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TCD 24 - Hypertension By Zak Mouyer x Maria Chowdhury zakariya.mouyer@student.manchester.ac.ukAdmin Stuff - Checkyourjunkmail - Checktheemailaddressthatyouregisteredforthezoomwith-that’sthe oneit’llbesentto - Pleasedon’tdmmexxx - YouwilleventuallygettheslidesIpromise(ifyoufilledoutfeedback forms) - BEPATIENTWITHUS(PLEASEEEEE) - Don’tworryaboutthenittygrittystuff,justtryandabsorbasmuchasyou can ILOs ThemainaimoftodayistoadheretothefaultlesswordsofLilPumpand‘Esketit’ - DefiningHTN - HypertensivePhysiology - AetiologyandSecondaryCauses - Diagnosis - GuidanceonHTNmanagement - HypertensiveEmergency - QRISK3 - SecondaryPrevention - Historytaking,explaining,examiningHypertension - who dat? Awise person once said: ‘I ain’t ever seen two pretty best-friends, one of them always gotta be hypertensive’ Wowtheculturalreferencesinthis 11.10 areasoldaszakDefinition plus les nombres - Clinically,hypertensionisdefinedas(oncecompleteandappropriate investigationisdone): - Clinicbloodpressureof140/90mmHgorhigher - andABPMdaytimeaverageorHBPMaverageof135/85mmHgor higher. - Forpatients: “Common,long-termconditionwherethepressureofbloodinthe arteriesistoohigh.Peopleusuallydon’tfeelanything,butitisstill importanttotreatbecauseitcanleadtocomplications,likeputting strainontheheartanddamagingbloodvesselsintheheart,brain,eyes andkidneys.Thecauseismostcommonlyunknown,butinrare instancestherecanbeanunderlyingcondition.Itistreatablewith lifestylechangesandtablets.” BTWGUYSTHISISREALLYFLIPPINGEASILYOSCE-ABLESOPLSLEARNITPLS THNXGUYSIAPPRECIATEITHAVENICEDAYHypertensive Physiology 11.15 How does blood pressure increase? Butonalegitnote,BPcangoupfor2reasons: - Physiologicallyviathesympatheticnervoussystem →arteriolar vasoconstriction - PathologicallyviatheRAASPhysiological BP Increase: CO=HRxSV BP=COxPVR SympatheticBPIncrease: Canbecome“reset”/sensitizedby 2majorbaroreceptorpopulationsin long-termHTN carotidsinusandaorticarch ● Archactivation->vagusCNX-> Thisisimportantsincethereceptorscan tractussolitarus allowincreasinglyhigherBPstobehit ● Carotidactivation->Hering’snerve-> beforetheaforementionedpathwayis glossopharyngealnerve/CNIX -> activated tractussolitarus ● Tractussolitarus->inhibitionof WELCOMETOESSENTIAL vasoconstrictioncentreand HYPERTENSIONLADIESANDGENTS excitationofvagus→THISWILL DECREASESYSTEMICBP Sidenote:Obesitycausesperivascular ImportantinmaintainingposturalBP adiposetissuewhichcanincreasePVRby changes(agechanges->syncope) decreasingarterialcontractilityPathological BP Increase: Renin-Angiotensin-Aldosterone-SystemPathological BP Increase: Renin-Angiotensin-Aldosterone-SystemCauses of Hypertension Howifeelboutthistopic(M) this is gonna RAAS your brains hehe 11.25 ThepneumonicROPEmighthelpu rememberthe2ndrycauses: Aetiologies of Hypertension R-Renaldisease O-Obesity P-Pregnancyinduced/Pre-eclampsia E-Endocrine Passmetheropehahax •Primary/Essential/IdiopathicHypertension-90%/95% •SecondaryHypertension-5%/10% ○ RenalDiseases ○ EndocrineDiseases ○ Drugs(Glucocorticoids,Oralcontraceptives,SSRIs,NSAIDs,EPO) ○ Other-preggolol Lolthewayhypertensionispasseddownforsomeofusitmightaswellbehereditary:0 Secondary Hypertension: Renal Causes RenalDisease→HypoperfusiontoJuxtaglomerularApparatus(JGA) ○ Intrinsic ■ Glomerulonephritides,PKD,PAN,SystemicSclerosis,Pyelonephritis,CKD ○ RenalArteryStenosis ○ FibromuscularDysplasia Secondary Hypertension: RenalArtery Stenosis •RenalArteryStenosis: ○ >50%reductioninrenalarterylumen ○ IschaemicnephropathycausesreducedeGFR ○ RenovascularhypertensionmediatedbyhighlevelsofreninandangiotensinII producedbyrenalhypoperfusedkidney ○ ThinkofOLD,FEMALE,SMOKERw/atheroscleroticriskfactors Dx: ■ DuplexUSS ■ Gadolinium-enhancedMRAngio/Renalangiography Rx: ■ AntiHTNtherapy+renalmonitoring ■ SecondaryPreventiontherapies ■ ConsiderRenalArteryStentingifonmultiplepharmaceuticaltherapiesSecondary Hypertension: Fibromuscular Dysplasia FMD ○ Non-inflam,Non-atherosclerotic ■ MultifocalFibroplasiaofallarterialbedsinthebody-commonlyRenals/Carotids ■ SegmentsofStenosesfollowedbyAneurysmaldevelopments(basicallynarrowingand enlargement) ○ Thinkmiddle-agedwomen ○ Sympx(bothrenalandcerebral) ■ Migraines,PulsatileTinnitus,TIA,CVAs,Horner’s ■ SecondaryHTN(treatmentresistant-getsworseinwomenafterACEi)and evidenceof <eGFR ■ Generallybruitsmaybeaudibleonexam ○ DxisclassicallyDuplexUSS,MRAorCTA(thinkaboutkidneyfunctionhereuplebs) ■ ‘String-bead’signtypicallyseenonangiography ○ Highkey/Lowkeyguysinrelationto2ndaryHTN,thisformsatypeofRASbutisabitmoresaucy that’sall ○ Rx ■ AntiHTNtherapies ■ 2ndaryPreventionforriskofCVAs ■ ConsiderRenalArteryAngioplasty/Stenting Secondary Hypertension: Endocrine Causes EndocrineCauses: ○ Cushing’sSyndrome/Disease ○ PrimaryHyperaldosteronism(mostcommoncauseof2ndaryHTN) ○ Phaeochromocytoma ○ Acromegaly ○ Hyperparathyroidism-wewon’tcoverthistodayasit’scoveredinanotherTCD Secondary Hypertension: Cushing’s Thiswillbecoveredinalatercase, butbriefly Endresult:thereisanincreaseinserum corticosteroids Thisisclassedashavingtoomuchcorticosteroidvia: (glucocorticoids/mineralocorticoids) Cushing’sDisease:Pituitary-dependentcorticotropic ■ Highaldosterone→refertoRAAS→ adenoma(ACTHproducingpituitarytumour) incbloodvolume Cushing’sSyndromes: ■ Highcortisol→increaseSNS ● EctopicACTHproduction→endocrine activation→lossofdiurnalityin paraneoplasticsyndromefromaSmall-CellLung cortisolsecretiontoo Cancer ○ Whatotherparaneoplasticsyndromecan occurinSCLC? Mx: ■ SIADH Trytotreatunderlyingcauses ■ Cushing’s ● Excision/Chemotherapies/Radiotherapies ofadenomas/tumours ■ Lambert-EatonMyasthenicSyndrome ■ CerebellarDegeneration ● ExcludeIatrogeniccauses ● IatrogenicSteroid→exogenousandexcessive ● BeginAntiHTNtherapies steroidintake Secondary Hypertension: Hyperaldosteronism What is it? Toomuchaldosterone •PrimaryHyperaldosteronism: ○ Bilateralidiopathicadrenalhyperplasia-70%-mostcommon2ndaryHTN ○ Unilateraladrenaladenoma-Conn’sSyndrome-30% ○ AdrenalCarcinoma-rarerthanrare ○ FamilialHyperaldosteronism-DoE(exceedinglyrare) •Technically,RenalArteryStenosisandHeartFailurecancausea secondary hyperaldosteronism ○ CausedbyrenalhypoperfusionleadingtoactivationoftheRAASpathwaySecondary Hypertension: Hyperaldosteronism Features and RF ○ Uncontrollable,persistentHTN ○ Agebetween20and70 ○ Hypokalaemia ■ Lethargy ■ Paresthesias ■ Hypotonia,Hyporeflexia,Muscleweakness ■ Palpitations ■ Muscleweakness ■ DiabetesInsipidus ● Hypokalemiacausedamagestubules→reducestubularsensitivitytoADH→ nephrogenicdiabetesinsipidus(don’tworryabtdisrn) RiskFactors ■ FHofPA ■ Unexplained+earlyonsetHTN/Strokein1stDegreeFamilySecondary Hypertension: Hyperaldosteronism Diagnosis ○ Renin:AldosteroneRatio ■ HighAldostandLowReninsuggestPrimaryAldosteronism ■ HighAldostandHighReninsuggest2ndaryAldosteronism ○ BloodPressure ○ U&Es(HypokalemiaandHypernatremia) ○ ABG ■ Alkalosis(duetoH+leavingviaCD) ○ CT/MRIlookingforUnilateral/BilateralHyperplasias/AdrenalTumours ○ AdrenalVeinSampling ○ Consider: ■ RenalDopplerUSS ■ RenalMRA ■ RenalCTA ■ Why? ● 2ndaryHyperaldosteronismcausedbyrenalhypoperfusioninRASSecondary Hypertension: Hyperaldosteronism Management ○ AldosteroneAntagonists-bilateraladrenalhyperplasia ■ Eplerenone ■ Spironolactone ● Whataresomeissueswithspironolactonehere? ○ CancauseAldosterone-antagonistinducedhyperkalaemia ○ Chattomeabouthyperkalaemia... ○ AdrenalAdenectomy-adenoma/carcinoma ○ TreatanyunderlyingRenalArteryStenosisifpresentSecondary Hypertension: Phaeochromacytoma Background ○ Tumourofthecatecholamine-secretingchromaffincellsofAdrenalMedulla. ■ 10%arebilateral ■ 10%aremalignant ■ 10%areextra-adrenal(peri-aorticarch) ○ Causesasporadicreleaseofcatecholamines(adrenaline)Secondary Hypertension: Phaeochromacytoma Symptoms ● SustainedHTN ● Headaches-90% ● Diaphoresis-70% ● Palpitations-60% ● Anxiety ● Insomnia ● Diabetes(polyuriaandpolydipsia) ● Adrenalineincreasesglycogenolysisandinhibitsinsulinrelease ○ RFs:MEN2(2aand2b)includingitsotherassociatedcancerousrisks,NF1Secondary Hypertension: Phaeochromacytoma Diagnosis & Management ○ Dx:plasma thenurinarymetanephrines=gold,24-hoururinecollectionforcatecholamines =leastvalue ○ Mx: ■ Hypertensivecrisis:Phentolamine(potentalpha-receptorblockade)andIV Nitroprusside(vasodilator) ■ Non-crisis: ● alphaantagonists,betaantagonistsafter ● Surgicalexcisionoftumour(partial/totaladrenalectomy Secondary Hypertension: Acromegaly Features AnteriorPituitary(Somatotroph)TumoursecretingexcessiveGH s/s= ABCDEFGHIJ ■ -Arthralgia/arthritis. ■ -Bigboggyhands. ■ -Carpaltunnelsyndrome. ■ -DM. ■ -Enlargedorgans(tongue/heart). ■ -Fielddefect(bitemporalhemianopia). ■ -Gynaecomastia/galactorrhoea/GImalignancy(CRC)/greasyskin. ■ -HTN/headache. ■ -Increasedsize(rings/gloves/shoes/hat/dentures). ■ -Jawenlargement+prognathism(protrusion) ○ Complications: ● DM/HTN(atleast40%ofcases) ● Cardiomyopathy ● CRCSecondary Hypertension Acromegaly Diagnosis and Management ○ Dx: ■ WhynotjustmeasureserumGH? ■ SerumIGF-1 ■ ThenOGTT ■ MRIPit-toconfirmiguess ■ Considerotherpituitaryhormonetests(hypopituitarism) ○ Mx: ■ 1stline:trans-sphenoidalresections ■ 2ndline/Adjunct:SomatostatinAnalogue(-vefeedbacktingz)-OCREOTIDE ■ 3rdline:pegvisomant(GHRA)/bromocriptine/cabergoline(Dopamineagonist-prolactinoma??)Secondary Hypertension: Drugs and Other Causes OtherSecondaryCauses: ○ AorticCoarctation (renal Drugs: hypoperfusion) ○ Steroids ○ GestationalHTN ○ Cocaine ○ Pre-eclampsia ○ NSAIDs ○ Sleepapnoea ■ hypoxaemiatriggering ○ Amphetamines ○ MAO-i chemoreceptors→risein cortisolduringsleep additionallyDiagnosing Hypertension 11.42Hypertension Stages Diagnostic Process ●Aone-offclinicreadingjustisnotenough-‘whitecoatHTN’ ○ Alsoyoumustmeasurebotharms-why? ○ Technique,restingandrelaxationareneededforaccuratereadings ●Inclinicif>140/90but<160/100 ○ Offer24hrABPM/HBPM ●IfABPM>135/85but<150/95 ● Offernon-medicaltreatmentunless: ○ Stage1and<80y/oandoneof: ■ End-organDamage ■ RaisedCVDrisk ■ RenalDisease ■ T1DM/T2DM ■ QRISK3>10% ●IfABPM>150/95 ● OfferNormalMedicalHTNTherapies ●Inclinicif>160/100 ○ OfferNormalMedicalHTNTherapiesOther aspects of HTN diagnostics ○ CheckfastingglucoseandHb1AC ○ CheckLipidprofile ○ CheckEnd-organdamage: ■ ECG-AF+/-dilatedCM ■ ECHO-dilatedCM ■ URINALYSIS-proteinandblood ■ FUNDOSCOPY-retinaldamage ■ CVEXAM-coarctation Diagnostic Process Justtoreiterate,offerMedicalTreatmentto thefollowing: ○ <80y/ow/Stage1HTNandoneof: Reminder,iftreatmentresistant,considerthe ■ Stage1and<80y/o following: ■ End-organDamage ○ Conn’s-takeU&Es ■ RaisedCVDrisk ○ Hyperpara-takeCa2+ ■ RenalDisease ○ RAS-RenalUSS/Arteriography ■ T1DM/T2DM ○ Phaeo-24hrUrinaryMetanephrines ■ QRISK3>10% ○ AnyonewithStage2HTNHypertension Management 11.50Drugs lolmy fave is intranasal Benzoylmethylecgonine WhichHTNdrugscauseshyponatremia, hypokalemiaandhypercalcaemia? WhichHTNdrugscauseshyperkalemia? HTNRxinbadCKD? Drugs lol - my fave is intranasal Benzoylmethylecgonine ACEi/A2RBs?Ramipril/Linsopril/Candesartan - MOA - SE - CI - Monitoring ThiazideDiuretics?Indapamide(Thiazide-like)/Bendrolfufuorurouethaizeedfe - MOA(rip) - SE - CI HTN Lifestyle Changes •IndicatedwithStage1HTNin<80withnocomplications/RFs ○ HealthyDiet-NHSEATWELLGUIDE ○ <6gdailysaltintake-(1.5teaspoons) ○ SmokingCessation ○ RegularExercise ■ 150mins/weeksplitacross5x30minssessionsonseperatedays • Alsotheyshouldattendanannualreviewclinicforend-organdamage HTN Mx Stop ACEi if ↑↑ creatinine by 30%/K up to 5.5 1stLine:<55y/oORT2DM ○ ACE-i-ramipril ■ 1.25mgODPOupto10mgODPO ■ SE: ● Drycough,angioedmea,dizziness, hyperkalaemia,1stdose HYPOtension ■ IfACE-inottoleratedofferA2RB ● Candesartan8-32mgODPO ○ Contraindicatedin: ■ heartvalvedisease ■ cardiomyopathies ■ ACEi(duh) 1stLine:>55y/oorAfro-Caribbean ○ CalciumChannelBlocker- Amlodipine ■ 5-10mgPOOD ■ SE ● Diuretic-resistantankleswelling•2ndLine:A+C/DorC+A (2RBifb/Dck) •3rdLine:A+C+D ○ Thiazide-liDiuretic-Indapamide2.5mgODPO ○ ProximalDCTNa/Clinhibitor→keepsNa/H2Ointubule •4thLine:A+C+D+x ○ xdependsonserumK+levels ○ SerumK+<4.5mmol/L ■ Addanaldosteroneantagonist ● Spironolactone ○ Cancauseseverehyperkalaemiain combinationwithACE-i ○ NeedregularU&Es ○ CancauseGouttoo ○ SerumK+>4.5mmol/L ■ Addanalphablocker ■ ThenaddaBetablocker(Biso5-20mgPOOD) ● ContrawithAsthma ● Cancausebronchospasm,HR,Impotence •IFPREGNANT: ○ Nifedipine,Labetalol,Mehtyl-dopaHypertensive Emergency 11.55Hypertensive Urgencyvs. Emergency HypertensiveUrgency Hypertensiveemergency/MalignantHTN Noend-organdamage Endorgandamage Approx180/110 Usually180-200/120-130butcanbelower Symptoms: Symptoms: Headache,SOB,epistaxis,severeanxietyorcan Chestpain,SOB,backpain,numbness,weakness, beasymptomatic visionchange,difficultyspeaking Complications: Complications: Checksignsofend-organdamage Cerebraloedema,raisedICP->encephalopathy Management: Management: Outpatientoralmedicationsand48hrreview HDU,IVvasodilator,CCB,ß-blocker U&E Urinalysis Fundoscopy ECGHypertensive Emergency Mx •FirstlycheckforEnd-OrganDamage: ○ ECG,ECHO,Fundoscopy,Urinalysis •ReduceBPinacontrolledwayoverseveraldays ○ SuddenlydroppingBPcancauseaStrokeorHypoperfusionofVitalOrgans •InitiallygiveAtenololor CCB •IfpatientisEncephalopathic→admittoHDUstat ○ InsertAterialBPline ○ GiveLabetalol(alphaandbetablocker) ○ AlsoadministerIVNitroprusside(potentvasodilator)Hypertensive Complications ● IHD ● MI ● LVH ● HR ● Stroke ● Retinopathies ● HTNNephropathies ● ShrunkenKidneys ● DamagedGlomeruliQRISK3 ScoreQRISK 3 ●NICE:treatHTNifQRISK3is10%orgreater ○ Underestimatesriskinunder40yo’swithnoend-organdamagesoinvestigate forsecondaryHTNcausesinthem ●Assessesneedforprimarypreventiontreatment(%riskofstroke/MI in10years) ●If>10%,patientneedsAtorvastatin20mgPOODPM ○ AllpatientswithCKDorT1DM>10yearsshouldalsotakethis ○ Checklipids3months,andincreasedosetoaimfor>40%reductioninnon-HDL cholesterol(Checkadherencebeforeincreasingdose) ○ CheckLFTswithin3monthsofstartingstatinandagainat12months,noneed afterthat ○ ASTandALTcanrise,don’tneedtobestoppedunlessriseis3xupperlimitof normalHigh yield zak stuff 12.00 CAUSES OF CAUSES OFAF RAISED JVP ●-Mnemonic = TRIPPAH: ● Mnemonic = PPQRST ● -Thyrotoxicosis. ● -Rheumatic heart disease. ● -Pulmonary HTN. ● -Massive PE. ● -IHD. ● -Pneumonia. ● -Quantity overload. ● -RHF. ● -PE. ● -SVC obstruction (non-pulsatile). ● -Alcohol/anaemia. ● -HTN. ● -Tamponade.SIDE EFFE TS= CCUSHINGOIDP. ● -Cushing's syndrome. OF STEROIDS ● -Cataracts. ● -Ulcers/pancreatitis (GI). ● -Skin (striae/thinning/bruising). ● -HTN. ● -Immunosuppression. ● -Necrosis (avascular necrosis of femoral head). ● -Glycosuria. ● -Osteoporosis/Obesity (weight gain). ● -Infection. ● -Diabetes. ● -Psychosis/depression/mania. Resources - BMJBestPractice - Zerotofinals - KumarandClark’sClinicalPathologyChapteron‘howtostopmissingher’ - Geekymedics- - OHCM - DrugbankCa - ClinicalKnowledgeSummaries - MyownnotesThe final session, Very cri much sad, Gonna miss you guys so much lol, I learnt from you a lot more than you learnt from me, Don’t forget to do everything you do with ihsaan and you will succeed beyond yourwildest imagination, I love you all, Bye Bye manchester - Z z.mouyer@gmail.com zmouyer@doctors.org.uk(bigflexiknow,suemebishes)