Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

My email address: sr1220@ic.ac.uk Slides based off: Angelos Frisiras Adrenals – Shruti Rajendra MedEd Y3 Written Exam Lectures 2025SESSION STRUCTURE Aetiology History Presentation Investigations Management = Gold Standard = High YieldSESSION CONTENT 1. Adrenals structure & function 2. Cushing’s syndrome 3. Adrenal insufficiency – Addison’s disease Conditions 4. Primary aldosteronism - Conn’s syndrome 5. Phaeochromocytoma 6. PCOS 7. Hypogonadism 8. Hypo-/hyper-kalaemiaAdrenal structure & function Hormonesproduced Mineralocorticoids (aldosterone) Glucocorticoids (cortisol) Androgens (testosterone) Nursingtimes Catecholamines (norepinephrine, (Chromaffin cells) epinephrine)Cushing’s syndrome Definition: clinical syndrome due to high levels of cortisol in the body Aetiology: Causes of ↑ cortisol: a) ACTH-dependent (↑ ACTH): 1. ACTH-secreting pituitary adenoma (Cushing’s disease) -> bilateral adrenal hyperplasia 2. Paraneoplastic ACTH secretion -> bilateral adrenal hyperplasia b) ACTH-independent (↓ ACTH): Epidemiology: 1. Exogenous steroids -> ↓ACTH -> bilateral Higher incidence in females adrenal atrophy Overall most common cause: exogenous 2. Primary adrenal adenoma, hyperplasia or steroids carcinoma -> ↓ACTH -> atrophy of uninvolved Most common endogenous cause: adrenal Cushing’s diseaseCushing’s syndrome AnnaMarsh nutritionCushing’s syndrome Investigations: 1 line options: Overnight 1mg dexamethasone suppression test (DST) (↑ morning cortisol) / alternative is 48hr nd low dose DST 2 line options: SerumACTH - If low: adrenal CT 24hr urinary free cortisol (↑) If high: Late night salivary cortisol (↑) CSRF a) inferior petrosal sinusb) high dose DST: sampling (IPSS): elevated suppression in Cushing’s central/peripheral ACTH disease vsno suppression in ratio -> Cushing’s disease ectopic cause 3 line options: MRI of pituitary for Cushing’s disease CT chest/abdomen/pelvis to localise ectopic sourceCushing’s syndrome Management: ❑ Cushing’s disease: Transsphenoidal pituitary adenomectomy Consider medical therapy (eg somatostatin analogues, steroidogenesis inhibitors) prior to surgery or on its own ❑ Ectopic ACTH source: primary tumour management (resection/chemo-radio-therapy) Nationalcancer institute ❑ Adrenal mass: Surgery for adrenal carcinoma/ adenoma/ hyperplasia Complications: Consider medical therapy (eg somatostatin analogues, Cardiovascular disease, Hypertension, Diabetes, steroidogenesis inhibitors) prior to surgery or on its own Osteoporosis SBA 1 A 45-year old woman reports thatduring the pastmonth she has been bruising easier than before and has also gained weight despite no changes in her diet. On examination, her face is swollen, and there are striae on her abdomen. She denies any past medical or relevant family history. Given the most likely diagnosis, which of the following is the least likely cause of her symptoms? a) Pituitary adenoma b) Adrenal hyperplasia c) Tuberculosis d) Lung cancer e) Steroid medications SBA 1 A 45-year old woman reports that during the past month she has been bruising easier than before and has also gained weight despite no changes in her diet. On examination, her face is swollen, and there are multiple stretch marks throughout her legs. She denies any past medical or relevant family history. Given the most likely diagnosis, which of the following is the least likely cause of her symptoms? a) Pituitary adenoma b) Adrenal hyperplasia c) Tuberculosis d) Lung cancer e) Steroid medicationsCushing’s syndrome: Summary slide Aetiology: Investigations: ACTH-independent (↓ Overnight 1mg(DST) (↑ morning cortisol) ACTH-dependent (↑ ACTH): ACTh): ACTH-secreting pituitary adenoma (Cushing’s disease) Exogenous steroids Late night salivary cortisol Paraneoplastic ACTH secretion Primary adrenal adenoma, hyperplasia or carcinoma 24hr urinary free cortisol (↑) Central obesity, moon face, muscle Serum ACTH - If low: adrenalCT, If high: IPSS or ↑ dose DST History/Examination: weakness, striae, easy bruising, hypertension MRI pituitary or CT chest/abdomen/pelvis Management: Complications: Cushing’s disease: Transsphenoidal pituitary adenomectomy / medicaltherapy Cardiovascular disease, Hypertension EctopicACTH source: primary tumour management Osteoporosis Uni-/Bi-lateral adrenalectomy for adrenal adenoma/hyperplasia / medicaltherapy Diabetes Surgical resection or chemo-radio-therapy for adrenal carcinoma / medical therapyAdrenal insufficiency Definition: Impairment in adrenal gland function causing reduced levels of glucocorticoids and mineralocorticoids Aetiology &Epidemiology: Can be primary (Addison’s) or secondary/tertiary (HPA axisdefect) Autoimmune adrenal dysfunction most common cause in developed countries Tuberculosis most common cause in developingcountries Other causes: amyloidosis, metastatic tumours,infections Acuteadrenalinsufficiency/crisis: stressors (e.g. infection) in a patient with untreated Associations(Addison’s): autoimmune conditions, Addison’s can lead to acute crisis often occurs simultaneously with hypothyroidism Abdo pain,N/V,altered mental status,shockAdrenal insufficiency Signs/Symptoms: Investigations: Postural Hypotension Bloods (↓NA , ↑K , ↓glucose) Skin/mucosal pigmentation (not in 2 /3 )o Morning serum cortisol (↓) o o o Fatigue Plasma ACTH (↑ in 1 , ↓ in 2 /3 ) Weight loss SynACTHen test -> measure cortisol + ACTH -> give Salt cravings 250 micrograms ACTHIM/IV -> remeasure cortisol GI symptoms (N/V, abdo pain) at 30 & 60 mins (↓) Pigmentation mechanism: ↓cortisol -> ↑ACTH Management: Hormone replacement -> hydrocortisone & fludrocortisone (Treat cause if applicable) ACTH precursor isPOMC, with POMC also being a precursor ofMSH -> Complications: pigmentation Treatment-related Cushing’s / osteopenia / Altmeyers Encyclopedia HTN SBA 2 A 32-year old woman is referred to the endocrine clinic due to recent symptoms of fatigue, feeling dizzy after standing up and skin pigmentation for the last 2 months. Bloods carried out at the GP practice showed low serum sodium levels and high serum potassium levels. What investigation is going to be the most useful for diagnosing this patient? a) Aldosterone : renin ratio b) SynACTHen test c) 24hr urine sample d) Overnight 1mg dexamethasone suppression test e) ECG SBA 2 A 32-year old woman is referred to the endocrine clinic due to recent symptoms of fatigue, feeling dizzy after standing up and skin pigmentation for the last 2 months. Bloods carried out at the GP practice showed low serum sodium levels and high serum potassium levels. What investigation is going to be most useful for diagnosing this patient? a) Aldosterone : renin ratio b) SynACTHen test c) 24hr urine sample d) Overnight 1mg dexamethasone suppression test e) ECGAdrenal insufficiency: Summary slide Definition/Aetiolo History/Examination: Investigations: gy: Impairment in adrenal + + gland function causing PosturalHypotension Bloods (↓NA , ↑K , ↓glucose) Skin/mucosal pigmentation (not in 2 /3 ) Morning serum cortisol (↓) reduced levels of Fatigue glucocorticoids and mineralocorticoids Weight loss Plasma ACTH (↑in 1 , ↓ in 2 /3 ) o o Salt cravings Primary (Addison’s) or GI symptoms (N/V, abdo pain) SynACTHen test (cortisol ↓) secondary/tertiary (HPA axis defect) Management: Complications: Treatment-related Cushing’s / Hormone replacement -> hydrocortisone & fludrocortisone osteopenia / HTN (Treat cause if applicable)Primary aldosteronism (PA) Endocrinol Metab Clin N Am Definition: increased aldosterone production from the adrenal gland Aetiology: Main causes of ↑ aldosterone: a) Bilateral adrenal hyperplasia b) Adrenal adenoma (Conn’s syndrome) c) (Familial hyperaldosteronism) d) (Adrenal carcinoma) Epidemiology: most common cause of secondary Signs/symptoms: Treatment-resistant hypertension hypertension Fatigue Polyuria Mood disturbances (depression, anxiety)Primary aldosteronism (PA) Investigations: Management: + + Bloods (↑NA , normal or ↓K ) Conn’s: Aldosterone:renin ratio (ARR) (↑) Adrenalectomy CT adrenals Aldosterone antagonists (eplerenone), (Adrenal venous sampling) K sparing diuretics (spironolactone) either (Fludrocortisone suppression test) preoperatively or on their own Adrenal.com Bilateral adrenal hyperplasia: ↑ ARR: -ve feedback of Aldosterone antagonists (eplerenone) aldosterone on K sparing diuretics (spironolactone) renin Complications: Conn’s syndrome (adrenal adenoma) Cardiovascular & cerebrovascular disease due to HTN in a CT Drug-induced hyperkalaemiaPrimary aldosteronism (PA): Summary slide Definition/Aetiology: Investigations: Serum ↑NA , normal or ↓K + Increased aldosterone production from the adrenal gland Aldosterone:renin ratio (ARR) (↑) Bilateral adrenal hyperplasia Adrenal adenoma (Conn’s syndrome) CT adrenals (Familial hyperaldosteronism) (Adrenal carcinoma) (Adrenal venous sampling,Fludrocortisone suppression test) History/Examinati on: Treatment-resistant hypertension, Fatigue, Polyuria, Mood disturbances (depression,)anxiety Management: Complications: Conn’s: Bilateral adrenal hyperplasia: Cardiovascular & cerebrovascular disease due to HTN Adrenalectomy Aldosterone antagonists Aldosterone antagonists + K sparing diuretics Drug-induced hyperkalaemia K sparing diureticsPhaeochromocytoma Definition: Adrenal medulla tumour derived from catecholamines-producing chromaffin cells Aetiology: most sporadic, but germline mutations (MEN-2, VHL, NF-1) have been identified Symptoms occur due to episodic secretion of epinephrine, norepinephrine and dopamine Epidemiology: rare cause of secondary hypertension Rule of 10’s: 10% malignant 10% bilateral 10% extra-adrenal 10% calcify 10% in kids (not entirely accurate)Phaeochromocytoma Investigations: Management: Bloods (↑ plasma catecholamines & 1) Alpha-blockers (e.g. phenoxybenzamine): metanephrines) control hypertension 24hr urine sampling (↑ urine 2) Beta-blockers (e.g. atenolol):prevent catecholamines & metanephrines) arrhythmia 3) Surgicalresection Columbia surgery Wikipedia Complications: acute hypertensive crisis, neurological pathology (e.g. seizures) SBA 3 A 41-year old man presents to the emergency departmentwith sweating, palpitations and headaches lasting for the past45 minutes. He experienced similar symptoms a week ago, but he did not attend the hospital because they resolved within 10 minutes. Which of the following is true about the appropriate management of this condition? a) The patient should be immediately prepared for theatre b) Surgery is contraindicated c) Beta-blockers should be given before alpha-blockers d) Alpha-blockers should be given before beta-blockers e) The patient should be discharged with safety-netting since it is only the second time he is experiencing these symptoms SBA 3 A 41-year old man presents to the emergency departmentwith sweating, palpitations and headaches lasting for the past45 minutes. He experienced similar symptoms a week ago, but he did notattend the hospital because they resolved within 10 minutes. Which of the following istrue about the appropriate management of this condition? a) The patient should be immediately prepared for theatre b) Surgery is contraindicated c) Beta-blockers should be given before alpha-blockers d) Alpha-blockers should be given before beta-blockers e) The patient should be discharged with safety-netting since it is only the second time he is experiencing these symptomsPhaeochromocytoma: Summary slide Definition/Aetiolo History/Examination: Investigations: gy: Bloods (↑ plasma catecholamines & metanephrines) Adrenal medulla tumour derived from Headache, palpitations, perspiration, catecholamines- pallor, tremor, tachyarrhythmias, 24hr urine sampling (↑ plasma catecholamines & producing chromaffin hypertension cells metanephrines) Sporadic, but MEN-2, VHL, NF-1 mutations associated Rule of 10’s: Management: Complications: 10% malignant 10% bilateral Acute hypertensive crisis 10% extra-adrenal 1) Alpha-blockers (e.g. phenoxybenzamine) 10% calcify 10% in kids Neurological pathology (not entirely accurate) 2) Beta-blockers (e.g. atenolol) 3) Surgical resectionPolycystic ovary syndrome (PCOS) Radiopedia.org Definition: Endocrine disorder diagnosed based on 2/3 of: a) Polycystic ovaries on US, b) oligo-/amenorrhea, c) hyperandrogenism (hirsutism, acne) Epidemiology: approx. 20% of women have polycystic ovaries, but only around 5% also Risk factors: family history of PCOS, exhibit symptoms premature adrenarche Aetiology: peripheral insulin resistance, ↑insulin and disordered ↑ LH production → Associations: obesity, insulin resistance, ↑androgens → impaired folliculogenesis → type 2 DM, endometrial cancer, polycystic ovaries acanthosis nigricansPolycystic ovary syndrome Signs/Symptoms: Investigations: Hirsutism For oligo-/amenorrhea and infertility: Acne Prolactin (to exclude prolactinoma) Irregular menses TSH (to exclude thyroid dysfunction) Infertility LH / FSH → ↑LH, FSH, thus ↑LH:FSH Obesity Acanthosis nigricans For hyperandrogenism: Serum testosterone levels (↑) Transvaginal ultrasound: multiple small follicles Oral glucose tolerance test Obstetrics& Gynaecology (Impey)Polycystic ovary syndrome Management: InviTRA Weight regulation (if applicable) Metformin Oligo-/amenorrhea: oral contraceptive pill Infertility: clomiphene (blocks oestrogen Complications: receptors in hypothalamus and pituitary) Endometrial cancer (due to unopposed oestrogen from anovulation) Hyperandrogenism: antiandrogens (e.g. Miscarriages spironolactone) Type 2 diabetes (& gestational diabetes) SBA 4 A 25-year old woman presents to her GP . She complains of persistent acne throughout the last year and reports that she has nothad any periods in the last 4 months. She has a BMI of 31,denies the possibility of being pregnant and had her firstperiod when she was 7. No relevant family history apartfrom her mother being a type II diabetic. Considering the most likely diagnosis, which of the following is part of the diagnostic criteria for this disease? a) 25-years of age b) Acne c) Type II diabetic mother d) BMI of 31 e) Adrenarche at 7-years old SBA 4 A 25-year old woman presents to her GP . She complains of persistent acne throughout the last year and reports that she has nothad any periods in the last 4 months. She has a BMI of 31,denies the possibility of being pregnant and had her first period when she was 7. No importantfamily history apart from her mother being a type II diabetic. Given the most likely diagnosis, which of the following is partof the diagnostic criteria for this disease? a) 25-years old of age b) Acne c) Type II diabetic mother d) BMI of 31 e) Adrenarche at 7-years oldPCOS: Summary slide Definition/Aetiolo History/Examination: Investigations: gy: 2/3 of: Bloods: Prolactin,TSH, LH & FSH, testosterone Polycystic ovaries on US, Hirsutism, Acne, Obesity, Acanthosis oligo-/amenorrhea, nigricans, Irregular menses, Infertility hyperandrogenism Transvaginal ultrasound (hirsutism, acne) Risk factors: insulin resistance, Oral glucose tolerance test RF: family history of PCOS, premature ↑insulin, ↑ LH → ↑androgens. adrenarche Differentials: Management: Complications: Prolactinoma,Thyroid Weight regulation (if applicable) Endometrial cancer dysfunction Metformin Hypothalamic Miscarriages hypogonadism, premature oral contraceptive pill ovarian insufficiency clomiphene Androgen-secreting Type 2(& gestational) diabetes tumor Antiandrogens (e.g. spironolactone)Hypogonadism: Summary slide Definition: History/Examination: Investigations: Decreased function of Decreased libido, infertility, Bloods: LH & FSH, testosterone, GnRH, Prolactin gonads resulting in gynaecomastia (men) erectile reduced sex hormones dysfunction (men), amenorrhea levels (women) MRI pituitary, genetic testing Aetiology: Management: Primary (hypergonadotrophic) -> Kallman syndrome, HRT: testosterone (men), oestrogen/progesterone (women) cryptorchidism, infection, trauma, drugs Secondary (hypogonadotrophic) Treat secondary cause -> hyperprolactinaemia, pituitary tumoursHypo-/Hyper-kalaemia Hypokalaemia Hyperkalaemia Definition: serum potassium level <3.5mmol/L Definition: serum potassium level >5.0mmol/L Aetiology: Aetiology: 1) GI loss: vomiting, diarrhoea 1) Excessive intake 2) Renal loss: primary aldosteronism, 2) Decreased excretion: AKI, CKD, K sparing thiazide/loop diuretics, renal tubular acidosis, diuretics, NSAIDS, ACEi, ARB + hypomagnesemia,excess corticosteroids 3) Increased K entry into serum fromcells: 3) Redistribution into cells: insulin, beta- acidosis,DKA / lack of insulin, rhabdomyolysis agonists, metabolic alkalosis 4) Haemolysed sample Signs/symptoms: muscle weakness, arrhythmias, polyuria,polydipsia,constipation Signs/symptoms: muscle weakness, arrhythmiasHypo-/Hyper-kalaemia Hypokalaemia Hyperkalaemia Investigations: Investigations: Serum & urine K + Serum & urine K + serum Na , urea,glucose, Cl , urea,creatinine, Mg 2+ Serum Na , urea,glucose, Cl , urea,creatinine, Mg 2+ ECG ECG ABG ABG ARR Management: + K >5.5mmol/L with ECG changes or >6.5mmol/L: 1) 10% calcium gluconate(cardioprotective) Management: 2) Dextrose (drives K into cells) 3.0-3.5mmol/L: Oral KCl 3) Nebulised salbutamol(drives K into cells) <3.0mmol/L or unable to take oral KCl: IV KCl 4) Treat causeHypo-/Hyper-kalaemia JLPMHypo-/Hyper-kalaemia SBA 5 A 57-year old man at a medical ward receives a blood testto monitor his full blood count, U/Es and inflammatory markers two days after he was diagnosed with a heart failure exacerbation. His symptoms and inflammatory markers are improving but his potassium level has risen to 6.1 mmol/L, an increase which the doctors attribute to one of the medications prescribed for his heart failure. An ECG is also carried out, which shows characteristic hyperkalaemia changes. Which of the following will NOT be part of the appropriate management of this patient? a) Salbutamol b) Dextrose c) Calcium gluconate d) Reduce dose or change relevant medication e) Oxygen SBA 5 A 57-year old man at a medical ward receives a blood test to monitor his full blood count, U/Es and inflammatory markers two days after he was diagnosed with a heart failure exacerbation. His symptoms and inflammatory markers are improving but his potassium level has risen to 6.1 mmol/L, an increase which the doctors attribute to one of the medications prescribed for his heart failure. An ECG is also carried out, which shows characteristic hyperkalaemia changes. Which of the following will NOT be part of the appropriate management of this patient? a) Salbutamol b) Dextrose c) Calcium gluconate d) Reduce dose or change relevant medication e) OxygenHypokalaemia: Summary slide Definition: History/Examination: Investigations: Serum & urine K+ + Serum potassium level Muscle weakness, arrhythmias, serum Na , urea, glucose, Cl, urea, creatinine, Mg <3.5mmol/L polyuria, polydipsia, constipation ECG ABG ARR Aetiology: Management: GI loss Oral KCl Renal loss IV KCl Redistribution into cells (Treat cause)Hyperkalaemia: Summary slide Definition: History/Examination: Investigations: + Serum & urine K Serum potassium level serum Na , urea, glucose, Cl, urea, creatinine, Mg >5.0mmol/L Muscle weakness, arrhythmias ECG ABG Aetiology: Management: Excessive intake 10% calcium gluconate (cardioprotective) Dextrose (drives K into cells) Decreased excretion Nebulised salbutamol (drives K into cells) + Increased K entry into serum from cells (Treat cause) Haemolysed sampleFeedback