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Zia Kanji and Sandra Benny Learning Outcomes Diabetes Adrenal Thyroid Parathyroid And many more...Mohammedpresents to the emehe has beenexcessivelythirstyand passing largeamounts of urine.st day. He complains that beforethis, On examination,he has dry mucous membranes,a prolonged capillary refill time anddeep,labouredbreathing. His blood results are: Serumglucose : 27 mmol/L ( <11) Serumketones:5mmol/L ( <3) What typical finding willbe seenon an ABG? A- Mixed respiratory and metabolic acidosis B- Normal anion gap metabolic acidosis C- Raised anion gap metabolic acidosis D- Reduced anion gap metabolic acidosis E- Respiratory acidosisMohammedpresents to the emergency department complaining of nauseaand vomiting over the past day. He complains that beforethis, he has beenexcessivelythirstyand passing largeamounts of urine. On examination,he has dry mucous mHis blood results are:apillary refill time anddeep,labouredbreathing. Serumglucose : 27 mmol/L ( <11) Serumketones:5mmol/L ( <3) What typical finding willbe seenon an ABG? A- Mixed respiratory and metabolic acidosis B- Normal anion gap metabolic acidosis C- Raised anion gap metabolic acidosis D- Reduced anion gap metabolic acidosis E- Respiratory acidosis DKA DKA is a life-threatening diabetic emergency Lack of insulin= cells Release of glucagon and Ketonaemia Metabolic instarvationmode cause gluconeogenesis, >3mmol/L due to lack of and lipolysis. Production of acidosis absorptionof glucose leads to metabolic acidosis High osmolality of the The increase influid DKA Osmotic blood results in fluid inthe intravascular intracellular → osmotic diuresis ina Diuresis Intravascular spaces the kidneys. Acidosis with Hyperglycaemia Aelectrolytes are Leads to HCO3<15.0mmo >11.0mmol/L Electrolyte also dragged out depletion of K+. l/L of the filtrate and Masked imbalances excreted hypokalemia DKA SYMPTOMS DIAGNOSTIC CRITERIA MANAGEMENT Nausea Vomiting Lab glucose pH<7.3 Fluids-isotonic >11.0mmol/L saline(0.9%NaCl) Polyuria Polydipsia Insulin(0.1 Ketones >3mmol/L unit/kg/hour) Abdo pain Kussmaul or ketonuria breathing Potassium- Pear drop importanttomonitor breath Headache cardiacfunction DKA-resolution Ketonemiaand acidosisshould have settledwithin 24 hours. If not → ENDOCRINOLOGIST Ketones pH>7.3 <0.6 mmol/L Visual Focal Headache? Irritabilitydisturbance? neurology? HCO3 >15.0 mmol/L Potential cerebral oedema? Children and young adults are more vulnerable to this followingfluidresuscitation(usually4-12 hours after) If above criteriaare metand the patient is CT HEAD AND SENIOR REVIEW! eating and drinking,move them to SC InsulinRahul , a 6 year old boy is brought to the GP because he has recently startedto wet the bed again. Se gained continence overnight at age 4, and has been fine overnight since, but has wet the bed everynight for the last 2 weeks. Also, he is always pesteringhis parents for water and juice. Otherwise, he is a healthy boy and is getting on well at school. On pasta.oning, his father notes his son has lost weight recently. His mother has a thyroidcondition and can't eat bread or On examination, the boy appears thin. A urine dipstick shows glucose ++. Which cell type has been destroyedby the immune system? A- Thyroid Follicular Cells B- Pancreatic delta Cells C- Pancreatic Beta Cells D- Pancreatic Alpha cells E- Villous enterocytesRahul , a 6 year old boy is brought to the GP because he has recently startedto wet the bed again. Se gained continence overnight at age 4, and has been fine overnight since, but has wet the bed everynight for the last 2 weeks. Also, he is always pesteringhis parents for water and juice. Otherwise, he is a healthy boy and is getting on well at school. On pasta.oning, his father notes his son has lost weight recently. His mother has a thyroidcondition and can't eat bread or On examination, the boy appears thin. A urine dipstick shows glucose ++. Which cell type has been destroyedby the immune system? A- Thyroid Follicular Cells B- Pancreatic delta Cells C - Pancreatic Beta Cells D- Pancreatic Alpha cells E- Villous enterocytes Type 1 Diabetes Characterised byan inabilityto produce/secreteinsulindue to autoimmunedestructionof the beta-cells(productionsiteof insulin)inthe pancreatic isletsof Langerhan. The absenceof insulinleadsto an increasein the rate of glucoseproductionfrom the liverand reduced peripheral uptake of glucose.Thisis exacerbated by the highlevelsof glucagonand othercounter-regulatoryhormones.Thisresultsin an osmotic diuresis Fastingglucose>7mmol/L Polyuria Weight Or Polydipsia loss Random glucose>11mmol/L If asymptomatic,mustbe demonstratedon 2 Urine dip for ketones and Random and ICA (Islet occasions fasting glucose cell glucose autoanti MANAGEMENT bodies) Anti GAD → Multiple dailybasal-bolus insulinregimen C peptide and (Antibodies → Twice dailyinsulindetemir HbA1c not to acidamic → BMI> 25= considermetformin accurate for use diabetic auto IAA decarboxInsulinoma in T1D antibodies (Insulin ase) associated-2 used auto- autoantibodie BLOOD GLUCOSE TARGETS: antibodi s) On waking=5-7 mmol/L presentation includes some atypical features (for example, age 50 years or prodrome)I of 25 kg/m² or above, slow evolution of hyperglycaemia or long Before meals and other times of the day=4-7 mmoL/Priya, a 63 year old diabetic woman is admitted to hospital in order to have intravenous antibiotics for community acquired pneumonia. On day 3 of admission she becomes confused and drowsy after which she has a short seizure which spontaneously resolves.Her capillary glucose is noted at 3.1mmol/L and she is unconscious. What is the most appropriate immediate management of this patient? A- IV Glucagon B- Oral glucosetablets C- IM Glucagon D- IV lorazepam E- Stop all diabeticmedicationPerina, a 63 year old diabetic woman is admitted to hospital in order to have intravenous antibiotics for community acquired pneumonia. On day 3 of admission she becomes confused and drowsy after which she has a short seizure which spontaneously resolves.Her capillary glucose is noted at 3.1mmol/L and she is unconscious. What is the most appropriate immediate management of this patient? A- IV Glucagon B- Oral glucosetablets C- IM Glucagon D- IV lorazepam E- Stop all diabeticmedication Hypoglycaemia Glucose <4mmol/L Blood Autonomic Sweating CONSCIOUS AND CAN SWALLOW →15- symptoms due to Shaking glucose the release of Hunger 30mgfast actingcarbohydrate, glucose <3.3mmol/L gadrenalined Nauseay tablets and drink Blood Neuroglycopenic Weakness CONSCIOUS AND CAN’T SWALLOW syinadequate to Vision changes →Glucosegelaround the teeth(eg glucose glucose supplyto Confusion glucogelordextrogel) <2.8mmol/L the brain Dizziness Severe and UNCONSCIOUS→Enable IVAccess and uncommon Seizures give an IV glucoseload. Consider1mg IM Coma Glucagon if difficultto establishaccess featuresdrowsinessand confusion. He has recentlybeen startedon oral antibioticsby his general practitioner for a urinary tracting infection.His past medical history includes type two diabetes mellitus and hypertension.His medication historyincludes Motor 6). He is apyrexial,tachycardic and hypotensivewith dry mucus membranes and decreased skin turgor.es 3 Voice 4 Which of the followinginvestigationresults would confirm a diagnosis of hyperosmolar hyperglycaemic state (HHS)? A- Serum Bicarbonate 10mmol/L B- Urinalysisketones+++ C- Serum osmolality330 mOsm/kg D- Blood glucose14mmol/L E- ABG pH 7.21drowsinessand confusion. He has recentlybeen startedon oral antibioticsby his general practitioner for a urinary tracting infection.His past medical history includes type two diabetes mellitus and hypertension.His medication historyincludes Motor 6). He is apyrexial,tachycardic and hypotensivewith dry mucus membranes and decreased skin turgor.es 3 Voice 4 Which of the followinginvestigationresults would confirm a diagnosis of hyperosmolar hyperglycaemic state (HHS)? A- Serum Bicarbonate 10mmol/L B- Urinalysisketones+++ C- Serum osmolality330 mOsm/kg D- Blood glucose14mmol/L E- ABG pH 7.21 HyperosmolarHyperglycaemicState ACUTE DIABETIC EMERGENCY IN PATIENTS WITH T2DM Fatigue, lethargy, → Thelack of insulin is coupled with a rise in nausea, vomiting, General POLYURIA AND counter-regulatory hormones (cortisol, growth POLYDIPSIA hormone and glucagon) → profound rise in glucagon A certain amount of insulin Is Altered retained which prevents the consciousness, development of ketosis that headaches, defines DKA Neurological papilloedema, weakness OSMOTIC DIRUESIS → Leadingto loss of electrolytes (kidneysonly havea certain capacity for glucose reabsorption) Hyperviscosity of the blood → Haematological Potential stroke, PAD, infarctions Dehydration If they fail to and reduced compensate circulating Compensatory for renal water Dehydration, volume → mechanisms loss, HYPEROSMO eg ADH release hypovolemia Cardiovascular hypotension, LARITY AND and thirst occurs →AKI, tachycardia HYPERGLYC Hypotension, AEMIA comaHyperosmolarHyperglycaemic State Fluid and Swif osmolalityisn’t Hypovolemia electrolyte IV 0.9% NaCl declining (more replacement hypotonic solution) Rapidchanges in Increased serum Monitor osmolarity→ plasmasodium shouldof Cardiovascular not exceed10 mmol/L Hyperglycaemia osmolality(>320 management cpontine myelinosis in24 hours. >30mmol/l (with mosmol/kg) no ketosis or acidosis) KETONEMIA PRESENT (fixedrate insulin Insulin Chif insulinneeded.e startedat time zero KETOENMIA ABSENT= NO INSULINwith diabetes and has trialled lifestyle changes. Today, her HbA1c is 58 mmol/mol. At the time of diagnosis, her HbA1c was 51 mmol/mol. Her past medical history comprises chronic kidney disease - with an estimated glomerular filtration rate (eGFR) of 22mL/minute/1.73 m2 - and chronic pancreatitis. She recently underwent a percutaneous coronary intervention. What is the most appropriate management option? A-Book another appointment in 6 months B-Prescribecanagliflozin C-Prescribegliclazideand then canagliflozin D-Prescribemetformin E-Prescribemetformin and then canagliflozin Asiya, a 62 year old female presents to her general practitioner for a diabetic review. She was recently diagnosedwith diabetes and has trialled lifestyle changes. Today, her HbA1c is 58 mmol/mol. At the time of diagnosis, hered HbA1c was 51 mmol/mol. Her past medical history comprises chronic kidney disease - with an estimated glomerular filtration rate (eGFR) of 22mL/minute/1.73 m2 - and chronic pancreatitis. She recently underwent a percutaneous coronary intervention. What is the most appropriate management option? A-Book another appointment in 6 months If metforminiscontraindicated + patient B-Prescribecanagliflozin hachronic heart failure→ SGLT-2VDor monotherapy C-Prescribegliclazideand then canagliflozin D-Prescribemetformin E-Prescribemetformin and then canagliflozin Type 2 Diabetes Repeatedexposureto glucoseand insulin makes the PRE DIABETES → Bodystrugglesto get bloodglucoseina cellsresistant to the effects ofinsulin. This results in the normal range even after a prolongedperiodof not eating pancreas becomingfatiguedand producelessinsulin → carbohydrates CHRONICHYPERGLYCAEMIA Impaired fastingglucose –6.1-6.9 mmol/L Fatigue Polydipsiaand Polyuria Impaired glucose tolerance–plasma glucose at 2 hrs 7.8-11.1 mmol/L on an OGTT HbA1c–42-47 mmol/mol RF’s( Ethnicity, family history,obesity,high Unintentional weight loss carbohydrate diet, sedentarylifestyle) MANAGEMENT OF T2D: 1) Lifestylemeasures 2) Lifestyle+ metformin When HbA1C>= 58 → Addseconddrug Fasting glucose > 7mmol/L 3) Lifestyle+ hypoglycaemiacausingdrug (Sulfonylurea. Random glucose > 11.1 mmol/L Pioglitazone,SGLT2 Inhibitor) HbA1c >48 mmol/mol 4) Add another drug fromprior listorinsulinbased treatment HbA1c >48 METFORMIN If they have establishedCVD or HF, STANDARD offeran SGLT2i + Metformin(after IF METFORMIN CI’d: RELEASE metformintolerabilityisconfirmed) With HF or CVD: SGLT2 monotherapy If not: DPP-4 , HbA1c>58 Sulfonylurea,pioglitazone Metformin Metformin + DPP-4 + SGLT2i Metformin Metformin + sulfonylurea + Pioglitazone HbA1c>58 Triple therapy with above drugs If not effective,not tolerated or BMI>35 who have problemswith contraindicated: obesity Or Metformin+ BMI <35 and weight losswould Sulfonylurea+GLP- help co morbidities 1 agonistif..Type 2 Diabetes- tips about the drugs METFORMIN: PIOGLITAZONE (thiazolidinediones) GLP-1eg Exenatide-given as injection Weight neutral Weight gain Weight loss Doesn’t cause hypos Doesn’t cause hypos Doesn’t cause hypos SE’s: SE’s SE’s: - Diarrhea/abdo pain (Modified release ELBOW -GI upset -Weight loss can be given) 1) Edema-fluid retention - Lactic acidosis 2) Liver impairment -Dizziness - CONTRAINDICATIONS: 3) Bladdercancer Considered iftripletherapyineffective: - Lactic acidosis 4) Osteoporosis (fractures) BMI >35 and problems with high weight - Caution in renal impairment Acute 5) Weight gain BMI <35 and insulin unacceptable/ weight metabolic acidosis CI= Heart failure,Active bladdercancer loss would help DPP-4 eg Sitagliptin SGLT2 inhibitors eg dapagliflozin Weightneutral Sulfonylurea Weightloss Weightgain Doesn’t causehypos Doesn’t causehypos Causeshypos SE’s: SE’s: - GI tract upset Avoided in pregnancy - Urinary and genital infection (glucosuria)–fourniers gangrene - URTI - Normoglycaemicketoacidosis - Pancreatitiskilograms in the last month, despite exercising and a balanced diet. Additionally, she noticed an increase in her body hair and new-onset acne on her face. corticosteroids for her adhesive capsulitis of the shoulder.e has recently been prescribed regular oral Given the most likely diagnosis, what acid-base imbalance would you expect? A- Hyperchloremicmetabolicacidosis B- Hyperkalemicmetabolic acidosis C-Hyperkalemicmetabolic alkalosis D- Hypochloraemicmetabolic alkalosis E- HypokalemicmetabolicalkalosisHannah, a 42-year-old woman presents to her general practitioner complaining of weight gain. She has gained 10 body hair and new-onset acne on her face.cising and a balanced diet. Additionally, she noticed an increase in her On examination, centrally localised adiposity is noticed. She has recently been prescribed regular oral corticosteroids for her adhesive capsulitis of the shoulder. Given the most likely diagnosis, what acid-base imbalance would you expect? A- Hyperchloremicmetabolic acidosis B- Hyperkalemic metabolic acidosis C-Hyperkalemicmetabolic alkalosis D- Hypochloraemic metabolic alkalosis E- Hypokalemic metabolic alkalosis Cushing’s Signsand symptomsthat occurafter the prolonged exposure to elevated cortisol.Thiscouldbe due to exogenousor endogenous causes ACTH Dependent ACTH Independent Cushings disease : Most Prolongedexposure to PRESENTATION: common → Pituitary exogenous steroids is the ‘Roundinthe middle adenoma usually most common cause of Cushings syndrome withthin limbs’ →Round‘moonface’ Ectopic ACTH production:Adrenal tumours eg →Central obesity paraneoplastic syndromesadenomas, carcinomas and →Abdominalstriae eg lung cancers hyperplasias result in cortisol excess →Buffalohump(fat pad onupper back) Ectopic CRH production: -->Proximallimb CRH producedbymalignant tissue musclewasting → Easybruising → Reduced libido →Amenorhea INVESTIGATIONS : 24 Hour urinarycortisol Low andhighdose dexamethasone suppressiontestCushing’s NORMAL RESPONSE= DexamethasonesuppressingACTH due to negative feedback on the hypothalamus and pituitarygland, leadingto lowerlevelsof cortisol LOW DOSE DEXAMETHASONE SUPPRESSIONTEST= Using 1mg of dexamethasone. No suppressionof cortisol,sofurther investigationrequired HIGH DOSE DEXAMETHASONE SUPPRESSIONTEST= Using8mg of dexamethasone. Adrenal Ectopic ACTH Pituitary adenoma tumour adenoma Cortisol productionis Neither ACTH or 8mg is enough to separate frompituitary, Cortisol suppressed suppress both as it is coming fromthe here. This ACTH cortisol and ACTH via adrenal glands. productioncomes Suppressionof ACTH is fromoutside of the negative feedback seenthroughnegative axis and is unaffected feedback, but cortisol by the levels stayhigh. dexamethasone. CORTISOL= HIGH CORTISOL= HIGH CORTISOL= LOW ACTH= LOW ACTH= HIGH ACTH=LOW Cushing’s Dexamethasone Highdose Low dose High cortisol Low cortisol Highcortisol Low cortisol LOW HIGH ACTH ACTH Cushings Adrenal EctopicACTH NORMAL Cushings adenoma secretion syndrome diseaseCushing’s- management Important to not EXOGENOUS Withdrawal of stop abruptly → CUSHINGS the corticosteroid Addisonian crisis CUSHINGS Transspenoidal resection of the Ipituitary MRIo a DISEASE pituitary ECTOPIC Surgical removal CT Tap is of source + important ACTH CAUSE Chemo ADRENAL or resection of CT Tap is LESIONS the tumour importantshe has complained of fatigue, weight loss and dizziness on standing. She has a range ofs, blood tests and the following result is found to be significant. 9am cortisol : 312 nmol/L (>500 nmol/L) What is the next best step in management? A- Adrenal antibody test B-CT Abdo C- Dexamethasonesuppressiontest D-Glucocorticoidreplacement E- Short synacthen testshe has complained of fatigue, weight loss and dizziness on standing. She has a range ofs, blood tests and the following result is found to be significant. 9am cortisol : 312 nmol/L (>500 nmol/L) What is the next best step in management? A- Adrenal antibody test B-CT Abdo C- Dexamethasonesuppressiontest D-Glucocorticoidreplacement E- Short synacthen test Addisons disease Caused by destructionor dysfunctionof the adrenal cortex CAUSE INTHE UK :Autoimmuneadrenalitis CAUSE WORLDWIDE :TB CLINICAL FEATURES Primary adrenal Secondaryadrenal Tertiaryadrenal insufficiency insufficiency insufficiency Non-specific symptoms e.g lethargy, weakness, Salt craving •Addisons •ReductioninACTH •ReductioninCRH anorexia (also vitiligo) •Destruction/dysfunction •Affecting the pituitary •Affecting the of adrenal cortex gland hypothalamus •Seenas part of •Seen followingchronic Hyperpigmentation in panhypopituitarism, glucocorticoiduse the palmarcreases isolateddeficiency,after (important to know this HYPOnatremia and •CORTISOL : LOW brain injury ordue to doesn’t happen in HYPERkalemia •ACTH :HIGH drugs secondary insufficiency) •CORTISOL : LOW •ACTH:LOW ADDISONIAN CRISIS: •CORTISOL : LOW Hypotension and Shock, abdominalpain, •ACTH:LOW hypoglycaemia severe electrolyte abnormalitiesAddisons disease-investigationsand management SHORTSYNACTHENTEST: Acute management of Addisonian crisis SyntheticACTH given in the morning • IV hydrocortisone and serum cortisol is measured 0, • Fluidresuscitation 30 and 60 minutes after • For patientsalreadydiagnosedwith Addisons, administration. the glucocorticoiddose should be doubledand Normal individuals → cortisol level the fludrocortisonedose remainthesame doubles in responseto synacthen ADDISONS= Failure of cortisol to risChronic Addisons disease (less than double the baseline) • Hydrocortisonein2 or 3 divideddoses →20- 30mgper daywiththe majoritygiveninthe first Othertests: halfof theday → Adrenal antibodies-21 hydroxylaseFludrocortisone deficiency • PATIENT EDUCATION:Notmissingdoses, → VBG/ABG hydrocortisoneforInjection,MedicAlert → U&E braceletsand steroidcardsAli, a 48-year-oldman presents to his GP with a 3-year history of hypertensionthat has been difficult to bring under control. No medication has been successful in reducing his blood pressure significantly.Accompanying the high blood pressure are muscle weakness and nocturia. On examination, his blood pressure is 164/82 mmHg. Bloodtests demonstrate low potassium and high aldosterone-to- renin ratio. Given the likelydiagnosis, which of the followingis the most likely cause of this patient's presentation? A - Adrenal Adenoma B-Adrenocortical carcinoma C-Bilateral idiopathic adrenal hyperplasia D- Ectopic aldosterone producing adenoma E-Unilateral adrenal hyperplasiaAli, a 48-year-oldman presents to his GP with a 3-year history of hypertensionthat has been difficult to bring under control. No medication has been successful in reducing his blood pressure significantly.Accompanying the high blood pressure are muscle weakness and nocturia. On examination, his blood pressure is 164/82 mmHg. Bloodtests demonstrate low potassium and high aldosterone-to- renin ratio. Given the likelydiagnosis, which of the followingis the most likely cause of this patient's presentation? A - Adrenal Adenoma B-Adrenocortical carcinoma C-Bilateral idiopathic adrenal hyperplasia D- Ectopic aldosterone producing adenoma E-Unilateral adrenal hyperplasia Primary Hyperaldosteronism ↑ ALDOSTERONE PRIMARY = High 1) Aldosterone:Renin aldosterone, lowrenin ratio SECONDARY= High aldosterone, high renin ↑ Na+ ↑ H+ secretion reabsorption ↑ K+ secretion from the from distaltubule from distaltubule collectingducts 2) HighresolutionCT scanof the adrenal gland ADRENAL ADENOMA: Hypertensionand Hypokalemiaand Alkalosis Surgery 3) Adrenal Venous Sampling-invasive BILATERAL ADRENAL HYPERPLASIA (most common):Aldosterone antagonist eg spironoloactone Priya is a 74yr old female with end-stage renal failure who presentsto the ED with severe abdominal pain, constipatCorrected calcium level= 3.54mmol/Lu(2.1-2.6mmol/L)t week.Blood tests show: Phosphate 2.8mmol/L (0.8-1.4mmol/L) PTH level = 24.7pmol/L (1.6-6.9pmol/L) Given the most likely diagnosis, what is the definitive treatment for this patient's hyperparathyroidism? A - Remove the parathyroid adenoma B – Fluid resuscitation with isotonic saline C - Intravenous bisphosphonates D – Parathyroidectomy E – Oral furosemide 40mg once daily Priya is a 74yr old female with end-stage renal failure who presentsto the ED with severe abdominal pain, constipatCorrected calcium level= 3.54mmol/L(2.1-2.6mmol/L)st week.Blood tests show: Phosphate 2.8mmol/L (0.8-1.4mmol/L) PTH level = 24.7pmol/L (1.6-6.9pmol/L) Given the most likely diagnosis, what is the definitive treatment for this patient's hyperparathyroidism? A - Remove the parathyroid adenoma B – Fluid resuscitation with isotonic saline C - Intravenous bisphosphonates D – Parathyroidectomy E – Oral furosemide 40mg once daily PARATHYROID HORMONE Parathyroidhormone is secreted by the chief cells in the thyroid glandby responding to hypocalcaemia RoleofPTH Symptoms of hyperparathyroidism – remember mnemonic Increases Increases calciumand "stones, bones, groans, activation of reabsorptioninthe moans" osteoclasts bone - Stones --> Renal stones - Bones--> Bone pain Increases Inhibits reabsorptionof reabsorption of PO4 in PCT leadingtreabsorptionatthe - Groans --> Abdominal groans calcium from m– decreasingPO4 POascendingloopand e.g., constipation, nausea and levels DCT the kidneys vomiting - Moans --> Psychiatric moans Increasing e.g., depression, fatigue and calcium absorption vitamin D from the gut psychosis activity PARATHYROID DISORDERS Hyperparathyroidism Cause PTH Calcium Phosphate VitaminD Primary Tumourof High High Low High hyperparathyroidism parathyroid glands Secondary Lowvitamin D High Low/normal High Low hyperparathyroidism or CKD Tertiary Hyperplasiaof High High Low/normal Low hyperparathyroidism PT gland OTHER MSK CONDITIONS MSK conditionsassociated with calcium levels – need to look over: • Renal osteodystrophy – complication of chronic renal failure with hypocalcaemia and hyperparathyroidism • Osteomalacia - metabolic bone disease where there is incomplete mineralisation of the underlying bone • Pagets Disease - disorder of bone turnover due to increased activity of osteoclasts and osteoblasts (everything is normal aside from ALP) Hannah is 35yr old lady under the care of the neurosurgeons for treatmentof a pituitary adenoma. Following endocrine testingthis is found to be non-functional.However, prior to surgery she is found to have a high serum calcium level of 3.8 nmol/l. A diagnosis of hyperparathyroidism is then made. It is suspectedthat What investigation should you undertake next?ultiple parts of her body. A - CT Adrenals B – CT Chest C - CT Pancreas D – Upper GI endoscopy E – Thyroid Ultrasound Hannah is 35yr old lady under the care of the neurosurgeons for treatmentof a pituitary adenoma. Following endocrine testingthis is found to be non-functional.However, prior to surgery she is found to have a high serum calcium level of 3.8 nmol/l. A diagnosis of hyperparathyroidism is then made. It is suspectedthatWhat investigation should you undertake next?multiple parts of her body. A - CT Adrenals B – CT Chest C - CT Pancreas D – Upper GI endoscopy E – Thyroid UltrasoundMultiple EndocrineNeoplasia (MEN) MEN are a group of condition where there is formation of hormone producing tumours in different organs around the body MEN Subtype Key features Multiple EndocrineNeoplasia - 1 - Mutation in MEN-1 gene - Affectsfollowing: - Parathyroid = hyperplasia/adenomas - Pancreas = gastrinoma,insulinoma - Pituitary = prolactinoma Multiple EndocrineNeoplasia – 2a - Mutation in the RET gene - Affectsfollowing: - Thyroid = medullary thyroid cancer - Adrenal = phaeochromocytoma - Parathyroid = hyperplasia/adenomas Multiple EndocrineNeoplasia - 2b - Mucosal neuromas - Affectsfollowing: - Thyroid = medullary thyroid cancer - Adrenal = phaeochromocytoma - Parathyroid = hyperplasia/adenomasJoanna, a 33-year-old female has been unwell for some time with symptoms of fatigue, headaches, double vision and intermittent blackouShe recoversfrom these episodes when she takes sugary snacks.m blood glucose of 2.2 mmol/l. It is suspected that she has an insulinoma. What is the best test for establishing the diagnosis? A - Measuring serum insulin levels B – Glucagon test C - Insulin tolerance test D – 72hr fast test E – 3x 15hr fast testsand intermittent blackouts. She has been found on the latest occasion to have a random blood glucose of 2.2 mmol/l. She recoversfrom these episodes when she takes sugary snacks. It is suspected that she has an insulinoma. What is the best test for establishing the diagnosis? A - Measuring serum insulin levels B – Glucagon test C - Insulin tolerance test D – 72hr fast test E – 3x 15hr fast tests Jamal is an 18 year old boy is >97th percentilefor height and is on the 75th percentilefor weight. He reports headachesand greasy skin with acne. He recnight.presented to the GP complaining of pain in his hands, especially at He deniesdiarrhoea and has a normal bowel habit. He deniesfeeling hot or cold. His blood pressure is 150/85 mmHg. What is the most appropriate initial investigation to supportthe diagnosis? A - Thyroid function tests B – Serum IGF-1 C - MRI head D – Chromosome analysis test E – Growth hormone test Jamal is an 18 year old boy is >97th percentilefor height and is on the 75th percentilefor weight. He reports headachesand greasy skin with acne. He renight. presented to the GP complaining of pain in his hands, especially at He deniesdiarrhoea and has a normal bowel habit. He deniesfeeling hot or cold. His blood pressure is 150/85 mmHg. What is the most appropriate initial investigation to supportthe diagnosis? A - Thyroid function tests B – Serum IGF-1 C - MRI head D – Chromosome analysis test E – Growth hormone test Luke, a 25 year old man presents to the GP with episodesof flushing and sweats. He describes these occuring intermittently and reports that he has periods of diarrhoea that coincide with these symptoms. During these episodeshe feels that his heart is racing. He does not reportvomiting or a temperature. On examination of his abdomen aWhat is the single most likely diagnosis?. He is normotensive. A - Hepatocellular Carcinoma B – Infective gastroenteritis C - Carcinoid tumour D – Phaeochromocytoma E – Carcinoid syndrome Luke, a 25 year old man presents to the GP with episodesof flushing and sweats. He describes these occuring intermittently and reports that he has periods of diarrhoea that coincide with these symptoms. During these episodeshe feels that his heart is racing. He does not reportvomiting or a temperature. On examination of his abdomen What is the single most likely diagnosis?t. He is normotensive. A - Hepatocellular Carcinoma B – Infective gastroenteritis C - Carcinoid tumour D – Phaeochromocytoma E – Carcinoid syndromeACE! Quick Conditions! Carcinoid Insulinoma Acromegaly Syndrome Key symptoms ❑ Whipple'striad Key symptoms: - signsand symptomsof hypoglycaemia - Bitemporalhemianopia - Diarrhoea,flushing,wheeze - serumglucose < 2.2 - Prominentforehead,largehandsand feet - Abdominalpain - symptomreversalupon etc. glucoseadministration Test= 24hrurinary5HIAA ❑ Investigation=72hrfastingglucose Test= IGF-1 is initial,thenOGTT (highC-peptideandinsulin) Management=Octreotideorsurgical DefinitiveTreatment=transsphenoidal resection surgerymeasures 2cm x 2cm. It is firm and moves on swallowing, but not on tongue protrusion. She has also noted that some of the 'glands' in her neck are enlarged, and lymphadenopathy is palpated in the anterior neck. What is the most likely diagnosis? A - Thyroid lymphoma B – Medullary thyroid cancer C - Anaplastic thyroid cancer D – Follicular thyroid cancer E – Papillary thyroid cancermeasures 2cm x 2cm. It is firm and moves on swallowing, but not on tongue protrusion. She has also noted that some of the 'glands' in her neck are enlarged, and lymphadenopathy is palpated in the anterior neck. What is the most likely diagnosis? A - Thyroid lymphoma B – Medullary thyroid cancer C - Anaplastic thyroid cancer D – Follicular thyroid cancer E – Papillary thyroid cancer A 37 year old lady presents with sweating, palpitations, tachycardia and acute confusion. On examination she is warm to touch, has an irregular pulse, a heaving apex, evidenceof pulmonary oedema and a smooth symmetrical swelling of the anterior neck. What is the most appropriate initial managementof this patient? A - IV diltiazem B – IV propanolol C - IV thyroxine D – Lugol's iodine E – IV hydrocortisone A 37 year old lady presents with sweating, palpitations, tachycardia and acute confusion. On examination she is warm to touch, has an irregular pulse, a heaving apex, evidenceof pulmonary oedema and a smooth symmetrical swelling of the anterior neck. What is the most appropriate initial managementof this patient? A - IV digoxin B – IV propanolol C - IV thyroxine D – Lugol's iodine E – IV hydrocortisoneMANAGEMENTOF THYROID STORM DEFINITION = acute, life-threatening state where the body produces excessive thyroid hormones – can often be precipitated by infection, surgery and trauma Main presenting symptoms ➢ Pyrexia Step 3: Treat any ➢ Hypertension Step 2: Reducethyroid complications ➢ Tachycardia activity - Heart failure ➢ Delirium - 1st line = Propylthiouracil - Hyperthermia (inhibits peripheral thyroxine conversion) - Lugol's iodine 4hrs later Step 1: Symptoms - 2nd line = Control Carbimazole/Methimazone - First line: IV Propanolol - IV hydrocortisone (reduces - Second line: IV Digoxin (if thyroid inflamamtion) propanolol is CI e.g., asthma, low BP)Priya is a 45yr old lady being seen in the endocrinology clinic. She complains of a one-month history of always feeling hot, sweating constantly TSH = 0.2mU/Lingp0.5-5.5?ons. The followingtests were carried out Free thyroxine (T4) =34pmol/L9.0-18 TSH receptorstimulating antibodies = +ve What other finding would support the most likely diagnosis ? A - Smooth enlarged tender goitre B – Multinodular goitre C - Pretibial myxoedema D – Weight gain E – Thinning of hairPriya is a 45yr old lady being seen in the endocrinology clinic. She complains of a one-month history of always feeling hot, sweating constantly TSH = 0.2mU/Lingp0.5-5.5?ons. The followingtests were carried out Free thyroxine (T4) =34pmol/L9.0-18 TSH receptorstimulating antibodies = +ve What other finding would support the likely diagnosis ? A - Smooth enlarged tender goitre B – Multinodular goitre C - Pretibial myxoedema D – Weight gain E – Thinning of hairA 35 year old woman with a history of Graves disease has had a previous thyroidectomy. She is on levothyroxine 75mcg/day. She admits to poor compliance with therapy. Choose from below the thyroid function tests you would expect to see. A - Normal T4/T3, Normal TSH B – Low T4/T3, Low TSH C - Normal T4/T3, Low TSH D – Normal T3/T4, Raised TSH E – High T4/T3, Suppressed TSHA 35 year old woman with a history of Graves disease has had a previous thyroidectomy. She is on levothyroxine 75mcg/day. She admits to poor compliance with therapy. Choose from below the thyroid function tests you would expect to see. A - Normal T4/T3, Normal TSH B – Low T4/T3, Low TSH C - Normal T4/T3, Low TSH D – Normal T3/T4, Raised TSH E – High T4/T3, Suppressed TSH THYROID TESTS Hypothyroidism Hyperthyroidism TSHlevel TSHlevel High -> check Low-> check High -> check Low-> check T4 and T3 T4 and T3 T4 and T3 T4 and T3 LowT3 and T4 Normal T3 and LowT3 and T4 High T3 and T4 Normal T3 and HighT3 and T4 = primary T4 = sub- = secondary = secondary T4 = sub- = primary hypothyroidism clinical hypothyroidism hyperthyroidism clinical hyperthyroidism hypothyroidism hyperthyroidismOTHER CONDITIONS TO LOOK OVER... Myxoedema coma – hypothyroid state (key symptoms = hypothermia, SIADH bradycardia + confusion) Diabetes Insipidus Prolactinoma Congenital adrenal hyperlplasiaACE! Phaeochromocytoma Diagnostic Pathophysiology Symptoms Criteria ❑ Adrenaline= producedbychromaffin cells in adrenalmedulla Anxiety ❑ Phaeochromocytoma= tumourof Sweating o 24hrurinecatecholamines the chromaffincellsleadingtoincreased Headaches o Plasmafreemetanephrines–betteras secretionof adrenaline Hypertension tells you how muchadrenalineis ❑ Adrenalineissecretedin bursts– Palpitations,tachycardiaandparoxysmal secretedduringthe24hrperiod symptomsareworse at certainpoints AF Management Alpha blockerse.g., phenoxybenzamine Once on alpha blockers, add beta-blockers Definitive management = adrenalectomy to remove tumourACE! Diabetes Insipidus Pathophysiology Symptoms Management o Treating underlyingcause ❑ Lack of ADHor lack of responseto ADH Polyuria o Desmopressin can be given in ❑ Can be nephrogenicorcranial Polydipsia cranial ❑ Nephrogenic=when the CDs of the Hypernatremia kidneys donot respondtoADH Dehydration o Low salt/protein diet, thiazides ❑ Cranial= when hypothalamusdoesnot Posturalhypotension can be given in nephrogenic produceADH Investigations & Diagnosis Investigations–low urineosmolalityandhighserum osmolality Diagnosis= waterdeprivationtest–pt does not drinkfluids for 8hrs, then syntheticADH(desmopressin)isgiven, and urineosmolalityis measured8hrslater - Cranialdiabetes:initially= urineosmolalityis low aftersyntheticADHadministration=urineosmolalityhigh - Nephrogenicdiabetes:initially=urine osmolalitylow aftersyntheticADHadministration=urine osmolalitystilllow HYPERKALAEMIA Definition=when potassiumlevels are> 5.5mmol/L Causes Management Impaired excretion from cells • 10mls over 10mins as this stabilises the • AKI, CKD, ACEi, NSAIDs, Addison's Calcium cardiac membrane ... gluconate Increased release from cells • Insulin causes K+ to shift intracellularly • Lactic acidosis, rhabdomyolysis, • Glucose is required to prevent insulindeficiency,tumourlysis IV insulin hypoglycaemia syndrome... 25g glucose Other causes • Haemolysis,delayed analysis of blood, contaminationwith K+ Nebulised • K+ intracellular shift salbutamol ECG changes: tall tented T-waves, flat P-waves and prolonged PR interval HYPERCALCAEMIA Definition=when calciumlevels are> 2.65mmol/L Causes Management • Correctsdehydration Primary • Protectskidneys hyperparathyroidism Malignancy IV fluid• Increasescalcium excretion • E.g., zolendronate Osteolyticbone Medicatione.g., Bisphosphonates lesions lithium, thiazides • Radiotherapy for tumours Prevent • Chemotherapy recurrence Steroids for sarcoidosis Thyrotoxicosis