Respiratory

Question 1

What is silicosis ?

Occupations at risk?

Features?

Answer 1

Silicosis is a fibrosing lung disease caused by inhalation of fine particles of crystalline silicon / silica.

Occupations at risk - Miners, slate works, potteries, foundry worker ( metal casting)

Features - upper zone fibrosing lung disease

“Egg shell” calcification of hilar lymph nodes

Question 2

Common causes of IECOPD

NICE guidance on mx

Answer 2

Bacterial - haemophilus influenza, streptococcus pneumoniae and moraxella catarrhalis.
Viral - Rhinovirus most important pathogen.

NICE guidance:
Increased freq of bronchodilator and consider giving via nebuliser.
Prednisilone 30 mg OD for 5 days
Oral abx only if sputum is purulent or there are clinical signs of pneumonia. 1st line abx –> amoxicillin, clarithromycin or doxycyline.

Question 3

NICE recommendation for admission with IECOPD?

Answer 3

Severe SOB
Acute confusion / reduced concious level
Cyanosis
o2 sats < 90%
Social reasons - living alone or unable to cope at home
Significant comorbidity e.g cardiac or insulin dependent diabetes.

Question 4

Hospital mx of IECOPD

Answer 4

Controlled oxygen therapy. All patients on high flow o2 via non rebreathe if hypoxic. ABG should be completed to determine if pt is CO2 retainer. ( CO2 retainers have lost hypercapnic drive for respiration and rely on hypoxia to drive RR, if giving too much o2 can suppress resp drive). If non retainer, aim sats 94-98%, CO2 retainer 88-92%.

Nebulised bronchodilators - salbutamol and ipratroprium
Steroid therapy - Oral prednisilone or IV hydrocortisone
IV theophylline if failure to respond to above.
Abx - 1st line Amoxicillin / 2nd line if pen allergy - doxycycline, if received abx recently in past 5 days co trimoxazole (5 day course)

Development of T2RF - NIV. Typically for pts with respiratory acidosis pH 7.25- 7.35. BTS state NIV can be used in patients who are more acidotic but HDU monitoring required. BiPaP typically used with initial settings - EPAP 4-5 cm H20 and IPAP 10-15 cm

Question 5

Pneumothorax mx

Primary PT

Secondary PT

Iatrogenic PT

Answer 5

Primary PT: No underlying respiratory disease.

If rim of air < 2cm & patient asymptomatic then d/c considered.
If < 2cm but symptomatic then aspiration should be considered.
If aspiration fails or remain SOB then chest drain should be inserted.

Secondary PT:
If > 50 yrs old, rim of air > 2cm and / or pt SOB then chest drain should be inserted.
If rim of air 1-2cm then aspiration. If aspiration fails then chest drain. All patients admitted for at least 24 hours
If PT < 1cm then o2 and observation for 24 hours.

Iatrogenic PT:
Less likelihood of recurrence than Spont PnT
Majority resolve with observation, if treatment required then aspiration used.
Ventilated pts need chest drains / COPD pts.

Question 6

Recommendation for persistent pneumothorax

Answer 6

If persistent air leak/ insufficient lung re-expansion or recurrent pneumothoraces then video assisted thorascopic surgery ( VATS) should be considered to allow for mechanical/ chemical pleurodesis +/- bullectomy

Question 7

D/C advice for patients with PT?

Answer 7

Smoking - avoid to reduce further risk of PT
Flying - not before 6 weeks or for 1 week post a check xr
Diving - never unless surgical BL pleurectomy and normal lung function and CT scan post op.

Question 8

2WW referral for lung cancer when?

Answer 8

CXR suspicious for lung cancer
> 40 yrs and unexplained haemoptysis.

Question 9

Offer urgent CXR ( 2 weeks) for ? Lung cancer when?

Answer 9

> 40 YRS and they are a non smoker with two of the following unexplained symptoms or smoker with one of the following unexplained symptoms:

Cough
Fatigue
SOB
Chest pain
WL
Appetite loss

Question 10

Consider an urgent chest x-ray (to be performed within 2 weeks) to assess for lung cancer in people aged 40 and over with any of the following..?

Answer 10

Persistent/ recurrent chest infections
Finger clubbing
Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
Chest signs consistent with Lung cancer
Thrombocytosis *raised platelets > 450 x 10 9

Question 11

Lung CA RF’s

Answer 11

Smoking - increases risk by 10 x
Asbestos - increases risk by 5 x
Both smoking & asbestos are synergistic ( if both 50x risk)

Others:
Arsenic / radon/ nickel
Aromatic hydrocarbons
Cryptognic fibrosing alveolitis

NOT related is COAL dust.

Question 12

Sleep apnoea - Predisposing factors?

Presentation?

Answer 12

RF’s:
Male
Middle aged
Obesity
Macroglossia - acromegaly, hypothyroid, amyloidosis
Large tonsils
Marfans syndrome
Alcohol intake

Ob sleep apnoea - episodes or partial or complete airways obstruction. Episodic obstruction is associated with oxyHG desaturation and arousal from sleep.

Presentation:
-often noticed by partner, excessive snoring & may report periods of apnoea.
Chronic snoring & gasping
Unrefreshing sleep
Morning headache
Daytime somnolence
Reduced concentration
Insomnia and restless sleep
Depression and anxiety
Compensated respiratory acidosis and hypertension.

Question 13

AX of sleep apnoea?

Answer 13

Epworth scale
Referral to ENT for polysomnography studies - overnight oximetry

Question 14

Mx of sleep apnoea

Answer 14

Conservative - lifestyle modification including weight loss, reduced alcohol and stop smoking

Medical mx - CPAP 1st line for moderate to severe OSA.
CPAP improves survival, sleepiness and mood. Needs pt education and adherence, proper facial mask fitting.
2nd line if CPAP not tolerated intra oral devices or for mild OSA with no daytime sleepiness.

• DVLA need to be informed if daytime sleepiness *

Question 15

Indications for BiPAP?

Answer 15

COPD with resp acidosis pH 7.25-7.35.
T2RF secondary to chest wall deformity, Neuromuscular disease or OSA.
Cardiogenic pulmonary oedema unresponsive to CPAP.
Weaning from tracheal intubation.

Bipap - cycle of high and low prssure to corrspond with inspiration and expiration.
Insipiratory PAP - prssure to force air into lungs 10-15 cm
Expiratory PAP - to keep airways open during expiration 4-5 cm

Question 16

Main indications for placing chest drain in pleural infection?

Answer 16

Frankly purulent / turbid/ cloudy pleural fluid on sampling.
The presence of organisms identified by Gram stain and/or culture from a non-purulent pleural fluid sample indicates that pleural infection is established and should lead to prompt chest tube drainage.
Pleural fluid pH < 7.2 in patients with suspected pleural infection indicates a need for chest tube drainage.

Question 17

Define pleural effusion

Pathophysiology of pleural effusions

Answer 17

Pleural effusion = abnormal collection of fluid within the pleural space commonly detected on CXR as blunting of costophrenic angles / consolidation with a meniscal line.

Pathophysiology:
Pleura is formed of mesothelial cells and connective tissue. Two layers, the visceral layer ( covering lung tissue) and parietal layer ( covering chest wall) and between them the pleural space. Pleural space normally contains around 10 mls fluid & lubricates the surfaces allowing for easier respiration and generates surface tension ( pulling the parietal and visceral pleura together).

Under normal circumstances there is a constant balance between fluid entry and exit into the pleural space. Related to three things 1) Hydrostatic pressure in vessels 2) oncotic pressure of vessels 3) lymphatic drainage.

Increase in fluid entry:
1) increased vasc permeability - infection or malignancy
2) increased microvascular pressure - e.g. HF or cirrhosis
3) reduced plasma oncotic pressure - Nephrotic syndrome/ cirrhosis

Reduced fluid exit:
Altered lymph drainage after radiotherapy or extrinsic physical compression.

Question 18

Causes of pleural effusion split into transudate vs exudate

Answer 18

Exudate - protein content > 35g/L or 3.5 g/dL with high protein and cellular content.
Due to increased vascular permeability or reduced lymphatic drainage. Causes:
1) Parapneumonic effusion
2) malignancy
3) Trauma
4) TB
5) PE
6) Pancreatitis
7) Radiation pleuritis
8) Systemic inflammation - RA or SLE

Transudate - low protein content ( < 25g/L or 2.5g / dL). Due to increased hydrostatic pressure or reduced oncotic pressure:

Heart Failure
Cirrhosis
Nephrotic syndrome
Meig’s syndrome - Triad of benign ovarian tumour, pleural effusion and ascites.
Peritoneal dialysis

Question 19

Presenting sx of pleural effusion

Answer 19

Pleuritic CP
SOB
Cough - productive favours parapneumonic , dry favours transudative cause.
O2 requirement
Reduced Ex Tol

Examination :
Reduced chest expansion
Stony dullness to percussion
Reduced breath sounds
Decreased vocal resonance
Tracheal deviation if large ( > 1L)
Clubbing - lung cancer.

Question 20

Imaging in pts with suspected pleural effusion?

Answer 20

PA & lateral CXR - Key findings blunting of costophrenic angles, meniscus level, fluid in fissures, tracheal/ mediastinal deviation with large effusions. Complete white out seen in large effusions.

Pleural USS- increases likelihood of successful pleural aspiration and sensitive for detecting pleural septations.
Contrast CT - for underlying cause in exudative effusions.

Question 21

Outline investigation in Pleural effusion

Answer 21

Bedside - Sputum sample and gram stain
Bloods - FBC/ CRP/ U&ES/ LFTs / NTproBNP/ Blood cultures if ? infective
Imaging. - CXR, pleural USS , CT CAP. ECHO for ? HF.

Special tests:
Pleural aspiration / drainage.
Generally BL pleural effusions are assumed to be transudative and pleural aspirations not done unless unsuccessful trial of treatment / cause unclear.
If unilateral pleural effusion, pleural tap usually done to confirm if transudative vs exudative.

Question 22

What is sent for from pleural fluid during a pleural paracentesis?

Answer 22

USS guided pleural aspiration done to avoid complications. Fluid is sent for:
1) pH - pleural fluid alkaline pH ( 7.6). pH < 7.3 abnormal - parapneumonic effusion. pH < 7.2 - empyema.
2) Protein - transudate vs exudate. Transudate < 30g/ L , exudate > 30g/L. IF intermediate level of protein ( 25- 35) use Lights criteria.
3) LDH - Part of lights criteria, High in exudate, low in transudate.
4) MCS - gram stain, culture, sensitivity & TB
5) Cytology - ? malignant cells
6) Glucose - Glucose < 3.3 mol/L suggests parapneumonic/ empyema/ malignant/TB/SLE
7) Haematocrit - > 50% = haemothorax
8) WCC - high neutrophils in parapneumonic effusion , high leucocytes in TB/lymphoma/sarcoid
9) Amylase - high in pancreatitis / oesphageal rupture or malignancy
10) Lipids - > 110 / dL - chylothorax

Question 23

What is Lights criteria and when is it used?

Answer 23

Used to distinguish between exudate and transudate when there is intermediate levels of protein ( 25-35 g/L) .
Exudate if:
Pleural fluid protein / serum protein ratio > 0.5
Pleural fluid LDH / serum LDH > 0.6
Pleural fluid LDH more than 2/3rds upper limit of normal serum LDH

Question 24

Other characteristic pleural fluid findings:
low glucose: ? differentials
raised amylase: ? differentials
heavy blood staining: ? differentials

Answer 24

low glucose - TB / Empyema/ RA

Raised amylase - pancreatitis, oesphageal perforation

Heavy blood staining - mesothelioma, PE, TB

Question 25

Characteristic of pleural fluid in: 1) Parapneumonic effusion 2) Empyema 3) TB 4) HF 5) Malignant

Answer 25

Parapneumonic - Turbid/ straw coloured, pH < 7.3, High protein, +ve gram stain, LOW glucose < 3.3 Empyema - Pus on aspiration, pH < 7.2, high protein, low glucose < 3.3 , +Ve gram stain TB - Turbid/bloody/straw coloured, Very high protein, Very low glucose, low pH & +ve for acid fast bacilli. HF - straw colourd, low protein count, negative MCS, normal glucose Malignant - blood stained fluid, high protein , LOW glucose. -ve mcs, Cytology positive for malignant cells

Question 26

When should a chest drain be placed in suspected pleural infection?

Answer 26

All patients admitted with sepsis or pneumonic illness should have diagnostic pleural fluid sampling. if pleural fluid is cloudy/ purulent or turbid a chest drain should be placed. If fluid is clear but pH less than 7.2 chest tube should be placed.

Question 27

Management of pleural effusions?

Answer 27

Treat the cause. Dependent on size may need aspiration or drainage. Small asymptomatic effusions often do not need intervention. Large effusion ( > 1L) - therapeutic and diagnostic paracentesis or chest drain. Recurrent pleural effusions - Pleurodesis after drainage via chest drain using sclerosing agents ( fibroses the pleural space). OR surgical management - if pleural biopsy is required, video assisted thorascopic surgery ( VATS) for biopsy, washout and pleuredectomy. Empyema - always requires chest drain and empirical abx. ( coamoxiclav + metronidazole or Tazocin).

Question 28

Asthma management in adults

Answer 28

1) New diagnosis - SABA 2) Not controlled on previous step OR new diagnosis with symptoms >= 3x / week OR night time waking --> SABA + Low dose ICS 3) SABA + low dose ICS + Leukotriene receptor antagonist ( LRTA). 4) SABA + Low dose ICS + LABA . Can continue LRTA if benefit. 5) SABA +/- LTRA. Switch ICS/LABA for one inhaler, MART ( maitenance and reliever therapy) which includes a low dose ICS & fast acting LABA e.g. formoterol. 6) SABA +/- LTRA + medium dose ICS MART . Or consider changing back to fixed dose Moderate ICS and separate LABA. 7) SABA +/- LTRA and one of the following: - Increase ICS to high dose ( not as MART as part of fixed dose regime). -Trial LAMA (tiotroprium) or Theophylline ( methylxanthine / PDE inhibitor) -Referral to secondary care for specialist advice.

Question 29

Low vs Med vs High ICS dosing?

Answer 29

Low dose - < = 400 micrograms budesonide 400-800 micrograms moderate dose budesonide > 800 micrograms - high dose budeosonide

Question 30

What is intersitial lung disease? What is the most common type?

Answer 30

Interstitial lung disease - umbrella term for group of conditions that lad to progressive fibrosis and scarring of the lung tissue. Leads to restrictive disease and impaired gas exchange. Most common type is idiopathic pulmonary fibrosis

Question 31

Pathophysiology of interstitial lung disease

Answer 31

Inflammation and scarring of the lung interstitium. Some diseases driven mainly by inflammation that may respond to treatment, once scarring has occurred it is irreversible. Repeated injury of lung tissue leadings to fibroblast activation and laying down of new ECm. In ILD genetic mutations in fibroblasts leads to excess ECM depositing and scarring. The lung interstitium is thicker which increases the diffusion distance and compromising gas exchange.

Question 32

Causes of interstitial lung disease?

Answer 32

Idiopathic - IPF Autoimmune / connective tissue disease - sarcoidosis, RA, SLE/ Sjogrens/ systemic sclerosis/ Alpha 1 antitrypsin/ UC Environmental: Asbestosis Silicosis Occupational: Hypersensitivity pneumonitis Bird fanciers lung ( droppings) Farmers lung ( mouldy spores in hay) Mushroom workers lung Malt workers lung ( mould on barley) Infective: - mycoplasma pneumonia / pneumocystis pneumoniae Drugs : BANSMe Bleomycin Amiodarone Nitrofurantoin Sulfasalazine Methrotrexate

Question 33

Investigations of ILD

Answer 33

Bloods - FBC ( chronic anaemia ) , CRP, ESR ( raised) , U&E ( vasculitis) & autoimmune screen. ( RF/AntiCCP RA, ANA SLE). Imaging- CXR --> reticular fine opacities. HRCT - Ground glass appearance, later honeycombing ( destruction of airspaces) , traction bronchiectasis ( dilated airways pulled apart by fibrosis) .Reticular opacities with thickening of lung interstitium. Special tests - BAL / Transbronchial biopsy or surgical lung biopsy

Question 33

Common features of ILD

Answer 33

Symptoms: Progressive exertional SOB & Reduced exercise tolerance ( progresses over weeks - months) Chronic dry cough General fatigue and malaise Symptoms of CTD e.g. arthralgia, dysphagia, dry eyes etc Examination features: Clubbing Skin - raynauds ( systemic sclerosis) / erythema nodosum ( sarcoidosis) Bibasal fine end inspiratory crackles Dullness to percussion and pleural effusion Painful joints

Question 34

Causes of upper zone fibrosis - CHARTS

Answer 34

Coal worker pneumoconiosis Hypersensitivity pneumonitis Ankylosing spondylitis / ABPA Radiation TB Silicosis / sarcoidosis

Question 35

Causes of lower zone fibrosis

Answer 35

RASIO RA Asbestosis SLE/Scleroderma/Sjogren IPF Other- drugs

Question 36

Mx of Interstitial lung disease

Answer 36

Conservative --> Avoidance of causes/ drugs/ toxin Stop smoking Pulmonary rehabilitation Annual influenza and one off pneumococcal Medical mx: IPF --> antifibrotic drugs ( Pirfenidone) Sarcoidosis --> Prednisilone Connective tissue disease/ autoimmune --> steroid, azathioprine, mycophenolate extrinsic allergic alveolitis --> steroid LTOT if sats < 88% & paO2< 7.3 kPa

Question 37

Define Idiopathic pulmonary fibrosis Who is typically affected?

Answer 37

Chronic lung condition where there is progressive fibrosis of the lung tissue with no clear cause. Typically seen in men ( 2x common) and over 50 yrs ( 50-70yrs).

Question 38

Key features of IPF RFs for IPF

Answer 38

Insidious onset > 3 montsh with progressive SOB on exertion and dry cough. Constitutional sx - fatigue / reduced appetite/WL/arthralgia. OE - bibasal fine end inspiratory crackles & clubbing RFs - male, 50-70 yrs, family history, smoking, exposure to asbestosis/ metal / dust/ livestock

Question 39

Ky findings in the investigation of IPF

Answer 39

Restrictive pattern on Spirometry - Reduced FVC, normal / reduced FEV1 , FEV1/FVC ratio > 0.7. Reduced TCLO ( impaired gas exchange) Imaging - bL interstitial shadowing ( small irregular peripheral opacitities) ( ground glass) later progressing to honeycombing/ traction bronchiectasis. HR CT imaging of choice. BAL - high lymphocytes ( good prognosis) , high PMN / eosinophils (poor prognosis) Bloods - Raised CRP/ESR, Raised IgG's. ANA + ve / RF +ve.

Question 40

Mx of idiopathic pulmonary fibrosis

Answer 40

Smoking cessation Pulm rehab LTOT Antifibrotic

Question 41

Scoring systems used in Risk assessment of pneumonia 1) Community score 2) Hospital score Other point of care test ?

Answer 41

CRB 65 in community : Confusion RR > 30 BP < 90 systolic or < 60 diastolic 65 - 1 point if over 65 0- low risk - consider treatment in the community 1-2 - intermediate risk - consider hospital assessment 3- high risk > 10% mortality risk) transfer to hospital for assessment and treatment CURB65 Confusion Urea > 7 mmol RR > 30 BP systolic < 90 or < 60 diastolic 65 yrs Score 0-1 consider treatment at home ( low risk, less than 3% mortality risk) Score 2>= intermediate risk ( 3-15% mortality risk) Score 3>= - high risk (> 15% mortality risk). Another point of care test is - CRP. Recommendations made with regards to abx therapy. CRP < 20 mg/L - not routinely offered abx CRP 20-100 - consider delayed abx prescription CRP > 100 - offer abx therapy

Question 42

Mx of low / moderate/ high severity CAP?

Answer 42

Low severity CAP - 1st line amoxicillin 5 -7 days. If pen allergic then macrolide/ tetracycline. ( Clarithromycin or doxycycline) Moderate CAP - dual abx therapy with amoxicillin and macrolide. (Clarithromycin) 7-10 day course recommended. High severity CAP - Penicillin cover with Co amoxiclav, ceftriaxone or Pip Taz PLUS macrolide 7-10 day course.

Question 43

Mx of HAP

Answer 43

Depends on local guidance and timing of onset after hospital admission. Generally if early in admission and no previous abx been prescribed ( therefore low risk of resistance) - Oral Amoxicillin or IV amoxicillin. If early onset ( , 5 days) and abx have been given in the last two weeks then - Cotrimoxazole 960 mg BD 5 days ( IV or PO) Late onset > 5 days and no abx in past 2 weeks - cotrimoxazole 960 mg BD 5 days ( IV or PO) Late onset and abx given in past 2 weeks - Piperacillin with tazobactam 4.5 g TDS IV D days If concern about MRSA - add vancomycin iv 5-10 DAYS

Question 44

When is Prophylactic antibiotic tx offered in COPD management? What investigations are required before?

Answer 44

Azithromycin prophylaxis is recommended in COPD patients who: - Have optimised therapy - Freq exacerbations with sputum production - Prolonged exacerbations with sputum production -Hospitalisation from exacerbation CT thorax ( exclude bronchiectasis), ECG ( azithromycin prolongs QT interval), LFT ( Azithromycin can cause liver derangement) and sputum cultures ( rule out atypical infections) prior to starting azithromycin.

Question 45

What is mesothelioma ?

Answer 45

Mesothelioma - epithelial malignancy of mesothelial cells of pleural cavity strongly associated with asbestos exposure. Unlike asbestosis, mesothelioma can occur with only short term exposure ( and is not related to the amount of exposure). Commonly seen in construction workers , electricians, plumbers, shipyard workers.

Question 46

Features of mesothelioma?

Answer 46

SOB ( progressive over months) WL / anorexia Chest wall pain Clubbing Chronic cough 30% present as painless pleural effusions & only 20% have pre existing asbestosis. History of asbestos exposure in 85-90% , latent period of 30-40 yrs.

Question 47

Ix of mesothelioma

Answer 47

CXR - features suspicious for mesothelioma / asbestos exposure. Lower zone fibrosis, pleural plaques, pleural thickening or pleural effusion/ pleural mass. Pleural CT Pleural aspiration - exudative with malignant cells. Local anaesthetic thoracoscopy increasingly used to ix cytology negative exudative effusions ( high diagnostic yield) - camera inserted into pleural space to visualise and take biopsy. If pleural nodularity is seen on CT then image guided pleural biopsy.

Question 48

Mx of mesothelioma

Answer 48

Often has metastasised by diagnosis making it inoperable. Very poor prognosis with median survival 8-14 months. Chemotherapy +/- radiotherapy Surgery if operable Industrial compensation Symptomatic management - morphine, oxygen , LTOT

Question 49

Outline the pharmacological management of COPD

Answer 49

Step 1: SAMA ( ipratroprium) or SABA ( salbutamol or terbutaline) as required Then - any features of asthma? Includes previous diagnosis of asthma or atopy, raised eosinophil count, FEV variation or PEFR diurnal variation > 20%. For Asthmatic features: Step 2 - SABA/ SAMA PRN & Regular LABA + ICS. Step 3 - Remain symptomatic or freq exacerbations then Above PLUS LAMA. ( SABA / LABA/ LAMA / ICS For no Asthmatic features: Step 2 : SABA PRN, LABA + LAMA Step 3 : if remaining symptomatic Add ICS trial for 3 months, if no improvement revert back.

Question 50

Additional medical mx of COPD if previous therapy failed ( At end of step 3)

Answer 50

1) Oral theophylline - only after trials of short and long acting bronchodilators 2) Oral carbocistiene - considered in patients with chronic productive cough 3) Long term prophylactic abx - Azithromycin ( as previous ) 4) PDE 4 inhibitors - Oral PDE 4 inhibitors such as Roflumilast reduced the risk of COPD exacerbations in patients with severe COPD ( FEV < 50%) and hx of freq exacerbations ( > 2 in last 12 months despite maximal therapy) .

Question 51

What is sarcoidosis? What are the risk factors ?

Answer 51

Sarcoidosis is a chronic granulomatous disorder. Granulomas are inflammatory nodules full of macrophages and cause of granulomas is unknown. Usually presents as a respiratory disease 90% but has many extra pulmonary manifestations. Commonly skin manifestations are tested - erythema nodosum and lupus pernia Risk factors: Female Aged 20-40 or 60 Black ethnic origin or Scandinavian origin Fhx

Question 52

Presenting features of Sarcoidosis

Answer 52

Resp - Dry cough, SOB & chest pain ( due to development of pulmonary nodules, fibrosis and mediastinal lymphadenopathy). Constitutional - WL, anorexia, swinging fever, lymphadenopathy MSK - arthralgia Skin - Erythema nodosum ( multiple erythematous tender nodules on shins) or lupus pernio ( pathognomonic for sarcoid, purple nodules or plaques on nose/cheeks/chin/ears) Eyes - painful red eye ( uveitis) / loss visual acuity and photophobia Hypercalcaemia - ( macrophages inside granulomas increases conversion of vitamin D to active form) - renal colic/ stones

Question 53

Lofgrens syndrome?

Answer 53

Specific presentation of sarcoidosis with classic triad: Erythema nodosum BL Hilar lymphadenopathy Polyarthralgia

Question 54

Heerfordt's syndrome

Answer 54

Heerfordts syndrome - Parotid enlargement, fever and uveitis secondary to sarcoidosis.

Question 55

Investigations in sarcoidosis?

Answer 55

Bedside -ECG to exlude cardiac involvement ( half of patients have abnormal conduction). Urine dipstick to screen for proteinuria. Bloods: ACE level --> macrophages within the granulomas produce ACE, levels increase in active sarcoidosis. FBC ( anaemia) CRP/ESR raised ( inflammatory condition) U&Es - renal involvement Bone & calcium - granulomas increase active vit D - hypercalcaemia LFTs - look for hepatic involvement Imaging: CXR - BL hilar lymphadenopathy ( classical finding). DDx - TB/ Lung Ca/ Lymphoma HRCT - Hilar LN , pulm nodules, fibrosis affecting middle & upper lobes Spirometry - restrictive pattern Bronchoscopy & biopsy --> Gold standard for confirmation of diagnosis = non caseating granulomas

Question 56

Mx Sarcoidosis

Answer 56

Sarcoidosis is largely a benign disease with the majority of patients showing clinical regression or stabilisation. Treatment started in severe disease. No treatment is 1st line in patients with no to mild sx as the condition often resolves spontaenously. Monitoring with LFTs and CXR 6 m . Treatment required if: BL HLN & infiltrates on CXR, hypercalcaemia or eye/heart/neuro involvement. Oral steroid 6-24 m if treatment required plus bisphosphonates to protect against Osteoporosis. 2nd line methotrexate and azathioprine

Question 57

1) What is varenicline 2 ) Use 3) SE's

Answer 57

Varenicline is a partial agonist of the nicotinic AchR Used as an aid in smoking cessation. Should be started 1 week before patients target date to stop. Recommended course is 12 weeks. SE - nausea, secondary to release of dopamine leading to GI disturbance N&V. Other SE headaches, insomnia and abnormal dreams. Caution - depression or self harm Contraindication - pregnancy and breast feeding

Question 58

General management tips for smoking cessation

Answer 58

Offer NRT, varenicline or buproprion. 1 agent should be offered as part of a commitment to stop smoking on or before a particular date ( target stop date). Prescription should be sufficient to last only 2 weeks after target stop date. Further prescription only to pts who have demonstrated attempt to quit is continuing. If unsuccessful using NRT / varenicline or buproprion no repeat prescription within 6m

Question 59

Recommendations for NRT Adverse effects

Answer 59

NICE recommend offering a combination of NRT - patches plus another form ( gum/ inhlator/ lozenge or spray) to those who have found single forms of NRT inadequate in the past. Adverse effects - N&V, headaches, flu like symptoms

Question 60

What is Buproprion Use? Risks Contraindications?

Answer 60

Bupropion is a NA/DA reuptake inhibitor and nicotinic antagonist. Should be started 1-2 weeks before pt target date to stop smoking. Small increased risk seizures CI - epilepsy, pregnancy and breastfeeding / Eating disorder

Question 61

Smoking cessation management in pregnancy?

Answer 61

NICE recommnd all pregnant women are testing for smoking using Carbon monoxide detectors ( CO reading of 7ppm) / current smokers, those who have quit in last two weeks should be referred to NHS stop smoking services. 1st line - CBT/ motivational interviwing 2nd line NRT Varenicline and buproprion are contraindicated

Question 62

Features of moderate asthma

Answer 62

PEFR 50-75% best or predicted Speech normal RR < 25 / min Pulse < 110 bpm

Question 63

Features of severe asthma

Answer 63

PEFR 33-50% best or predicted HR < 110 RR > 25 Inability to complete sentences ( sats remain above 92%, LOW paCO2 < 4.6, maintaining normal paO2).

Question 64

Features of life threatening asthma

Answer 64

CHEST Confusion / Coma + Cyanosis / CO2 " Normal" ( 4.6-6.0) Hypotension & Hypoxia ( PaO2 < 8kpa Sats < 92%) pEFR < 33% best or predicted, exhaustion Silent chest /feeble resp effort Tachycardia - HR > 110 & Tachypnoea RR > 25

Question 65

Features of near fatal asthma

Answer 65

-Raised pCO2 > 6 kPa ( indicates tiring & exhaustion) --> requires intubation and mechanical ventilation

Question 66

Management of acute asthma : Admission criteria

Answer 66

Anyone with lifethreatening features Anyone with severe features failing to respond to Treatment Presentation at night Pregnancy Presenting with worsening symptoms despite being on oral steroid already. Lower threshold: under 18 yrs Recent hospital admission or severe attack Concern over ability to cope at home

Question 67

Management of acute severe/ lifethreatening / near fatal attacks in hospital

Answer 67

1) Oxygen 15L non rebreathe , aim 94-98% 2) Salbutamol nebuliser " back to back" 2.5 mg - 5mg 20 mins apart over 1 hour. 3) may need to add ipratroprium bromide ( 0.5mg) after 1st nebuliser if no effect or if attack is severe/life threatening. Ipratroprium can be used every 2O mins up to 2hrs if required. 4) oral prednisilone 50 mg ( should be continued for a minimum of 5 days ) or IV hydrocortisone 100 mg 5) IV magnesium sulphate ( 1.2g -2g ) infusion over 20 mins 6) IV aminophylline ( can cause arrhythmia therefore needs cardiac monitoring) / IV salbutamol ( can cause hypokalaemia, tachycardia, tremor and lactic acidosis) ( requires ICU admission) 7) Mechanical ventilation / ECMO

Question 68

When should a referral to ICU be done for acute severe asthma?

Answer 68

Failing to respond despite treatment & Evidence of tiring or exhaustion: Rising CO2/ Falling O2 levels Acidosis Confusion / reduced concious level Poor respiratory effort --> resp arrest Deteriorating PEF

Question 68

Discharge criteria for asthma patients

Answer 68

Stable for 24 hours off all treatment ( no nebulisers or oxygen) Inhaler technique checked and recorded PEFR > 75% Informed GP and FU in 48 hours Oral steroids to continue until 5 days post attack Resp clinic FU if admitted within 1 month , if ICU admission life long follow up

Question 69

Fill out the table

Answer 69

Question 70

COPD - reason for using inhaled corticosteroids

Answer 70

Reduced frequency of exacerbations. Evidence from numerous clinical trials, which have shown that ICS use in COPD patients reduces the rate of exacerbations, especially in those with a history of frequent exacerbations. This therapeutic benefit can significantly improve patient's quality of life and decrease hospital admissions.

Question 71

Fill out the values

Answer 71

Question 72

Causes of BL hilar lymphadenopathy

Answer 72

Most common causes are TB and sarcoidosis Other causes: Lymphoma Malignancy Pneumoconiosis ( any lung disease caused by inhalation of organic or non organic airborne dust and fibres) Fungi - histoplasmosis , coccidiodiomycosis

Question 73

Key facts to inform patients of if found with pleural plaques?

Answer 73

Pleural plaques are benign. They are the most common form of asbestos related lung disease, they do not undergo malignant change and do not increase your risk of lung cancer or mesothelioma. No FU required and patient can be reassured. Ongoing FU of asbestos related disease encouraged.

Question 74

What are the common forms of asbestos related disease?

Answer 74

1) Pleural plaques - benign, do not undergo malignant change, most common form of asbestos related disease, generally occur after latent period of 20-40 yrs. 2) Asbestosis - fibrosis of lung secondary to asbestos 3) Mesothelioma - Malignant disease of pleura secondary to asbestos exposure 4) Pleural thickening -Asbestos exposure may cause diffuse pleural thickening 5) lung cancer -lung cancer is actually the most common form of cancer associated with asbestos exposure. It also has a synergistic effect with cigarette smoke in terms of the increased risk.

Question 75

Asbestosis : Severity related to? Latent period Causes what type of fibrosis? Who is at risk? Patho phys Symptoms IX Mx

Answer 75

Asbestosis = lung fibrosis related to asbestos exposure. Asbestos is fibrogenic & oncogenic. Severity of asbestosis is related to length of exposure ( in contrast to mesothelioma where limited exposure can cause disease). Latent period 15- 30 yrs post exposure. Normally causes lower lobe fibrosis ( RASIO) Asbestos including in building/ ship construction/ textile industry. ( carpenter/ roofer/ plumber/ shipyard worler/ mechanics/ welder) , family members also at risk of secondary exposure. Pathophys - alveolar macrophages attempt to ingest asbestos fibres, release cytokines and GFs, inflammation and excess ECM. scarring. Sx - Progressive SOB on exertion, chronic cough, chest pain, WL, Fatigue. Signs - BL end insipiratory crackles & clubbing Lung function tests - restrictive pattern and reduced TLCO Mx - conservative. Risks - increased risk of NSCLC ( adenocarcinoma). Smoking and asbestos are synergisitic.

Question 76

Define acute bronchitis Presentation Causes Exam

Answer 76

Acute bronchitis is a self limiting lower respiratory tract infection & is the result of inflammation of the trachea and major bronchi. It is associated with oedema of airways and production of sputum. Acute onset < 3 weeks of Cough - productive or not Sore throat Rhinorrhoea Wheeze SOB Low grade fever . * Key onset of cough alongside viral symptoms * Normally resolves within 3 wks although 25% will still have a cough beyond this time. Common in autumn and winter. Viral causes most common. Majority of pts have normal examination , some may present with wheeze/ rales/ low grade fever

Question 77

Mx of acute bronchitis

Answer 77

Analgesia Good oral intake Consider abx therapy if pts systemically unwell, or preexisting comorbidities OR point of care CRP testing: CRP 20-100 mg ( offer delayed prescription), CRP > 100 mg offer abx immediately Doxycyline 1st line ( not in children or pregnant women ) , alternative is amoxicillin.

Question 78

What is bronchiectasis Causes

Answer 78

Permanent & irreversible dilatation and thickening of bronchial walls due to destruction of the muscular and elastic components. Often secondary to recurrent infections or underlying disorder. Causes: Recurrent / severe infections - TB/ Pertussis/ Influenza Immune deficiency - HIV Genetic - Cystic fibrosis, Ciliary dyskinetic syndromes ( Kartagner's/ primary ciliary dyskinesia) Connective tissue disease - RA/ EhDlos/ Marfans/ Sjogrens Obstructive disease - COPD/ Asthma 50% idiopathic

Question 79

What are some of the most common organisms isolated from bronchiectasis patients?

Answer 79

Haemophilus influenzae Pseudomonos aeruginosa Klebsiella Streptococcus pneumoniae

Question 80

Pathophysiology of bronchiectasis

Answer 80

Vicious cycle --> initial infection with pathogen, leads to inflammation of airways, activation of neutrophils and release of elastase --> impaired mucociliary clearance --> airway mucus hypersecretion and obstruction --> microbial colonisation / infection ---> further inflammation and bronchial dilatation / airways destruction

Question 81

Symptoms of bronchiectasis

Answer 81

Chronic productive cough with copious sputum production SOB Haemoptysis Wheeze Chest pain Freq chest infections & Rhinosinusitis Hx of childhood respiratory infections/ asthma Constitutional sx - fever/ fatigue/ WL -often absence of smoking history and younger age than COPD.

Question 82

Examination features of Bronchiectasis

Answer 82

Clubbing Wet cough Wheeze Coarse inspiratory crackles and crepitations. ( high pitched squeaks and pops) Chest hyperinflation

Question 83

Investigation of bronchiectasis

Answer 83

Sputum culture: Haemophilus / pseudomonas/ aspergillus fumigatus ( ABPA) Spirometry with bronchodilator reversibility --> obstructive pattern common Bloods: FBC/CRP/U&Es - look for infective cause, raised eosinophils in ABPA. Autoimmune screen --> RhF Immunoglobulins ( immune deficiency) HIV ab test Alpha 1 anti-trypsin imaging - CXR --> tramline opacities on XR HR CT --> *Signet rings * due to thickening & dilation of airways.

Question 84

Management of bronchiectasis

Answer 84

Conservative: 1) Chest physiotherapy for inspiratory muscle training, postural drainage. ( postural drainage is a technique using gravity to clear mucus from the lungs) 2) Annual flu and one off pneumococcal 3) Smoking cessation Medical management: Treating underlying cause. Bronchodilators - esp those with pre-existing asthma/ COPD Mucolytics - Prophylactic abx - particularly if there is evidence of chronic infection ( pseudomonas) or frequent exacerbations ( Azithromycin) Surgical - lobectomy if localised disease

Question 85

Key features of Klebsiella pneumonia

Answer 85

Klebsiella - gram -ve rod part of normal gut flora. Typically causes pneumonia following aspiration. More common in alcoholics and diabetics. May occur after aspiration " Red currant jelly sputum" Often affects upper lobes Commonly causes lung abscess and empyema Mortality is high 30-50%

Question 86

Outline the severities of COPD and FEV1 predicted values

Answer 86