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Respiratory medicine

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Respiratory medicine

  1. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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)

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