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Endocrinology Dr Deepshikha Kumar and Dr Yi Sim Question 1 A 65-year-old man is admitted to the intensive care unit for Sepsis secondary to Community Acquired Pneumonia. He has a past medical history of insulin dependent type 2 diabetes mellitus and hypertension. Over the past 48 hours,on this information what he has gradually become more bradycardic, fatigued anis the most likely underlying intolerant to cold. Blood tests are performed as part of his evaluation and reveal the following: cause: A) Subclinical Hypothyroidism ● CRP: 125 mg/L (<5) ● Albumin: 26 g/L (35–50) B) Hashimoto’s Thyroiditis ● Procalcitonin: 5.8 µg/L (<0.5) C) Sick Euthyroid Syndrome ● HbA1c: 52 mmol/mol (20–42) D) Myxoedema Coma ● Sodium: 134 mmol/L (135–145) ● Potassium: 4.1 mmol/L (3.5–5.0) E) Primary Hypothyroidism ● TSH: 0.8 mU/L (0.4–4.0) ● Free T4: 10.2 pmol/L (9.0–25.0) ● Free T3: 2.1 pmol/L (3.1–6.8) Question 1:T ypes of Hypothyroidism A 65-year-old man is admitted to the intensive care unit for Sepsis secondary to Community Acquired Pneumonia. He has a past medical history of insulin dependent type 2 diabetes mellitus and hypertension. Over the past 48 hours,on this information what he has gradually become more bradycardic, fatigued anis the most likely underlying intolerant to cold. Blood tests are performed as part of his evaluation and reveal the following: cause: A) Subclinical Hypothyroidism ● CRP: 125 mg/L (<5) ● Albumin: 26 g/L (35–50) B) Hashimoto’s Thyroiditis ● Procalcitonin: 5.8 µg/L (<0.5) C) Sick Euthyroid Syndrome ● HbA1c: 52 mmol/mol (20–42) D) Myxoedema Coma ● Sodium: 134 mmol/L (135–145) ● Potassium: 4.1 mmol/L (3.5–5.0) E) Primary Hypothyroidism ● TSH: 0.8 mU/L (0.4–4.0) ● Free T4: 10.2 pmol/L (9.0–25.0) ● Free T3: 2.1 pmol/L (3.1–6.8)A deficiency of Thyroid Hormone (T3 and T4) in the body. Symptoms: ● Fatigue ● Weight Gain ● Constipation ● Menorrhagia ● MSK Pain, Arthralgia ● Reduced Cognitive function ● Depression ● Cold Intolerance ● Oedema ● Hoarse Voice Examination: ● Coarse Face (rounded, thickened) ● Goitre: Also present in HyperThyroidism ● Dry Skin ● Alopecia ● HyporeflexiaHypothyroidism TSH = High T4 = Low Treat with Levothyroxine 50 micrograms (lower dose to start in elderly at 25 micrograms) Subclinical TSH = High Hypothyroidism T4 = Normal If presented with Monitor TFTs 6 monthly to spot potential progression (Especially in Pregnancy!) Sensironeural Hearing Loss Consider offering levothyroxine if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart Sick Euthyroid TSH = Normal (Otoacoustic testing Syndrome T4 = Low from birth) = TSH is between 5.5 - 10mU/L and the free thyroxine level is within the normal range PENDRED ● if < 65 years consider offering a 6-month trial of levothyroxine if: SYNDROME ❏ the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart,and Seen in acute illness Supportive care + Monitor TFT till underlying cause Tx: levothyroxine + ❏ there are symptoms of hypothyroidism and resolves, then review hearing aids ● in older people (especially those aged over 80 years) follow a 'watch and wait' strategy is often used fasting/malnutrition Hashimoto’s TSH = High Thyroiditis T4 = Normal M:F ratio 1:5 anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies → Raised Pituitary Mass TSH = Low T4 = Low Thyroid Peroxidase helps bind Iodine to Will be accompanied by other hormonal deficiencies Thyroglobulin alongside other signs (e.g BiTemporal Hemianopia). during Thyroxine production in the Thyroid Gland Pituitary MRI needed TSH = High Myxoedema Coma T4 = Low (Emergency) Hypothermia, Hyporeflexia, Low BMI, Bradycardia, Pancreatitis, Psychosis, Seizures, Comatose condition is precipitated by Tx: exposure to cold, ● A to E usually in poorly ● High Flow O2 heated houses, ● Bear Hugger (to warm) infection, or ● IVF (corrects Hyponatraemia <130) and IV Glucose sedative drugs e.g. ● T3 + T4 IV replacement phenothiazines, ● Steroids narcotics, anaesthetics.Question 2 A 58-year-old man with a 40-pack-year smoking history presents to the emergency department with haemoptysis, proximal muscle weakness, and unintentional weight gain to a BMI of 42 over the past three months. He also reports new-onset acne and easy bruising. On examination, you notice he has a dorsocervical fat pad, purple striae and plethoric face with Acne Vulgaris What would be the most underlying cause of the above? A) Squamous Cell Carcinoma of the Lung B) Small Cell Carcinoma of the lung C) Adrenal Cushing’s D) Long term use of Methylprednisolone E) Cushing’s DiseaseQuestion 2:Causes ofCushing’s A 58-year-old man with a 40-pack-year smoking history presents to the emergency department with haemoptysis, proximal muscle weakness, and unintentional weight gain to a BMI of 42 over the past three months. He also reports new-onset acne and easy bruising. On examination, you notice he has a dorsocervical fat pad, purple striae and plethoric face with Acne Vulgaris What would be the most underlying cause of the above? A) Squamous Cell Carcinoma of the Lung B) Small Cell Carcinoma of the lung SCLC ● SIADH C) Adrenal Cushing’s ● Cushing’s D) Long term use of Methylprednisolone E) Cushing’s Disease ● Lambert Eaton ● Chemo sensitive Symptoms ● Unintentional weight gain ● Mood Swings ● Acne A group of conditions causing excess Cortisol secretion. F:M ● Hirsutism ● Reduced Libido/Female Virilisation is 3:1 ● Irregular Menstrual Cycles ● Proximal Muscle Weakness Causes: ● Unexplained Low energy fractures (Early age Osteoporosis) 1) Iatrogenic; Excess ● Recurrent Achilles Tendon Rupture Glucocorticoids ● New onset HTN medication → Cushing’s Clinical Signs Syndrome ● Dorsocervical Fat Pad (Buffalo Hump) 2) ACTH Pituitary Tumour ● Moon Facies + Plethora → Cushing’s Disease ● Truncal Obesity + Thin upper limbs (“Lemon on a stick”) 3) Primary Adrenal Gland Adenoma/Carcinoma → ● Purple Striae on Abdomen ● Visible Bruising (due to thinned skin) Adrenal Cushings ● Hirsutism 4) Ectopic ACTH → Small Cell Lung Cancer If Cushing’s Disease - Headache - Visual Field DefectInvestigations Bedside: Obs, 24 hour Urinary Free cortisol (NB excess ETOH and Anxiety can also falsely raise) Bloods: FBC, U+Es, CRP, LFTs, TFTs (rule out thyroid), Bone Profile, 9am Cortisol, ACTH levels (low in exogenous steroids, raised in others), Serum Testosterone +/- LH and FSH (rule out PCOS), Blood Glucose (Hyperglycaemia) ● VBG: Hypokalaemic Hypochloraemic Metabolic Alkalosis, Hypernatraemia Special Tests ● Dexamethasone suppression test - 1st line; Low-dose dexamethasone suppression test (LDDST): In this test, 1mg of dexamethasone is administered at night with serum cortisol measured the following morning. A normal response would be to suppress serum cortisol to less than 50 nmol/L. Failure to suppress indicates Cushing's syndrome. - High-dose dexamethasone suppression test (HDDST): This test helps differentiate between pituitary and ectopic causes of Cushing's syndrome. After administration of 8mg dexamethasone at night, failure to suppress serum cortisol suggests an ectopic source while suppression indicates a pituitary cause. ● Late-night salivary cortisol: Normally cortisol drops at night. If stays elevated above normal Cushing’s is likely. Imaging ● MRI Pituitary ● Visual Fields Testing ● CTAP; Adrenal Cushing’sManagement ● Manage HTN and Glycaemic Control 1) Excess Glucocorticoids = Taper off steroids and monitor 2) Cushing’s Disease = Transsphenoidal Surgery 3) Adrenal Cushing’s = Adrenalectomy 4) Ectopic ACTH = - Find underlying cause e.g SCLC - Can be controlled by Mifepristone + Azole (Fluconazole) medications until location identifiedQuestion 3 A 52-year-old woman presents to her GP with progressive fatigue, weight loss, dizziness on standing. The GP does the below observations: ● HR: 92 bpm ● BP: 98/64 mmHg (drops to 82/55 mmHg on standing) ● RR: 16 bpm ● SpO₂: 98% on RA ● Temp: 36.2°C ● CBG: 3.5 mmol/L O/E: Appears visibly nauseous. Increased pigmentation of her skin, particularly around her palmar creases and buccal mucosa are noted. The GP suspects Addison’s Disease. Which of the below is not a cause of Addison’s Disease? A) Meningococcal Septicaemia B) Autoimmunity C) Tuberculosis D) Lymphoma E) Thymic HyperplasiaQuestion 3:Causes ofAddison’s A 52-year-old woman presents to her GP with progressive fatigue, weight loss, dizziness on standing. The GP does the below observations: ● HR: 92 bpm ● BP: 98/64 mmHg (drops to 82/55 mmHg on standing) ● RR: 16 bpm ● SpO₂: 98% on RA ● Temp: 36.2°C ● CBG: 3.5 mmol/L O/E: Appears visibly nauseous. Increased pigmentation of her skin, particularly around her palmar creases and buccal mucosa are noted. The GP suspects Addison’s Disease. Which of the below is not a cause of Addison’s Disease? A) Meningococcal Septicaemia B) Autoimmunity C) Tuberculosis D) Lymphoma E) Thymic Hyperplasia: associated with Myasthenia Gravis Symptoms General: ● N+V Condition causing Cortisol and ● Abdominal Pain Aldosterone deficiency from Adrenal ● Diarrhoea Cortex. ● Dizziness, Muscle Weakness ● Depression, Causes Psychosis ● Anorexia 1) Primary → Adrenal Cortex Destruction ● “Salt cravings” ● Most common in UK → Autoimmune ● TB Examination: ● Hyperpigmentation ● Lymphoma (in attempt to ● Haemorrhage → produce ACTH POMC Waterhouse-Friderichsen Syndrome is cleaved, which also (due to Meningococcal Septicaemia) produced Alpha-MSH ● Congenital which causes pigmentation): 2) Secondary → Acute, sudden withdrawal of steroid medication Palmar Creases, Buccal Mucosa and People with Coeliac Disease, T1DM and scars Sarcoidosis are more at risk of developing ● Loss of Axillary and Add signs of Shock +/- Addison’s Disease Pubic Hair Comatose = Addisonian Crisis ● VitiligoInvestigations Bedside: Obs (BP = Hypotension), Finger prick glucose (hypoglycaemia), 12 Lead ECG (electrolyte imbalances) Bloods: FBC, U+Es (Hyponatraemia, Hyperkalaemia), CRP, ESR, 9am Cortisol ● VBG Special Tests: ● SynACTHen test = Synthetic ACTH given, then Cortisol levels are monitoring at the 9am mark, then at 30min and 60 min mark. No increase in Cortisol = Addison’s ● 21 Hydroxylase Adrenal Antibodies → Autoimmune cause Imaging: ● CT AdrenalManagement Non-Acute: replace steroids with supportive management ● Hydrocortisone ● +/- Fludrocortisone (mineralocorticoid) if postural hypotension Discussion with patients on adjusting hydrocortisone doses during illness e.g Infection is important ● consider MedicAlert bracelets and steroid cards Addisonian Crisis: Hydrocortisone + Fludrocortisone + IVF + IV GlucoseQuestion 4 A 45-year-old man presents to his GP with complaints of excessive sweating, vision loss and headaches over the past few years. On examination, he has prominent supraorbital ridges, prognathism, frontal bossing and spade like hands. What would be the most appropriate DIAGNOSTIC investigation? A) Insulin Like Growth Factor 1 B) Oral Glucose Tolerance Test with Growth Hormone measurement C) Random Growth Hormone level D) Magnetic Resonance Imaging of the Pituitary Gland E) Requesting photos from the patient over the past 5 yearsQuestion 4: Investigations to proveAcromegaly A 45-year-old man presents to his GP with complaints of excessive sweating, vision loss and headaches over the past few years. On examination, he has prominent supraorbital ridges, prognathism, frontal bossing and spade like hands. What would be the most appropriate DIAGNOSTIC investigation? A) Insulin Like Growth Factor 1 B) Oral Glucose Tolerance Test with Growth Hormone measurement C) Random Growth Hormone level D) Magnetic Resonance Imaging of the Pituitary Gland E) Requesting photos from the patient over the past 5 yearsAn excess of growth hormone. Symptoms: ● Jewelry, Shoes etc. gradually not able to fit ● Headaches; Pituitary Adenoma ● Visual disturbances: B/L Hemianopia ● Weight Gain ● Excessive Diaphoresis ● Snoring (OSA) ● Arthralgia + Back Pain ● Amenorrhoea ● Hoarse voice; Laryngeal Dyspnoea Examination: ● Wide Nose ● Big Supraorbital ridges ● Spade Hands ● Features of Carpal Tunnel: Phalen’s and Tinel’s +ve ● Frontal Bossing: Large forehead ● Prognathism: Overbite ● Macroglossia: Large tongue ● Puffy Lips, eyelids ● Widely spaced teeth ● Dark toned skin Associations: ● Cutis Verticis Gyarta: Expanding but tethered (leathery, floppy) skin ● HTN ● Skin Tags ● Congestive Heart Failure ● Hepatomegaly ● Dilated Cardiomyopathies ● Increased IHD and Stroke Risk ● Increased risk of Colorectal Cancer: +/- Colonoscopy screeningInvestigations Bedside: Obs, 12 lead ECG, Blood Glucose, Urine sample (for calcium) Bloods: FBC, U+Es, Glucose, Bone Profile (High Serum + Urine Ca2+, High PO4-) ● IGF-1 levels: Raised ● GH levels: raised ● Oral Glucose Tolerance Test: if GH >0.4 mcg/L +/- IGF-1 raised - Glucose should suppress GH normally. In Acromegaly it doesn’t - Lowest level of GH is >1 mcg/L to confirm Acromegaly Special Tests ● Regular GH Glucose at intervals of 30 mins (30, 60, 90, 120, 150) Gigantism When this condition occurs in ● Old Photos: To see chronological changes in physical looks to show progression into features of Acromegaly childhood then there is stimulation of ● Epworth Sleepiness scale: OSA epiphyseal growth. Patients are excessively tall; and often there is Imaging associated sexual immaturity and mental retardation. ● MRI Pituitary: GHoma ● TTE; Cardiomyopathies Slipping of the upper femoral ● Endoscopy: Visualise true vocal cords epiphysis may occur.Management Transsphenoidal Surgery: Removes GHoma in pituitary If surgery fails to correct GH/IGF-1, or unfit for surgery: ● Somatostatin Analogues: Octreotide/Ianreotide IM - S/E Pain at injection sides, abdominal cramps, flatulence, loose stools, impaired glucose tolerance) ● If intolerant to Somatostatin Analogues → GH Antagonists: Pegvisomant (however small risk of recurrence of tumour) External Beam Radiotherapy may be used as adjuvant treatment from above (however may take years to show effect)Question 5 A 25-year-old woman presents to her the Emergency Department after a fall from standing height where she broke her right leg. She noted this happened as she couldn’t concentrate while having frontal headaches. She also noted irregular periods and nipple discharge. She has no significant past medical history and is not on any regular medications.On examination, there is bilateral galactorrhoea on breast expression. Visual field testing reveals a slight reduction in peripheral vision bilaterally. Her right leg shows no Neurovascular compromise or tenting Which of the following is the first-line Investigation results: treatment for this condition? ● Prolactin: 4,200 mU/L (<500) ● TSH: 1.2 mU/L (0.4–4.0) A) Transsphenoidal surgery ● Free T4: 14.8 pmol/L (9.0–25.0) ● LH: Low B) Temozolomide ● FSH: Low C) External Beam Radiotherapy D) Bromocriptine ● Estradiol: Low E) Brachytherapy ● Random GH: 1.2 µg/L (<1.0) B-HCG: -ve Right Tibia and Fibula Radiograph AP and Lateral: Complete Oblique fracture of Right Tibia. MRI pituitary: 8 mm pituitary lesion with no cavernous sinus invasion.Question 5: Management of Prolactinomas A 25-year-old woman presents to her the Emergency Department after a fall from standing height where she broke her right leg. She noted this happened as she couldn’t concentrate while having frontal headaches. She also noted irregular periods and nipple discharge. She has no significant past medical history and is not on any regular medications.On examination, there is bilateral galactorrhoea on breast expression. Visual field testing reveals a slight reduction in peripheral vision bilaterally. Her right leg shows no Neurovascular compromise or tenting Which of the following is the first-line Investigation results: treatment for this condition? ● Prolactin: 4,200 mU/L (<500) ● TSH: 1.2 mU/L (0.4–4.0) A) Transsphenoidal surgery ● Free T4: 14.8 pmol/L (9.0–25.0) ● LH: Low B) Temozolomide ● FSH: Low C) External Beam Radiotherapy D) Bromocriptine ● Estradiol: Low E) Brachytherapy ● Random GH: 1.2 µg/L (<1.0) B-HCG: -ve Right Tibia and Fibula Radiograph AP and Lateral: Complete Oblique fracture of Right Tibia. MRI pituitary: 8 mm pituitary lesion with no cavernous sinus invasion. Symptoms: Hyperprolactinaemia Prolactinoma Men ● impotence 1) Physiological 1) Pituitary ● loss of libido - Pregnancy Tumours ● Reduced facial hair - Breastfeeding - Microprolactin - Prolonged oma: <1cm ● Galactorrhoea; Gynaecomastia ● Osteoporosis stress - Macroprolactin Women 2) Drugs; oma: >1cm ● amenorrhoea Dopamine 2) Trauma: Antagonists Haemorrhage ● infertility - 1st generation 3) Iatrogenic ● galactorrhoea Antipsychotics Damage: ● Osteoporosis e.g Surgery Haloperidol, - Pituitary stalk If Prolactinoma Risperidone injury ● Visual Disturbance; Bilateral Hemianopia - Antiemetics: ● Headache Metoclopramid e (not domperidone; Investigations doesn’t cross Bedside: Obs, Beta-HCG Test (ALWAYS TEST PREGNANCY IN FEMALES 1st) BBB) Bloods: FBC, U+Es, Serum Prolactin, Serum Testosterone/Oestrogen/LH and FSH (rule out other androgen deficiencies) Special Tests: Visual Fields Testing, IgG bound prolactin (macroprolactinaemia) Imaging: MRI PituitaryManagement Hyperprolactinoma: Stop underlying drugs, manage pregnancy etc 1) Microprolactinoma (<1cm): ● Dopamine Agonist → Bromocriptine (S/E: Depression, Postural Hypotension; give ON), Cabergoline (fewer S/E, but unknown risks in pregnancy). ● Both drugs can rarely cause Cardiac Fibrosis → +/- TTE monitoring 2) Macroprolactinoma or if visual field compromised (>1cm): Skull base Surgery +/- RadiotherapyQuestion 6 A 34 F in who is 12 weeks pregnant with her 1st child presents with medication resistant hypertension and muscle cramps. As part of her routine blood work up in investigating this, she is found to have an electrolyte imbalance and her ECG shows U wave. She also has low renin levels. Based on the diagnosis, which area of the adrenal gland is responsible for the hormonal change in this patient? A: Zona glomerulosa of the adrenal cortex B: Zona reticularis of the adrenal cortex C: Zona fasciculata of the adrenal cortex D: Adrenal medulla E: Adrenal CortexQuestion 6 A 34 F in who is 12 weeks pregnant with her 1st child presents with medication resistant hypertension and muscle cramps. As part of her routine blood work up in investigating this, she is found to have an electrolyte imbalance and her ECG shows U wave. She also has low renin levels. Based on the diagnosis, which area of the adrenal gland is responsible for the hormonal change in this patient? A: Zona glomerulosa of the adrenal cortex B: Zona reticularis of the adrenal cortex C: Zona fasciculata of the adrenal cortex D: Adrenal medulla E: Adrenal CortexQuestion 6: Explanation-Conn’s She has Conn’s Syndrome: Medication resistant HTN, Hypokalaemia U wave, muscle cramp→ Hypokalaemia Primary hyperaldosteronism→ increased Na reabsorption, increased K excretion and H + extraction H+ excretion → Metabolic alkalosis High BP leads to less renin production as JG cells suppress renin release Where is aldosterone produced: Zona glomerulosa of the adrenal cortexQuestion 6:PrimaryhyperaldosteronismQuestion 7 A 37 male is about to have surgery for removal of tumors from his adrenal glands. 1 month prior he attended his GP with palpitations, recurrent headaches, tremors and feeling flushed. His 24 hr urine collection tested positive for metanephrines. His initial BP of 165/100 was managed with propranolol and in the interim period managed his symptoms well. However after successful resection of the tumor intra op, he went into cardiac arrest due to a hypertensive emergency. He has ROSC after resuscitation. Which drug ought to have been started in the Pre-op phase? A: Higher dose of propranolol B: An Alpha blocker C: Doxazocin D: Phenytoin E: HydrocortisoneQuestion 7 A 37 male is about to have surgery for removal of tumors from his adrenal glands. 1 month prior he attended his GP with palpitations, recurrent headaches, tremors and feeling flushed. His 24 hr urine collection tested positive for metanephrines. His initial BP of 165/100 was managed with propranolol and in the interim period managed his symptoms well. However after successful resection of the tumor intra op, he went into cardiac arrest due to a hypertensive emergency. He has ROSC after resuscitation. Which drug ought to have been started in the Pre-op phase? A: Higher dose of propranolol B: An Alpha blocker C: Doxazocin D: Phenytoin E: Hydrocortisone Question 7: Pheo-chromo-cyt-oma Dark colour cell tumor Tumor of the adrenal medulla Treatment: Surgery BUT tumor manipulation and insufflation during Increased levels of adrenaline/ noradrenaline laparoscopy leads to release of catecholamines→ HTN Occurs in 3rd - 5th decade crisis→ STROKE/MI THEREFORE PRE-OP NON SELECTIVE ALPHA BLOCKER ( Phenoxybenzamine) is vital to pre-op. Why does it happen: Phenoxybenzamine: Familial: MEN type II, neurofibromatosis and von Hippel-Lindau syndrome ● Non-selective, irreversible alpha-adrenergic antagonist. How does the tumor present: ● Blocks both α1 and α2 receptors, leading to vasodilation and decreased blood pressure. 10% Bilateral ● Start 1-2 weeks pre-op with close monitoring and 10% malignant 10% extra-adrenal (most common site = organ of warn of SE e.g hypotension, reflex tachycardia ( Zuckerkandl, adjacent to the bifurcation of the aorta) unopposed B adrenergic activity), nasal congestion. Start with 10mg and totrate up as per response.Question 8 A 30 yr female pregnant with her first pregnancy is at her 28 week antenatal appointment. She has polyuria and polydipsia. She is otherwise fit and well. Which of the following are diagnostic criteria for gestational diabetes? A: Blood glucose level 5.6 mmol/l or above 2 hours post glucose load B: Fasting blood glucose level 6.0 mmol/l or above C: Fasting blood glucose level 7.8 mmol/l or above D: Blood glucose level 7.8 mmol/l or above 2 hours post glucose load E: Fasting glucose is >= 5.5 mmol/LQuestion 8 A 30 yr female pregnant with her first pregnancy is at her 28 week antenatal appointment. She has polyuria and polydipsia. She is otherwise fit and well. Which of the following are diagnostic criteria for gestational diabetes? A: Blood glucose level 5.6 mmol/l or above 2 hours post glucose load B: Fasting blood glucose level 6.0 mmol/l or above C: Fasting blood glucose level 7.8 mmol/l or above D: Blood glucose level 7.8 mmol/l or above 2 hours post glucose load E: Fasting glucose is >= 5.5 mmol/L Question 8:Gestational diabetes (G-DM) Risk factors: Mx Gestational DM: Mx of pre existing DM in BMI > 30 Previous macrosomnic baby (>4.5kg) pregnancy: 1st degree relative with DM Newly diagnosed women: Joint DM/ antenatal Previous G-DM clinic Rv in less than a week BMI of > 27 : weight loss Patient education: self-monitoring of BM/ Previous unexplained stillbirth dietary advice/ exercise advice Stop oral hypoglycemic agents Higher Prevalence DM except for metformin & start ethnicity: caribbean, south asian, middle eastern Fasting plasma glucose level is < 7 mmol/l: Screening programme: trial diet and exercise insulin Oral glucose tolerance test (OGTT) Glucose target not met in 1-2 weeks of diet/ Folic acid 5 mg/day till 12 weeks of Previous G-DM: OGTT after booking appt AND exercise: start metformin 24-28 weeks if first test is normal Target still not met: diet/exercise/ metformin + conception Risk factors present: OGTT at 24-28 weeks Detailed anomaly scan at 20 Dx criteria: insulin( short acting NOT long acting) Fasting glucose is >= 5.6 mmol/L Fasting plasma glucose level is > 7 mmol/l: weeks: including four-chamber 2-hour glucose is >= 7.8 mmol/L Start insulin view of the heart and outflow Target BMs for pregnant women: Plasma glucose level: 6-6.9 mmol/l: tracts Fasting: 5.3 mmol/L Complications such as macrosomia or Tight glycaemic control reduces 1 Hr post meal: 7.8 mmol/L hydramnios→ insulin should be offered complications 2hr post meal: 6.4 mmol/L Glibenclamide: only offered if metformin not tolerated or not meeting glucose targets with Treat retinopathy as can worsen metformin but decline insulin treatment during pregnancyQuestion 9: A 50 yr old woman recently diagnosed with depression is started on citalopram. She complains of A: Myeloma increased thirst and increased frequency of urination and feeling constipated. She feels this is all related to her new antidepressants. Full blood count and B: Parathyroid hyperplasia electrolytes are normal. Her bone profile: C: Lung Cancer Ca : 2.8mmol/L (raised), D: Drug induced PO4: 0.7mmol/L( low). E: Parathyroid Adenoma PTH: 5.0 micromol/L ( normal) What is the best explanation of the above results?Question 9: A 50 yr old woman recently diagnosed withPsychic depression is started on citalopram. She moansains A: Myeloma of increased thirst and increased frequency of urination and feeling constipated. She feels this is B: Parathyroid hyperplasia all related to her new antidepressants. FAbdominal count and electrolytes are normal. groans C: Lung Cancer Her bone profile: Ca : 2.8mmol/L (raised), Bones, stones D: Drug induced PO4: 0.7mmol/L( low). PTH: 5.0 micromol/L ( normal) E: Parathyroid Adenoma What is the best explanation of the above results?Question 9: Parathyroidism Calcium/ PO4 haemostasis https://zerotofinals.com/medicine/endocrinology/hyperparathyroidism/Question 9: Hyperparathyroidism-Primary Causes: Features: Investigations Bloods: raised Ca, low PO4, PTH may be 80% asymptomatic inappropriately) raised OR normal. ● Polydipsia, polyuria Technetium-MIBI subtraction scan ● Depression ● Anorexia, nausea, constipation X-ray findings: Pepperpot ● Peptic ulceration skull/Osteitis fibrosa cystica ● Pancreatitis ● Bone pain/fracture Treatment: ● Renal stones Definitive management: total parathyroidectomy ● Hypertension Conservative management: if Ca < 0.25mmol/L Associations above upper limit of normal AND the patient > 50 ● Hypertension years AND no evidence of end-organ damage ● Multiple endocrine neoplasia: MEN I Patients not suitable for surgery: Treat with and II cinacalcet, a calcimimetic- 'mimics' action of calcium on tissues.Question 9: Hyperparathyroidism-Xrays Acro-osteolysis of terminal phalanges Pepperpot skullQuestion 10 A 45 yr old female with bipolar disorder attends Urine osmolaliUrine Cause the endocrinologist after suffering with after water osmolality after deprivation DDAVP polydipsia and polyuria for the last 1 month. A: Low Low Cranial DI She undergoes urine osmolality testing and a water deprivation test and subsequently trials B: Low High Primary DDAVP to help with her symptoms. She Polydipsia unfortunately continues to be symptomatic. C: Low Low Nephrogenic DI What was her urine osmolality results most likely to be and why? D: Low High Nephrogenic DI E: Low High Cranial DIQuestion 10 A 45 yr old female with bipolar disorder attends Urine osmolaliUrine Cause the endocrinologist after suffering with after water osmolality after deprivation DDAVP polydipsia and polyuria for the last 1 month. A: Low Low Cranial DI She undergoes urine osmolality testing and a water deprivation test and subsequently trials B: Low High Primary DDAVP to help with her symptoms. She Polydipsia unfortunately continues to be symptomatic. C: Low Low Nephrogenic DI What was her urine osmolality results most likely to be and why? D: Low High Nephrogenic DI E: Low High Cranial DIQuestion 10: Diabetes Insipidus Explanation Physiology: Causes: Ix: AVP-D: more common Water deprivation test Intracranial infections: meningitis/ Desmopressin trial ADH made in encephalitis Low urine osmolality (lots of hypothalamus→ stored in Vascular conditions: sickle cell disease water diluting the urine) Posterior pituitary→ ADH Genetic issues: Autosomnal dominant gene/ Wolfram syndroDIDMOAD is the High/normal serum osmolality on vasopressin 2 association of cranial Diabetes Insipidus, (water loss may be balanced by receptors in collecting Diabetes Mellitus, Optic Atrophy) increased intake) duct cells→ acts on More than 3 litres on a 24-hour AVP-R: urine collection Aquaporin 2 cells in Medications: particularly lithium (used in collecting duct cells → bipolar affective disorderdemeclocycline Management: water reabsorbed. Genetic mutations in the ADH receptor AVP-D: gene (X-linked recessive inheritance) Desmopressin Pathophysiology: Hypercalcaemia AVP-R: Hypokalaemia Thiazide/NSAIDS/ Low Na Kidney diseases (e.g., polycystic kidney C-DI: AVP-D (inadequate Renal stones) and protein diet ADH production) Pyelonephritis Correct underlying issues Haemochromatosis Alternative to offending drugs N-DI: AVP-R(inadequate renal response) SEEYOUNEXT https://linktr.ee/medtic.teaching THURSDAY! Sign up to our next session on MedAll Take part in our research survey See all our upcoming events www.medticteaching.com | Email: medticteaching@gmail.com | Youtube @medtic | Instagram @medtic.teaching | Tiktok @medticteaching