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Summary

The on-demand teaching session TCD 23 - Diabetes + Thyroid Disease highlights important concepts related to diabetes and thyroid disease for medical professionals. Attendees will gain insights into topics like Diabetes Refresher, T1DM, T2DM, Diabetes Complications, Diabetic Foot Examination, Practise Questions, and more. Additional focus will be on Thyroid diseases, including Hypothyroidism, Hyperthyroidism, Thyroid Cancer, and managing these conditions. This session will also delve into various complications linked with diabetes. The practical information offered in this session will equip healthcare providers with updated knowledge and strategies for managing and caring for patients with diabetes and thyroid issues.

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Learning objectives

  1. By the end of this session, participants will be able to identify the early signs and symptoms of Type I and Type II Diabetes.

  2. Participants will understand the difference between the two types of Diabetes and their underlying causes.

  3. Participants will have an understanding of the various treatment options for Diabetes, including lifestyle modifications and medication.

  4. Attendees will be able to identify the complications associated with Diabetes and their management.

  5. Participants will be familiar with diagnosing techniques and important parameters to monitor in patients with Diabetes.

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TCD 23 - Diabetes + Thyroid Disease By Marwan and Wayne With help from Zak Mouyer x Maria Chowdhury x zakariya.mouyer@student.manchester.ac.ukAdmin Stuff - Checkyourjunkmail - Checktheemailaddressthatyouregisteredforthezoomwith-that’sthe oneit’llbesentto - Pleasedon’tdmmexxx - YouwilleventuallygettheslidesIpromise(ifyoufilledoutfeedback forms) - BEPATIENTWITHUS(PLEASEEEEE) - Don’tworryaboutthenittygrittystuff,justtryandabsorbasmuchasyou canFeeding back to your feedback - Wewilldomorepolls - Notheycan’tbelonger - Notheycan’tbeshorter - Wedon’tdothelecturebeforeyourTCDsessiononFridayssothatyou canreallymakethemostofit - Zakcan’tbeanyslower,he’salreadyprettyslow - Thoseofyouthatsaidnothing-youarecorrect<3:DContent ➔ DiabetesRefresher ➔ T1DM ➔ T2DM ➔ DiabetesComplications ➔ DiabeticFootExamination(refertotheexaminationbook) ➔ ProgressPractiseQuestions ➔ OSCEs HereisaclassicpresentationofaZakariyainahypoglycemicstateContent ➔ ThyroidThrowback ➔ TacklingTFTs ➔ Hypothyroidism ➔ Hyperthyroidism ➔ ThyroidDiseaseManagement ➔ TouchingonThyroidCancer ➔ ProgressPractiseQuestions ➔ OSCEs ➔ ResourcesDiabetes Refresher 11.10 Which organs? Which Diabetes Mellitus? organs? ➔ DiabetesisageneraltermfordisorderscharacterisedbyPOLYURIA ➔ Mellitus,fromtheLatinmeaning“sweetenedwithhoney,” Soputthetwotogetheranditmeansyou’repissingoutlotsofsugar ➔ DMisavascular/endocrinediseasecausingmicrovascularandmacrovascularcomplications Themainreasonwemanageisto↓↓↓↓RISKOFTHESECOMPLICATIONS 8%ofthetotalNHSbudgetis nowspentonmanaging patientswithdiabetesmellitus Main Types ➔T1DM-Pancreasdoesn’tproduceinsulin ◆ before/aroundpuberty ◆ HLA-D3/4linked ◆ autoimmuneß-celldestruction(?CoxsackieBVirus,Enterovirus) ◆ polydipsia/-uria,weightloss,ketosis ➔T2DM-Bodybecomesresistanttoinsulineffect(insulinresistance) ◆ usuallyolder;metabolicsyndrome ◆ Insulinresistance(+ß-celldestruction) ◆ sometimesasymptomaticoronlycomplications ➔Gestational-diabetestriggeredbypregnancy…usuallyresolvesafter givingbirth.Itisaresultofreducedinsulinsensitivity. InsulinFunctions-Allowsuptakeof glucosefrombloodtogetusedby cells…Allowsliver/musclestostoreit asglycogen Causes of ↓insulin or insulin resistance? Trytosplitthisintodifferentcategories Haemochromatosis ➔ Pancreatic-Pancreatitis,surgery(>90%removed),trauma,pancreaticdestruction(bronzediabetes??, CF),pancreaticcancer ➔ Endocrine-Pregnancy,Cushing’s,acromegaly,pheochromocytoma,hyperthyroidism ➔ Medications-Steroids,anti-psychotics,anti-HIVdrugs ➔ Other(rare)-congenitallipodystrophy,glycogenstoragedisorders ➔ Othertypesofdiabetes:LADA,MODYT1DM (type I diabetes mellitus) 11.15T1DM ➔ Ketogenesis ◆ Bodythinksitdoesn’thaveenoughenergystores…livertakesfattyacidsandconverttoketoneacids ◆ Acetonebreath,urinalysis(dipstick),metabolicacidosis ➔ Firstpresentation ◆ Polydipsia/polyuriainchild ◆ Weightlossinchild ◆ DKA(lossofconsciousness,vomiting,abdopain)→LIFETHREATENING ◆ Hypokalemia→arrhythmias(theoretically) ◆ KussmaulBreathing(deephyperventilation→bodytryingtoreduceCO2→↓acidity) Ketones(DKA) Uremia Sepsis ➔ KussmaulBreathingVideo-https://www.youtube.com/watch?v=raEKXVfuWTo Salicylates Methanol Aldehydes LacticacidT1DM Long Term Management p1 ➔ Long-termtreatmentprinciples ◆ Patienteducation-lifelongcondition,beawareofwhattodoinhypo/hyperstates ◆ Monitoringdietarycarbohydrates,monitoringbloodsugars(Libre/fingerprick5x/d),monitoring forandmanagingcomplications ◆ BPTARGET-135/85 ◆ T1DM+albuminuriaor2ormorefeaturesofmetabolicsyndrome=130/80 ➔ Plantheinsulintosuitthelifestyle ◆ E.g.regularroutineBASAL-BOLUS: BDpen(Novomix30) ◆ E.g.morevarietyday-to-day:ODlongactingandTDSrapid-acting(Humalog,Novorapid)before meals ➔ MonitorHbA1c3-6monthly,BMself-monitoringT1DM Long Term Management p2 ➔ PatientbecomestheEXPERToftheirbloodglucose ◆ E.g.ifhyperglycaemic,mayknowthat1/uNovorapidusuallyreducestheirBM4mmol/landcan self-managethis…ortheyknowhowmuchameal/lucozadebottleincreasesBM ➔ DiabeticSpecialistNurseshelpwitheducationandfollowup ➔ We’lldiscussinsulintypeslateron ➔ Lipodystrophyifalwaysinjectinginsamesite ◆ Reducedinsulinabsorbancehere ◆ Cycleinjectionsites,checkforhardlumps Rushhiminandstartan ABCDEassessment Y ou’re the F1 in A&E A 8 y/o boy comes in with severe vomiting and abdo pain. He is dehydrated, drowsy and looks like he is going to pass out. His worried mum tells you he has T1DM. What are you guys gonna do next? Whatdoyouthinkthisis? DKAtriggeredbyinfection? ABCDE!!! SEPSIS Airways PatentAirways-He’sabletotalkalittle Breathing ClearChest,RR25,banghimonanO2mask, ABGshowsmetabolicacidosis Circulation HR135,BP90/50,ECGnormal…insert2wbcannulas Disability DEFG-Glucose17mmol/L,temp38.9 Everythingelse Norashes,bleeds,injury….urinedipshowsketonuria++ ComplicationsofDKA(+mistreatment) Type1Diabeticsbelike... ➔ DEATH Diabetic Ketoacidosis pt 1 ➔ gastricstasis ➔ thromboembolism ➔ arrhythmias EMERGENCYCOMPLICATIONOFT1DM-ACTFAST!!!! ➔ iatrogenicduetoincorrectfluid therapy:cerebraloedema*, ➔ Causes:Non-adherence,stoppinginsulinduringintercurrentillness,MI,”Diabulimia”,infectionpoglycaemia ➔ acuterespiratorydistress (sepsis),surgery,MI,pancreatitis,chemotherapy,antipsychotics syndrome ➔ acutekidneyinjury ➔ Symptoms/Signs:Gradualdrowsiness,vomiting,dehydration,abdopain,polyuria/dipsia, lethargy,anorexia,ketoticbreath,Kussmaulbreathing,coma(ABCDE–BM!) ➔ Diagnosis: - ◆ AcidosispH<7.3orHCO <15m3ol/L) ◆ Hyperglycaemia>11mmol/LorknownDM ◆ Ketosis≥3mmol/Lorketonuria+++ondipstickEMERGENCYCOMPLICATIONOFT1DM-ACTFAST!!!! WhatwillkillDKApatients→ dehydration,potassiumimbalanceand acidosis. Diabetic Ketoacidosis pt 2 DKApatientdeplete5-8litres,sopriorityisfluidresuscitationto correctthedehydration,electrolytedisturbanceandacidosis.Then giveinsulininfusionsocellscanuseglucoseandstopproducing ketones. ➔ ECG,CXR,urinedipandMSU,bloods(BMandlabglucose,pH,ketones,U&E,HCO ,osmolality,FBC, cultures)=ABCDEapproach 3 ➔ Treatment:(followlocalprotocol)→REMEMBER“FIG-PICKA”FORDKATREATMENT ◆ F–Fluids–IVfluidresus→IV0.9%salinewithpotassium1Lover1h,2x(1Lover2h),2x(1Lover 4h),1Lover8h ◆ I–Insulin–Addaninsulininfusion(e.g.Actrapidat0.1Unit/kg/hour) ClassicProgressQuestion ◆ G–Glucose–MonitorBMhourlyandadddextroseinfusionifbelow14/15mmol/l ◆ P–Potassium–Monitorserumpotassium(e.g.4hourly)andcorrectasrequired(potassium shouldnotbeinfusedatarateofmorethan10mmolperhour) Why?Cancause ◆ I–Infection–Treatunderlyingtriggerssuchasinfection hyperkalemia→cardiac ◆ C–Chartfluidbalance arrest ◆ K–Ketones–Monitorbloodketoneshourly(orbicarbonateifketonemonitoringisunavailable) ◆ A-Acid-VBGevery2hrs(ABGifthey’reveryunwell) ➔ Establishthepatientontheirnormalsubcutaneousinsulin regimepriortostoppingtheinsulinandfluid infusion.. Signs?Howtomanage? Complication of DKA Complications Mnemonic = CHAAAV. (of DKA + Mx) -Cerebral oedema (esp. children/teens --> neuro-obs). -↓↓ K (due to insulin). + -Arrythmias (due to ↓↓ K ). -AKI (due to hypovolaemia). -ARDS. -VTEMetabolic Acidosis □ Low pH, low HCO3- Causes; □ DKA □ Liver/renal failure □ Drug overdose □ Renal tubular acidosisAnion Gap ([Na+] + [K+]) – ([Cl-] + [HCO3-]) Normal range = 10-18mmol/LCauses of Raised Anion Gap; LUKA □ Lactic acidosis (shock, sepsis) □ Urate (renal failure) □ Ketones (DKA, alcohol, starvation) □ Acid Poisoning ■ Salicylates ■ Biguanides (metformin) ■ Ethylene glycol ■ MethanolCauses of Normal Anion Gap; □ Pancreatic fistula □ GARA □ GI loss of bicarb (D not V !!!) □ Addison’s □ Renal Tubular Acidosis □ Ammonium chloride ingestion CausesofHyperkalemia ➔ AKIorCKD Hyperkalaemia (Progress Test Basics) ➔ Drugs:potassiumsparingdiuretics,ACE inhibitors,angiotensin2receptorblockers, spironolactone,ciclosporin,heparin Whydoweneedtomanage? ➔ metabolicacidosis Cancausearrhythmias(BAD!),leadstocardiacarrest ➔ Addison'sdisease(adrenalinsufficiency) ➔ Tumourlysissyndrome(chemoSE) ➔ Rhabdomyolysis SignsonECGandwhatlevelK+doweseethis@? Above6mmol/L→TalltentedT-waves,Loss/Flat Pwaves,BroadQRS,ARRHYTHMIA Mainwaytotreat? 1. STOPANYDRUGScausing↑K+(ieACEi,spironolactone) 2. InsulinandDextroseinfusion(why?) 3. CalciumGluconatein>6.5mmol/L(or>6mmol/LwithECGchanges)tostabilizecardiacmembrane OtherwaystoreduceK+? 1.SalbutamolworkslikeinsulintodriveK+intocells….2.Sodiumbicarbusedinrenalfailurepatients…3. calciumresonium(oral/enema)ORloopdiuretictoexcreteexcessK+...4.resistanttotreatment→consider dialysisQuick Quiz ➔Namesomecausesofhyperglycemia? ➔Whatadvicedoyougivetopatientstoavoidlipodystrophy? ➔Namesomecausesofkussmaulbreathing ➔Whatarethe3thingsthatwillcauseaDKApatienttodie?Howdowemanage? ➔MnemonicforDKAtreatment? ➔4thingsyouseeonhyperkalemiaECG? ➔Maintreatmentforhyperkalemia ➔ResistantHyperkalemia→whatdoyouconsider?T2DM (type II diabetes mellitus) 11.35T2DM ➔ Riskfactors ◆ age,ethnicity,FH,obesity,sedentarylifestyle,high-carbdiet ➔ Presentation ◆ Asymptomatic…usuallyanincidentalfinding ◆ Fatigue,polydipsia/uria,unintentionalweightloss,opportunisticinfections(UTIs..why?),slow healingwounds,glucosuria,complainingofcomplications(ieulcers,visionissues,lossof sensationsetc) T2DMverylikelytocomeupasanOSCE - Morelikelyasinformation-giving,sobesureaboutthedefinitionandmanagement - NEXTSESSIONWEWILLCOVER TATTHISTORY→Lesslikelyashistory(buthavesome differentialsupyoursleevee.g,thyroiddisorder,DM,addisons,depression) - Thinkofwhatquestionsyoucanasktorulein/outdiseasesT2DM (Explanation Station) ➔“T2DMisacommon,long-termconditionwhereyourbodycan’tcontrolthe sugarsinyourbloodaswellasitusedto:)...Becauseofthehighsugarsinyour system,thisiswhyyouareexperiencingXYZ (polyuria,tirednessetc etc)...Thankfullyitiseasilymanagedusinglifestylechangesandmedication andmostpeoplewiththisconditionlivenormalhealthyhappylives.It’s importantwecontrolyourbloodsugarlevelssowecanpreventsomeofthe seriouslongtermcomplications associatedwithyourcondition.” ➔Management ◆ Diet(vegandoilyfish,lowglycemic,highfibre) ◆ Optimiseriskfactors(exercise,weightloss,smokingcessation,treatotherdiseasese.g.ramipril (140/90target),20mgatorvastatinsimvastatin(QRiskscore>10%)) ◆ Monitorforcomplications(retinopathy,nephropathy,diabeticfoot) st ◆ Metforminis1 line,otherhypoglycemicsaddedon,?insulinifneededUsethisasatemplateandgothroughalltheprevious cases. 1. Takebriefhistory 2. Nameofcondition+common/rare+short/longterm 3. VERYSIMPLEexplanationofdisease(LAYTERMS.. DON’TDIGYOURSELFAHOLE) 4. Linktotheirsymptoms(sopatientmakesa correlation) 5. “It’seasilymanagedusinglifestylechangesand medication” 6. Whathappensifyoudon’tmanageCriteria for Diagnosing T2DM ➔Bloodtests ◆ HbA1c>48mmol/mol(notinpregnancy,children,T1DMorHb-opathies) ◆ Randomglucose/OGTT>11mmol/l x2 or x1withhyperglycemia symptoms ◆ Fastingglucose>7mmol/l ➔Pre-diabetes ◆ HbA1c42-47mmol/mol ◆ Fastingglucose6.1-6.9mmol/l ◆ RandomGlucose/OGTT7.8-10.9mmol/lT2DM Management SIGNGuidelines2017,NICEGuidelines2015 ➔ HbA1c48mmol/molfornewT2DM ➔ HbA1c53mmol/molfordiabeticstreatedwithmorethanmetformin ➔ Treatment ◆ 1 line(48mmol/mol):Lifestylechanges nd ◆ 2 line(48mmol/mol):Lifestyle+Metformintitratedupastolerated(start500mgOD) ◆ 3 line(53mmol/mol):addsulfonylurea,pioglitazone,DPP-4inhib.orSGLT-2inhib. th ◆ 4 line(58mmol/mol)tripletherapy(metformin+2ofabove)ormetformin+insulinDrug Name Mechanism ofAction Side Effects (progress potential questions in bold) Biguanide-Metformin Increasesinsulinsensitivity,decreaseshepaticglucose ➔ Diarrhea production ➔ Abdodiscomfort(dosedependent) ➔ Lacticacidosis ➔ NB:don’tprescribeifeGFR<36 Sulfonylurea -Gliclazide Stimulatepancreaticinsulinrelease ➔ Weightgain ➔ Hypoglycaemia ➔ SIADH/lowNa+ ➔ ↑CVdiseaseandMIrisk Pioglitazone- Increasesinsulinsensitivity,decreaseshepaticglucose ➔ Weightgain Thiazolidinedione production ➔ Fluidretention ➔ Osteoperosis ➔ LiverDysfunction ➔ Bladdercancer ➔ Pancreatitis DPP-4i-Sigagliptin Increaseinsulinsecretion,inhibitglucagonproduction,slowGI ➔ GITupset/fulltummy absorption ➔ URTIsymptoms SGLT-2i-empagliflozin StopglucosereabsorptionfromSGLT-2proteininPCTofkidney ➔ Glucosuria ➔ UTIrisk ➔ weightloss ➔ DKA(rare) GLP-1mimetics-liraglutide Increaseinsulinsecretion,inhibitglucagonproduction,slowGI ➔ weightloss, absorption ➔ dizziness, ➔ (lowhypoglycaemiarisk)Insulin (don’t need to know specifics, but know there are different types) Special Interest Content to look at (ifyou’re a neek) ➔ Rapid-acting(10min-4h) ◆ E.g.Novorapid,Humalog,Apidra ➔ Short-acting(30min-8h) ◆ E.g.Actrapid,Humulin-S,InsumanRapid `➔ Intermediate-acting(1h-16h) ◆ E.g.Insulatard,Humulin-I,InsumanBasal ➔ Long-acting(1h-24h) ◆ E.g.Lantus,Levemir,Degludec(upto40h) ➔ Combination(intermediate:rapid-acting) ◆ Humalog25(25:75),Humalog50(50:50),Novomix30(30:70) p.s whilst I was editing these slides I realised the opposite of keen is neek!Diabetes Emergencies 12.001. Diabetic Emergencies - Hyperosmolar Hyperglycaemic State ➔T2DM;days-weeks ➔Symptoms:Dehydration,weakness,legcramps,reducedGCS,visionproblems ➔Causes:Infection,stroke,trauma,MI,medications,non-adherence ➔Investigations:BM>30mmol/L,Osmolarity>320mOsm/kg,ketones+/trace/none or<3mmol/L(whylol), pH>7.3 ➔Management:IVfluids,insulin,LMWH,Abxifinfection ➔Approx.15%mortality -HHS: -DKA: Onset -Onset --> Rapid (hours) -Onset --> slow -More likely in T1DM -More likely in T2DM Investigation -BM --> ↑↑ (>11) -BM --> ↑↑↑↑ (>30) s -Ketones/acidosis --> ↑↑ -Ketones --> normal -φ --> ↑↑ -φ --> ↑↑↑↑ (>320 mosmol/kg) Management -IVF --> IV glucose. -IVF --> IV glucose. -Insulin (0.1 u/kg/hr). -~Insulin (0.1 u/kg/hr). -K replacement. -~K replacement. 2. Diabetic Emergencies - Hypoglycemia ➔ Diabeticscauses:Insulin/sulfonylurea/(GLP-1?),increasedactivity,accidental/deliberate overdose ➔ Non-diabeticscauses(ExPLAIN):Exogenousdrugs(e.g.alcohol,insulin(bodybuilders),Pituitary insufficiency,Liverfailure/enzymedefects,Addison’sdisease,InsulinomaorImmune hypoglycaemia(anti-insulinreceptorinHodgkin’s),Non-pancreaticneoplasm(e.g.fibrosarcomas, haemangiopericytomas) ➔ Symptoms:Tremor,sweating,irritability,dizziness,pallor,reducedGCS,coma,death ➔ BloodTest:BM≲4mmol/L ➔ Management ● Ifconscious:rapidactingglucosee.glucozade+sloweractingcarbohydratee.g.biscuit andtoast ● Ifunconscious:IVdextrose(200ml10%),intramuscularglucagonDiabetes Complications @thoseofyouwithfootfetishes,youcanwakeupnow :0 12.10Long-Term Complications ➔Microvascular ◆ Retinopathy ◆ Neuropathy ◆ Nephropathyesp.glomerulosclerosis ➔Macrovascular ◆ Coronaryarterydisease ◆ Peripheralischaemia(poorhealing,ulcers,diabeticfoot) ◆ Stroke ➔(HigherriskofUTIs,pneumonia,skin/softtissueinfectionesp.feet,fungal infectionse.g.oralandvaginalcandidiasis)Microvascular Complications lowrisk=noretinopathyon2successive screenings ➔ Retinopathy–checkevery2yearsforthose atlowriskofsightlossandat leastannuallyforeveryotherdiabetic ◆ Capillaryleakage->haemorrhages/oedema/hardexudates->lossofcentralvision ◆ Capillaryocclusion->newvesselformation->haemorrhage/fibrosis/retinal detachment/glaucoma->totalblindness ➔ Neuropathy–checkfeetaccordingtorisk,MDT–podiatry,vascular surgery ◆ Mainlyperipherallossofsensation,pain(orboth);alsoautonomic,vasomotor,glucosemetabolism unawareness,mononeuritisofCNIIIorVI ◆ Treatw.capsaicincream,tricyclicantidepressants,anticonvulsants,analgesics ➔ Nephropathy–ScreenA:CrandeGFRannually ◆ CommonestcauseofESRD,damagetoendotheliumbyRAASactivation/growthfactors/advanced glycosylationendproducts/oxidativestress/↑glomerularpressure ◆ Microalbuminuriaisfirstsign(A:Cr3-30mg/mmol);dipstickMacrovascular Complications (CoronaryArtery Disease) ➔BloodPressureControl ◆ Lifestyleadvice ◆ Reviewmedications ◆ Maintainthefollowingbloodpressuretargets ➔ LipidModification ◆ doesnothaveestablishedCVD-offeratorvastatin20mgODfor primarypreventionofCVD ◆ establishedCVD-offeratorvastatin80mgODforsecondaryprevention ofCVD ◆ aimfor>40%reductioninnonHDLcholesterolOsteomyelitis ➔ (Neuropathy+PVD+reducedimmunefunction)→ Cellulitis+/- Osteomyelitis ➔ X-Rayfoot(althoughMRIisgoldstandardfordiagnosis) ➔ Youwanttotreatpain+bloodsupplytofoot+infection(commonstaphaureus) ◆ Analgesia,Statins(?Referraltovascularsurgery),Abx,Allowmechanicalhealinge.g. crutches/well-fittingshoes ➔ Assessdiabeticfootriskwhendoingdiabeticfootexamination ◆ Low(nothingwrongorjustcallus)-reassessannually ◆ Moderate(1ofdeformity,neuropathy,non-criticalischaemia)-reassess6-8wkly ◆ High(2ofaboveorprev.ulcer/amputation/RRT)–reassess2-4wkly ◆ Activediabeticfootproblem(ulcerorspreadinginfectionorcriticallimbischaemiaor gangreneorsuspicionofacuteCharcotarthropathy(painlessunexplainedhotswollenfoot) FootUlcers-Ithinkthisisthe mostdisgustingpartofmedicine… ifyouhaveanendocrineblock prepareyourself…lotsofulcers andamputations(NOTFUN!!) Patientslosesensationinfeet,can GuesswhichoneisZak’sfoot…? accidentallysteponsomething andnotrealise..sitegetsinfected beforetheyevenrealise Alwaysagoodpointtoscarethe patientintotakingtheirdiabetes meds!!!Scarethemwithfoot amputationsQuick Quiz ➔FirstlinetreatmentforT2DM?HbA1ctargets? ➔WhichT2DMmedcancausebladdercancer? ➔Namesomecausesofhypoglycemia(orthemnemonicatleast?) ➔Howtotreathypoglycemicattack? ➔Whatarethe3thingsthatwillkillaDKApatient? ➔Whatarethe3thingswearetreatingforinosteomyelitis?Progressively Depressive Progress Practise Questions 12.25-gliptin→DPP4i MetabolicAcidosiswith partialrespiratory compensation DKADDx(drowsiness (Refertocase2slidesonABG) +abdopain) - Aspirinoverdose - Sepsis - Bowel obstruction - HHS - Anycausesof acuteabdomenRemember0.1 units/kg/hourOSCEs (the stuffyou’ve been waiting for)Potential OSCE Stations ➔ TATT-“TiredAllTheTime”History→ThinkofyourDDx(Anaemia,Diabetes,Hypothyroid, Depressionetc) ➔ ExplainingDiagnosisandManagementofT1DM/T2DM ◆ Talkaboutcomplicationofdiseases,checkpatientadherence,modifiablefactorsadvice ◆ Explainingmetforminandhowtotake ➔ DIABETICFOOTEXAMINATION-PRACTISEPRACTISEPRACTISE→talkthroughitby yourself/withmateandbeslik!Becomfortablefeelingafoot,sointheosceyou’renot weirdedout ◆ incl.ABPI,peripheralvascularexaminationincl.dopplerUSS(KNOWHOWTOUSE DOPPLER) ➔ DataInterpretation-Bloods:HbA1c,glucose,nephropathy/CKD,hyperlipidaemia,metabolic syndrome?Take Home Messages 1. Diabetes is a common long term condition that you will probably see on a daily basis 2. DKA is a life threatening acute condition → knowwhat do there and then… ABCDE approach and DEFG!!! 3. Knowyou hyperkalemia diagnosis/treatment algorithm… lots of conditions cause this electrolyte abnormality 4. Explaining T2DM to a patient is important and you need them to fully understand WHY they’re taking their medication… you won't die ofT2DM, you will die of the complications, make that very clear!!! 5. PRACTISE your diabetic foot examination… be slick and smooth i know feet are weird but you have to know it!Thyroid Throwback or maybe it’s your first time 👀 11.10Thyroid Anatomy Anendocrineglandlocatedatthebaseoftheneck!Asyoucanseeit lieslowerthanthethyroidcartilage!Thishasimplicationsforyour examinations;youprobablyneedtofeellowerthanyouthink. Embryologically,itdevelopsviathethyroglossalductofthetongue–a remnantmarkerbeingtheforamencaecum.Whatarethepathological implicationsofthis? Improperclosureofthischannelcanleadtoathyroglossalcysts. Manymusclesoverlieit.Theinfrahyoidmusclescomefromlandmarks onthepectoralgirdleandattachontothehyoidboneorthyroid cartilages.Whataretheimplicationsofthiswithregardstoagoitre? Goitresarelimitedintheirexpansionsuperiorly,andtendtoexpand inferiorlyandlaterally.What is a goitre? (you’ve goitre know this!) ANY swellingofthethyroidgland Doesn'thavetobeallofthethyroid:itcanbediffuseor uninodular Arethyroidnodulesthesame?Notnecessarily->whenthey becomebigenoughtoseewecancallthemgoitres  Howdoesagoitreactuallyarise?Dependsonthecause: ➔ Iodinedeficiency=thyroidgrowstomakeupforlowactivity ➔ Hashimoto's=thyroidisinflamedandbeinginfiltratedby lymphocytes ➔ Grave's=overstimulationofthethyroidleadsittogrowThyroglossal Cyst? ➔ Afibrousstructureresultingfromincompleteclosureofthethyroglossalduct ➔ Canthereforeoccuranywhereinthemidlinebetweenthetongueandsuprasternalnotch ➔ MovesonswallowingANDstickingtongueout(agoitrewillnotmoveontongueout) ➔ Canbecomeinfectedorformafistula,andareremovedsurgicallyTry to palpate at least ONE goitre/enlarged thyroid in your time in 3rd year. Don’tforgetthat theparathyroid glandsexist! The Thyroid - Physiology (thisisjustareminder,youdon’tneedtoknowitindepthatall) Thyroidproducesthyroidhormonesusingiodineandtheenzymethyroid peroxidase(TPO);knowninshortasT3andT4.T3istheactivehormone, andT4isreadilyconvertedaroundthebody. EVERYSINGLECELLisaffectedbythyroxine(T3). ● AlotofT3=fastmetabolism–everythingspeedsup ● AlotofT4=slowmetabolism–stuffslowsdown ● Why? Whatotherhormoneismadeinthethyroid? Calcitonin made by C-cells (parafollicular cells) helps regulate levels of calcium and phosphate in the blood, opposing the action of parathyroid hormone Hypothalamic-Pituitary-Thyroid Axis Thyroid Physiology - the HPTAxis ➔ Aswithmostendocrineorgans,thehypothalamus kickseverythingoff. ➔ Thereleaseofthyroidreleasinghormone(TRH) triggerstheanteriorpituitarytoreleasethyroid stimulatinghormone(TSH). ➔ TSHthencausesthereleaseofT4andT3fromthe thyroid. ➔ Anincrediblyimportantaspecttorememberisthat thereisnegativefeedbackfromT4/T3onproduction ofTSH(andTRH). ➔ The“FLAThormones”causemore Pituitary Refresher hormonereleasefurtherdown. ➔ The“PEG”onesdon’t. ➔ Livesonthesellaturcicaofthesphenoidbone ➔ Releasesabunchofhormonesthattriggerthereleaseofevenmore ➔ Theanteriorandposteriorpartshavedifferentfunctions LH Prolactin FSH TSH FLATPEG Endorphins (anterior pit. hormones) Growth Hormone ACTH ➔ Whathormonesdoestheposteriorpituitaryrelease? ADHandoxytocinarebothmadebythehypothalamusbutarereleasedbytheposteriorpituitaryTackling TFTs Thyroid Function Tests 11.20 ➔ TSH - (0.4 – 4 mU/L) Thyroid Function Tests ➔ Free T4 - (9 – 25 pmol/L) ➔ Free T3 - (3.5 – 7.8 nmol/L) Principles: You don’t need to remember ➔ ThethyroidreleasesaLOTmoreT4thanT3, normalvalues andT4isconvertedtoT3intheperipheries Anoteonthyroid-relatedantibodies: ➔ Hence,T4isabettermarkerofthyroid function,sowetendtolookatitratherthan T3ontests ➔ Hashimoto’s=↑anti-TPO+ anti-thyroglobulin ➔ T4hasahalflifeofaroundaweek,sowewait severalweeksbeforerepeatingTFTstosee theimpactofinterventions ➔ Grave’s=↑TSH-receptorantibodies and↓anti-TPO ➔ Asasidenote,thevastmajorityofT4isbound tothyroid-bindingglobulin,sowe’re measuringthefreeT4thatisn’tbound ➔ TSH - (0.4 – 4 mU/L) ➔ Free T4 - (9 – 25 pmol/L) Summary ofTFTs ➔ Free T3 - (3.5 – 7.8 nmol/L) You don’t need to remember normalvalues e.g. Hashimoto’sHypothyroidism (aka myxedema) We'll break this up OSCE style: used to describe extreme hypothyroidism but also some of the effects hypothyroidism has on - History & Explanation the body - Physical Examination Findings - Management and Treatment 11.15What would you expect in a history of hypothyroidism? (i.e. things the patient would complain about [not signs!]) Hypo=slowdown - tired Whatdoyounoticeabout Appropriate differentials for these symptoms: - lowmood thesesymptoms? ➔ Anaemia -hairloss ➔ Depression They'renotspecificatall! ➔ Addison's (later case) -goitre(possibly) ➔ Diabetes (last week case) -constipation "Tiredallthetime"(TATT)is -heavyperiods averycommonscenarioand Thinkaboutwhatcanweasktorulein/out -feelingcold iscausedbymanyconditions. theseconditions? Whataresomedifferentials -cramps thatstickouttoyou? Familyhistory!Thyroidconditionsare - weightgain commonlyautoimmune,andautoimmune -memory/concentrationproblems -beingfemale conditionshavegeneticlinks–soask,"has anyoneinyourfamilyeverhadthyroid problems?",aswellasaskingaboutother autoimmuneconditionssuchasdiabetes (type1). Anti-arrhythmicdrugusedin tachycardias ➔ TFT,LFT,U&E,CXRpriorto treatment Causes of Hypothyroidism Why? ➔ TFT,LFTevery6months ➔ TFTs-Cancause ➔ Mostcommonworldwide? Iodinedeficiency hyper/hypothyroid ➔ U&Es+LFTs-Cancauseliver Hashimoto's(goitre);primaryatrophic ➔ Autoimmunecauses? hypothyroidism(nogoitre) fibrosis/hepatitis ➔ CXR- Cancausepulmonary fibrosis ➔ Whichdrugscancauseit? Amiodarone,anti-thyroiddrugs(overtreatmentofhyperthyroidism),lithium ➔ Whatissubacutethyroiditis? Hypothyroidismfollowinghyperthyroidism:thethyroidhasreleasedallitsstored hormoneinonebiggoandnowhasnoneleft.Duetoviralinfection. Anyformoftreatmentfor ➔ Secondarycause? Hypopituitarism -rare!!shouldn'tbeyourfirstdifferential hyper cancauseit!E.g.thyroid surgeryorradiationtherapy. ➔ Howmightpregnancybeinvolved? Sheehan'sorpost-partumthyroiditis Canbehyper,hypo,orboth(usuallyhyper beforehypoI.e.subacutethyroiditis). Occursin12monthperiodafterparturition andisusuallyself-resolvingbutcanbecome permanenthypothyroidism Sheehan's Syndrome Extra Content for the Class Neeks ➔ Pregnancyisanextremelyhormonalstate.Inordertoprovidethosehormones,thepituitary glandhypertrophies(mainlythelactotrophsthatproduceprolactin)withoutanincreasein correspondingbloodsupply. ➔ Ifpost-partumhaemorrhageoccurs,thepituitaryreceiveslessbloodthanneededtosupply ` itsmetabolism. ➔ Thisrelativeischaemialeadstonecrosis,andthepituitaryglandcanbecomeinfarcted. ➔ Lactotrophs(prolactinproducingcells)areprimarilyaffectedandsothecommonestsymptom isagalactorrhea(difficultywithlactation).Dependingontheextentoftheinfarct,othercells maybeaffectede.g.thethyrotrophsthatproduceTSH;leadingtohypothyroidism. ➔ Itonlyaffectstheanteriorpituitarygland…Patientwillhave ➔ Agalactorrhea(lackofprolactin) hypopituitarismsymptoms! ➔ Amenorrhea(lackofLHandFSH) ➔ Whichhormonesaffected?RememberFLATPEG ➔ AdrenalInsufficiency(lackofACTH) ➔ Whichhormonesaren’taffected? ➔ Hypothyroidism(lackofTSH)Hashimoto's ➔ Th◆ Middleagedwomencausesofhypothyroidisminthedevelopedworld. ➔ AutoimmuneCondition-Thyroidisslowlydestroyedbytheimmunesystem. ➔ Takesawhiletocausesymptomsandformagoitre.Thegoitreisdueto fibroidtissueratherthanthethyroidtissueitselfhypertrophying. Whatantibody(ies)is/arAnti-TPO! / Anti-thyroglobulin WhatTFTresultswouldyouexpect? ↑TSH + ↓T4What would you expect to find on examination? (Hypo) (this is the easier one, less signs!!) General Inspection Face + Eyes ➔ High(er)BMI(say"increasedbody ➔ "Peachesandcreamcomplexion" habitus") ➔ Puffyeyes Pemberton Sign* ➔ Dressedverywarmlye.g.manylayers ➔ Hairlossonscalp ➔ Hairlossonouter1/3rdofeyebrow Hands + Wrists Neck ➔ Coldandclammyperipheries ➔ Onycholysis(splittingofnailfromnail Thendoyourneckinspection,palpation(don’tforget bed–morecommonwithhyper) lymphnodes!),percussion,andauscultation.Thendothe ➔ Bradycardia "othertests",whereinyoumayfind: ➔ slowreflexes ➔ nonpitting peripheraloedemaSigns of Hypothyroidism Onycholysis Peaches and Cream - splitting of the nail Loss of Outer Eyebrow Complexion from the nail bed - aka Queen Anne's - yellow and pink blotches sign - harder to see on ethnic - aka Hertoghe's sign peopleOSCE Pointer condition/finding in OSCEsthat you may be asked to examine someone FOR a certain For example, instead of doing a ‘thyroid exam’ you may be asked to “examine someone for look for, to the scenario!nstances, cater what you say out loud, and what features you This applies to everything! When you're practising with friends (which you should be doing by now!), instead of asking them to do an abdo exam over and over again, ask them to examine you for signs of alcoholism. Resp exam? Try examining for a pleural effusion. Cardio? Examine for signs of aortic stenosis.Scars!! know👏your👏scars👏 TheyLOVEtogiveyoupatientswithnormalfindingsexceptformaybeascarhereorthere. Kocher,Lanz,Rutherford-Morrisonthemainscarsandwhatsurgeriesthatmaybeusedfore.g. Forcardio:midlinesternotomy(withorwithoutasaphenousharvestgraft…whereareyoulooking?) Andforthyroidtheymayhavebeenapreviouspatientwhohadtheirthyroidremoved!Quick Quiz ➔ Howdoyoudifferentiatebetweenagoitreandathyroglossalcyst? ➔ Whathormonesdoesthepituitaryglandrelease? ➔ WhatTFTresultswouldyouexpectforsecondaryhypothyroidism? ➔ Differentialsforhypothyroidism? ➔ Whatissubacutethyroiditis? ➔ WhatantibodieswouldyouexpectinHashimoto‘sandGraves‘? ➔ Givetwosignsyoumayseeinthefaceforsomeonewithhypothyroidism? ➔ Sideeffectsofamiodarone? Presenting your Examination GeneralStructure ➔ Getstraightintoit-“Iperformedthis____examinationon33y/oPatientX ➔ RapidGeneralInspection-“Fromendofthebedthepatientseemedwell…The patienthasanincreasedbodyhabitus…NAMETHEOBVIOUSTHING(insome cases)etc.” ➔ Hands-Nameanypositivesigns(leaveoutnegative) ➔ Face-Nameanypositivesigns(leaveoutnegative) ➔ Organ-IPPA( Inspection,Palpation,Percussion,Auscultation) ◆ NameALLpositivesignsandimportantnegativesigns ◆ HaveastructureforeachphysicalexaminationsIPPA ➔ Tocompletemyexamination..? Learn to present normal examinations too!! ie equal air entry to base of both lungs, soft and non-tender to touch, no signs of hepatosplenomegaly etc etc If you can’t find anything in hands/face - “There were no peripheral signs of thyroid/CV/respiratory disease” Give your positive findings, but also give important negatives! E.g. if you did a resp exam and the only thing you Presenting found was a high resp rate, you would still include the fact there was no wheeze or crepitus or dullness to percussion – to prove that you checked! Sointhisinstance… inspectionIsawalargegoitre.Herpulsewas52beatsperminuteandregularandher peripherieswerecold.Therewassomehairlossonthescalpandtheouterthirdofthe eyebrow.Onexaminationoftheneck,hergoitremoveduponswallowingBUTnotupon protrusionofthetongue.Therewerenootherpositivefindings:forinstanceherreflexes werenormal,therewasnoretrosternaldullness,therewerenochangestotheeyes. Tosummarise,thiswasanabnormalthyroidexamination,withfeaturessuggestiveof hypothyroidism.” Tocompletemyexamination… What you’re more likely to say in an OSCE “TodayIperformedathyroidexaminationon56yearoldMargaretJones.Ongeneral peripheralstigmataofthyroiddisease.Oninspectionandpalpation,therewasno goitreorthyroglossalcyst.Reflexeswerepresentandnormalandtherewerenosigns ofproximalmyopathy. Tosummarise,thiswasanormalthyroidexamination Tocompletemyexamination…To complete my examination… Aftercompletinganyexamination,thankthepatient,helpthemredressifneedbe,andwashyour hands. Then,theexaminer/doctorshouldaskyoutopresentyourexamination.Youshouldpresentand thenexplainwhichtests/investigationsyouwoulddotocompleteyourexamination. Testsandinvestigationsthatarealwaysuseful: ➔ Takingafullhistory ➔ Takingafullsetofobservations(BP,temp,sats,etc) ➔ FBC(checkforanemia/signsofinfection) ➔ Liverfunctiontests(toensurewecanusedrugsexcretedbytheliver) ➔ TFTs ➔ Ureaandelectrolytes(getabaseline,wemayneedtodoCT) ➔ Anyotherspecifictestsyoumaywant IFTHEEXAMINERDOESN’TPROMPTYOU,DOITANYWAY! Use this as a base for all physical examination and add/remove when needed… write up a template for main examinations and PRACTISE!To complete my examination Thisisn’tthegoldstandardfor post-thyroidexamplansbytheway!You arewellwithinyourrightstoinclude Think:bedside,bloods,andimaging. anythingASLONGASYOUCANJUSTIFY IT! Whatwouldbeappropriatefollowingathyroidexam? Setofobservations,anECG(iftherewasanirregularpulse!),buttobehonest,youcansayanythingifyou Bedside: canjustifyit!Andafullhistorytoo!Otherrelevantexaminationse.g.cardioexamifyoufindpittingoedema TFTs,LFTs,U&Es,lipidprofile(hypothyroidismcancausehighLDLs),FBC(infectioncouldcause Bloods: lymphadenopathywhichisadifferential) Imaging: Ultrasoundscan,considerFNAC(fineneedleaspirationcytology)Is hypothyroidism a big deal? Shortanswer:YESit’saverybigdeal ➔ Longanswer: ◆ Pregnancy:itcancausecomplicationssuchaseclampsia,prematurity,lowbirthweight,and evenstillbirths  ◆ Itcanraisethelipidprofileofapatient,increasingtheircardiovasculardiseaserisk ◆ Myxoedemacoma:thisisthehypothyroidstatethatprecedesdeath.Thepatienthas hypothyroidsymptomsaswellashypothermia,seizures,psychosis,andthencoma.Itcan bebroughtonbyinfection,MI,stroke,etc. ● TheyneedtobetreatedonICUwithlevothyroxine,steroids,abxifnecessary,fluids, andoxygenifnecessary. ● (Youdon'tneedtoknowloadsaboutthis–justbeaware!)Treatment Whatisthemaindrugusedtotreathypothyroiddisease?  Levothyroxine:prettysimple–theydon'thaveenoughT4,sowegivethemT4! Whatcautionsdoyouneedtotake?  Youmustconsidertheriskofprecipitatingamyocardialinfarctionorworseninganginaintheelderlyorthosewith knownischaemicheartdisease. So: -healthyyoungpatient:levothyroxineanywherebetween0-100microgramsaday -old/IHDpatient:alwaysstartat25microgramsaday,adjustby25micrograms every4weeks.Maintenancedose is50-200microgramsoncedaily Howdoyoutakeit?  Take30-60minsbeforebreakfast,caffeineandanyothermedicationMonitoring Treatment DuetothelonghalflifeofT4,andthelogarithmiceffectithasonTSH,wewait4weeksafterthefirstdose toseeifTSHhasnormalised. Oncewe'rehappywiththedose,checkyearly. Sometimespeoplearen'tgoodwithadherence.Theymaynottaketheirmedicationuntilafew daysbeforetheirappointment.Whatwouldtheir TFTresultsshow? HighTSHwithnormal/highT4(dependshowmanydosestheytook!). It'simportanttoruleoutnon-adherence,asotherwisetheseresultscouldpointtowards morecomplexmechanismsatplay,thatwouldrequiremoremoneyforinvestigations, appointments,etc.Hyperthyroidism (thyrotoxicosis) Again we'll break this up OSCE style: - History - Physical Examination Findings - Management and Treatment Hyperthyroidism - Overproduction of thyroid hormone by the thyroid gland. Thyrotoxicosis - Abnormal quantity of 11.40 thyroid hormone in the body.What would you expect in a history of hyperthyroidism? (i.e. things the patient would complain about [not signs!]) Hypo=speed up AppropriateDDxforthesesymptoms? -overactive -irritabilityandmoodswings ➔ Anxiety -eyeproblems(possibly) ➔ Psychosis/bipolar  ➔ Atrialfibrillation -goitre(possibly) -diarrhea -palpitations Onceagain,familyhistoryisimportant here. -oligomenorrhea -feelinghot -itchiness - weightloss(sometimesweightgain)  -psychosis -beingfemaleCauses of Hyperthyroidism MostcommonintheUK? Graves'disease Other causes? Toxicmultinodulargoitre(mostcommon);toxicadenomas("hotnodules");thyroiditis (postpartum,druginduced,dequervains) Whoisnormallyaffectedbytoxicnodules? Theelderly Complicationsofhyperthyroidism? Heartfailure(thyroidcardiomyopathy),atrialfibrillation Whatdrugscancauseit? Amiodarone(AGAIN!),thyroidreplacementdrugs(overtreatmentof hypothyroidism)Thyroid Nodules ➔ Nodule=non-visible.Theycanbefibrouschangestothethyroidorsometimesswellings (hyperplasia,neoplasms,ormalignancy).Theymayormaynotproducehormones;wecando radionuclidescanstoseetheactivityofanodule. ◆ Hot=producingmorehormonethanusual ◆ Warm=producingnormalamounts ◆ Cold=producingloweramounts ➔ Manynodulesallproducinghormone,thiscancauseatoxicmultinodulargoitrewith hyperthyroidism. ➔ Ifwehaveasingleadenomaproducingahormone,wemightrefertoitasasingletoxic nodule. ➔ Ifwehaveasinglecoldnodule,itisextremelylikelytobemalignant.Graves' Disease asagoitre.gantibodiesactivatetheTSHreceptorscausingthereleaseofhormonesaswell Whatantibody(ies)is/arefound? ↑TSHrAb + ↓Anti-TPO WhatTFTresultswouldyouexpect? ↑T4, ↓TSH ItmayalsocauseGraves’eyedisease;what’sthebiggestriskfactor? Smoking!What would you expect to find on examination? (Hyper) (more signs so watch out!!) Signs-againlet’sbesystematic Red=Complicationofgraves Whatorderarewegoingin? Face + Eyes General Inspection ➔ Proptosis:abletoseewhitesofeyespast eyelidsfromlookingdownatpatientand ➔ Low(er)BMI(say"decreasedbody fromtheside habitus") ➔ Chemosis-periorbitaloedema ➔ Inappropriatelydressedfortheweather ➔ Painoneyemovements,lidlag e.g.wearingshortsandashirtduring Neck Hands + Wrists Thendoyourneckinspection,palpation(don’tforget ➔ Hotperipheries lymphnodes!),percussion,andauscultation(Graves’may ➔ Onycholysis haveabruitduetoincreasedvascularity).Thendothe ➔ TachycardiaorAF "othertests",whereinyoumayfind: ➔ Clubbing(acropachy) ➔ Briskreflexes ➔ Palmarerythema ➔ Pretibialmyxoedema ➔ Sweaty ➔ Proximalmyopathy(can’tstandfromsittingwithout ➔ FineTremor usingarms–althoughmaybeacommonfindingin elderlypeopleforotherreasons) ➔ PembertonSigns of Hyperthyroidism Onycholysis Acropachy Proptosis/exophthalmos Pre-tibial Myxoedema - splitting of the nail - New bone formation Sclerae visible above and - “Orange-peel” skin from the nail bed around the below the iris changes metacarpals and - Protrusion of sclerae phalanges beyond eyelidsGraves’ Eye Disease JustbecauseyouhaveGraves’hyperthyroidism,doesn’tmeanyou’llhaveeyediseasetoo- biggestriskfactorfordevelopingeyediseaseis Smoking! Thisisreallyreallyawfulforthepatient.Ithurtstolookaround,theireyesfeelgritty,anditcan beextremelypainful.Sometimestheyareunabletoblinkandtheircorneacanulcerate.They mayalsogetdoublevisiontoo. Insomecasesitcanonlybereversedwithsurgery,andwemustwaitforthyroidfunctionto returntonormalbeforeoperating,as,ifthepatientstillhasactivedisease,thechangesmay recur.Thesurgeryisverygoryandinvolvesremovingtheconnectivetissuethathasbeen depositedintheretrobulbarspace.Quick Quiz ➔ WhatTFTresultswouldyouexpectforprimaryhyperthyroidism? ➔ Differentialsforhyperthyroidism? ➔ WhatisSheehan‘ssyndrome? ➔ Howdowetreathypothyroidism? ➔ Givethreesignsyoumayseeinthehandsforsomeonewithhyperthyroidism? ➔ Cautionswhentreatingsomeonewithhypothyroidism?Hyperthyroid Disease Management 12.00Treatment Whatarethe3maintreatmentoptionsfor hyperthyroidism? 1. Pharmacological 2. Radiotherapy 3. SurgeryPharmacologicalTreatment Whatdrugsareregularlyused? Beta-blockersforsymptomaticrelief.Carbimazoleandlevothyroxineforthyroidfunction. Propylthiouracil(2ndline) Howarethesedrugsused? 1) Titration:givecarbimazoledailyfor4weeksandthencheckTFTsevery4-8weeksandreduce asneeded 2) BlockandReplace:givecarbimazoleandlevothyroxine(toreducechanceofhypothyroidism)in thesametimeline Bothareequallyeffective.InGraves’however,dotheseregimensfor12-18months,thenwithdraw. 50%willrelapsehowever,andneedsurgeryorradiotherapy. Sideeffectsandrisks? Treatmentisn’tguaranteedtoworkesp.forGrave’s.Hypothyroidismifovertreated. Rarely,carbimazolecancauseagranulocytosis:severeleukopenia.Henceyoumustwarnpatientsto stopmedicationandseekmedicalhelpiftheyhavesignsofillnesse.g.EVENASORETHROAT!Radioiodine Treatment Yougivethemradioactiveiodinewhichisabsorbedbythethyroidandbasicallykillsit. Contraindications? Pregnancyandlactation Extra Content to impress OSCE examiner There’sabunchofrulestofollowtooe.g.avoidgettingpregnant,closecontact,sleepalone, washyourclothesseparate,flushthetoilettwice,etc–youdon’tneedtoknowallofthese BUT,youmayhaveastationwhereyouneedtoexplaintreatmentoptionsfor hyperthyroidism.ItwouldbeusefultoKNOWAFEWOFTHESEGUIDELINESandthensay “formoredetailedinformationIcangiveyoualeaflet.” http://www.snmmi.org/AboutSNMMI/Content.aspx?ItemNumber=5609 Furthermore,asthistreatmenteffectivelydestroysthethyroidgland,themajorityofpatientswill becomehypothyroidafter. All of the intrinsic larynx Surgery: Thyroidectomy muscles except cricothyroid (which is done by external laryngeal) Canbehemi-thyroidectomybutisusuallytotal.Guaranteedtocause hypothyroidismafter.Hasriskshowever,whatarethey? ➔ Damagetotherecurrentlaryngealnerve (whichmuscle(s)doesthisinnervate bytheway?)whichcancausepermanentvoicechanges ➔ Hypoparathyroidism ➔ Bleeding,infection,DVT(usualsurgerystuff) ➔ Thyroidhaematoma–aftertheoperationapatientmayhavenewonset hoarsenessduetoahaematomabuildingupandcompressingthetrachea.This canleadtorespiratorydistressandevendeathifnottreated(viasurgical decompression/removingthestitchesonthewoundtorelievepressure)Thyroid Progress Test Honourable Mentions 12.10 Triggers -Thyroid/non-thyroidal surgery. Thyroid Storm -Trauma. -Infection. ➔ Untreatedhyperthyroidismcanlead -Acute iodine load (e.g. CT contrast/radioiodine). tothisrarecomplication. -Pregnancy. ➔ Youdon’treallyneedtoknowaboutit S/S -Fever > 38.5ºC. butIwantedtomentionitbecauseit’s gotacoolname. -Tachy/HTN. -Confusion/agitation. ➔ Itwillcauseahypotensiveshock -N/V. followingaheartattackandorheart -HF. -Abnormal LFTs + ~jaundice. failure,whichwillleadtodeath. ➔ Patientwillbeextremelyfebrile, confused,restlessnessandagitated Management -Treat underlying cause. (usually)andveryhypertensive. -IV propranolol. -Methimazole/propylthiouracil. -Lugol’s solution (aqueous iodine + potassium iodide). -Dexamethasone (prevents conversion of T4 --> T3)Subclinical Disease ➔ HighTSHandnormalT4?Thinksubclinicalhypothyroid.Subclinicalbasically meansthepatienthasnosymptomsetc,butsomethingisoffabouttheir pathology.Inthisinstance,theirthyroidisalittlebithypothyroid,buttheTSHis compensatingbyincreasingtoamplifyT4output. ➔ Theymayprogresstohypothyroidism. ➔ LowTSHandnormalT4?Theoppositeishappening!Thinksubclinical hyperthyroid.Pregnancy and Thyroid Disease ➔ Reminder:thisisforthemostpartveryspecialistandyouwon’tbe dealingwiththisasafoundationdoctor–butstuffaboutmedications candefinitelycomeupinprogresstest. ➔ Hypothyroidismisprettystraightforward ◆ thepatientisonlevothyroxineandjustneedstohaveregularcheckstoensureTFTsare normalandthey’reeuthyroid. ◆ Uncontrolledhypothyroidismcancausealotofproblemssuchaspre-eclampsia, prematurity,andstillbirths. ➔ Hyperthyroidismismorecomplex ◆ Antithyroiddrugsareforthemostpartteratogenic,andtheGraves’diseaseantibodies arecapableofcrossingtheplacenta,andaffectingthefetus.Thyroid Meds and Pregnancy ➔ Carbimazoleisnotrecommendedtouseinthefirsttrimesterofpregnancy(itisnot absolutelycontraindicatedbutitoftencauseshypothyroidismand,extremelyrarely, aplasiacutisofthenewborn) ➔ Itisrecommendedthatwomenoncarbimazoleshouldusecontraceptiontoavoid pregnancy ➔ Thereisalotoutthereonwhethertousepropylthiouracilinthefirsttrimester,and thenswappingtomethimazoleafterthat,butthisisextremelyspecialisedand abovemedstudentlevel.Don’twasteyourtimelearningmorespecificsbecausethis isconsultantlevelstuff–thereareprosandconstousinganti-thyroidmedications inpregnancy:somecausesideeffectsinthemotherbutsparethebaby,andsome aretheopposite.Touching on Thyroid Cancer 12.20Types 5types,whatarethey? Extra Content for Progress Test Usefulmnemonic(inorderofprevalence): ➔ Please(papillarycarcinoma) ` ➔ Find(follicularadenomaorcarcinoma) ➔ My(medullarycarcinoma) ➔ Auntie(anaplasticcarcinoma) ➔ Lauren(lymphoma)Cancerous thyroid cancer facts! Extra Content for Progress Test ➔ Papillaryandfolliculararehandledinthesameway:totalthyroidectomyandradiation treatmenttogetridofanyresidualcells.YearlyfollowupforTPOantibodies. ➔ MedullaryisrelatedtoMEN2(moreonthisnextslide).Canbeassociatedwithapoor prognosis. ➔ Anaplastic:worseprognosis,oftencanonlytreatwithpalliation. ➔ Lymphoma:rarestandcanresultfromHashimotosMEN2 Extra Content for Progress Test ➔ MENstandsformultipleendocrineneoplasia.Hereditarydisease. ➔ Type2causesmedullarythyroidcancerandpheochromocytomas(cancerofadrenalmedulla). ◆ Splitsintotype2Aor2B ➔ Type1affectsparathyroid,pituitary,andpancreas. ➔ “Apatientisdiagnosedwithathyroidtumour.Herfamilyhistoryispositivefordiabetes, ` hypertension,andherbrotherhasbeentreatedforapheochromocytoma,whattypeoftumourisshe likelytohave?” Why did the endocrinologist break up with his wife? Theyweren’t MEN-2BFinal Quiz ➔What3waysdoweusetowetreathyperthyroidism? ➔Howisitdonepharmacologically? ➔Sideeffectsofpharmacologicaltreatment? ➔WhataresignsspecifictoGraves‘hyperthyroidism? ➔Whatsortofnoduleislikelytobemalignant? ➔Whatcanhappenifhypothyroidismisn‘ttreated? ➔Whatarethetypesofthyroidcancer?Practise Questions➔ TSH - (0.4 – 4 mU/L) ➔ Free T4 - (9 – 25 pmol/L) ➔ Free T3 - (3.5 – 7.8 nmol/L) You don’t need to remember normalvaluesVERYCHE👀KYQUESTIONOSCEs (the stuffyou’ve been waiting for)Explaining Thyroid Conditions - CarAnalogy Thethyroidisanorganinyourneckwhichcontrolsyourmetabolism.Your thyroidissimilartotheacceleratorinyourcar. ➔ Whenthethyroidisworkingtoomuch,it’slikepushinghardonthecar acceleratormakingeverythingmovefaster….that’swhyyouhavebeen gettingthesesymptomssuchasdiarrhoea,palpitations,weightloss, lumpinyournecketc. ➔ Whenthethyroidissluggishandunderactive,it’ssimilartopushing downonthebrakesmakingeverythingmoveslower...that’swhyyou havebeenfeelingsleepy,lowinmood,feelconstipatedetc. ALWAYSRELATEBACKTOTHEIRSYMPTOMS!!!!Potential OSCE Stations ➔Thyroidexam(eithergeneralortargetedforhyper/hypothyroidsigns) ◆ Gothroughthemotions,washyourhands,introduceyourself,bepoliteandbeslick! ◆ Completeyourexamin6minutes(orless!–thistakesalotofpracticesogoannoyyour friends)andthenimmediatelysummariseyourfindingsandsayhowyou’dcompletethe examination ➔Explainingadiagnosis(caranalogy) ➔TFTinterpretation ➔Explainingtreatmentoptions (thinkaboutrisks,chunkandcheck,pros andcons!) ➔History:makesureyouaskaboutfamilyhistoryofautoimmunedisease andthinkaboutthedifferentialswediscussed!Afteryourhistory,you shouldbeaskedfor3differentials,andthenyourmostlikelydifferential!Thanks. Any Questions?