Endocrinology Flashcards
What is acromegaly?
- Excess growth hormone, normally secondary to pituitary adenoma
- Spade like hands and feet, large tongue, excessive sweating, raised prolactin, protruding jaw
- Sometimes features of pituitary tumour: headaches, bitemporal haemianopia
Investigations of acromegaly?
- IGF1 levels initially then OGTT as gold standard (GH will not be suppressed)
- Pituitary MRI
Management of acromegaly?
- Trans-sphenoidal surgery
- Somatostatin analogues which inhibit GH release e.g Octreotide
- Pegvisomant which is GH receptor antagonist
- Dopamine agonists e.g. bromocriptine
What is Addisons disease?
- Autoimmune destruction of darnel glands causing primary hypoadrenalism
- Reduced cortisol and aldosterone
- Lethargy, anorexia, weight loss, hyperpigmentation, ‘salt craving’
- Hyponatraemia and Hyperkalaemia
Other causes of hypoadrenalism?
- TB
- Metastases
- HIV
- Antiphospholipid
How to tell difference between primary Addisons and secondary adrenal insufficiency?
- Hyperpigmentation is only in primary Addisons
Investigations for Addisons
- 9am serum cortisol
- Synacthen test (gold standard): cortisol levels will not increase adequately
Management of Addisons
- Replacement glucocorticoid (cortisol): hydrocortisone
- Replacement mineralocorticoid (aldosterone): fludrocorticoid
- Doses given to mirror cycle of release in body
- Patient education around illness and symptoms of adrenal crisis
Addisonian crisis
- Causes by sepsis, surgery, haemorrhage or steroid withdrawal
- Hypotension, shock, delirium, abdo pain, vomiting, headaches, fever
- Managed with IM/IV Hydrocortisone, IV fluids
What is Bartter’s syndrome?
- Inherited cause of severe hypokalaemia due to defective chloride absorption at the loop of Henle
- Presents with failure to thrive in childhood/diabetes like symptoms
Corticosteroid Groups
- Mineralocorticoid: Fludrocortisone
- Glucocorticoid: Hydrocortisone, Dexamethasone, Betamethasone
Steroids side effects
- Impaired glucose regulation
- Increased appetitie/weight gain
- Hirsutism
- Hyperlipidaemia
- Cushings syndrome (moon face, buffalo hump)
Steroids management
- Doses should be doubled in intercurrent illness for those on long-term steroids
- Should not be withdrawn abruptly: Addisionian crisis
Cushings disease
- Pituitary adenoma secreting excessive ACTH which stimulates excessive cortisol from the adrenals
Causes of Cushings syndrome (high levels of glucocorticoids in the body)
- Cushings disease
- Adrenal adenoma (excess cortisol)
- Paraneoplastic syndrome
- Exogenous steroid use
Cushings syndrome presentation
- Moon face
- Central obesity
- Abdominal striae
- Buffalo hump
- Hirsutism
- Hyperpigmentation of skin in Cushings disease
Conditions associated with Cushings
- HTN
- T2DM
- Osteoporosis
- Dyslipidaemia
What sign helps to distinguish cushings diseases as a cause compared to steroids/adrenal adenoma?
Hyperpigmentation of skin (ACTH stimulates melanin production)
Management of Cushings
- High dose dexamethasone supression test
- Removal of pituitary/adrenal tumour
- Adrenalectomy plus lifelong steroid replacement
T1DM
- Pancreas stops producing adequate insulin
- Hyperglycaemia: polyuria, polydipsia, weight loss
Insulin production
- Beta cells in islets of langerhans in pancreas -> causes absorption of glucose by cells and promotes glycogenesis where glucose is stored as glycogen in liver
DKA Triad
- Ketoacidosis
- Dehydration
- Potassium imbalance
Presentation of DKA
- Polyuria
- Polydipsia
- N+V
- Sweet smelling breath
- Dehydration
- Weight loss
Treatment of DKA
- IV Fluids
- Insulin
- Glucose
- Potassium
- Infection
- Chart fluids
- Ketone monitoring
Long term management of T1DM
- Insulin via basal bolus (1 long acting and then short-acting before meals0
- Monitor blood sugar and complications
Hypoglycaemia
- Hunger
- Tremors
- Sweating
- Irritability
- Dizziness
- Pallor
- Tx with rapid acting glucose followed by slower acting carbohydrates
T2DM
- Fasting glucose >7
- Random glucose >11.1
- HBA1c > 48
T2DM Treatment
- Metformin
- SGLT-2 inhibitor e.g empagliflozin for patients with high risk of CVD
- DPP-4 inhibitor e.g. Sitagliptin
- Sulfonylurea e.g. Gliclazide
- Insulin
Metformin pharmacology
- increases insulin sensitivity/decreases glucose production
- Does not cause weight gain/hypoglycaemia
- S/E include GI symptoms and lactic acidosis
SGLT-2 Inhibitors pharmacology
- Blocks reabsorption of glucose from urine into blood causing it to be excreted
- Cause cause hypoglycaemia when used with sulfonylurea/insulin
- S/E include urinary frequency/urgency, thrush, weight loss, DKA
Sulphonylurea pharmacology
- Stimulate insulin release from pancreas
- S/E include weight gain and hypoglycaemia
DPP-4 inhibitor pharmacology
- Block action of DPP enzyme allowing increased incretin activity which increase insulin secretion, inhibit glucagon production
- S/E include headaches and low risk of acute pancreatitis
Hyperglycaemic Hyperosmolar state
- Hyperosmolality: concentrated blood
- Hyperglycaemia
- Absence of ketone
- Tx with IV fluids and monitoring
Diabetic Neuropathy
- Glove and stocking distribution
- Management of AMT, Duloxetine, Gabapentin, Pregabalin
- Topical capsaicin may be used for localised pain
What is Conn syndrome?
High levels of aldosterone caused by an adrenal adenoma producing too much aldosterone
RAAS Cycle
- Renin produced in afferent arterioles in kidney and is secreted from BP is low
- Renin converts angiotensiongen into angiotensin I
- ACE convers AG I into AG2 which stimulates release of aldosterone from adrenals
How does aldosterone increase BP?
- Increased sodium reabsorption in DT
- Increase potassium secretion from DT
- Increase hydrogen secretion from ducts
Causes of primary and secondary hyperaldosteronism?
Primary
1. Bilateral adrenal hyperplasia
2. Conns
Secondary
1. Renal artery stenosis
2. Heart failure
Management of Conns
- Ald:Renin ratio (high Ald and low renin)
- CT/MRI to look for andenoma
- Tx includes spironolactone/surgery to remove adenoma
Hypothyroidism
Primary: Pathology at thyroid: High TSH, low T3/T4
Secondary: Pathology at pituitary: Low TSH, low T3/T4
Most common causes of hypothyroidism
Primary: Hashimotos in developed, Iodine deficiency in developing
Secondary: Tumours, Surgery, Sheehans
Presentation of Hypothyroidism
- Weight gain
- Fatigue
- Dry skin
- Cold intolerance
- Coarse hair/loss
- Constipation
- Heavy/irregular periods
- Goitre
Hashimotos
- Anti TPO antibodies and anti-TG antibodies
Hyperthyroidism
Primary: thyroid pathology: high T3, T4, low TSH
Secondary: pituitary/hypothalamus pathology: high T3/T4, high TSH
Causes of hyperthyroidism
Graves
Inflammation
Solitary toxic thyroid nodule
Toxic multinodular goitre
Presentation of hyperthyroidism
- Anxiety and irritability
- Sweating and heat intolerance
- Tachycardia
- Weight loss
- Fatigue
- Diarrhoea
- Sexual dysfunction
Graves specific features
- Diffuse goitre
- Graves eye disease: proptosis
- Pretibial myoxedema: waxy, appearance often on shins
Graves
- TSH receptor antibodies
De Quervains thyroiditis
- Thyrotoxicosis
- Hypothyroidism
- Return to normal
- Self limiting conditions, which requires supportive management
Thyroid Storm
- Rare presentation of hyperthyroidism with fever, tachycardia and delirium
- Can be life threatening
- Requires fluid resus, anti-arrhythmic
Tx of Hyperthyroidism
- Referral to secondary care if Graves
- Carbimazole for 12-18 months with either maintenance for life or block and replace with levothyroxine
- Propylthiouracil
- Radioactive iodine to block and replace
- Propranolol
- Surgery to remove then replace
S/E of Carbimazole/Propylthiouracil
Carbimazole: Risk of acute pancreatitis, agranulocytosis
Propylthiouracil: agranulocytosis, liver reactions
Parathyroid physiology
- PTH glands produce PTH in response to hypocalcaemia
- PTH increases osteoclast activity (calcium reabsorption via bones), increases reabsorption in kidneys and increases vit D which increases calcium absorption in intestines
Symptoms of hypercalcaemia
- Kidney stones
- Painful bones
- Abdominal groans (constipation, N+V)
- Psych moans (fatigue, depression and psychosis)
Hyperparathyroidism
Primary: uncontrolled PTH production by PTH tumour causing hypercalcaemia, treated with removal
Secondary: insufficient vit D/CKD causes hypocalcaemia and so excess PTH, treated with treat cause
Tertiary: secondary HPT of occurs for long time causes hyperplasia and high PTH and hypercalcaemia, treated with removal of some parathyroid
Hypoparathyroidism
Primary: decreased PTH, low calcium and phosphate, tx with alfacalcidol
Presentation of hypoparathyroidism
- Muscle twitching, cramps and spasms
- Prolonged QT interval
- Perioral paraesthesia
- Chvostek sign: tapping over parotid causes facial twitch
- Trousseau sign: carpal spams when brachial artery occleded
SIADH
- Increased release of ADH from posterior pituitary which increases water reabsorption and causes euvolemic hyponatraemia
- High urine osmolality and high urine sodium
Causes of SIADH
- Post op
- Pneumonia/Lung abscess
- Brain pathology
- Iatrogenic e.g SSRI/Carbamazepine
- Malignancy - small cell lung cancer
Presentation of SIADH
- Headaches
- Fatigue
- Muscle aches and cramps
- Confusion
- Seizures if severe
Management of SIADH
- Clinical features from bloods/urine dip
- Exclude other causes
- CTTAP if suspect cancer
- Tx includes treat cause, fluid restriction and tolvaptan (blocks ADH receptors but works very quickly so needs close monitoring)
Complication of severe hyponatraemia
- Central pontine myelinolysis/osmotic demyelination syndrome
What is diabetes insipidus?
- Lack of ADH (cranial)
- Lack of response to ADH (nephrogenic)
- Causes polyuria, polydipsia, postural hypotension
Nephrogenic Causes
- Idiopathic
- Medications e.g lithium
- Genetic mutations
- High calcium/low potassium
- Renal disease
Cranial causes
- Idiopathic
- Brain tumours/injury/surgery/infection
- Genetic mutations
Investigations for DI
- Low urine osmolality, high/normal serum osmolality
- Water deprivation test:
Cranial: Low UO after water deprivation, high after desmopression - Nephrogenic: Low UO after both
Tx of DI
Cranial: Desmopressin
Nephrogenic: Fluids, high dose desmopressin, diuretics, NSAIDs
Phaeochromocytoma
- Tumour of chromaffin cells which secretes excessibe adrenaline
- Common with MEN2, NF1 and von Hippel-lindau
Presentation of phaeochromocytoma
- Anxiety
- Sweating
- Headache
- Tremor
- Palpitations
- HTN
Management of phaeochromocytoma
- Plasma free metanephrine/24 hoururine catecholamines
- CT/MRI to confirm tumour
- Tx includes alpha blockers e.g doxazosin, beta blocks and surgical removal
Thyroid eye disease
- Smoking is the most important risk factor
- Can be with hypo/hyper
- Proptosis, optic disc swelling, conjunctival oedema
- Tx with topical lubricants, steroids, radiotherapy
Thyroid nodules
- Requires exclusion of thyroid cancer
- Benign include: Goitre, thyroid adenoma, cysts
- Malignant include: Papillary carcinoma, follicular carcinoma
- US is imaging of choice
- Malignancy treated with thyroidectomy, radioiodine and yearly thyroglobulin levels
Which diabetes medication causes weight loss?
SGLT-2 inhibitors e.g. empaglioflozin
GLP-1 agonists e.g semaglutide
Electrolyte abnormality found in Addisons?
hyperkalaemia, hyponatraemia, hypoglycaemia
