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Sachi Parikh scp21@ic.ac.uk Slides adapted from lecture delivered in 2023 Diabetes & Pituitary MedEd Y3 Written Exam Lectures 2025SESSION STRUCTURE Aetiology History Presentation Investigations Management = Gold Standard = High YieldSESSION CONTENT • Diabetes Mellitus (DM) • Diabetes insipidus (DI) • Complications of Diabetes Mellitus • Syndrome of inappropriate ADH (DM): secretion (SIADH) • Hypoglycaemia • Hyponatraemia • Diabetic Ketoacidosis (DKA) • Hypernatraemia • Hyperosmolar Hyperglycaemic State (HHS) • Pituitary adenomas • Microvascular complications SBA 1 A 58-year-old man with a 15-year history of type 2 diabetes presents with fatigue, and impaired sensation in the lower extremities. His observations reveal a blood pressure of 145/94 mmHg. Proteinuria is positive on urine dipstick, and blood tests reveal an eGFR of 78 mL/min/1.73 m2 (>90). A random plasma glucose is 19mmol/L (<11.1) and fingerpick HbA1c is 65mmol/L (<48). He takes metformin andsitagliptin. What is the next most appropriate step in the patient’s management? a) Prescribe lisinopril and review diabetes medications b) Stop metformin and begin SGLT-2 inhibitor c) Commence insulin therapy d) Prescribe amlodipine and review diabetes medications e) Arrange for an ambulance to transfer the patient to A&E SBA 1 (answer) A 58-year-old man with a 15-year history of type 2 diabetes mellitus presents with fatigue, and impaired sensation in the lower extremities. His observations reveal a blood pressure of 145/94 mmHg. Proteinuria is positive on urine dipstick, and blood tests reveal an eGFR of 78 mL/min/1.73 m2 (>90). A random plasma glucose is 19mmol/L (<11.1) and fingerpick HbA1c is 65mmol/L (<48). He takes metformin and sitagliptin. What is the next most appropriate step in the patient’s management? a) Prescribe lisinopril and review diabetes medications b) Stop metformin and begin SGLT-2 inhibitor c) Commence insulin therapy d) Prescribe amlodipine and review diabetes medications e) Arrange for an ambulance to transfer the patient to A&EDiabetes Mellitus (DM) Definition: TWO types: Type 1 Type 2 Associated with HLA DR3/4 Associated with obesity, hypertension Inadequate secretion of insulin Insensitivity to insulin Due to autoimmune destruction of Due to reduced peripheral sensitivity pancreatic β-cells to insulin → leads to reduced insulin production (over time) Elevated plasma glucose concentration (hyperglycaemia)Diabetes Mellitus (DM) Presentation: TWO types: Type 1 Type 2 <20-years-old >40-years-old FHx of autoimmune disease RFs: obesity, hypertension, South Asian/Afro-Caribbean ethnicity, FHx Polyuria + polydipsia (osmotic diuresis) Weight loss and fatigue Often asymptomatic Polyuria + polydipsia DKA SIGNS – nausea and vomiting, abdominal pain, kussmaul breathing Examination findings: acanthosis nigricans, (deep hyperventilation), sweet-smelling symptoms of micro/macrovascular breath (ketonaemia) complications of T2DMDiabetes Mellitus (DM) Table 1: Normal Prediabetes Diabetes Type 1: Random <11.1 N/A ≥11.1 ▪ Urine dip for glucose & ketones(common Fasting <5.5 5.5-6.9 ≥7.0 in T1 but not T2) 2hr post <7.8 7.8-11.0 ≥11.1 ▪ Specific antibodies prandial found in T1although HbA1c* <42 (6%) 42-47 (6-6.4%) ≥48 (6.5%) not required for diagnosis: Anti-GAD (80%) and Islet cell Table 1: Diagnosis (for Type 1 & 2) antibodies (ICA) (70- Symptoms + 1 of above tests 80%) Asymptomatic + 2 different tests, on 2 different daysType 1 Diabetes Mellitus Management of T1DM: INSULIN! ▪ Highly personalised to the patient ▪ Monitored day-to-day using capillary glucose (finger prick test) ▪ Monitored over time using HbA1c (overall glucose control over 3 months) Basal-bolus = long acting + short acting (before meals) E.g., insulin glargine E.g., insulin lispro or aspart (subcutaneous injection OD) (subcutaneously pre-meal)Type 2 Diabetes Mellitus Management of T2DM: Diet, exercise, education! Glycaemic control BP management • Step 1: Metformin ifHbA1c >48 despite • Step 1: ACEi OR ARB lifestyle advice • Step 2: Add CCB orthiazide • Step 2: Add another drug (DPP-4 inhibitor, • Step 3: ACEi/ARB + CCB + thiazide pioglitazone, SU, SGLT-2i) Check potassium, consult specialist • Step 3: Add further drug or try insulin based • Step 4: If K<4.5add spironolactone, if K>4.5 treatment add b-blocker Lipid management Antiplatelets • Aspirin 75mg for patients with • Atorvastatin 20mg OD if 10-year cardiovascular event ≥ 10% IHD/CVD/peripheral artery disease • Atorvastatin 80mg OD if IHD/CVD/peripheral artery diseaseDiabetes MellitusDIABETES MELLITUS : Summary slide Aetiology: Examination: Investigations: Type 1 – autoimmune Type 2 – acanthosis Symptoms + 1 test Table 1: Normal PrediabetesDiabetes destruction of B cells nigricans → inadequate insulin OR Random <11.1 N/A ≥11.1 Type 2 – insensitivity Differentials: Asymptomatic + 2 Fasting <5.5 5.5-6.9 of ≥7.0 tests on 2 different investigations if to insulin 2hr post <7.8 7.8-11.0 ≥11.1 Obesity Diabetes insipidus days prandial applicable) Hypertension FHx Psychogenic HbA1c* <42 (6%) 42-47 (6- ≥48 (6.5%) polydipsia 6.4%) History: Management: Complications: Polydipsia Polyuria ✶ T ype 1: insulin (long acting + short acting) ✶ DKA Nocturia ✶ T ype 2: glycaemic control, BP management with ✶ HHS ACEi, lipid management ✶ Hypoglycaemia SBA 2 A 21-year-old man with known type 1 diabetes mellitus is brought into A&E in the morning following a seizure athome after a heavy night out yesterday. He injected insulin this morning but fell back to sleep before eating. He was drowsy in the ambulance but now cannotbe roused. The ambulance staff performed a capillary glucose, which read 1.4 mmol/L (>3.6). What is the most appropriate first step in the management of this patient? a) IV insulin b) IM glucagon c) 500mL 0.9% saline d) Oral glucose gel e) IV 5% dextrose SBA 2 (answer) A 21-year-old man with known type 1 diabetes mellitus is broughtinto A&Ein the morning following a seizure at home after a heavy nightout yesterday. He injected insulin this morning but fell back to sleep before eating. He was drowsy in the ambulance but now cannot be roused. The ambulance staff performed a capillary glucose, which read 1.4 mmol/L (>3.6). What is the most appropriate first step in the management of this patient? a) IV insulin b) IM glucagon c) 500mL 0.9% saline d) Oral glucose gel e) IV 5% dextroseComplications of DM Acute metabolic disturbances: Long term complications: ▪ Hypoglycaemia (resultof treatment) ▪ Diabetic ketoacidosis (mainly T1DM) Microvascular: ▪ Hyperosmolar hyperglycaemic state ▪ Retinopathy ▪ Neuropathy ▪ Nephropathy Macrovascular: (covered in a different lecture!) ▪ Ischaemic heart disease ▪ Cerebrovascular disease ▪ Peripheral artery disease Hypoglycaemia Definition: Low plasma glucose (<3.6 mmol/L) Treatment: GIVE SUGAR! Causes: ▪ Inappropriate insulin regime Conscious: ▪ Missed meals ORAL Glucose (solution/tablet) AND ▪ Unaccustomed exercise complex CHO ▪ Drugs (sulfonylureas, SGLT-2 inhibitors etc.) Impaired consciousness: Signs: PARENTERAL: 1mg glucagon IM ▪ Palpitations (tachycardia), tremor, If fails, IV dextrose e.g., 10% glucose sweating, pallor, anxiety infusion ▪ Drowsiness, confusion, altered behaviour (aggression), comaHyperglycaemia Acute metabolic hyperglycaemic complication of diabetes mellitus (DM) Diabetic Ketoacidosis Hyperosmolar Hyperglycaemic State Associated with T1DM Associated with T2DM Lack of insulin → lack of glucose uptake into NOKETOACIDOSIS! – insufficient, NOT absent cells → break down of fats for energy use → insulin production ketone production TRIAD: TRIAD: Hyperglycaemia Hyperglycaemia withoutketoacidosis Hypovolaemia Hyperosmolality Ketonaemia Metabolic AcidosisDiabetic Ketoacidosis Key metabolic triad: Hyperglycaemia, ketonaemia, metabolic acidosis Presentation: + Insulin Prevents K+ moving into cells Total b+dy K always low in DKA ▪ Acidosis → N&V, deficiency Blood K varies hyperventilation Hyperglycaemia Ketonaemia ▪ Abdominal pain diuresis ▪ Ketotic breath – Dehydration Metabolic acidosis fruity smell Reduced renal perfusion Vomiting Hyperventilation + Impaired excretion of HDKA vs. HHS DKA (more common in T1DM) HHS (more common in T2DM) Pathophysiology Absolute lack of insulin and increased stress Also hyperglycaemia but NO ketonaemia (asstill some insulin to suppress lipolysis+ ketogenesis) hormones cause: hyperglycaemia, ketonaemia and metabolic acidosis Dehydration causes increased osmolality Causes Initialpresentation, infection/other acute illness, non-adherence to diabetes medications S&S Collapse/confusion, S&S of dehydration, kussmaul Collapse/confusion, S&S of dehydration, breathing, abdominal pain, N&V hyperventilation, N&V NO abdominal pain! Ix Ketones > 3mmol/L, pH<7.3 (high anion gap Ketones < 3mmol/L, pH normal (7.35-7.45), plasma metabolic acidosis), plasma glucose >11 glucose >30 Mx Fluids must be started first (normal saline) + potassium chloride (if K <5.5) IV insulin after fluids and only when K not <3.5 Include dextrose in fluids if glucose falls <14 Treat underlying cause (e.g., Abx)DKA Mx Please scan to give feedback! 21 SBA 3 A 55-year-old man presents to his general practitionercomplaining of sudden bouts of vision loss. He describes it as if a dark curtain is obscuring his vision. His past medical history consists of type 2 diabetes mellitus that is currently being managed with metformin. The GP performs a capillary glucose, which gives a random plasma glucose concentration of 18mmol/L (<11.1). Which of the following is the most appropriate management option? a) Add an ACE inhibitor b) Initiate insulin therapy c) Initiate statin therapy d) Intravitreal VEGF (vascular endothelial growth factor) inhibitors e) Pan retinal laser photocoagulation SBA 3 (answer) A 55-year-old man presents to his general practitionercomplaining of sudden bouts of vision loss. He describes it as if a dark curtain is obscuring his vision. His past medical history consists of type 2 diabetes mellitus that is currently being managed with metformin. The GP performs a capillary glucose, which gives a random plasma glucose concentration of 18mmol/L (<11.1). Which of the following is the most appropriate management option? a) Add an ACE inhibitor b) Initiate insulin therapy c) Initiate statin therapy d) Intravitreal VEGF (vascular endothelial growth factor) inhibitors e) Pan retinal laser photocoagulationDiabetic Retinopathy On fundoscopy: Management: Background: blot and dot Improve glycaemic control haemorrhages/hard exudates Pre-proliferative: background + cotton Pan-retinallaser wool spots photocoagulation Proliferative: non-proliferative + new Pan-retinallaser vessels on disk (neovascularisation) photocoagulation Maculopathy: hard exudates (i.e., Intravitreal VEGF (vascular endothelial background retinopathy) happens growth factor) inhibitors to be near macula Neovascularization is often associated with retinal detachment and vitreous hemorrhage → Visual lossDiabetic Retinopathy Background DR Pre-proliferative DRDiabetic Nephropathy Common cause of chronic kidney disease (CKD) Presentation: ▪ Oedema, polyuria, lethargy, hypertension Investigations: ▪ First line – urinalysisalbumin:creatinine ratio (ACR) = microalbuminuria ▪ Gold standard – Renal biopsy showing Kimmelstiel-Wilson nodules (rarely done in practice) Management: ▪ ACEi/ARB (renoprotective) ▪ Improve glycaemic controlDiabetic Neuropathy Commonest cause of neuropathy Mononeuropathy Caused by blockage of vasa nervorum Sudden motor loss usually E.g., wrist drop, foot drop, 3 nerve Peripheral neuropathy palsy (eye down and out) “glove andstocking distribution” Loss of sensation (particularly feet) May not sense injury to foot Autonomic neuropathy INSPECT FEET! GI tract: difficulty swallowing, delayed gastric emptying, bladder Monofilament on lower limb exam dysfunction Loss of ankle jerk/vibration Postural hypotension (collapse on standing) sense/fractures (Charcot’s joint) Cardiac autonomic supply Mx: Glycaemic control If painful, use neuropathic pain agent e.g., duloxetine, pregabalin or gabapentin SBA 4 A 33-year-old man presents to the GP as he is going to the toilet all the time, and throughout the night. There is no weight loss or sign of infection, and his examination is normal. A finger-prick capillary glucose reveals a plasma glucose concentration of 7.2mmol/L (<11.1). The GP then orders a test to assess urine osmolality, which reveals urine osmolality is low. A water deprivation test is performed. Which of the following is the most likely diagnosis? a) Syndrome of inappropriate ADH b) Cranial diabetes insipidus c) Nephrogenic diabetes insipidus d) Diabetes mellitus e) Psychogenic polydipsia SBA 4 (answer) A 33-year-old man presents to the GP as he is going to the toilet all the time, and throughout the night. There is no weight loss or sign of infection, and his examination is normal. A finger-prick capillary glucose reveals a plasma glucose concentration of 7.2mmol/L (<11.1). The GP then orders a test to assess urine osmolality, which reveals urine osmolality is low. A water deprivation test is performed. Which of the following is the most likely diagnosis? a) Syndrome of inappropriate ADH b) Cranial diabetes insipidus c) Nephrogenic diabetes insipidus d) Diabetes mellitus e) Psychogenic polydipsia Arginine vasopressin deficiency & resistance (= Diabetes insipidus) Definition: TWO types: Arginine vasopressin deficiency Resistance Cranial / Central DI Nephrogenic DI Inadequate secretion of vasopressin (ADH)OR Insensitivity to vasopressin (ADH) Production of dilute urine (hypotonic polyuria) Note new terminology: Arginine vasopressin deficiency & resistanceArginine vasopressin deficiency & resistance (= Diabetes insipidus) INCREASED SERUM Water deprivation OSMOLALITY Osmoreceptors stimulated REDUCED URINE VOLUME, Posterior pituitary releases vasopressin (ADH) INCREASE IN URINE OSMOLALITY REDUCTION IN INCREASED WATER SERUM REABSORPTION FROM RENAL COLLECTING DUCTS OSMOLALITYArginine vasopressin deficiency & resistance (= Diabetes insipidus) Water deprivation INOSMOLALITYRUM Osmoreceptors stimulated REDUCED URINE Posterior pituitary releases VOLUME, vasopressin (ADH) INCREASE IN URINE OSMOLALITY REDUCTION IN INCREASED WATER SERUM REABSORNEPHROGENICRENAL OSMOLALITY COLLECTIN DUCTSArginine vasopressin deficiency & resistance (= Diabetes insipidus) Aetiology: Cranial / Central DI Inadequate secretion of vasopressin (ADH) from the posterior pituitary Causes: pituitary tumour/surgery, traumatic brain injury (TBI), infection (meningitis), sarcoidosis/TB Nephrogenic DI Collecting ducts insensitive to vasopressin (ADH) Causes: lithium therapy, electrolyte imbalance (↑Ca2+, ↓K+), idiopathic, ureteric obstruction, inherited (AVPV2 gene),Arginine vasopressin deficiency & resistance (= Diabetes insipidus) Presentation: Investigations: ▪ Polyuria (including nocturia) ▪ Polydipsia General: U&Es (Ca/K for cause, Na (rarely raised), ↑ urea), glucose (to ▪ Dehydration: exclude DM) tachycardia/reduced tissue turgor/dry Plasma osmolality = high mucous membranes Urine osmolality = low (>700 excludes ▪ Signs of the cause DI) (e.g., bitemporal hemianopia) Diagnostic: water deprivation testArginine vasopressin deficiency & resistance Water deprivation test: NOTE: STOP the test if the fall in body weight is > 3% ▪ Water is restricted for 8hours ▪ Plasma and urine osmolality are measured every hour ▪ After 8 hours, give desmopressin (ADH analogue) and measureurineosmolality During water restriction Desmopressin causes… Normal Rise in ADH → ↑ urine osm Little change (urine already Urine osm >600 (concentrated) concentrated) DI – cranial No ADH release → no concentration Rapid concentration of urine of urine (>50% rise in urine osm) DI – ADH insensitivity → no concentration Urine remains unconcentrated nephrogenic of urine (<45% rise in urine osm)Arginine vasopressin deficiency & resistance (= Diabetes insipidus) Management: 1. Treat the underlying cause 2. Cranial: intranasal desmopressin (should not drink large amounts of water on this medication) 3. Nephrogenic: thiazide diuretic or NSAIDsArginine vasopressin deficiency & resistance (DIABETES INSIPIDUS): Summary slide Aetiology: Examination: Investigations: Water deprivation test Cranial – inadequate During water restriction Desmopressin causes… S&S dehydration secretion ofADH Normal Risein ADH → ↑ urineosm Littlechange(urine already Nephrogenic – Urineosm >600 (concentrated) concentrated) insensitivity toADH Differentials: DI – cranial No ADH release → no Rapid concentration of urine concentration of urine (>50% risein urine osm) Pituitary tumours Diabetes mellitus applicable) Infection DI – ADH insensitivity → no Urineremains TBI Psychogenic nephrogenic concentration of urine unconcentrated Lithium therapy polydipsia (<45% risein urine osm) History: Management: Polyuria ✶ Cranial – intranasal desmopressin polydipsia ✶ Nephrogenic – thiazide diuretic OR NSAIDs SBA 5 A 67-year-old-patient was admitted yesterday with bacteria community acquired pneumonia. She has been receiving IV amoxicillin and clarithromycin and received 1L saline and oxygen yesterday. The most recent blood report reveals a plasma sodium concentration of of 122 mM (135-145), a normal plasma glucose and no other electrolyte abnormalities. The patient has no signs of dehydration or fluid overload, and her thyroid function tests from yesterday were normal. What is the most appropriate management for this patient? a) Return to IV 0.9% saline b) Nil by mouth c) Restrict fluid intake to 1L per day d) Initiate hypertonic IV saline 3% e) Initiate oral demeclocycline SBA 5 (answer) A 67-year-old-patient was admitted yesterday with bacteria community acquired pneumonia. She has been receiving IV amoxicillin and clarithromycin and received 1L saline and oxygen yesterday. The most recent blood report reveals a plasma sodium concentration of of 122 mM (135-145), a normal plasma glucose and no other electrolyte abnormalities. The patient has no signs of dehydration or fluid overload, and her thyroid function tests from yesterday were normal. What is the most appropriate management for this patient? a) Return to IV 0.9% saline b) Nil by mouth c) Restrict fluid intake to 1L per day d) Initiate hypertonic IV saline 3% e) Initiate oral demeclocyclineSIADH Syndrome of inappropriate antidiuretic hormone (SIADH) Definition: continued secretion of ADH, despite the absence of increased serum osmolality or decreased blood volume Pathophysiology: Think of as – Opposite of DI! Excess ADH secretion → expansion of ECF volume, ↓ plasma osmolality (and hyponatraemia), concentrated urine (↑ urine osmolality, ↑ urine Na) Causes: ▪ CNS: SAH, stroke, tumour, TBI ▪ Pulmonary: pneumonia, bronchiectasis ▪ Malignancy: small cell lung cancer ▪ Drugs: carbamazepine, SSRI ▪ Idiopathic SIADH is not a final diagnosis – need to find the causeSIADH Syndrome of inappropriate antidiuretic hormone (SIADH) ▪ N&V ▪ Concentrated urine Presentation of SIADH ▪ Hypertension ▪ Dizziness / confusion / seizures Management: Treat underlying cause Fluid restriction to 1L per day – for hyponatraemia If ineffective: oral demeclocycline (makes collecting ducts less responsive to ADH) / IV vaptans For ACUTE and SEVERE hyponatraemia e.g. seizing, reduced GCS: slow* IV hypertonic saline + fluid restriction + furosemide *rapid changes in Na+ concentration can lead to central pontine myelionylysisSodium abnormalities ▪ Normal range 135-145 mEq/L ▪ A measure of water status rather than total body salt content Normal Na+ Low Na+ High Na+ Reflects relative excesswater Reflects relative waterdeficit + Na+ Na+ Na+ Na Na + Na+ Na+ Na+ + Na Hyponatraemia Definition: Serum Na <135 mEq/L Assess volume status Hypovolaemic Euvolaemic Hypervolaemic Presentation: S&S of dehydration: tachycardia, Peripheraloedema, bibasal crackles, reduced skin turgor, dry membranes, low BP, postural raised JVP hypotension Hypothyroidism TFTs Heart failure Causes: Vomiting/diarrhoea Adrenalinsufficiency Short synacthen test Diuretics SIADH Cirrhosis ↓plasma and ↑urine osmolality Nephrotic syndrome Management: Volume replacement Fluid restriction Fluid restriction with 0.9% saline Treat underlying cause Treat underlying cause For ACUTE and SEVERE hyponatraemia e.g. seizing, reduced GCS: slow* IV hypertonic saline + fluid restriction + furosemide *rapid changes in Na+concentration can lead to central pontine myelionylysis Hypernatraemia Definition: Serum Na >145 mEq/L Causes: Much less common ▪ Unreplaced water loss: ▪ GI losses: diarrhoea, vomiting Presentation: ▪ Sweat loss ▪ Renal losses:osmotic diuresis (e.g., ▪ S&Sof dehydration HHS), diabetes insipidus ▪ Lethargy / weakness / irritability ▪ Sodiumoverload (rare): ▪ Cushing’s Management: ▪ Primary aldosteronism CORRECT water deficit – 5% dextrose ▪ Iatrogenic (hypertonic saline) CORRECT ECF volume depletion – 0.9% ▪ Patient cannot control water intake saline (e.g., children, elderly, cognitively Measure Na+ every 4-6 hours impaired)SIADH: Summary slide Aetiology: Examination: Investigations: Continued secretion ofHypertension •SIADH DIAGNOSIS: ADH o Low plasma osmolality Differentials: (<270mOsmol/kg)  One of these + CNS: SAH, stroke, o Low serum [Na+] (<135 mmol/L) Pulmonary: pneumonia o Increased urine osmolality absence of Malignancy: small cellDehydration (>100mosmol/kg) hypovolaemia lungcancer o High urine Na+ (>30 mmol/L) Drugs: carbamazepine Idiopathic History: Management: Complications: Dizziness / ✶ Restrict fluid intake to 1L per day ✶ Hyponatraemia → confusion / seizures, reduced GCS ✶ Severe + acute hyponatraemia → slow IV seizures hypertonic saline + fluid restriction + furosemide N&V Concentrated urine SBA 6 A 45-year-old man presents with loss of libido and some erectile dysfunction. He has no other relevant past medical history. On physical examination he has mild bilateral gynaecomastia and normal testes. Laboratory work-up reveals a highly elevated prolactin level of 46,000 mIU/L (<300), low testosterone, LH and FSH levels. An MRI scan depicts a large 32 mm pituitary macro- adenoma with suprasellar extension and optic chiasmal compression. What is the most appropriate next step in the management of this patient? a) Trans-sphenoidal surgery b) Sellar radiotherapy c) Dopamine agonist d) Dopamine antagonist e) Somatostatin analogue SBA 6 (answer) A 45-year-old man presents with loss of libido and some erectile dysfunction. He has no other relevant past medical history. On physical examination he has mild bilateral gynaecomastia and normal testes. Laboratory work-up reveals a highly elevated prolactin level of 46,000 mIU/L (<300), low testosterone, LH and FSH levels. An MRI scan depicts a large 32 mm pituitary macro-adenoma with suprasellar extension and optic chiasmal compression. What is the most appropriate next step in the management of this patient? a) Trans-sphenoidal surgery b) Sellar radiotherapy c) Dopamine agonist d) Dopamine antagonist e) Somatostatin analoguePituitary adenomas Definition: benign tumours of the pituitary gland TWO types: Non-functional Functional Do NOT release hormones Release hormones Often picked up incidentally Symptoms related to excess hormone secretion Can be asymptomatic Acromegaly (GH secreting) Prolactinoma (prolactin secreting) Cushing’s disease (ACTH secreting) Pituitary adenomas cancompress: ▪ Other partsof the pituitary gland → hypopituitarism (more common in non-functional) ▪ Optic chiasm → bitemporalhemianopiaNon-functioning pituitary adenomas Investigations: Bloods – check all the hormones TSH, cortisol and ACTH, LH and FSH, prolactin, GH, IGF-1 Pituitary MRI Management: Microadenoma (<1cm): observation Macroadenoma (>1cm) without mass effect: observation + evaluation for transsphenoidal surgery + HRT Macroadenoma (>1cm) with mass effect: transsphenoidal surgery + HRTHyperprolactinaemia NORMALLY HYPERPROLACTINAEMIA ↑ prolactin → supresses GnRH pulsatility → ↓ LH and FSHHyperprolactinaemia Causes: Physiological: Pathological: ▪ Pregnancy ▪ Prolactinoma ▪ Breastfeeding ▪ Primary hypothyroidism Presentation: Loss of libido Infertility / subfertility – prevents Erectile dysfunction sperm production in men, egg Galactorrhoea Hypogonadism release in women (lactation outside Gynaecomastia Osteoporosis – low testosterone / breast-feeding) Reduced beard growth oestrogen Secondary Mass effect – tumour size → amenorrhoea / bitemporal hemianopia, oligomenorrhoea headaches MEN WOMENProlactinoma Investigations: ▪ Pregnancy test (exclude physiological hyperprolactinaemia) ▪ TFTs ▪ Basal serum prolactin – if >6,000 mU/L, almost certainly prolactinoma ▪ Pituitary MRI Management: ▪ 1st line medical management: ▪ Dopamine receptor (D2) agonists e.g., oral bromocriptine, cabergoline (oral administration) → reduce prolactin secretion and tumour size ▪ 2 line: Transsphenoidal surgery (if needed) ▪ 3 line: sellar radiotherapyPITUITARYADENOMAS: Summary slide Aetiology: Investigations: Management: Benign tumour of the Serum prolactin – for ✶ Non-functioning: pituitary gland prolactinoma Microadenoma (<1cm): observation Pituitary MRI Macroadenoma (>1cm) without mass effect: observation Can be non-functioning OR functioning: + evaluation for transsphenoidal surgery + HRT - Prolactinoma Macroadenoma (>1cm) with mass effect: transsphenoidal - GH secreting surgery + HRT - Cushing’s disease ✶ Prolactinoma: History: Complications: 1st line medical management: dopamine receptor (D2) agonists e.g., oral bromocriptine, cabergoline (oral May be ✶ Loss of vision administration) reduce prolactin secretion and tumour asymptomatic if non-functioning size 2nd line: transsphenoidal surgery (if needed) Mass effect e.g. 3rd line: sellar radiotherapy bitemporal hemianopia Prolactinoma: loss of libido, Infertility