Endocrinology Flashcards
What are the 4 types of diabetes mellitus?
T1DM, T2DM, MODY, LADA
What is T1DM?
Absolute insulin deficiency, autoimmune destruction of pancreatic beta cells.
When does T1DM normally present?
Presents ages 5-15.
What percentage of diabetes is T1DM?
10%
What are the four risk factors for T1DM?
HLA DR2-DQ3, HLA DR4-DQ8, other autoimmune disease, environmental infection.
What is the pathophysiology of T1DM?
Autoimmune destruction of pancreatic beta islets, resulting in hyperglycaemia and low cellular glucose.
What are the 6 main symptoms/signs of T1DM?
Weight loss, nocturia, glycosuria, polyuria, polyphagia, polydipsia.
What is the typical patient that presents with T1DM?
Lean and young, with rapid weight loss, polydipsia, polyuria, nocturia, ketosis, FHx of autoimmune disease.
How is T1DM diagnosed?
By RPG (random), FPG (fasting for 8+h) and HbA1c (48+).
What are the values of RPG and FPG in T1DM?
RPG - >11mmol/LFPG - > 7mmol/L
What is the value of HbA1c in T1DM?
> 48mmol/L
Compare RPG/FPG and HbA1c.
RPG/FPG = Instant results.HbA1c = Slower but more accurate.
What is the treatment for T1DM?
Insulin - Fast acting (4-6h) and slow acting (12-24h).
What is the main complication of T1DM?
Diabetic ketoacidosis (DKA)
How does diabetic ketoacidosis occur in T1DM?
Often from undiagnosed/poorly managed T1DM. Maybe from infection/illness.
What is the pathophysiology of diabetic ketoacidosis?
Absolute insulin deficiency from T1DM, so there is lots of lipolysis and gluconeogenesis. Not all is used so it is converted to ketones (acidic).
What are the signs and symptoms of DKA?
Sx of T1DM and:
-Kussmaul breathing - Blow off CO2 (acidic blood)
-Pear drop breath - Fruity ketone smell
-Hypotension, N+V, tachycardia, weight loss, pain.
How is diabetic ketoacidosis diagnosed?
Same symptoms and RPG/FPG as T1DM and:
-High ketones, >3mmol/L.
-Acidosis, <7.35pH.
-Ketonuria.
What is the first line treatment for diabetic ketoacidosis?
After ABCDE - IV fluids (prevent dehydration).
What is the second line treatment for diabetic ketoacidosis?
Insulin and restore electrolytes.
What is T2DM?
When patients gradually become insulin resistant or pancreatic beta cells fail to secrete enough insulin, or both.
When does T2DM normally present?
Later in life (40+) and is more common in males.
What are the seven risk factors for T2DM?
Genetic link, smoking, obesity, hypertension, sedentary lifestyle, alcohol, Asian men.
What are the two main causes of T2DM?
Reduced insulin secretion /+ increased insulin resistance.
Others = Steroids, gestational, Cushing’s.
What four conditions is T2DM a risk factor for?
Hypertension, silent MI, nephrotic syndrome, CKD.
What are the seven main symptoms of T2DM?
Obese, hypertensive, nocturia, polydipsia, polyuria, glycosuria, blurred vision.
How is T2DM diagnosed?
Same as T1DM - RPG (>11mmol/L), FPG (>7mmol/L) and HbA1c (>48mmol/L).
What states are there in T2DM that there isn’t in T1DM?
Prediabetic states - impaired glucose tolerance (IGT) and impaired fasting glucose (6.1-6.9).
What is the treatment for prediabetes?
Lifestyle changes - healthier diet, exercise, modify RFs.
What is the first line treatment for T2DM?
Lifestyle changes - Healthier diet, more exercise, less alcohol, stop smoking, regular monitoring.
What is the second line treatment for T2DM?
Medications.
What is the first medication for T2DM and how does it work?
Metformin - increases sensitivity to insulin.
When is the 2nd line medication given for T2DM and what is it?
If HbA1c - 58+mmol/L.
Add another drug to metformin such as sulfonylureas (gliclazide) which increases insulin secretion.
When is a 3rd line medication given for T2DM and what is it?
If HbA1c levels remain persistently high - Add a 3rd drug to metformin and sulfonylureas:
-DPP4 inhibitor.
-SGLT-2 inhibitors
What is the last resort medication for T2DM?
Insulin.
What are some complications to T2DM?
Macrovascular - MI, ischaemic stroke, PVD.
Microvascular - Retinopathy, neuropathy (Charcot foot), nephropathy (CKD).
What is a serious complication to T2DM?
Hyperosmolar hyperglycaemic state (HHS).
What is HHS and how does it present?
Excessive hepatic gluconeogenesis - glucose is osmotically active, so an excess means hyperosmolar blood.
Often precipitated with undiagnosed/uncontrolled T2DM and infection/illness.
What are the five main symptoms of HHS?
Severe T2DM, lethargy, decreased consciousness, severe dehydration, confusion.
How is HHS diagnosed?
Heavy glycosuria, increased plasma osmolality with hyperglycaemia. NO ketosis/ketonuria.
How is HHS treated?
Insulin, IV fluids, LMWH.
Why is an anticoagulant given as a treatment for HHS?
Hyperosmolar blood is thicker so to prevent clots.
What is diabetes insipidus?
Decreased ADH secretion or action with more than 3L of urine daily.
What are the two types of diabetes insipidus?
Cranial - decreased ADH secretion.
Nephrogenic - decreased kidney response to ADH.
What is the pathophysiology of diabetes insipidus?
Decreased ADH means increased losses of H2O in urine, producing urine with dilute high volumes.
What are the main three symptoms of diabetes insipidus? What are four severe symptoms?
Polyuria, polydipsia, hypernatraemia.
Severe = Lethargy, confusion, coma and severe dehydration.
When would diabetes insipidus be suspected?
When there is more than 3L of urine daily.
What is the gold standard test to diagnose diabetes insipidus and what are the results?
Water deprivation test (no fluid for 8h).
Normally, serum osmolality test remains the same as urine osmolality increases but it’s the opposite in diabetes insipidus:
-Serum osmolality rises while urine osmolality is unchanged.
How is cranial and nephrogenic diabetes insipidus differentiated?
By injecting IM desmopressin (synthetic ADH).
-Cranial: urine osmolality rises (ADH works on kidney).
-Nephrogenic: urine osmolality is unchanged (ADH has no effect).
What are the five main causes of cranial diabetes insipidus?
Idiopathic, congenital, tumour, trauma, infection.
What are the four main causes of nephrogenic diabetes insipidus?
Inherited, drugs (lithium), metabolic, CKD.
How is mild diabetes insipidus treated?
Conservatively - stay hydrated.
How is cranial diabetes insipidus treated?
Desmopressin (synthetic ADH).
How is nephrogenic diabetes insipidus treated?
-Thiazide diuretics and NSAIDs to stop kidneys producing as much urine.
What is hyperthyroidism?
The clinical effects of excess thyroid hormone.
What is the difference between primary and secondary hyperthyroidism?
Primary - Abnormally increased thyroid function.
Secondary - Abnormally increased TSH production.
Who is hyperthyroidism most common in?
Young women aged 20-40.
More common in women to men 9:1.
What is the main cause of primary hyperthyroidism?
Graves’ disease - 70%
What are some other primary causes of hyperthyroidism?
Toxic adenoma, toxic goitre, drugs, cancer.
Which drugs can cause primary hyperthyroidism?
Amiodarone, lithium, iodine.
What is a secondary cause of hyperthyroidism?
TSH secreting pituitary tumour.
What is the pathophysiology of hyperthyroidism?
Increased T3 increases metabolic rate, which increases CO, bone resorption and activates the SNS.
What are the four risk factors for hyperthyroidism?
Smoking, stress, HLA-DR3 and other autoimmune diseases (T1DM, Addison’s).
What are the five main symptoms of hyperthyroidism?
Heat intolerance/sweaty, diarrhoea, weight loss, hyperphagia, anxiety.
What are four signs of hyperthyroidism?
Goitre, tachycardia, fine tremor, muscle wasting.
What is first used to diagnose hyperthyroidism?
Thyroid function tests (TFTs).
How is primary and secondary hyperthyroidism differentiated?
TFTs:
-Primary: Decreased TSH, increased T4/T3.
-Secondary: Increased TSH, increased T4/T3.
What other tests are used to diagnose hyperthyroidism?
Thyroid USS, CT of head and anti-TPO antibodies.
Which drugs used are used for symptom relief in hyperthyroidism?
Beta blockers (block adrenaline of SNS).
What is the first line treatment for hyperthyroidism and how does it work?
Carbimazole - blocks T4 synthesis.
What is the second line treatment for hyperthyroidism?
Propylthiouracil (prevents T4-T3 conversion).
What is a less common treatment for hyperthyroidism?
Radioiodine.
What is the last resort treatment for hyperthyroidism?
Thyroidectomy.
What is the pathophysiology of Grave’s disease?
IgG autoantibodies bind to TSH receptors to increase T4/T3 production. (70% of hyperthyroidism).
What are signs and symptoms of Grave’s disease?
Sx of hyperthyroidism and:
-Thyroid eye disease (eyelid retraction, periorbital swelling and proptosis - eye bulging).
-Pretibial myxedema: waxy, skin discolouration.
-Thyroid acropachy: nail clubbing, finger/toe swelling.
What is hypothyroidism?
Clinical effect of lack of thyroid hormone.
What is the difference between primary and secondary hypothyroidism?
Primary - Abnormally low thyroid function.
Secondary - Abnormally low TSH production.
What is the most common cause of primary hypothyroidism worldwide?
Iodine deficiency.
What is the most common primary cause of hypothyroidism in the developed world?
Hashimoto’s thyroiditis - autoimmune thyroid destruction, inflammation leads to goitre.
What is a cause of primary hypothyroidism that doesn’t cause a goitre?
Primary atrophic hypothyroidism.
What four other things cause primary hypothyroidism?
Postpartum thyroiditis, drugs, post-thyroidectomy and radioiodine.
What causes secondary hypothyroidism?
Hypopituitarism - less TSH released.
Pituatry adenomas.
What is the pathophysiology of hypothyroidism?
Not enough T3 to increase metabolic rate for normal bodily functions.
What are four symptoms of hypothyroidism?
Cold intolerance, constipation, weight gain, lethargy.
What are four signs of hypothyroidism?
Bradycardia, slow reflexes, cold hands, goitre.
What is first used to diagnose hypothyroidism?
Thyroid function tests (TFTs).
How is primary and secondary hypothyroidism differentiated?
TFTs:
-Primary: Increased TSH, decreased T4/T3.
-Secondary: Decreased TSH, decreased T4/T3.
What other tests can be used to diagnose hypothyroidism?
Anti-TPO autoantibodies are increased and maybe anaemic.
How is hypothyroidism treated?
Levothyroxine (T4) - same for primary and secondary.
What can hypothyroidism treatment cause?
Iatrogenic hyperthyroidism.
What is a complication of hypothyroidism?
Myxedema coma - rapidly decreased T4 and severe hypothyroidism.
Sx - hypothermia, LOC, heart failure.
Tx - Levothyroxine, hydrocortisone.
What are the three main types of thyroid cancer?
Popullary (70%), follicular (25%) and anaplastic (worst prognosis).
How does thyroid cancer present?
Hard and irregular thyroid lump, compression may cause hoarse voice.
How is thyroid cancer diagnosed?
TFTs, USS of thyroid and aspiration biopsy.
How is thyroid cancer treated?
Popullary/follicular - thyroidectomy, radioiodine.
Anaplastic - palliative.
What is Cushing’s syndrome?
Long term exposure to excessive cortisol homorne which is released by the adrenal glands - hypercortisolemia.
What is Cushing’s disease?
Cushing’s syndrome (hypercortisolemia) that is caused by an ACTH secreting adenoma.
What are the two types of causes of Cushing’s syndrome?
ACTH dependent (pituitary adenoma, SCLC) and ACTH independent (adrenal adenoma/iatrogenesis).
What are some ACTH dependent causes of Cushing’s syndrome?
Cushing’s disease and ectopic CTH (SCLC).
What are some ACTH independent causes of Cushing’s syndrome?
Iatrogenesis and adrenal adenoma.
What is the most common cause of Cushing’s syndrome overall?
Iatrogenesis (steroids).
What are the main eight signs and symptoms of Cushing’s syndrome?
Moon face, buffalo hump, obesity, striae, acne, muscle atrophy, weight gain, hypertension, hirituism.
What is the first step of diagnosing Cushing’s syndrome?
Rule out if on steroids - if so, stop.
What is the first line at diagnosing Cushing’s syndrome and what are the results?
Overnight dexamethasone suppression test:
-Low dose = Synthetic cortisol should be suppressed via negative feedback but in Cushing’s syndrome there is little/no suppression.
-High dose = If suppressed it is Cushing’s disease.
If not suppressed measure plasma ACTH.
What has to be measured before first line test in Cushing’s syndrome?
Random serum cortisol test at 12am, if this is high then it is very abnormal (cortisol is lowest at 12am).
What else is measured in Cushing’s syndrome if the first line test is positive?
Measure plasma ACTH and urinary free cortisol.
What can be interpreted if plasma ACTH is high in Cushing’s syndrome?
ACTH dependent - potential Cushing’s disease or SCLC.
What can be interpreted if plasma ACTH is low/normal in Cushing’s syndrome?
ACTH independent - consider adrenal adenoma.
How is Cushing’s syndrome treated if iatrogenic cause?
Stop medications.
How is Cushing’s disease treated?
Transsphenoidal resection of pituitary adenoma.
How is Cushing’s syndrome treated if caused by adrenal adenoma?
Unilateral adrenalectomy.
How is Cushing’s syndrome treated if caused by ectopic ACTH?
If tumour causing - remove tumour (SCLC).
What are some medications used to treat Cushing’s syndrome?
Cortisol synthesis inhibition - metyrapone and ketoconzole.
What are two complications of Cushing’s syndrome?
Osteoporosis and secondary diabetes.
What is acromegaly?
Release of excess GH and overgrowth of all systems.
What is the difference between acromegaly and gigantism?
Acromegaly is in adults after epiphyseal fusion.
Gigantism is in children before epiphyseal fusion.
What is the main cause of acromegaly?
Functional pituitary adenoma (99%).
What is a rare cause of acromegaly?
Secondary to lung cancer - ectopic GH (1%).
What is the pathophysiology of acromegaly?
GH acts directly on some tissues (liver, muscle, bone and fat) and indirectly through IGF-1.
What are the five signs of acromegaly?
Large hands and feet, large nose and tongue, prominent forehead/brow, box jaw, deep voice.
What are the symptoms of acromegaly?
Sweating, sleep apnoea, vision defects.
What is the 1st line test for acromegaly?
Test IGF-1 serum level - increased.
What is the gold standard test for acromegaly?
Impaired glucose test.
What other tests can be used to diagnose acromegaly?
Pituitary fossa MRI, serum GH level.
What is the 1st line treatment for acromegaly?
Transsphenoidal resection of pituitary adenoma.
What is the 2nd line treatment for acromegaly?
Somatostatin analogue - octreotide.
What is the 3rd line treatment for acromegaly?
GH antagonist - pegvisomant.
What is the 4th line treatment for acromegaly?
Dopamine antagonist - cabergoline/bromocriptine.
What are the three main complications of acromegaly?
T2DM, obstructive sleep apnoea and erectile dysfunction.
What is a prolactinoma?
A benign pituitary adenoma that causes hyperprolactinemia.
What are the two types of prolactinoma and how common are they?
Micro (<10mm) - 90%.
Macro (>10mm) - 10%.
What is another cause of hyperprolactinemia?
Antidopaminergic drugs.
What are the main 7 signs and symptoms of prolactinoma?
Decreased libido, visual field defect.
Women - Amenorrhoea, galactorrhoea.
Men - Erectile dysfunction, gynecomastia, decreased testosterone.
How is a prolactinoma diagnosed?
Increased serum prolactin and CT head.
What is the first line treatment for prolactinoma and why?
Dopamine antagonists (inhibits prolactin).
What is the gold standard treatment for prolactinoma?
Transsphenoidal resection of tumour.
What is Conn’s syndrome?
Hyperaldosteronism - excess aldosterone independent of RAAS system. Caused by an adrenal adenoma.
How many cases of hyperaldosteronism are caused by Conn’s syndrome?
2/3rds
What is the other less common cause of hyperaldosteronism?
Bilateral adrenal hyperplasia (1/3rd).
What condition most commonly causes secondary hypertension?
Hyperaldosteronism (Conn’s syndrome).
What is the pathophysiology of hyperaldosteronism (Conn’s)?
Excess aldosterone - high Na+ and H2O retention with increased K+ excretion (hypokalaemia).
What are the main five symptoms of Conn’s syndrome?
Resistant hypertension (unfixable with ACE-i/Bb), hypokalaemia, muscle weakness, polydipsia, polyuria.
What is the first line test for Conn’s syndrome (hyperaldosteronism)? What are the results?
Aldosterone to renin blood test ratio - Increased.
Low renin = Primary hyperaldosteronism.
High renin = Secondary hyperaldosteronism.
What does hyperaldosteronism (Conn’s) show on ECG?
Hypokalaemia.
What is the 1st line treatment for Conn’s/hyperaldosteronism?
Spironolactone - aldosterone inhibitor.
What is the gold standard treatment for Conn’s syndrome?
Laparoscopic adrenalectomy.
What is Addison’s disease?
Primary adrenal insufficiency. Destruction of adrenal cortex and decreased production of glucocorticoids (cortisol) and mineralocorticoids (aldosterone).
Who is Addison’s disease most common in?
Females with other autoimmune diseases.
What is the most common cause of Addison’s disease in the developed world?
Autoimmune destruction.
What is the most common cause of adrenal insufficiency worldwide?
TB
What are other causes of adrenal insufficiency?
Adrenal metastases or adrenal haemorrhage.
What is a cause of secondary adrenal insufficiency?
Main cause is loss or damage of the pituitary gland.
What is the difference between primary and secondary adrenal insufficiency?
Primary - Destroyed adrenal cortex - Increased ACTH, decreased adrenal hormones.
Secondary - HPA axis suppression - Decreased ACTH, decreased adrenal hormones.
What are the five main symptoms and two main signs of adrenal insufficiency?
Symptoms - Nausea/abdo pain, fatigue, cramps, reduced libido.
Signs - Hyperpigmentation (primary) and postural hypotension.
What is the gold standard test used to diagnose Addison’s?
Short synacthen test - synacthen is synthetic ACTH, with Addison’s this results in high ACTH and low cortisol/aldosterone.
-Normally, cortisol/aldosterone should be high and ACTH should decrease.
How is primary and secondary adrenal insufficiency differentiated?
Primary - ACTH increased
Secondary - ACTH decreased
What other tests can be used to diagnose Addison’s?
CXR (exclude TB), 21-hydroxylase adrenal autoantibodies.
How is Addison’s disease treated?
Replace steroids; hydrocortisone (cortisol), fludrocortisone (aldosterone).
What is a complication of Addison’s disease?
Adrenal crisis.
What is SIADH?
Syndrome of inappropriate ADH. Inappropriately large amounts of ADH released causing water to be reabsorbed in collecting duct.
What are the causes of SIADH?
SIADH:
SCLC, infection, abscesses, drugs (SSRI, sulfonylureas, thiazides), head trauma.
What are the six symptoms of SIADH?
Sx of hyponatraemia:
N+V, headache, muscle weakness/cramps, confusion, brainstem herniation.
Which condition causes dilute euvolemia?
SIADH - less Na+ (hyponatreaemia)
What is the first line test for SIADH and what does it show?
U+E - Hyponatraemia and normal K+.
-High urine Na+ and osmolality.
What type of diagnosis is SIADH?
Diagnosis of exclusion:
-Causes of hyponatraemia need to be excluded.
What four things need to excluded before SIADH is diagnosed?
Adrenal insufficiency, no D+V, no diuretic use, no AKI/CKD.
What is the DDx of SIADH and how is it tested?
Na+ depletion - when IV saline is given, serum should normalise (in Na+ depletion) but in SIADH it won’t.
What is the 1st line treatment for SIADH?
Fluid restriction and hypertonic saline to concentrate the blood. (Also treat underlying cause).
What is the treatment for chronic SIADH?
Drugs - ADH antagonist (tolvaptan).
What is hyperkalaemia?
High blood potassium level (>5.5mmol/L).
What is the emergency hyperkalaemic serum K+ level?
> 6.5mmol/L.
What are the three types of causes of hyperkalaemia?
Impaired excretion, shift to intracellular and increased intake.
What three things can cause impaired excretion and hyperkalaemia?
Renal disease, drugs (NSAIDs, spironolactone, ACE-i), Addison’s.
What are the three symptoms of hyperkalaemia?
Palpitations, muscle weakness and paralysis.
What two tests are used to diagnose hyperkalaemia and hypokalaemia?
Bloods (FBC, U+E) and ECG.
What are the features of a hyperkalaemic ECG?
Absent P waves, prolonged PR, wide QRS and tall tented T waves.
What is the urgent treatment for hyperkalaemia?
Calcium gluconate - protects myocardium.
How is non urgent hyperkalaemia treated?
Insulin and dextrose, treat underlying cause.
What is hypokalaemia?
Low blood potassium level (<3.5mmol/L).
What is the emergency serum hypokalaemic level?
<2.5mmol/L.
What are the two main types of hypokalaemia causes?
Increased excretion and decreased intake.
What five things can increase excretion of K+ in hypokalaemia?
Thiazides and diuretics, GI losses (D+V), Conn’s, AKI/CKD.
What are the three main symptoms of hypokalaemia?
Asymptomatic, maybe muscle weakness and paralysis.
What are the features of a hypokalaemic ECG?
Prolonged PR, ST depression, flat T waves, prominent U waves.
What is the main treatment for hypokalaemia?
Treat underlying cause, IV K+ replacement.
Which drugs can treat hypokalaemia?
Aldosterone antagonist - spironolactone.
What is hyperparathyroidism?
Excessive secretion of parathyroid hormone (PTH).
What are the three types of causes of hyperparathyroidism?
Primary, secondary and tertiary.
What is primary hyperparathyroidism?
Excess PTH secretion from parathyroid glands.
What are the two causes of primary hyperparathyroidism?
Parathyroid adenoma (80%) and hyperplasia (20%).
What is secondary hyperparathyroidism?
Increased secretion of PTH to combat hypocalcemia.
What are the two causes of secondary hyperparathyroidism?
CKD/low vitamin D.
What is tertiary hyperparathyroidism and how is it caused?
Autonomous secretion of PTH after many years of secondary hyperparathyroidism (CKD).
What are the four symptoms of hyperparathyroidism?
Sx of hypercalcaemia:
-Bones (bone pain), stones (kidney stones), groans (abdominal pain/constipation) and moans (depression and anxiety).
How are primary, secondary and tertiary hyperparathyroidism differentiated and what are the results?
By PTH/bone profile:
-Primary - Raised calcium.
-Secondary - Low serum calcium, high PTH.
-Tertiary - Raised calcium and PTH.
What other tests can be used to diagnosed hyperparathyroidism?
DEXA scan, USS throat, ECG.
What does hyperparathyroidism show on ECG?
Hypercalcaemia - short QT interval.
What is the treatment for primary hyperparathyroidism?
Removal of adenoma/parathyroidectomy and bisphosphonates.
What is the treatment for secondary and tertiary hyperparathyroidism?
Treat cause and correct calcium.
What is hypoparathyroidism?
Reduced PTH secretion - hypocalcaemia.
What are the two main types of causes of hypoparathyroidism?
Primary - PTH glands failure.
Secondary - After surgery (parathyroidectomy).
What can cause primary hypoparathyroidism?
Autoimmune destruction or congenital (DiGeorge syndrome - 22q11 deletion).
What are the symptoms of hypoparathyroidism?
Sx of hypocalcaemia - CATS go NUMB:
-Convulsions, arrhythmia, tetany, spasm, numbness.
What are the two signs of hypoparathyroidism?
Chvostek’s sign - Facial nerve trap induces spasm.
Trousseau’s sign - BP cuff/torniquet causes wrist flexion and fingers to pull together.
How is hypoparathyroidism diagnosed?
PTH/bone profile and ECG.
What are the PTH/bone profile results of someone with hypoparathyroidism?
Decreased PTH, decreased Ca2+, increased phosphate.
What does an ECG look like of hypoparathyroidism?
Hypocalcaemia - Long QT and ST segements.
How is hypoparathyroidism treated?
IV/supplements of calcium, vitamin D3, synthetic PTH if required.
What is hypoglycaemia?
Abnormally low blood glucose.
What can cause hypoglycaemia?
Diabetic drugs (insulin, sulfonylureas), liver failure, Addison’s.
How is hypoglycaemia treated?
IV glucose, if no IV access, then IM glucagon.
What is a pheochromocytoma?
An adrenal medullary tumour which secretes catecholamines (noradrenaline/adrenaline).
What causes pheochromocytoma?
Usually inherited.
What are the symptoms of pheochromocytoma?
Activated SNS - hypertension, pallor, sweaty, tachycardia.
How is pheochromocytoma diagnosed?
Plasma metanphrines/normetanephrines.
How is pheochromocytoma treated?
Drugs - alpha/beta blockers.
Surgery to excise tumour.
How does a high dose dexamethasone suppression test differentiate the causes of Cushing’s syndrome?
Low cortisol (suppression) = Pituitary adenoma (disease).
High cortisol, high ACTH = SCLC.
High cortisol, low ACTH = Adrenal adenoma.
What is the difference between primary and secondary hyperaldosteronism?
Primary = Adrenal glands release too much aldosterone (hyperplasia/adenoma).
Secondary = Excessive renin stimulate the release of excess aldosterone (renal artery stenosis/obstruction).
How is tertiary adrenal insufficiency caused?
Abruptly stopping being on long-term steroids that have the suppressed the hypothalamus of releasing CRH.
What are carcinoid tumours?
Malignant tumours of enterochromaffin cell which produce serotonin (5-HT).
Where are carcinoid tumours found?
GI tract, liver and lungs.
What is the difference between carcinoid tumours and syndrome?
Tumours - neoplastic cells without symptoms.
Syndrome - when tumour metastasises to liver and causes symptoms.
What are 4 symptoms and one sign of carcinoid syndrome?
Flushing, diarrhoea, RUQ pain and respiratory problems.
Sign - tricuspid incompetence.
What is the gold standard diagnostic test for carcinoid syndrome?
5HIAA in the urine.
What other two investigations are done in carcinoid syndrome?
Liver USS to confirm mets.
CT/MRI to locate the primary tumour.
How is carcinoid syndrome treated?
Surgically excise primary tumour.
Octreotide (SST analogue) which blocks serotonin.
What is a complication of carcinoid syndrome?
Carcinoid crisis.
What are the side effects of biguanides and sulphonylureas?
Biguanide (metformin) - GI upset.
Sulphonylureas (gliclazide) - hypoglycaemia and weight gain.
What electrolyte abnormalities does Addison’s disease result in?
Hyperkalaemia and hyponatraemia.
