Endocrine slides
Summary
Join Dr. Catherine Clarke in her 'Foundation 2 Finals' lecture as she dives into the complex world of Endocrinology and Diabetic foot disease. Expand your understanding of various disorders like Electrolyte abnormalities, Thyroid disease, Cushing’s syndrome, Adrenal insufficiency, and Diabetes, including emergencies. Equip yourself with essential knowledge regarding effective diagnosis and treatment plans of the above disorders. Additionally, focus will be given to Diabetic foot complications. Gear up for an interactive session comprising of case-based learning, discussions, and MCQ practice to aid retention and application of the learned concepts. This lecture is sure to be a valuable learning experience for all aspiring medical professionals.
Learning objectives
- To develop an understanding of different electrolyte abnormalities, their causes, implications on health, and management strategies.
- To gain in-depth knowledge of different thyroid diseases such as hypothyroidism, hyperthyroidism, and thyroid cancer, their potential causes, symptoms, diagnostic procedures, and treatment methods.
- To comprehend Adrenal Insufficiency, its causes, effects on the body, methods to diagnose it and manage the potential health risks associated with it.
- To study about Cushing's Syndrome, its causes, symptoms and diagnose it followed by various treatment strategies.
- To understand the pathology of diabetic foot disease, related complications with an insight on therapeutic approaches as well as preventative measures.
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Endocrinology & Diabetic foot disease 1. By Dr Catherine Clarke FY2 2. ‘Foundation 2 Finals’ lecture 3. Jan 2025Objectives 1) Electrolyte abnormalities 2) Thyroid disease 3) Adrenal insufficiency 4) Cushing’s syndrome 5)Acromegaly 6)Phaeochromocytoma 7) Diabetes including emergencies 8) Diabetic foot 9) MCQ practice Not coveredin detail: -Osteoporosis --Hyponatraemia – DI, SIADH - Other Pituitary disease -Hyperaldosteronism (Conn’s Syndrome) -Hypertension -Gestational diabetes (Obs &Gynae) -Puberty & growth disorders 1) Electrolyte abnormalities - establish cause, replace and treat • Magnesium oftencauses imbalanceof other electrolytes – Na, Ca2+ and K+ • Common causes: • Medications – STOP/START criteria - PPIs can cause both hypomagnesaemia and hyponatraemia • Fluid depletion via diarrhoea+/- vomiting – low K+ • Poor oral intake – monitor for *Refeeding syndrome* - hypophosphatemia;hypokalaemia; hypomagnesaemia;low serum Albumin can indicate malnutrition • Tumour Lysis syndrome – hyperkalaemia, hyperuricaemia, hyperphosphatemia,hypocalcaemia. Hypocalcaemia • Adjusted serum Calcium – <2.2 (normal range: 2.2-2.6) Causes: 1. Poor intake - hypomagnesaemia; Vit D deficiency; medications i.e. phenytoin (increased metabolism of vitamin D) 2. Redistributed – hyperphosphatemia; Pancreatitis; TLS; Rhabdomyolysis; Decreased bone turn-over; hypoparathyroidism; Medications – Bisphosphonates;; PPIs, SSRIs, Gentamycin 3. Output increased e.g. urinary – ethylene glycol poisoning, cisplatin, loop diuretics; non-urinary – bleeding, plasmapheresis etc. Symptoms: • perioral numbness • seizures • paresthesias • tetany • muscle cramps • collapse • mild mental status changes (irritability) • to find cause: diet, drugs Investigations: -Bloods: Bone Profile, Mg2+, LFTs, U&E, PTH, Vit D, CK and Uric acid level, Amylase -ECG – Prolonged QTc **these patients should be on cardiac monitoring** O/E: Positive Chvostek’s sign Management – treat cause e.g. correct hypomagnesaemia, review medications Positive Trousseau sign -Oral Calcium replacement +/- Vitamin D replacement -IV Calcium Gluconate – involve seniors; these patients may need ICU support if refractory hypocalcaemia Hypercalcaemia • Adjusted serum Calcium – >2.6 (normal range: 2.2-2.6) Causes: • Intake: : Diet- excess Ca2+, Vit D or Vit A, hypoMg2+, hypovolaemia, TPN • Redistribution: 1) Commonest cause – Malignancy due to inappropriate release of PTH-related peptide from tumour cells. 2)Immobilization, primary hyperparathyroidism, sarcoidosis, lithium, adrenal insufficiency;endocrine causes (thyrotoxicosis, acromegaly, phaeochromocytoma) • Output: Urinary – thiazide diuretics Investigations: -Bloods: U&E, BP, Mg2+, Amylase +/- Lipase; ALP (to assess bone turnover); PTH, Vit D -ECG: Shortened QTc interval; presence of ‘Osbourne J waves’ -Imaging:X-rays; CTCAP, PET scan Management – depends on severity: -First: Treat cause – correct diet; stop thiazide diuretics - IV Fluids - IV Bisphosphonate (consult Endocrine) - IV Corticosteroids - Calcitonin - IV Denosumab Can cause seizures** - Genetic testingHyperkalaemiaHyponatraemia (Adults >16yrs)Thyroid disease • Hyperthyroidism • Hypothyroidism • Thyroid cancer • Thyroid status exam Thyroid disease – Hyperthyroidism Primary: problem with thyroid gland • Low TSH, high T3/T4 Secondary: problem with hypothalamus/pituitary: excess TSH • High TSH, high T3/T4 Features: anxious, irritable, sweaty, heat intolerance, tachycardia, weight loss, fatigue, loose stools, sexual dysfunction, amenorrhoea Thyroid Storm • Thyrotoxic crisis • Pyrexia, tachycardia and delirium • AdmitHyperthyroidism - Causes 1. Grave’s disease: Autoimmune: TSH receptor antibodies: commonest cause of hyperthyroidism • Pathognomonic signs: exophthalmos, pretibial myxoedema, diffuse goitre 2. Toxic multinodular goitre: (Plummer’s): thyroid nodules continually produce excess thyroid hormone 3. Thyroiditis: De Quervain’s, postpartum, drug-induced Management • Carbimazole: 1st line • Titrate and block or block and replace • Propylthiouracil: 2 line • Radioactive iodine, propranolol, surgeryThyroid disease - Hypothyroidism • Hashimoto’s - Commonest cause in developed world - Anti-TPO antibodies - Goitre then atropy • Iodine deficiency (rare in Western world) - IaCarbimazole/PTU, lithium, amiodarone • Secondary hypothyroidism • Hypopituitarism e.g. due to tumour, infection, Sheehan syndrome, radiation Hypothyroidism Features: • weight gain • Menorrhagia • Reduced libido • fatigue • peaches and cream complexion, • Dry skin • loss of outer 1/3 of eyebrow; hair loss constipation, • Fluid retention cold Management • Levothyroxine Myxodema Coma: LIFE-THREATENING Medical Emergency • Acute presentation: hypothermia, reduced mental status and may experience seizures • Cause: Undiagnosed or insufficient treatment of hypothyroidisim • Usually triggered by a stressful event – surgery, infection or trauma • Rx: IV levothyroxine and steroids Thyroid Cancer Lesion Features Management Papillary thyroid carcinoma • Most common thyroid neoplasm; • Total thyroidectomy approximately 70% of all thyroid cancers • Radio-iodine to ensure removal of • History of head and neck radiation – RF neoplastic cells • Lymphatic spread is more likely than • Annual assessment with thyroglobulin haematogenous spread levels to assess for recurrence • Excellent prognosis Follicular thyroid Carcinoma • 15% of thyroid cancer • Total thyroidectomy • Haematogenous spread • Radio-iodine to ensure removal of neoplastic cells • Annual assessment with thyroglobulin levels to assess for recurrence • Excellent prognosis Medullary carcinoma of the thyroid • May be part of Multiple Endocrine • Screen for MEN 2 Neoplasia (MEN) Type 2 syndrome • Total thyroidectomy • Arises from parafollicular cells; • Radio-iodine to ensure removal of calcitonin may be elevated neoplastic cells Anaplastic carcinoma of the thyroid • Least common thyroid neoplasm • Very poor prognosis • More likely to occur in women and the • Treatment options are generally palliative elderlyThyroid Status Exam - OSCE Inspect: clothing, irritability/anxiety, weight gain/loss, expose the neck, hoarse voice • Hands: thyroid acropachy (Grave’s), onycholysis, palmar erythema, peripheral tremor, tachycardia • Face: - Hypo: dry skin, peaches and cream complexion, loss of outer 1/3 of eyebrow - Hyper: sweating, exophthalmos, lid retraction/lid lag, eye inflammation, abnormal eye movements • Gland: swallow, tongue, palpate, palpate lymph nodes, trachea, percuss, auscultate • Peripheral: proximal myopathy, reflexes (just one), proximal myopathy Adrenal • Adrenal Insufficiency • Steroids • Addisonian CrisisAdrenal Insufficiency • Lack of cortisol and aldosterone • Addison’s: damaged adrenal glands: autoimmune: primary adrenal insufficiency • Secondary adrenal insufficiency: inadequate ACTH due to pituitary gland problem e.g. tumour/infection; XRT; recent surgery; Sheehan’s syndrome • Tertiary adrenal insufficiency: inadequate CRH by hypothalamus: Iatrogenic: pt on long-term oral steroids-suppresses natural feedback PC: fatigue, nausea, cramps, abdominal pain, decreased libido Bronze hyperpigmentation, hypotensionAdrenal Insufficiency: Investigations and Treatment Hyponatraemia +/- hyperkalaemia Hypoglycaemia Raised Creatinine and Urea –due to dehydration • Short synACTHen test: > Less than double indicates primary adrenal insufficiency (i.e. Addison’s) • ACTH • Check Autoimune antibodies: - 21-hydroxylase antibodies and adrenal cortex antibodies Treatment • Steroids • Hydrocortisone to replace cortisol • Fludrocortisone to replace aldosteroneAdrenal Crisis • Severe presentation of adrenalinsufficiency (LIFE-THREATENING) • Symptoms: - Reduced consciousness - Hypotension - Hypoglycaemia and hypocalcaemia - Hyponatraemia and hyperkalaemia If suspecting: -ABCDE approach - Treat immediately with IM or IV steroids (100mg hydrocortisone, followed by infusion or 6hrly doses) - IVF • Correct hypoglycaemia • Monitor fluid balance and U&EsCushing's Syndrome •Cushing’s Syndrome & Cushing’s Disease •Dexamethasone Suppression Test •Other investigations •ManagementCushing’s syndrome – multi-system condition Prolonged elevated cortisol • Cushing’s Disease (80%): Pituitary adenoma secretes excess ACTH causing Cushing’s syndrome Causes: • ACTH dependent: Cushing’s disease, ectopic ACTH (paraneoplastic) • ACTH independent (exogenous steroids, adrenal adenoma)Cushing’s Syndrome Investigations Management 24-hr urinary free cortisol Treat the cause • Rarely done now as difficult to do FBC, U&E • Trans-sphenoidal surgery for • Low potassium pituitary adenoma MRI brain • Surgical removal of adrenal • Pituitary adenoma tumour CT chest • SCLC • Treatment of cancer for paraneoplastic Cushing’s Abdominal CT • Adrenal tumours syndromeAcromegaly Excessive growth hormone • Usually due to pituitary adenoma Symptoms: • Bitemporal hemianopia • Headaches, frontal bossing, macroglossia, prognathism, bilateral carpal tunnel syndrome, HTN, T2DM, skin tags, sweating ++ Investigations: IGF-1 (elevated), OGTT, MRI brain Treatment: trans-sphenoidal removal of pituitary adenoma Meds: Somatostatin analogues (ocreotide), Dopamine agonists (bromocriptine);Pegvisomant (growth hormone receptor antagonist)Phaeochromocytoma • Rare, catecholamine-secreting tumour • Symptoms: Palpitations; Sweating; Hypertension; arrhythmias • Rule of 10s: -10% Bilateral -10% Malignant -10% occur in children -10% occur outside the adrenal medulla • Investigations: Urinary metanephrines; CT/MRI adrenals followed by MIBG scan • Genetic testing: associated with MEN Type II; Neurofibromatosis or Von Hippel-Lindau Syndrome Treatment: -Surgical excision -Alpha blockade pre-operatively (phenoxybenzamine) Diabetes •Type 1 vs Type 2 •Diagnosis •Management •Complications •OSCE TopicsDiagnosis - **Common MCQ** Symptomatic diabetic: • fasting glucose >7.0 OR • Random glucose >11.1 OR • 2 hr plasma glucose >11.1 after an oral glucose tolerance test (OGTT) • HbA1c greater than 48mmol/L (6.5%) Asymptomatic: • • As above but must be demonstrated twice Pre-Diabetic Conditions - **Common MCQ** Impaired Glucose Tolerance: • • 2hr post-prandial reading between 7.8 and 11.1 Impaired Fasting Glucose: •Fasting glucose between 6.1 and 7.0 • HbA1c 42-47mmol/L = pre-diabetes Management: • Diet & lifestyle • Diabetes prevention programme • Annual review with bloods • Metformin if no improvementManagement of Type 1 Diabetes Insulin • Basal-bolus regime • ‘Basal’: base-line insulin: once daily long-acting insulin e.g. Lantus or Levemir (never omit even when sick) with: • Bolus’: rapid acting insulin before meals or snacks e.g. Novorapid or Apidra (can be adjusted for each meal if carb counting) • Diet & lifestyle – yearly eye screening; 6 monthly HbA1c check • Target glucose 4-7mmol (five to drive) • Monitor before every meal, before bed and before driving • Increased monitoring if sick, exercising or after hypoComplications – Short-term • Hypoglycaemia • DKA • HHSHypoglycaemia Hypoglycaemia kills - if in doubt, give glucose! • Hypoglycaemia: glucose <4mmol/L • Unconscious: 200ml of 10% IV glucose STAT • (Glucagon IM if no IV access) – don’t give glucagon in patients with severe Liver disease • Conscious but cannot swallow: 2tubes 40% glucose gel around gums • Can swallow: 15-20g fast acting carbs • Check CBG in 10minsDiabetic KetoacidosisHHS - 'HONK'Diabetic Foot Examination – OSCE station 1. Introduction 2. Inspection: -Footwear: pattern of wear on soles; ?correct size; 4. Examine: no materials inside shoe causing injury -Touch sensation – light touch or pinprick -Gait: speed; stance; steps (?foot-drop); turning -Vibration sensation or Proprioception -Both feet: -Ankle Jerk reflex 3. Palpation: - Peripheral pulses Final tests: - Pallor -CBG - Peripheral cyanosis -Serum HbA1c - Venous ulcers or arterial ulcers -Lower limb exam – look for venous signs - Gangrene -Foot care advice - PEDIS score - Amputated toes/limbs/finger - Cap refill - TemperatureOSCE FeedbackThank you for listening! Thank you for listening! ☺ Not covered - Osteoporosis • Any Questions? - Hyponatraemia – DI, SIADH - Other Pituitary disease cclarke48@qub.ac.uk - Hyperaldosteronism (Conn’s Syndrome) - Hypertension - Gestational diabetes • Evaluation link - Puberty & growth disordershttps://forms.office.com/r/GYpBbyqWmW