Respiratory Pathology Flashcards

Question

What are the Clinical Features of Lung Cancer?

Answer 1

* 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

Answer 2

* 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

Answer 3

* 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

Answer 4

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)

Answer 5

* 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

Answer 6

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

Answer 7

• 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

Answer 8

* 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

Answer 9

* 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

Answer 10

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

Answer 11

• 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

Answer 12

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

Answer 13

• 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)

Answer 14

• 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

Answer 15

* Air in pleural cavity | * Common, occasionally fatal

Answer 16

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

Answer 17

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

Answer 18

* 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

Answer 19

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

Answer 20

* 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

Answer 21

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

Answer 22

• 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

Answer 23

* 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

Answer 24

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

Answer 25

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)

Answer 26

• 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

Answer 27

• 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

Answer 28

* 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

Answer 29

* 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

Answer 30

• 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!

Answer 31

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

Answer 32

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)

Answer 33

• 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

Answer 34

• 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)

Answer 35

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

Answer 36

• 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

Answer 37

• 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

Answer 38

• 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

Answer 39

* 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

Answer 40

* 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)

Answer 41

* 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

Answer 42

* 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

Answer 43

* 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

Answer 44

• 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

Answer 45

• 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

Answer 46

``` 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) ```

Answer 47

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)

Answer 48

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§

Answer 49

• 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)

Answer 50

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

Answer 51

• 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

Answer 52

• 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

Answer 53

* 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

Answer 54

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

Answer 55

* 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).

Answer 56

• 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

Answer 57

• 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

Answer 58

• 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

Answer 59

* 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

Answer 60

* 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

Answer 61

* 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).

Answer 62

* 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

Answer 63

* 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.

Answer 64

* 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)