchi then subsequent spread to surrounding alveoli
o Lobar pneumonia- affects a large part/ entirety of a lobe - 90% due to S.pneumoniae

69
Q

What are the different types of Pneumonia?

A

• Community acquired pneumonia (CAP)
• Hospital acquired pneumonia (HAP)
o Pneumonia developing >48hrs after hospital admission
o Additional causative organisms to CAP, especially if >5days after admission: enterobacteriaceae
o In hospitals- have superbugs in env so have diff pop of organisms to think about , enterobacteriaceae (gut bacteria)
• Ventillator acquired pneumonia (VAP)
o Subgroup of hospital acquired
o Pneumonia developing >48hrs after ET intubation & ventilation
o Pseudomonas spp. may be implicated
o Some people have strep pnumoniae in their throat normally so if put a tube down will push this bacteria into lungs
• Aspiration pneumonia- e.g. in stroke patient
o Pneumonia resulting from abnormal entry of fluids e.g. food, drinks, stomach contents, etc. into lower resp tract
o Patient usually has impaired swallow mechanism
o Anaerobes may be implicated

70
Q

What is Community Acquired Pneumonia?

A 
Community Acquired Pneumonia (CAP)
•	Do HIV test in someone that presents with this- could be HIV presentation 
•	From env- legionella pneumonia 
Epidemiology 
•	Incidence: 1 per 1000 ppl/yr (common!)
•	20-40% cases need hospital admission 
•	Peak age 50-70 yrs
•	Peak onset midwinter- early spring
•	Acquisition of organisms;
o	Person-to-person or from a person’s existing commensals (S.pneumoniae, H.influenzae) 
o	From the environment (L. pneumophilia) 
o	From animals (C.psittaci)
71
Q

What are the Causative Organisms of Community Acquired Pneumonia?

A

see table of typical and atypical bacteria.

Causative Organisms: CAP
• Bacterial causes often divided into ‘typical’ & ‘atypical’
• Aytypical pneumonia- described cases and no organism could be identified which failed to respond to penicillin (organisms with atypical or no cell wall))- caused by atypical organisms (clinical presentation & treatment slightly diff)
• Atypical- didn’t respond to penicllin, no causative organism found, now think of atypical pneumonia as if present unwell e.g. ; malaise, headache, diarrhoea (not as easy to identify)

72
Q

What is the CURB score?

A

CRURB 65 score- for severity of Pneumonia
Confusion: No 0 Yes+1
Urea : > 7 mmol/L
Respiratory Rate ≥ 30 No 0 Yes+1
Systolic BP < 90 mmHg or Diastolic BP ≤ 60 mmHg
No0 Yes+1
Age ≥ 65

0/1=low 2 moderate 3-5= high severity§

73
Q

What are the Investigations for Inpatients with Community Acquired Pneumonia?

A

• Chest x-ray- may be clinically resolve but chest x-ray findings take longer to resolve (up to 6wks +)
• Legionella- affected liver tests
• Recommended for all moderate- severe CAP based on CURB65 score >2;
o Sputum culture
o Blood culture
o Pneumococcal urinary antigen
o Legionella urinary antigen
o PCR or serology for:
 Viral pathogens e.g. influenza (PCR of respiratory samples)
 Mycoplasma pneumoniae (PCR of respiratory samples preferable, complement fixation: interpret with caution)
 Chlamydophila sp. (complement fixation test most widely available – on blood)

74
Q

What is the Management of CAP/HAP/VAP & Aspiration Pneumonia?

A

With any unwell/ septic patient;
• A= airway- ensure open, patent & maintained airway
• B= breathing- assess resp rate & saturations, provide supplemental oxygen to reach prescribed target
• C= circulation- assess BP & heart rate, gain iV access & give IV fluids if haemodynamically unstable, urinary catheter (monitor urine output)
Then PROMPT empirical antibiotic therapy

75
Q

What are the complications of Pneumonia ?

A

• 3-5% Pleural effusion: – clear fluid +/- pus cells +/-organisms
• 1% Empyema: pus in the pleural space (-loculated)
• Lung abscess: – suppuration + destruction of lung parenchyma
o Single (aspiration) anaerobes, Pseudomonas
o Multiple (metastatic) Staphylococcus aureus

76
Q

What is Influenza?

A

• Usually influenza causes uncomplicated disease; fever, headache, myalgia, dry cough/ clear sputum, sore throat- convalescence takes 2-3wks
• Primary viral pneumonia- more commonly in patients with pre-existing cardiac & lung disorders ;
o Cough, breathlessness, cyanosis
o 2ndry bacterial pneumonia then may develop after initial period of improvement- S.pneumoniae, H.influenzae, S.aureus
• Complication; 2ndry bacterial pneumonia
• Swab- test this for influenza
• Diagnosis: viral antigen detection in resp samples using PCR

77
Q

What is VZV pneumonia?

A
  • Complication of VZV (chicken pox) infec
  • Rare in children, signif morbidity & mortality in adults with varicella
  • Those at greatest risk; immunocompromised, adults with chronic lung disease, smokers & pregnant women (preg women not more at risk of getting virus but is more severe when they do get it (need supportive care; oxygen, fluids then give acyclovir))
  • Insidious onset 1-6 days after rash with symptoms of progressive tachypnoea, dyspnoea & dry cough.
  • Tests: Chest X-ray typically reveals diffuse bilateral infiltrates
  • Treatment: Supportive & prompt administration of IV acyclovir
78
Q

What is Rhinovirus?

A
  • Responsible for most common colds
  • Can cause LRTI & trigger exacerbations of asthma
  • Tests: PCR on NPA/throat swab
  • Treatment: supportive
79
Q

What is CMV pneumonia?

A
  • Rarely in immunocompetent hosts
  • Can cause severe illness in transplant recipients & HIV patients (uncommon)
  • Tests: Chest-Xray, Broncho-alveolar lavage (can put a scope down & get fluid from alveolus) & viral load PCR
  • Treatment: supportive, anti-viral (e.g. ganciclovir) &; consider immunosuppression reduc (transplant pts).
80
Q

What is a LRTI with Bronchiectasis?

A

• Acquired disorder of major bronchi & bronchioles- permanent abnormal dilatation & destruction of bronchial walls
• Chronic cough, mucopurulent sputum production & recurrent infecs (e.g. S.aureus, H.influenzea, Pseudomonas aeruginosa, viruses).
• Exacerbation investigations: SpO2, CXR, FBC, U&Es, LFTs, CRP, review previous sputum culture
• Antibiotics recommended for exacerbations with acute deterioration with worsening symptoms
• Non-Antimicrobial Management;
o Effective clearance of respiratory secretions e.g. physiotherapy, postural drainage
o Nutritional support
o Identification and treatment of underlying cause - Annual influenza vaccination

81
Q

What is a LRTI with Cystic Fibrosis?

A

• CF- inherited disease caused by a genetic mutation on chromosome 7 causing abnormal produc & function of cystic fibrosis transmembrane conductance regulator (CFTR).
• Defective CFTR chloride channel function results in viscous secretions.
• Colonising organisms & resistance change over time:
o Staphylococcus aureus in childhood
o Pseudomonas aeruginosa in childhood/early adolescence (attempts will be made to eradicate)
o Burkholderia cepacia complex: very resistant & transmissible (need to avoid this in CF patients!)
o Non tuberculous mycobacteria & Fungi
• Acute exacerbations:
o Use most recent sputum culture results to guide treatment (often infected with normal flora)
o Prolonged antibiotic courses (3-4 weeks not uncommon)
o General measures: postural drainage, deep breathing, coughing, exercise, aerosolised DNAase etc+ Influenza and Pneumococcal vaccinations. Lung transplant.
• Colonising Organisms & resistance change over time- treated by diff antibiotics

82
Q

What is the Prevention of LRTIs?

A

• Pneumococcal vaccination (S. pneumoniae);
o Patients with chronic heart, lung and kidney disease
o Patients with splenectomy
o Infant vaccination schedule
o May repeat after 5 years in certain populations
• Influenza vaccination for vulnerable groups (annually); 2- 17 year olds, Over 65s, chronic disease, multiple comorbidities

83
Q

What is Aspergillosis?

A
  • Immunocompromised- will get infec
  • Aspergillosis is an infec caused by Aspergillus (mold- type of fungus) that lives indoors & outdoors
  • Most people breathe in Aspergillus spores every day without getting sick
  • Immunocompromised patients & those with lung disease at a higher risk of developing health probs due to Aspergillus
  • Types of health problems caused by Aspergillus; allergic reacs, lung infecs, and infecs in other organs
84
Q

What is Allergic Bronchopulmonary Aspergillosis?

A
  • In people with a background of atopy, asthma & cystic fibrosis
  • Presents with worsening asthma & lung function
  • Diagnostic features; high total IgE, specific IgE to Aspergillus & positive serum IgG to Aspergillus
  • CT imaging of the thorax may demonstrate central bronchiectasis
  • Treatment: corticosteroids and antifungal therapy
85
Q

What is Aspergilloma (pulmonary)?

A
  • Compilation: massive haemotyptysis (blood loss if it goes through one of their vessels)
  • Mobile mass (of Aspergillus) within a pre-exisiting lung cavity
  • Old cavities left by previous TB or sarcoidosis become colonised with Aspergillusspp.
  • Symptoms: cough, haemoptysis, weight loss, wheeze & clubbing. Some asymptomatic.
  • Can be demonstrated on chest X-ray or CT thorax.
  • Diagnosis can be confirmed by a positive test for Aspergillus IgG antibody
  • Sputum culture may be positive for Aspergillusspp
  • Complication: Massive haemoptysis
  • Treatment: 10% cases resolve spontaneously, surgical resection, antifungals (injected into the cavity, or orally for symptom relief).
86
Q

What is Pneumocystitis jiroveci pneumonia?

A
  • Disease of immunosuppression e.g. in HIV patients
  • Is a fungus but no ergosterol in its cell wall & not susceptible to a number of antifungals.
  • Ubiquitous in the env
  • Transmission: airborne route
  • Pneumonia: insidious onset of fever, dyspnoea, non-productive cough & reduced exercise tolerance.
  • Exercise induced hypoxia (shortness of breath on exercise)
  • Specimens: rarely isolated from expectorated sputum, can be found in induced sputum, broncho-alveolar lavage increases the diagnostic rate.
  • PCR to detect P.jiroveci DNA overtaken immunofluorescence techniques.
  • Supportive care, antimicrobials (including co-trimoxazole) and steroids.
  • Some at risk groups including HIV-infected patient with a CD4 count
87
Q

What is Nocardia Asteroides?

A
  • Genus of bacteria found in env
  • Pulmonary nocardiasis acquired via inhalation of organism
  • More common in immunosuppressed & those with pre-exisiting lung disease (esp. alveolar proteinosis)- but still rare
  • Presentation & clinical;/ radiological findings variable- diagnosis difficult
  • Lung abscesses can develop
  • Suitable specimens; sputum, or broncho-alveolar lavage or biopsy
  • Treatment: as with all pneumonic infections supportive Rx (ABC) & then antibiotics (several months). Co-trimoxazole most commonly used.
88
Q

What is Mycobacterium Tuberculosis?

A
  • Latent disease- interferon gamma
  • Infects 1/3 of the world’s pop (most frequent infectious cause of death worldwide)
  • Most cases occur in developing world (not limited to there)
  • Infec acquired by inhalation of infected resp droplets, bacilli lodge in alveoli & multiply- formation of a Ghon focus
  • Depending on host’s immune response infec either become quiescent or progress &/or disseminate
  • 90% of primary infections are asymptomatic
  • Risk of disease progression highest at extremes of age & in immunocompromised (inc. HIV)
  • Reactivation of disease may occur later in life, particularly in the immunocompromised
  • Pulmonary TB most common; chronic productive cough, haemoptysis, weight loss, fever, night sweats
  • Can disseminate (milary TB) or affect almost any other organ
  • Diagnosis: clinical features + supportive radiology + detection of acid-fast bacilli or culture of M. tuberculosis from clinical specimens (usually sputum).
  • PCR-based tests may be used to detect MTB in clinical specimens.
  • Interferon gamma release assays (IGRA) +/- Tuberculin skin test – Mantoux can be used (do not differentiate active from latent disease)
  • Treatment: combined chemotherapy for several months (usually 6/12)
  • Notifiable disease & contact tracing
  • Prevention: BCG given to infants & children in high prevalence areas (or parents & grandparents from high prevalence area)

Clinical Pathology (11 decks)

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