RESPIRATORY MEDICINE

1. Topics2. OSCE scenarios

ASTHMA:

Definition: Common chronic inflammatory disease of the airways characterised by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm.

Signs and Symptoms:

SYMPTOMS SIGNSIntermittent dyspnoea TachypnoeaWheeze Audible wheezeCough (often nocturnal) Hyperinflated chestSputum Hyperresonant percussionPrecipitating factors

Emotion, cold, allergens etcDiminished air entry

Diurnal variation

Investigations: FBC, U&E, CRP ABG: / Pa02 and PaCO2• Monitor PEF: >20% diurnal variation on 3 or more days per week (chronic

asthma) • Spirometry: Obstructive changes (FEV1/FVC; RV)• Bronchodilator reversibility (>15% improvement in FEV1)• Allergen skin prick tests: identify triggers• Aspergillus serology• CXR – hyperinflation: CXR > 6 anterior ribs

A B CAsthma Bronchiectasis PCP/HIVCOPD Interstitial lung diseaseLung Cancer SarcoidPE Sleep apnoeaPleural effusionPneumoniaPneumothoraxResp. failure – ABG profilesTBURTIs

Management:

ACUTE: 1. Assess severity:

– Severe Attack - Can’t finish sentences; HR >110 bpm; RR > PEF 33 - 50% predicted

– Life-threatening Attack - Silent chest; cyanosis; bradycardia; exhaustion; PEF <33% predicted; confusion; feeble respiratory effort

2. Sit patient up3. High-dose O2 in 100% via non-rebreathing bag4. Salbutamol 5mg + ipatropium bromide 0.5mg nebulised with O2

5. Hydrocortisone 100mg IV or prednisolone 40-50mg PO or both6. Consider Magnesium sulphate7. CXR

Safe to discharge? Stable on discharge meds for 24hrs Inhaler technique checked Peak flow rate > 75% predicted Own PEF meter and management plan GP appointment within a 1/52

CHRONIC: BTS Guidelines (just know this)

• Step 1: Occasional short-acting inhaled ß2-agonist as required for symptom relief. (Salbutamol)

• Step 2: Add standard-dose inhaled steroid. (Beclometasone)• Step 3: Add long-acting ß2-agonist (Salmeterol). If benefit but still inadequate

control, increase steroid dose• Step 4: consider trials of: beclometasone up to 1000 μg/12h; modified-release

oral theophylline; modified-release oral ß2-agonist.• Step 5: Add regular oral prednisolone. Refer to asthma clinic

COPD:

Definition: Common progressive disorder characterised by airway obstruction (FEV1 < 80% predicted; FEV1/FVC < 0.7) with little or no reversibility.

“Umbrella term for emphysema and chronic bronchitis” Emphysema – defined histologically as enlarged airspaces distal to

terminal bronchioles with destruction of alveolar walls. Bronchitis defined clinically as cough, sputum production on most

days for 3/12 of 2 successive years.

BronchitisEmphysema

Signs and Symptoms:

SYMPTOMS SIGNSCough Resp. distress –

TachypnoeaUse of accessory musclesNasal flaring

Sputum – white and frothy HyperinflationDyspnoea HyperresonantWheeze Quiet breath sounds

WheezeCyanosis

Investigations:

FBCABG – PaO2 +/- hypercapniaSpirometry – obstructive (FEV1<80%, FEV1/FVC<0.7) TLC, RV.CXR – hyperventilation, flat diaphragms, Large central pulmonary vasculatureECG – RAH + RVH (right axis deviation)Blood cults.Sputum cults.

Management: ACUTE: Look for cause – infection, pneummthorax

1. Controlled oxygen thx – start at 24 – 28% (aim for PaO2>8.0kPa + rise in PaCO2<1.5kPa

2. Nebulized bronchodilators – Salbutamol + Ipatropium3. Steriods – IV hydrocortisone + PO prednisolone4. Broad spectrum Abx to cover S. pneumonia, H. influenza and M. catarrhalis.

E.g. amoxicillin & trimethoprim, doxycycline or cefuroxime

NO RESPONSERepeat nebs and consider aminophylline

STILL NO RESPONSEConsider nasal intermittent positive pressure NIPPV if RR>30 or pH<7.35

Or consider intubation + ventilation if pH<7.26 and rising PaCO2

CHRONIC/STABLE:

Life style advice – smoking cessation, exercise, dietary advice, vaccines etc

MILD = FEV1 50-80% of predictedAntimuscarinic – Ipratropium bromide or B2 agonist Salbutamol PRN

MODERATE = 30-49% of precicted Regular anticholinergic – Ipratropium bromide/tiotropium (long acting) +/- long acting B2 agonist Salmeterol + inhaled corticosteroids – beclomethasone (NB// Seretide – combines corticosteroid + LABA)

SEVERE = FEV1<30% of predictedLABA + inhaled corticosteroid + anticholingeric Consider PO prednisolone trial

EXTRA:

Consider long term oxygen therapy (LTOT) if:Clinically stable non-smokers PaO2 <7.3kPA satble on two separate occasionsOr if PaO2 7.3-8.0 kPa + pulmonary hypertension + cor pulmonale

TUBERCULOSIS:

Definition: Common infectious disease caused by a variety of strains of Mycobacterium,

most commonly Mycobacterium tuberculosis and Mycobacterium Bovis, spread by airborne transmission

Worldwide epidemic - 1/3 of the world’s population is thought to be infected with M. tuberculosis

Accounted for 1.8 millions deaths worldwide in 2007, with 13 millions chronic/active cases in existence

Pathogenesis & Progression:

TB = granulomatous inflammatory conditionTB pulmonary alveoli and invade and replicate in alveolar macrophagesThey are then taken up by dendritic cells and can spread to lymph node GHON COMPLEX

T and B lymphocytes, macrophage and fibroblasts all aggregate and surround the infected macrophages to form a granuloma (granuloma is formed to prevent spread)Abnormal cell death at the centre caseous necrosis. Can remain dormant or be reactivated and spread

10 TB (pulmonary) 20 TB (post 10) – result of reactivation Progressive TB

75% cases active cases termed pulmonary TB25% active cases can move from lungs to other sites e.g. upper airways and gutDisseminated TB = mammillary TB

Primary TB (10)

First contact with BacillusInitial lesion in the parenchyma and subpleural spaceInvolvement of draining hilar lymph nodesLeads to formation of the GHON COMPLEXUsually asymptomatic and most cases heal by scar formation

Secondary TB (20)

Result of activation of latent 10 TB.GHON COMPLEX ASSMAN FOCUS

Signs and Symptoms:

Investigations:

Latent TB – Mantoux test if +ve consider interferon gamma testingActive TB – CXR = Consolidation, cavitation, fibrosis + calcification esp. in the apices. If CXR suggestive take sputum samples. At least 3 sputum samples (one in morning) and send for acid fast bacilli (consider bronchoscopy and lavage – obtain samples)Active non-pulmonary TB – find relevant clinical sample and send for cultures + CXR to exclude co-existing pulmonary TB

Management: START WITHOUT CULTURE RESULTS!Test colour vision – ishihara plates and stress COMPLIANCE – consider direct observed thx.

R - RifampicinI - IsoniazidP -PyrazinamideE - Ethambutol

SIDE EFFECTS: MUST KNOW

RIP

EXTRA –

ETHAMBUTOL - (EYE) Optic neuritis – 1st sign = colour vision damage RIFAMPICIN - Red/orange discolouration of tears and urine + inactivation of

the OCP + flu-like syndrome ISONIAZID - Neuropathy, agranulocytosis ( WCC – mainly neutrophils) PYRAZINAMIDE – Arthalgia (CI = Acute gout or porphyria)

PE:

Definition:

Continuation phase – further 16 weeks (24/52 on R & I in total)

Initial phase - 8 weeks

ALL = HEPATITS (small AST OK, if bilirubin STOP thx)

Thrombus usually formed in systemic veins embolized into the pulmonary arterial system.

90% of cases arise from DVT. DVT present in 70% of patients with proven PE.

Silent PE present in 50% of patients with proximal DVT

Signs and Symptoms:

Small PE: SYMPTOMS SIGNS

Unexplained dyspnoea Tachypnoea Pleuritic chest pain Pleural rub

Haemoptysis Crackles

Massive PE:SYMPTOMS SIGNS

Sudden collapse Tachycardia Severe central chest pain Hypotension

Peripheral shutdownRaised JVP (prominent A wave)

Investigations:

Well’s Score to assess probability:

o <2 = low probabilityo 2-6 = moderate probabilityo >6 = high probability

CTPA V/Q scan Duplex US with compression (for DVT) Pulmonary angiography ECG: S1Q3T3 CXR ABG: Decreased pO2 and pCO2

D-dimer

Management:

Admit Non-massive:

o IV LMW heparin (until INR = 2-3 for 2 consecutive days), o Warfarin continued for 6 months

Massive:o Thrombolysiso Unfractionated heparino Warfarin min. 6 months

PLEURAL EFFUSION – EXUDATES VS TRANSUDATES:

Definition: Excessive accumulation of fluid in the pleural space. Divided into two types depending on their protein concentration:

o Transudate effusion < 30g/Lo Exudate effusion > 30g/L

Pleural fluid: Serous fluid produced by normal pleura, contained within the cavity to aid lung function.

Signs and Symptoms:

Asymptomatic

OR:

SYMPTOMS SIGNSDyspnoea Signs of associated disease

Pleuritic chest pain – sharp & localised

Investigations:

CXR:

Management: Drainage < 2L/24h Pleurodesis - if recurrent Thorascopic talc pleurodesis Surgery

PNEUMONIA:

Definition: Defined as the inflammation of lung parenchyma, usually as a result of

infection. It is a clinically acute illness typically presenting with cough, purulent sputum

and fever.

Both physical signs and radiological changes are consistent with consolidation of the lungs.

Classification:o CAP vs. HAPo Lobar vs. Interstitialo Typical vs. Atypical

CAP: Pneumonia presenting in the community or within 48 hours of attending hospital. Mainly caused by bacteria, although can also be caused by viruses.

HAP: Acute pneumonia presenting 48hrs or more after admission to hospital. Occurs in up to 5% of all admissions. Ventilator Associated pneumonia is a subset of HAP and has a mortality of between 50-60%.

CAP organisms:o TYPICAL

Streptococcus pneumonia, Haemophilus influenzae, Moraxella influenzae, Staphylococcus aureus

o ATYPICALS Mycoplasma pneumonia, Legionella pneumophilia

(Legionnaires), Chlamydia species, Pneumocystis jirovecio VIRAL

RSV (especially in 2<yrs and elderly, risk of secondary bacterial infection)

HAP organisms:o 20% - Staphlococcus aureuso 60%- Pseudomonas aeruginosa, Acinetobacter spp, E. coli.o 20%- Other plus respiratory viruses in the immunosuppressed

Signs and Symptoms:

SYMPTOMS SIGNSFever Temp. up to 39.5 °C

Pleuritic chest pain Rigors, Malaise, AnorexiaDry cough progressing to a rusty-sputum producing cough

Purulent sputum

Rapid shallow breathing Reduced O2 SatsCVS: Tachycardia, hypotensive, cyanosis

Resp: Dyspnoea, tachypnoea, signs of consolidation (reduced expansion, dull percussion note, increased resonance, bronchial breathing, pleural rub)

Investigations:

CXR: Chest X-ray will show consolidation. Imaging can lag behind clinical presentations. Similarly, consolidation can remain despite resolution of symptoms

Lobar Pneumonia:

Focal area of consolidation. This can be difficult to differentiate from pulmonary oedema and fluid accumulation

Try to spot air bronchiograms. These can be hard to spot but they are essentially round black areas surrounded by white consolidation (representing consolidation surrounding bronchioles).

Oxygen saturation (ABGs) ECG? Blood tests (FBC, U+Es, LFTs, CRP, blood cultures, tailor to presentation) Sputum (microscopy and culture) Check urine antigen for legionella in severe cases

Management:

Oxygen (prevent respiratory failure O2< kpa)

IV fluids (hypotensive, dehydrated, hypovolemic shock) Analgesia (eg. Paracetamol) Antibiotics (empirical then adjust to results of cultures) Check for progression/ complications F/U at 6 weeks (repeat CXR)

CURB65 to assess severity:o Confusion (abbreviated mental test <8)o Urea (> 7mmol/L)o Respiratory Rate (>30/min)o Blood pressure (systolic< 90, diastolic< 60)o 65 yrs and above

0-1 = Mild 2 = Moderate 3-5 = Severe 0-1 treat as an outpatient, 2 consider a short stay in hospital or watch very

closely as an outpatient 3-5 requires hospitalization possibly ITU

MILD/MODERATEo Amoxicillin or Clarithromycin

SEVEREo Cefuroxime plus clarithromycino Benzylpencillin plus clarithromycino Clarithromycin plus rifampicin for Legionnaires

This treatment is empirical until organism sensitivities can be elicited

Prevention:

o Vaccination and pencillin prophylaxis in those at high risk (HIV, Cystic fibrosis, lymphomas, leukaemias, cytotoxic drugs and corticosteroids)

o Hand washing and VAP precautionso Hyperchlorination of water and heating (prevent legionaires)o Stop smoking (mucocillary paralysis etc…)

PNEUMOTHORAX:

Definition:

• A collection of air in the pleural cavity between the lung and the chest wall.• Tension pneumothorax: A breach in the lung surface acts as a valve, allowing

air into the cavity but not out.• Causes:

o Spontaneous - thin young men

o Traumao Iatrogenico Secondary to e.g. Asthma; COPD; pneumonia; lung abcess; carcinoma;

cystic fibrosis

Signs and Symptoms:

SYMPTOMS SIGNSNone Reduced chest expansion

Sudden onset dyspnoea Hyper-resonant percussionPleuritic chest pain Reduced Breath soundsIf 2˚ to asthma/COPD – sudden deterioration

Tension Pneumothorax:

SIGNSDeviated trachea and apex away from pneumothoraxHypotensionDistended neck veinsRespiratory distressTachycardia

Investigation:

If a tension pneumothorax is suspected, no tests as immediate treatment required

Otherwise, expiratory CXR to confirm Dark area devoid of lung markings, peripheral to edge of collapsed lung ABG if patient is dyspnoeic or has chronic lung disease.

Management:

BRONCHIECTASIS:

Definition: • “Abnormal and permanently dilated airways”• Classification: OBSTRUCTIVE*

LOWER respiratory tract• Aetiology: the airways become dilated secondary to a chronic, destructive

(hence irreversible), inflammatory process.• Causes:

o Congenital: Cystic fibrosis, Primary ciliary dyskinesiao Acquired: Post-infective bronchial damage. Major organisms: H.

influenza; Strep. Pneumoniae; Staph. Aureus; Pseudomonas aeruginosa; Klebsiella

o Mechanical bronchial obstruction. Extrinsic ( tumour, lymph nodes) or Intrinsic (foreign body)

Signs and Symptoms:

SYMPTOMS SIGNSPersistent cough Copious purulent sputum

Frequent production of green sputum SOBIntermittent haemoptysis Clubbing

Coarse inspiratory crepitationsWheeze

Investigations:

• CXR: Cystic shadows, thickened bronchial walls. Can be normal

• CT: Dilated cygnet-ring appearance airways. Use to assess extent and severity.• Sputum culture essential for treatment• Spirometry: obstructive pattern. Assess reversibility

Management:• Postural drainage: BD• Abx: ciprofloxacin 500mg 2x;

o Flucloxacillin 500mg per 6 hours in cases of Staph. Aureus. • (Bronchodilators)• (Anti-inflammatory agents e.g steroids)

INTERSTITIAL LUNG DISEASE:

Definition:

• A group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). i.e alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues.

• Are classified as a restrictive lung disease• Prolonged ILD may result in pulmonary fibrosis, but this is not always the

case.

Causes:

• Inhaled substances – inorganic (e.g. asbestosis) or organic (e.g. Hypersensitivity pneumonitis)

• Drug induced e.g. statins, methotrexate, amiodarone • Connective tissue disease • Infection e.g. Atypical pneumonia or TB • Idiopathic – Sarcoid or IPF • Malignancy - Lymphangitic carcinomatosis

Signs and Symptoms:

• Pneumoconiosis:

SYMPTOMS SIGNSSOB End inspiratory crackles

Cough WheezeFever

Occur hours after antigen exposure.

• Pulmonary fibrosis:

SYMPTOMS SIGNSProgressive breathlessness as disease becomes more severe

Progressive cyanosis

Resp. failurePulmonary hypotensionCor pulmonaleGross finger clubbing (2/3 patients)Fine bilateral end-inspiratory crackles

Investgations:

• Restrictive pulmonary spirometry with decreased DLCO.• Decreased VC and TLC• FVC and FEV1 decreased to similar degree therefore FEV1/FVC normal or

even raised.• CXR:

o Pneumoconiosis: upper zone fibrosis and/or honeycomb lung.o Pulmonary fibrosis: shows irregular reticulonodular shadowing

• CT: o Pulmonary fibrosis: Typically ground glass opacification – best seen at

the bases. Honeycomb lung in severe cases – represents cystic air spaces which are dilated and thickened terminal bronchioles.

Management:• Depends on type. • Pneumoconioses/Hypersensitivity pneumonites: Remove source of allergen.

Damage present is irreversible.

SARCOIDOSIS:

Definition:

• A multisystem non-caseating granulomatous disorder• Granuloma: An organised collection of macrophages• Unknown aetiology• Can affect almost any organ. 90% cases lung

Signs and Symptoms:

SYMPTOMS SIGNSNone Erythema nodosum

Cough & exertional breathlessness

Superficial lymphadenopathy

Respiratory & constitutional symptoms

Restrictive pattern of spirometry due to decreased lung compliance and gas exchange

Arthralgia Clear chest auscultationOcular symptoms

Investigations:

• Lymphopenia• LFTs• Hypercalcaemia (increased formation of calcitriol by macrophages)• Hypercalciuria• Raised serum ACE• CXR: symmetrical BHL, paratracheal nodes• FEV1/FVC• Biopsy (non caseating granuloma)• Bronchoscopy: cobblestone

Management:

• If acute illness, NSAIDS• If severe, steroids• Most have spontaneous remission• If hypercalcaemia, pulmonary impairment, renal impairment, uveitis then

PREDNISOLONE• Strong sunlight avoidance• Poor prognosis: afrocaribbean, >40, symptoms more than 6 months, more than

3 organs, lupus pernio. Use methotrexate, azathioprine. Single lung transplant• Overall mortality is low and reflects cardiac involvement or pulmonary

fibrosis.

2. OSCE

a) Respiratory historyb) Respiratory examc) Presenting a chest x-rayd) Inhaler technique/PEAK flowe) Explaining a procedure such as a chest drain

a) Respiratory History: Key things to remember

SOCRATES if pain = Pleuritic or cardiacAssociated symptoms =

WheezeSOBCough – character + productivePhlegm – colour and volume or blood?Night sweatsWeight lossPND – wake up gasping

Systemic symptomsTravel historyIf female – COCP?

b) Respiratory exam

Notes The Set-up

Washes handsIntroduces themselves to the patientAsks what the patient prefers to be called byExplains the examination and gets permissionAssesses pain status of the patientExposes patient from the waist upRepositions patient to 45

End of the bed

Checks for signs of breathlessness/wheeze/stridor/distressChecks whether the patient can speak in full sentences without breathing in betweenChecks surroundings for CPAP, oxygen tubing, peak flow meter, sputum pots, nebulisers, inhalers, cigarettes

Hands

Checks for temperature (warm in CO2 retention, cold with peripheral vasoconstriction or heart failure)Checks for tar staining (nicotine does no stain)Checks for peripheral cyanosis (poor perfusion to peripheries due to peripheral vascular disease, Reynaud’s phenomenon or vasoconstriction eg. in the cold)Checks for clubbing (respiratory causes are most commonly lung cancer, interstitial lung disease (importantly asbestositis) and suppurative lung diseases such as abscess, empyema, bronchiectasis. NOT COPD/asthma)Checks for fine tremor (caused by beta-agonists such as salbutamol)Checks for CO2 retention flap (late sign of CO2 retention)

Arms

Measurer radial pulse (Rate, rhythm and character. Bounding pulse present in CO2 retention)Measures respiratory rate subtly while taking pulse

Face

Checks eyes for anemia (pale conjunctiva)Checks eyes for Horner’s syndrome (compression of the sympathetic chain in the chest cavity interrupts sympathetic supply causing ptosis [relaxed superior tarsal muscle], anhydrosis and meiosis)Checks face for lupus pernio (purple swelling of sarcoid granuloma)Checks lips and tongue for central cyanosis (seen in severe pneumonia, COPD and pulmonary embolism)

Neck

Checks the JVP (raised in states of pulmonary hypertension and/or right-sided heart failure such as cor pulmonale, superior vena cava obstruction, cardiac tamponade, constrictive pericarditis and restrictive cardiomyopathy)Palpates the submental, submandibular, pre-auricular, post-auricular, cervical chain, supraclavicular, occipital and axillary lymph nodes

Inspecting the Chest

Checks for scars (such as a sternotomy or thoracotomy)Check for assymmetrical expansion (indicates lung disease on that side)Checks for visible veins (sign of superior vena cava obstruction)Checks for pectus excavatum (normal variant whereby sternum is depressed into the chest)Checks for pectus carinatum (abnormal deformity with chest wall protruding outwards caused by increased respiratory effort in childhood when bones are still malleable, eg. asthma)

Checks for barrel chest (rounded thorax caused by hyperinflation, a marker of smoking related lung disease)Checks for spinal deformities such as scoliosis or kyphosisChecks for the use of accessory muscles

Palpating the Chest

Palpates for tracheal deviation (deviated towards collapsed lung or localised fibrosis, deviated away from pneumothorax and large pleural effusion)Assesses chest expansion (unilateral reduction in expansion caused by pneumothorax, pleural effusion, pneumonia and collapsed lung)Assesses the tactile vocal fremitus by asking the patient to say “99” while feeling at 3 places each side of the chest using the ulnar edge of the hand (Increased over areas of consolidation eg. pulmonary edema, inflammatory exudate, blood or pus. Increased over areas of pleural effusion or pneumothorax as the filled pleaural space acts as a barrier to sound)

Percussing the Chest

Percusses the clavicle (without the flat hand)Percusses 3 areas of the lung on each side (Resonant=normal lung. Dullness=areas of increased density such as consolidation (eg. pneumonia), collapse, alveolar fluid, pleural thickening, fibrosis, peripheral abscess or neoplasm. Stony dullness=the unique extreme dullness heard over a pleural effusion. Hyper-resonant=areas of reduced density emphysema, pneumothorax, COPD)

Auscultation of the Chest

Asks patient to take deep breaths in through the mouth when stethoscope is placed on the chestAuscultates both sides of the chest (Normal “vesicular” sounds are produced by the large airways and then changed as they come through the normal small airways. Reduced sound is caused by an effusion, tumor, pneumothorax. Bronchial breathing occurs when consolidation, lung absesses and dense fibrosis cause the sound from the bronchi and larynx to be better transmitted to the chest wall and therefore sounds like breath sounds at the trachea. Added sounds include: 1) Wheeze is a whistling caused by a narrowed airways heard best in expiration. A polyphonic wheeze occurs in asthma as many airways are constricted. A monophonic wheeze occurs when a single airway is narrowed eg. foreign body or carcinoma. 2) Crackles (also called crepitations or rales) are caused by “popping open” of collapsed alveoli as air enters them. Fine crackles occur in small airways late in inspiration and are caused by fluid, infection or fibrosis usually at the lung bases. Coarse crackles sound like rice krispies and are in the larger

airways caused by infection or fluid. 3) Pleural rub occurs in both expiration and inspiration due to inflamed surfaces of the pleura rubbing together in pneumonia and pulmonary embolism with infarction.)Assesses vocal resonanceAssesses vocal pectoriloquy (whispering sound instead of “99”. If still loud, then consolidation is likely)

Back

Inspects the patient’s backPalpates the patient’s backPercusses the patient’s backAuscultates the patient’s back

Finishing off (SOAP)

Sends off a Sputum potChecks Oxygen saturationChecks for Ankle edemaMeasures Peak flowAsks if patient would like help getting dressed

c) Presenting a chest x-ray

DO NOT TOUCH THE FILM!!!!!!

Identify film

NAME DOBDATE OF FILMTYPE (AP/PA)

Quality of film:

R – rotation = position of clavicle headsI – inspiration > 6 anterior ribs = hyperinflationP – penetration = see thoracic spine through heartE – exposureF – framingL – lines or anything else

Then state the most striking abnormality.

Now Begin by looking at:

Trachea – central or displaced? Towards lesion = Collapse Away from lesion = Tension

Mediastinum – widened? Aneurysm Unfolded aorta LN enlargement – TB/ Sarcoidosis/ Lymphoma

Hila = L usually higher than R & compare shape and density Enlarged – Pulmonary artery HTN Calcified – Post TB/ Silicosis

Heart = CTR – 50% (hard to assess in AP film) – can you see the R and L heart borders

Diaphragm = Costophrenic angles – blunt or defined? Look for stomach bubble/ raised hemi-diaphragm

IF NOTHING SEEN – KEY AREAS:1. Behind the heart2. Pleura3. Apices4. Below diaphragms5. Bones

Finally summarise your findings, mentioning the important negatives and the stating the most consistent diagnosis.

d) Inhaler technique

WIPER Introduce and explain purpose of interviewCheck understanding of Asthma and rationale behind inhaler therapy

1. Stand up sit up straight before using inhaler

2. Remove cap and shake inhaler

3. Hold canister vertical for delivery of drug

4. Hold canister with middle finger and thumb

5. Put mouthpiece in mouth at start of inspiration

6. Inhalation should be slow and deep

7. Press canister down with index finger

8. Hold breath for 10 seconds

9. Wait about 30 seconds before administering the next dose

10. Close cap

Offer Spacer if still difficult. Same rules just breath normally through spacer

Spacer not dishwasher safe, just simply rinse and leave to dry.If steroid inhaler advise to do just before teeth – good mouth hygiene indicatedOffer leaflet and a follow up to answer questions they might have later on.

Rotahaler Capsule administration of drugTwist to release drug – inhale simultaneously Hold breath for 10 s

Other inhalers Easi-breath (teeth bite mouthpiece inhaler), Accuhaler (metered dosing)

e) Explaining a procedure such as a chest drain

Key to all explaining stations is to have a proforma that can be applied to all of them and avoid jargon. They are checking your communication not your knowledge.

WIPEREmphasis on explaining why here – that want to discuss proposed action and answer any of their questions. Say that this is a chance for them to ask you anything so feel free to interrupt me.

Then establish their knowledge base and what they want to know?

Background – reasons for doing procedure etc

Before – if there is any prep needed ie fasting etcDuring – on the day what to expect After – Can they leave straight after/ drive/operate machinery etc also will they need a friend or family member to pick them up

Risks and benefits

Results – when will they receive them and how

Any questions?

Ask them to repeat back what you have said and then offer leaflet and another chance to chat if they would like

NB// if this is a consent station bare in mind you must also offer alternatives and risks if patient choses not to have procedure.