1. 1
Respiratory Medicine
Thisguide isintendedtobe usedasa resource alongsidemanyothersources
Knowledge:
 Anatomy &Physiology
 Normal ranges
 Respiratory failure
 Pleural diseases
 Asthma
 COPD
 Bronchiectasis
 Cystic Fibrosis
 Pneumonia
 Tuberculosis
 Lung cancer
 Pulmonary Fibrosis
 Occupational
 Thromboembolism
 SleepMedicine

2. 2
Anatomy & Physiology
The lungsare linedbyvisceral pleurawhichiscontinuouswiththe parietalpleuraandfacilitates
movementforbreathing.Pleuralubricatedbysurfactactantproducedbytype IIpneumocytes.
23 generationsformbronchustoalveolarsacs,cartilage endsatgeneration12(bronchioles)
Trachea dividesatcarina@ T4
Rightbronchuswider,shorter&more vertical
Left lung– 2 lobesseparatedbyoblique fissure
 upper(mainlyanterior) –4 bronchial subdivisions
 lower(mainlyposterior)–4 bronchial subdivisions
Surface contacts
1. Aorticarch
2. Commoncarotid
3. Thoracic duct
4. Vagus& phrenicnerves
Right Lung – 3 lobes.U& M separatedbytransverse fissure,Lseparatedbyobliquefissure
 upper(mainlyanterior) - 4bronchial subdivisions
 middle (smallandonlyanterior) - 2bronchial subdivisions
 lower(mainlyposterior)- 5 bronchial subdivisions
Surface contacts
1. Oesophagus
2. IVC& SVC
3. Brachiocephalic&azygosveins
4. Vagus& phrenicnerves
Normal ABG Ranges
H+ - 35 - 45nmol/l (pH 7.35 - 7.45)
HCl- - 22 - 26 mmol/l
PaO2 - >10kPa
PaCO2 - 4.7 - 6.1kPa
Base Excess - -2 - +2 mmol/l

3. 3
Respiratory Failure
A ventilation/perfusionmismatchcausespulmonarygasexchange tofail tomaintainnormal oxygen
and carbon dioxidelevels.
Type 1 – Hypoxia(PaO2<8kPa)
Type 2 – Hypoxia&Hypercapnia(PaCO2>6.6kPa)
Causes
Type 1 Type 2
Acute Chronic Acute Chronic
H+
Normal/Raised Normal Raised Normal/Raised
HCl-
Normal Normal Normal Raised
Causes Acute asthma Emphysema Severe asthma COPD
Pulmoedema Fibrosis COPDexacerbation SleepApnoea
Pneumonia Lymphangitis Airwayobstruction Kyphoscoliosis
Pneumothorax Carconomatosa Acute paralysis Myopathies
PE Right-to-Leftshunt Narcotics Ankylosingspondylitis
ARDS Brain-stemLesion Primalveolarhypovent
Investigations
ABG
CXR
Management
Oxygen(maximumunlesssevere COPD (24-28% withventure mask))
Treat underlyingcondition
If worsening/noimprovementinABGpatientneedsmechanical ventilation.
Long TermOxygenTherapy(LTOT)
Indications(+smokingcessation)
-PaO2<7.3kPa& FEV1<1.5L
-7.3kPa < PaO2< 8kPa & PulmHypertension/Peripheral Oedema
Aimfor PaO2>8kPa withoutunacceptable rise inPaCO2
Therapy>15 hours/day

4. 4
Pleural Diseases
Pneumothorax–airinpleural space
Primary – occurs in absence of underlyinglungdisease(Male,20s,tall,thin,smokerw/apical blebs)
Secondary – occurs in presence of underlyinglungdisease(COPD&TB...othersalso)
Traumatic – causedby surgery,chestwall injuryetc.
Clinical features
Symptoms
Sudden,unilateral pleuriticchestpain
Breathlessness
Cough
Signs
Decreased/absentbreathsounds&vocal resonance
Hyper-resonantpercussion
Reducedexpansion
Tracheal deviation&mediastinal shift(Tension)
Investigations
CXR – complete translucency.Small <2cmLarge >2cm (>2cm = 49% hemi-thorax)
Management
Tension&secondary= Intercostal tube drainage (ICD)
Primary&>50 years old=ICD
Primary&<50 years old= Percutaneousaspiration
Primary&<15 % hemithorax =Observationfor6 hoursand follow upas outpatient
Videoassistedthoracoscopicsurgery(VATS) indicatedwhen:
Failure forlungto re-expand(5days)
1st
contralateral PTX
2nd
ipsilateral PTX
Spontaneousbilateral/haemothorax
Professionsatrisk
No flyingfor6 weeks
No diving(unlesspleurectomyperformed)
Pleural effusion– fluidinpleural space
Fluid- effusion
Pus– empyema
Blood– haemothorax
Clinical features
SOB
Underlyingdisease
Signs
Reducedexpansion/breathsounds&vocal resonance
Stonydull percussion
Investigation&Management
CXR - >200ml requiredbefore evident
USS – useful foraspiration
CT – distinguishesbetweenbenign&pleural disease
Aspiration
Microbiology - culture
Biochemistry –protein,glucose,LDH,pH
Pathology – cytology
Biopsy(Abram’sorVATS)
Histology
TB culture
Commoncauses
Pneumonia Ex
TB Ex
PE Ex (occasionallyTrans)
Malignancy Ex
Cardiac failure Trans
Renal problemsTrans
Light’sCriteria
Pleural FluidProtein:Serumproteinratio>0.5
Pleural FluidLDH:SerumLDHratio>0.6
Pleural FluidLDH> 2/3 of normal upperlimitserumLDH
Anypositive =Exudative (infection/malig/inflamm/PE)

5. 5
Asthma
No universal definition.Paroxysmal airwayobstructioncausedbyinflammationtriggered bya
specificstimulus.
Airwaynarrowingdue tobronchoconstriction&mucusplugging.Hypersensitive &increasedinflame
cells.Chronicleadstopermanentremodelling.
 Extrinsic– Specificallergenidentified.80%.IgE productionesptodustmites,pollenandpet
dander
 Intrinsic– Occurs inadultsand doesnotimprove
 Drug induced – NSAIDS(espaspirin) inhibitCOX= Leukotriene…thinkanti-leukotriene therapy
 Exercise induced –Hyperventilation=waterloss= mediatorproduction=asthmasymptoms
Epidemiology –8 milliondiagnosed(5.1Mon treatment).Prevalence increasing(300M worldwide)
possiblydue to central heating, pollution, processedfoods&hygiene hypothesis.1/6occupational.
Onset– Anyage, butcommonerinearlydecades.(Worse prognosisinadult-onset)
Symptoms – Breathlessness,chesttightness,wheeze&cough
Thinkof variability,timeof onset,provokingfactorsetc.
Diagnosis
Characteristichistory
 Diurnal symptoms(worse inearlymorning&disturbingsleep)
 Coughlasting>10 days& difficulttoclear
 Recurrentepisodesof wheezingesp.whenassociatedwithaprovokingfactor
FEV1>15% followingbronchodilator
>20% diurnal variation
FEV1>15% decrease following6minsof exercise
Management
Step 1 Step 2 Step 3 Step 4 Step 5
Education and environmental control
Β2 agonist (salbutamol)
Low dose ICS 200µg -
800µg (prednisolone)
Highdose ICS 2000µg Glucocorticosteroid
Low dose
Long actingβ-agonist
(salmeterol)
Leukotriene
antagonist/inhibitor
Anti-IgEtreatment
Theophylline
Considerif >2
exacerbationsonstep
1
Stepup to control symptoms.Bearinmindnon-complianceif symptoms worsening.
If symptomsstable,stepdowntherapy.
Acute exacerbations
Precededbyviral infections,moulds,pollen&pollution
Mild/Moderate–Generallyworseningsymptomsof PEF<60% of best
Doublingof ICSdose
Severe –PEF<50%

6. 6
Heart rate >110
Resprate >25
Inabilitytocomplete sentencesin1breath
Life threatening- PEF<33%
SpO2 <92%
Silentchest
Bradychardia
Cyanosis,exhaustion,confusion&coma
NearFatal - RaisedPaCO2 and/orrequiringmechanical ventilation
Immediate treatment
ABG
Oxygen– Highconcentrationaspossible.If notabove 92%,mechanicallyventilate
Bronchodilators –High dose salbutamol.Ipratropiumbromide inlife threateningcases
SystemicCorticosteroids –OPrednisoloneorIV hydrocortisone.Reduce inflame&hasten
resolution
Theophylline–monitorserumlevelsif givingregularly
IV fluids – Noevidence tosupport,butusuallynecessary.EspK,as serumKcan be low
If PEF remainsbelow30%,IV magnesium, aminophyllines&leukotriene RAs.
PEF measuredevery15-30 minsandthen4-6hrs.
Discharge 24hrs after PEF>75%
IndicationsforMechventilation
Coma,exhaustion,drowsiness
Resparrest
ABG deteriorationdespite besttherapy(PaO2<8kPa&fallingorPaCO2>6kPa& rising)
Pregnancy
1/3 getbetter, 1/3 remainthe same,1/3 getworse.90% no symptomsduringlabour
Biggestthreatto foetusisexacerbation,mostdrugsfine.
Occupational
Symptomsimprove atweekends/holidays.
Diagnosedbyrecording2-hourlypeakflows
Causative agents Occupations mostat risk
Isocyanates Paintsprayers
Flour& grain Bakers
Animals Nurses
Aldehydes Chemical workers
Colophony&fluxes Animal workers
Latex Welders
Wood dust Foodprocessingworkers
Timberworkers

7. 7
COPD
Airflowlimitationthatisnotfullyreversible.Characterizedby chronicbronchitis (cough&sputum
for >3 consecutive monthsover2 years) and/or emphysema(permanentenlargementof airspaces
distal toterminal bronchiolesw/wall destruction) whichcan be panlobular(Lowerlobe.α1 ATD) or
centrilobular(Upperlobe.Smokers)
Preventable&treatable withsignificantextra-pulmonaryeffects (muscleweakness,peroedema,
weightloss,osteoporosis).Progressivewithabnormal inflamresponse tonoxiousparticles/gasses.
Epidemiology
Directlyrelatedtotobaccosmoking(anduse of biomassfuelsinlow/middle income countries).
30,000 deathsperyear.5% of all deaths
1/8 of all hospital admissions.220,000 peryear
80 M worldwide
RiskFactors
Tobacco (95% of casesinUK) & cannabis smoke
Biomassfuels
Occupation – Coal miners
Airpollution
Low birthweight –Lower maximal lungvolume
Lung growth - Lowermaximal lungvolume (maternal smoking&
childhoodinfection)
Infections –Accelerate decline of lungfunction.HIV asx w/
emphysema
Genetic– α1-antiprotease deficiency.OtherCOPDgeneslikelytobe
identifiedinfuture.
Clinical Features
Chronicbronchitisand/orbreathlessness
Pulmonaryoedema
RR >20
Accessorymuscle use
Pursedlipbreathing
Chestwall abnormalities –Horizontal ribs,barrel shapedchest,protrudingabdomen, Intercostal in-
drawing,flattenedhemi diaphragm,decreasedcricosternal distance.(All hyperinflation)
Central cyanosis,signsof CO2 retention.
Peripheral oedema&weight/muscle loss
Investigations
X-ray– Eliminate othercauses:heartfailure,lungcancer&identifybullae
FBC – Eliminate anaemia&Documentpolycythaemia.Assay α1ATinyoungpatients.
Spirometry –FEV/FVC<70%. Nonreversible.
Transferfactor/diffusingcapacity.Lowgasexchange
Exercise testing
HRCT
α1-antiprotease deficiency
1/5000 live births
α1-AT aggregates in liver = liver
damage in some individuals
Emphysema <50 years old
Some individuals normal
Panlobar basal emphysema
Smoking cofactor

8. 8
Management
No COPDcure,but therapycan slowdisease progression,ease symptomsandreduce exacerbations.
Smokingcessationcritical &reductioninotherpossible RFs(e.g.pollution)
Β-agonist(betterinasthma) &anticholinergics (betterinCOPD) improvesymptoms&Spirometry.
Theophyllineimproves exercise testing&bloodgases.
Pulmonaryrehabilitationimprovesexercise tolerance andQoL.Noimpacton Lungfunction
Long termoxygentherapydecreasesmortality(>15hours/day).Criteria:COPD
PaO2<7.3kPa (whenwell)
Smokingiscontraindication
Surgery:Bullectomy
Lungvolume reductionsurgery
LungTransplantation
Exacerbations
Two of following three symptoms: Breathlessness
Lung volume
Change of sputumcolour
Management
Optimise bronchodilators(β-agonist+/- Ach+ Oral glucocorticoids)
Antibiotics(Thinksmall,Amoxicillin250mg/Doxycycline500mg or Clarithromycinif pennalleror Co-
amox if β-lactam+ve)
Oxygen(CheckABGwithin 60 minsof Oxygenadministrationoranychange)
Ventilation(Non-invasive better)
Factors asx w/ deathinacute onchronic respfailure
Age
Acidosis(H+
>55nmol/l
Hypotension
Uraemia
Breathelessness&exercise limitation
•SABA/SAACh
Exacerbationand/orpersistantbreathlessness
•FEV>50% - LAACh
•FEV<50% - LABA + ICS
Persistentexacerbations
•FEV>50% - LABA + ICS
•FEV<50% - LABA + LAMA + ICS

9. 9
Bronchiectasis
Abnormal dilationof the bronchi w/progressive scarring&lungdamage
Causes
 Congenital
 CysticFibrosis
 CiliaryDysfunctionSyndromes(primaryciliarydyskinesia&Kartanger’s)
 PrimaryHypogabbaglobinaemia
 Acquired – Children
 Pneumonia(complicatingwhoopingcough/measles)
 PrimaryTB
 Inhaledforeignbody
 Acquired – Adult
 Supprative pneumonia(pneumoniaw/pus& permlungdamage,asx w/ abscess)
 Allergicbroncho-pulmonaryaspergillosis(complicating
asthma)
 PulmonaryTB
 Bronchial tumours
Clinical Features
Cough– Chronicand productive of copiouspurulentsputum.Worse in
mornings& onchangingposture.Asx w/halitosis
Haemoptysis –Slightormassive.Usuallyasx w/ sputum& purulence.
Can be onlysymptom(drybronchiectasis)
Pneumonia&pleurisy –Inflammationcausesfever&malaise aswell
as a sharp painuponbreathing,
Poorgeneral health – weightloss,anorexia&failure tothrive.
Signs
Fingerclubbing
Coarse inspiratorycrackles
Wheeze
Investigation
Sputumculture (Routine,fungal &TB)
Bloodtests – FBC, U&Es, LFTs, Immunological
X-Ray– Notapparentunlesssevere
CT – May showBronchial dilation&wall thickening
Ciliarydysfunction –Saccharintest
Management
Smokingcessation
Antibiotics1st
line Amox 500mgTDS
2nd
line Clarithromycin500mgbd
Vaccination(annual flu&5yr pneumococcal)
Pulmonaryrehabilitation (>2timesdaily)
Pharmacology – SA-βA toimprove function,thenLA-βAif minimal improvement
ICS to reduce numberof infections
LT-Abx if >3 exacerbations/yearw/PsAeruginosa
Surgery – Onlyconsiderinpatientswithnoco-morbiditieswith localised,unresponsive &severe
bronchiectasis.(EmphysemaisaCI)
Mild– CXR normal
DiagnosisbyCT scan
Severe –CXR abnormal
-Cysticchanges
-Tramlining
-Collapse
Mucus plugging
DiagnosisbyCT scan
Bacterial colonisation
2/3 chronicallycolonisedby
H. influenzae β-lactam+ve Co-amox 375mg TDS
β-lactam-ve Amoxicillin500mgbd
S. Pneumonia Amoxicillin500mg bd
M. catarrhalis Co-amox 375mg TDS
S. Aureus Flucoxicillin250mgQDS
Ps.Aeruginosa See below
Sputum
Serous– frothy/clear. Pulmonaryoedema
Rusty- pneumococcal (lobar) pneumonia.
Mucoid - clear,white or grey.Asthma,
chronicbronchitisandinacute viral
respiratoryinfections
Mucopurulent– yellow/green/brown.
Pulmonaryinfection.Darker= serious
Ps.Aeruginosaeradication
Step1 Ciprofloxacin750mgBD 2 weeks
Step2 Anti-pseudomonal abx IV 2weeks
Step3 repeatciproflox 4weeks+nebulised
colomycin2MU bd3 months
Step4nebulisedcolomycin2MUbd 3 months

10. 10
Cystic Fibrosis
Mutationin CFTR (mostcommon ΔF508) gene (onchromosome 7) resultingin abnormal
sodium/chloridemovementand dehydrationinairwayepitheliumincreasingchancesof chronic
infection,ciliarydysfunction&bronchiectasis.
Epidemiology
Most commonfatal geneticdisorderinCaucasians.Autosomalrecessive.1/25carrier rate with
1/2500 live birthrate.
Clinical features
At birth,the lungsare macroscopicallynormal andlungfunctionnormal.
Respiratory
-Infectiveexacerbationsof
bronchiectasis
-SpontaneousPneumothorax
-Haemoptysis
-Nasal Polyps
-Respfailure
-Corpulmoale
-Lobar Collapse
GI
-Meconiumileus (14%)
-Malabsorption
-Steatorrhea
-Distal intestinal obstruction
syndrome
-Biliary cirrhosis&portal
hypertension
-Gallstones
-Rectal prolapse
Other
-Diabetes(25%)
-Delayedpuberty
-Male infertility (failure of vas
deferenstodevelop)
-Stressincontinence (dueto
persistentforcedcough)
-Osteoporosis
-Arthropathy
Investigations
Screening(detects~50% of affectedchildren)
Sweattest(increasedsodium chlorideinsweat)
Low elastase instools
Management
Similartosevere bronchiectasis
Pulmonaryphysiotherapy
S. Aureusinfectionsmanagedwithoral abx
Ps. AeruginosatherapymanagedwithIV abx (@home throughS/Cvascularport)
Regularnebulisedabx therapy(colomycin/tobramycin) betweenexacerbationstosuppresschronic
Ps A colonisation.
Many resistantstrainsdevelop&treatmentbecomestailoredtoeachpatient
Home Oxygen&NIV treat respfailure inlatterstagesof disease.
Lung transplantationwouldbe ideal,butlimitedbydonors.
Nonrespmanagement
Malabsorptiontreatedbyoral pancreaticenzyme supplements&vitamins.
Highcalorie diet
Somaticgene therapytoreplace faultygene withaworkingone isundertrial andis an exciting
researchfield.

11. 11
Pneumonia (Community Acquired)
A lowerrespiratorytractinfectionw/new X-rayshadowingwithnoothercause.
Epidemiology
5-11/1000
Mortality<1% in community
6-12% inhospitalisedpatient
>35% inITU
Clinical Features
Symptoms
Cough(92%)
Breathlessness(67%)
Pleuriticpain(62%)
Newsputumproduction(54%)
Haemoptysis(15%)
Signs
Fevers,rigors,tachypnoea,tachycardia,
hypotension,rigors
Coarse crackles,reducedexpansion,bronchial
breathing,pleural rub
Aetiology
Community Hospital
S. Pneumoniae 36% 39%
H. Influenzae 10% 5%
Legionella 0.4% 3.6%
Atypicals 2.6% 27%
Viruses 13% 13%
No cause 45% 31%
CURB65–used to predict30 day mortality (poorforverysick,veryyoung& veryold)
Confusion
Urea>7
RespRate >30
BP <90/60 (eitherone)
>65 yearsold
1 pointforeach
0-1 Outpatient(mort<2%)
2 In-patient;shortstay(mort~10%)
>3 In-patient;considerICU(mort15-40%)
Investigations
CXR – usuallyconfirmsdiagnosis.Opacityoccurswithin12-18hours of onsetinthe affectedlobe.
(May take 6 weekstoclear)
ABG
FBC (WCCveryhighin severe butmaybe normal whencausedbyatypical organisms) U&Es& LFTs
CRP usuallyelevated
Microbiology:
CURB 0-1– not necessaryinmildpneumonia
CURB 2 – Blood& Sputumculture
Pneumococcal urine antigentest
Pleural fluid(ifpresent) aspiratedformicroscopy&culture
CURB >3 – AsCURB 2
DIF foratypical pathogen(egM. pneumonia,adenovirus)
Management
Oxygen(>35%humidified)&IV fluids
Physiotherapy
Paincontrol (beware opiateswithpoorrespfunct)
Legionellasuspected?
 Urine for legionellaantigen
 Sputumsample forlegionellaculture
& Direct Immunofluorescence(DIF)
Abx 1st
line therapy
Low severity O amoxicillin500mg
Mod severity (within4hours) O amoxicillin500mg+
clarithromycin500mg
Verysevere (asap) IV co-amoxiclav1.2g+ clarithromycin
500mg
If Legionellasuspected,addinIV levofloxacin

12. 12
Tuberculosis
Infectioncaused predominantly byMycobacteriumtuberculosis(Mtb)
Epidemiology
~10/100,000 in UK. Mortality10%
1/3 worldwidehave latentMtbinfection with2-3milliondeaths/year
RiskFactors
TB contact
Veryyoung/elderly
Ethnicminorities
Immunosuppressed (HIV/chemotherapy)
Healthcare worker
Silicosis
Clinical Features
Several weeks/months
Weightloss/anorexia
Nightsweats
Cough+/-sputum+/- haemoptysis
General Malaise
Investigations
CXR – Upper lobespredominate (ΔΔsarcoid,oldinfection&infectionfromotherpathogen)
Consolidation,cavitation,military(<5mmnodules)
Bloodtests - ESR, Hb, Na, serumalbumin&derangedLFTs
Tuberculintest
Early morningurine
Sputumsamples
Diagnosis
Sputumx3 (includinganearlymorning sample)&bloodculture
Bronchoscopywithwashings(orBAL)
Gastric washing(usedforchildren)
Management
RifampicinR 6 months
Isoniazid H 6 months
Pyrazinamide Z 2 months
Ethambutamol E 2 months
PyridoxineB6 6 months
Differentregimesavailable basedonpatientresistance.
Multi-DrugResistantTBisresistanttoRifampicin&Isoniazid
Oral steroidstobe usedinextensive TBor withextensiveextra-pulmonaryfeatures(2-3months)
Control & prevention
Contact tracingto establishsource
Tuberculintest 0-5mm –ve (orv severe)
5-15mm immune
>15mm active TB (or strong
reactionto BCG)
Onlyuseful todifferentiate SarcoidfromTB
Resultread48-72 hours after
Extra-pulmonaryfeatures
Lymphadenitis
GI – esplowertract & acute abdomen
Pericardial –effusion&constrictive
CNS– meningeal disease(highmortrates)
Bone & joint– Lowerspine,hip&knee
GU- renal symptomsformany years
Side effects
R H Z E
P450 inducer P450 inhibitor Rash Retrobulbarneuritis
Bodilyfluidsorange Rash Hepatitis Dose halvedinCRF
Rash Hepatitis Arthralgia
Hepatitis Gout
Nausea& Vomiting

13. 13
Lung cancer
Malignanttumoursmore commonthan benign
Small cell lungcancer 20% (Many metastases)
Non-small cell lungcancer
Squamous 30-40%
Adenocarcinoma 20-30%
Large cell 10%
Undifferentiated 10%
Mixed/other <5%
Clinical Features
All 6
Hoarseness,Horner’s (apical tumour),armpain,SVCO
Investigation
CT scan betterthan CXR,usedforstaging
PET scan (mustbe done withCT)
Staging
TNM
PET scan more sensitive thanCT
Management
SCLC chemosensitive (80%responds)
Prolongssurvival from2– 16 months
NSCLC surgery(onlystage T1 &T2)
Radiotherapycanbe good,but can be bad
Mesothelioma
Presentsaspleural effusionw/chestwall pain
40 yearsbetweenasbestosexposure anddiagnosis
CXR – Pleural thickening
Thoracotomyto diagnose
Chemotherapymaybe useful
Survival 9-12 months
CXR Nodule differentiation
Benign Malignant
Small Large
Smooth Spiculated
Calcified Non-calcified
Equal distribution Upper lobes&Rightside
more common
TNMStaging
T1 Tumour<3cm
T2 Tumour>3cm &<7cm
T3 Tumour>7cm +/- invasionof diaphragm/chestwall
T4 Invasionof heart/greatvessels/mediastinum/trachea
N0 No nodal involvement
N1 Ipsilateral butclose
N2 Ipsilateral bitdistant
N3 Contralateral
M0 Nodistantmetastases
M1 Distantmetastases

14. 14
Interstitial Lung Disease (ILD)(>200 types)
CXR shadowing Bi-basal -IPF
ILD asx w/connective tissue disorder
Asbestosis
Bilateral mid-zone –Sarcoidosis
Bilateral upper–Sarcoidosis
Silicosis
Coal workers pneumoconiosis
Hypersensitivitypneumonitis
Peripheral bilateral–Eosinophilicpneumonia
Flittingshadows –Cryptogenicorganisingpneumonia(COP)
IdiopathicPulmonary Fibrosis(IPF)
Clinical Features
Breathlessness
Cough(dry)
Signs
Clubbing
Fine bi-basal mid&late crackles
Dull Percussion&Decreasedvocal resonance
Epidemiology
5-15/100,000. 4000-5000 newcasesper yearinUK (90 in Lothian)
Medianage presentation –68
M:F 2:1 Smokers:non-smokers
Investigations
Spirometry –Restrictive. Lung volume &gas transfer
HRCT – bi-basal sub-pleuralhoneycombcysts
Lung biopsy – if HRCT not conclusive,biopsyshowsdistortedlungarchitecture w/honeycombcysts
Management
No goodtherapy.UsuallyjoinanRCT & palliate withoxygen,opiatesetc.
Lung transplantif <65?
Mediansurvival 3-4 yearsafterpresentation
Sarcoidosis
Systemicdiseasecharacterisedbynon-caseatinggranulomas (small inflame nodules).Cause unknown
Clinical features
SOB
Cough(dry)
Fatigue&Skinlesions
Hypercalcemia
Investigations
Spirometry –Normal stage 1. Restrictive.ReducedTLC&KCO
Bloodtestsgenerallynormal.SerumACEmay monitordisease activity.
Tuberculinskintest –ΔTB
Biopsy – skin/lymphnode/lung.Noncaseatinggranuloma.
Management
Sarcoidosisisusuallyself-limiting.ICSpossible &lungtransplantiscurative
Staging
1 – Bi-hilarlymphadenopathy(BHL).Asympt.60-80%
spontaneouslyremitwith1year.ErythemaNodosum
2 – BHL + infiltrates(=parenchymal disease) remitsin50-60%
3 – Infiltrates.remitsin20-30%
4 – Fibrosis.Occursin5-10%. Irreversible.

15. 15
Occupational lung disease
Pneumoconiosis
Reactionof lungto inhaleddust
Coal Workers Pneumoconiosis (CWP) –small rounded opacitiesinupper&middle zones
Progressive Massive Fibrosis(PMF) –Irregularopacities
Riskof developingincreaseswithincreasingexposuretodusts
Silicosis
A pneumoconiosis causedbyinhalationof silica
Riskof developingincreaseswith increasingexposuretosilica
Progressive &irreversible
Can be complicatedbypulm hypertension&cor-pulmonale
Appears10 yearsafterexposure
Asbestosis
Tinyblue fibres
Requiresmuchasbestosexposure
15-30 yearsafterexposure before symptomsappear.

16. 16
Venous Thromboembolism (VTE)
PE & DVT – Most PEs arise fromlowerlimb.
Annual risk0.1-0.3%
Mortality1-2% (10% of hospital deaths)
RiskFactors
Major Surgery –major surgery
Obstetrics –late pregnancy,Csection
Lowerlimbproblem-fracture.Varicose veins
Malignancy
Immobility
PreviousVTE
Minor Cardio– Hypertension,CHF
Oestrogen
Loads others
Thrombophilia(egFactor V Leiden)
Foundin25-50% of VTE <50 years old.
Clinical Features
SOB
Pain
Cough
Haemoptysis
Signs
HS 4
Loud P2
Tachycardia
Investigations
ABG – Hypoxaemia&Hypocapnia
CXR – Normal/effusion/Westermarck’s/Hampton’shump
ECG –S wave inleadI,Q wave andT wave inversioninleadIII,andT wave inversionin leadsV1to
V4. More commonly,the ECGdemonstratesminornon-specificSTsegmentorT wave changes
D-Dimer– Useful forexclusion (if–ve,PEunlikely)
Well’sPEprobabilityscore >6= highchance
Ventilation/Perfusionscan
CTPA
DopplerUSS
Echo – trans-oesophageal.Useful inmassive PE
Management
LMW Heparin
Warfarin– 6 weeksto6 months
Thrombolysis –tPA.Use if patientisshocked
IVCfilter–if anticoagulationiscontraindicated.

17. 17
Sleep Apnoea (Obstructive Sleep Apnoea/Hypo-apnoea Syndrome (OSAHS))
Sleepdisruptiondue tobreathingpauses
Clinical features
Sleepiness
Snoring/apnoeas
Unrefreshingsleep
Awake choking
Poorconcentration
Depression
Nocturia
50% obese
Epidemiology
Affects1-2%of westernmiddle agedpeople
OSAHScommonestresppatientreferral
90& cases undiagnosed
Obstructionarisesfromnarrowpharynxwhichmaybe causedby: Retrognathia
Obesity
Alcohol
OSAHSis associated: Hypertension
Increasedchance of havingan RTA
Suddennocturnal death(!)
Cardiovascularevents
Diabetes
Liverdamage
Acromegaly
Hypothyroidism
Investigations&Diagnosis
EpworthSleepinessscore (>11=referral)
Overnightbreathingstudy(>15breathingpauses)
Management
Lifestyle –loseweight
ContinuousPositiveAirwayPressure (CPAP)therapy - 1st
line.Improvessymptoms&bloodpressure
Mandibularsplints –2nd
line
Othercausesof sleepiness
Insufficientsleep
Shiftwork
Drugs
Psychiatricillness
Narcolepsy(autoimmune)