Endocrinology Flashcards
List the hormones released by the anterior pituitary gland
Thyroid stimulating hormone
Adrenocorticotropic hormone (ACTH)
Follicle stimulating hormone (FSH) and Luteinising hormone (LH)
Growth hormone (GH)
Prolactin
List the hormones released by the posterior pituitary gland
Oxytocin
Antidiuretic hormone (ADH)
What stimulates anterior pituitary to release TSH
Thyrotropin releasing hormone (TRH)
When does cortisol peak
In the morning
When is cortisol at its lowest
Late in the evening
List the actions of cortisol on the body
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
What does growth hormone stimulate the release of?
Insulin like growth factor 1 (IGF-1) from the liver
What are the actions of growth hormone
Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs
What is parathyroid hormone released in response to
Low calcium
Low magnesium
High serum phosphate
What is the role of parathyroid hormone
Increase the serum calcium
Increases osteoclast activity - increases calcium reabsorption
Increases calcium reabsorption in kidney
Stimulates kidney to metabolise vitamin D into its active form calcitriol that promotes calcium absorption from the small intestine
What is renin
Released when there is low blood pressure
Enzyme that converts angiotensinogen into angiotensin 1
What happens to angiotensin 1
Converted into angiotensin 2 in lung by enzyme ACE
What does angiotensin 2 do?
Causes vasoconstriction
Increased BP
Aldosterone from adrenal glands
What does aldosterone do?
Mineralocorticoid steroid hormone which acts on the nephrons in the kidney to
- Increase sodium reabsorption from distal tubule - increase intravascular volume and increases BP
- Increase potassium secretion from distal tubule
- Increase hydrogen secretion from the collecting ducts
What is Cushing’s syndrome
Signs and symptoms thaqt develop after prolonged abnormal elevation of cortisol
What is Cushings disease
Pituitary adenoma secretes excessive ACTH
List some features of Cushings syndrome
- Round moon face
- Central obesity
- Abdominal striae
- Buffalo hump
- Proximal limb muscle wasting
- HTN
- Cardiac hypertrophy
- Hyperglycaemia
- Depression
- Insomnia
- Osteoporosis
- Easy bruising and poor skin healing
List some causes of Cushing’s syndrome
Exogenous steroids (prednisolone/glucocorticoids)
Cushing’s disease
Adrenal adenoma
Paraneoplastic Cushing’s - excess ACTH released from a cancer somewhere else - most common is small cell lung cancer causing ectopic ACTH
Describe the dexamethasone suppression test
Diagnose Cushing’s syndrome
Initially giving low dose test, if normal then Cushing’s excluded. If test is abnormal then high dose performed to distinguish cause
Dose of dexamethasone at night and their cortisol and ACTH is measured in the morning - find out if dexamethasone suppresses normal morning spike
Low dose - 1mg dexamethasone - dexamethasone suppresses release of cortisol is normal response. When cortisol not suppressed this is an abnormal result
High dose - 8mg, Cushings disease, pituitary shows response to negative feedback and this is enough the suppress the cortisol. Where there is adrenal adenoma the cortisol is not suppressed by ACTH is. Where there is ectopic ACTH, neither cortiosl or ACTH suppressed.
What is an alternative method of diagnosing Cushing syndrome to the dexamethasone suppression test?
24 hr urinary free cortisol
What investigations should be carried out if Cushing’s is suspected
Dexamethasone suppression test or 24hr urinary free cortisol
FBC - raised WCC
U&Es - potassium may be low if aldosterone also secreted by adrenal adenoma
MRI brain - pituitary adenoma
Chest CT - Small cell lung cancer
Abdominal CT - adrenal tumour
Describe the management of Cushing’s
Trans-sphenoidal removal of pituitary tumour
Surgical removal of adrenal tumour
Surgical removal of tumour producing ectopic ACTH
If surgical removal not possible, give replacement steroid hormones
What acid-base picture would be consistent with Cushing’s syndrome
Hypokalaemic metabolic alkalosis
What is adrenal insufficiency
Where the adrenal glands do not produce enough steroid hormones - cortisol and aldosterone
What is primary adrenal insufficiency
Addison’s disease
- Adrenal glands have been damaged resulting in reduced aldosterone and cortisol production
Autoimmune
What is secondary adrenal insufficiency
Low ACTH stimulating the adrenal gland - surgery, infection, loss of blood flow or radiotherapy or Sheehan’s (blood loss during childbirth causing pituitary necrosis)
Pituitary problem
What is tertiary adrenal insufficiency
Inadequate CRH release by hypothalamus
Long term oral steroids >3weeks causing suppression of the hypothalamus and when steroids stopped the body doesn’t start producing its own steroids
List the symptoms of adrenal insufficiency
Fatigue Nausea Cramps Abdominal pain Reduced libido
List some signs of adrenal insufficiency
Bronze hyperpigmentation to skin - ACTH stimulates melanocytes to produce more melanin
Hypotension -postural
List the investigations for adrenal insufficiecy
U&Es - hyponatraemia, hyperkalaemia
Early morning cortisol - often falsy normal
Short synacthen test - diagnose adrenla insufficiency
ACTH - primary adrenal failure, ACTH high as pituitary tryung hard to stimulate the adrenal glands without any negative feedback in the absocence of cortisol. In secodnary the ACTH is low
Adrenal autoantiboides - adrenal cortex antbides and 21-hydroxylase antibodies
CT/MRI adrenals or pituitary
Describe the short synacthen test
Adrenal insufficiency
Morning
Give synacthen (synthetic ACTH) and measure blood cortisol baseline, 30 and 60 mins. Should double in healthy individual. Failure of cortisol to rise indicates primary adrenal insufficiency
Describe the treatment of adrenal insufficiency
Hydrocortisone - glucocorticoid and used to replace cortisol
Fludricortisone - mineralococrticoid and used to replace aldosterone
Steroid card and emergeny ID tag - steroid dependent and important doses are not missed, doses are doubled during illness to match normal steroid response to illness
Describe Addisonian crisis
Severe Addisons where the abscence of steroid hormones leads to life threatening presentation
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
Patients can be very unwell
1st presentation of triggered by ilnness/ truama or sudden withdrawal of steroid
Describe the management of Addisonian crisis
Intensive monitoring
Parenteral steroid - IV hydrocortisone 100mg stat then 100mg every 6 hrs
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of fluid and electrolytes
How are the steroids given throughout the day in Addison’s
Hydrocortisone dose is split with the majority given in the first half of the days
Describe how Addison’s patients should adjust their steroids during illness
Double the glucocorticoid dose
Keep the mineralocorticoid (fludrocortisone) dose the same
Describe the thyroid results in hyperthyroidism
Low TSH and High T3 and T4
Describe the thyroid results in primary hypothyroidism
High TSH
Low T3 and T4
Describe the thyroid results in secondary hypothyroidism
Low TSH
Low T3 and 4
Give a cause of secondary hypothyroidism
Pituitary or hypothalamic cause
Which antibodies are present in Graves and Hashimotos thyroiditis
Antithyroid peroxidase (Anti-TPO) antibodies
Which antibodies are specific to Graves disease
TSH receptor antibodies
Describe some investigations for thyroid disease
Ultasound
Biopsy
Radioisotope scan - hyperthyroidism and thyroid cancer - the greater activity, the more radioisotope
Diffuse high uptake - Graves
Focal high uptake - toxic multinodular goitre and adenoma
Cold areas - cancer
Describe primary hyperthyroidism
Thyroid pathology
Describe secondary hyperthyroidism
Pituitary or hypothalamus pathology
What is thyrotoxicosis
Abnormal and excessive thyroid hormone
Describe Graves disease
Autoimmune condition
Antibodies to TSH receptor
Mimic TSH and stimulate TSH receptors on the thyroid
Describe toxic multinodular goitre (Plummers disease)
Nodules develop on the thyroid gland act indenpendently of the normal feedbkac system and continously produce excessive thyroid hormone
What is exopthakmos
Buldging of the eyeball due to graves disease
Inflammation and hypertroophy of tissue behind eyeball
What is pretibial myxoedema
Derm condition - deposits of mucin under the anterior aspect of the leg
Discoloured, waxy and oedematous appearance to the skin over this area
Specific reaction to the TSH receptor antibodies
List some causes of hyperthyroidism
Graves disease
Toxic multinodular goitre
Solitary toxic thyroid nodule
Thyroiditis
List the universal features of hyperthyroidism
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
List some unique features of Graves disease
Diffuse goitre
Graves eye disease
Bilateral exopthalmos
Pretibial myxoedema
List some unique features of toxic multinodular goitrew
Goitre with nodules
> 50 yo
Describe solitary thyroid nodule
Benign adenoma
Surgical removal
Describe De Quervains thyroiditis
Viral infection - fever, neck pain, tenderness, dysphagia and features of hyperthyroidism
There is a hyperthyroid phase followed by a hypothyroid phase as the TSH levels fall due to negative feedback
Symptomatic treatment with NSAIDs and beta blockers
Describe thyroid storm
Severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium
Supportive care and treatment of comlications such as AF
Describe management of hyperthyroidism
Carbimazole is 1st line
- Titration block
- Block and replace - block production then take levothyroxine
Propylthiouracil is 2nd line
Radioactive iodine - single drink which destroys proportion of the thyroid cells - remission takes 6 months and patient may be hypothyroid after
Beta blockers - propranolol is non selective
Surgery - post thyroidectomy patients will need to take levothyroxine replacement for life
How long does carbimazole take to produce a normal thyroid level
4-8 weeks
What is a complication of propylthiouracil
Hepatic reaction
What are some rules of radioactive iodine
Must not be pregnant and not allowed to get pregnant within 6 months
Avoid close contact with pregnant women and children for 3 weeks
Limit contact for several days
Describe hashimotos thyroiditis
Autoimmune inflammation of the thyroid gland associated with Antithyroid peroxidase anti-TPO antibodies and antithyroglobulin antibodies
List some causes of hypothyroidism
Hashimotos thyroiditis
Iodine deficiency
Secondary to hyperthyroid treatment
Lithium - inhibits thyroid hormone production
Amiodarone - interferes with thyroid hormone production and metabolism
Central causes (hypopituarism) - less TSH - tumour, infection, vascular (Sheehan syndrome), radiation
Describe the presenation of hypothyroidism
Weight gain Fatigue Dry skin Coarse hair and hair loss Fluid retnetion -oedema, pleural effusion, ascites Heavy or irregular periods
Describe the investigations for hypothyroidism
TFTs
Describe the TFT result of primary hypothyroidism
Low T3 and T4, High TSH
Describe the TFT result of secondary hypothyroidism
Low T3 and T4
Low TSH
Describe the management of hypothyroidism
Oral levothyroxine
Titrate until TSH levels are normal
Describe Type 1 diabetes
Pancreas stops producing insulin
Which viruses may be implicated in T1DM
Coxsackie B and enterovirus
What is the ideal blood glucose range
4.4-6.1
How does insulin reduce blood sugar level
Cells absorb glucose from blood
Muscles and liver absorb glucose from blood and store it as glycogen
Describe the action of glucagon
Catabolic hormone which breaks down glycogen into glucose - glycogenolysis
Tells liver to convert protein and fat into glucose - gluconeogenesis
Describe ketogeneies
When insufficient glucose supply
Fatty acids converted to ketones
Cross blood brain barrier
Describe the pathophysiology of diabetic ketoacidosis
Not producing insulin themselves and not injecting adequate insulin to compensate
Ketoacidosis - glucose can not enter the cells so body thinks it is staving, higher glucose, higher ketones.
Kidneys produce bicarbonate to counteract the ketones however eventually can not compensate and person becomes acidotic
Dehydration - hyperglycaemia - osmotic diuresis - polyuria and dehydration, stimulates thirst centre in the brain resulting in polydipsia
Insulin usually drives potassium into cells however without it the serum potassium can be normal or high and potassium is excreted in the urine however total body potassium is low as none in the cells - hypokalaemia - arrythmia
Describe how people in DKA present
Hyperglycaemia
Dehydration - poluruia and polydipsia, dehydration and hypotension
Ketosis - Acetone smell to breath
Metabolic acidosis
Potassium imbalance
Altered consciousness
Symptoms of underlying trigger
Nausea and vomiting
Describe management of DKA
Fluid resuscitation
Insulin infusion
Dextrose and potassium eventually
Look for infection
Chart fluid balance
Ketones- monitor
Establish the patient on their normal SC insulin prior to stopping insulin and fluid infusion
How is DKA diagnosed
Check with local guidelines
Hyperglycaemia (glucose >11)
Ketosis (ketones >3)
Acidosis (pH <7.3)
How fast can potassium be infused at
<10mmol/L/hr
Describe the long term management of type 1 diabetes
SC insulin regimes
Monitor carb intake
Monitor blood sugar levels on waking, each meal and before bed
Monitor and manage complications
What can injecting insulin at the same spot cause
lipodystrophy - sc fat hardens and insulin not absorbed properly
What are some short term complications of T1DM
Hypoglycaemia
Hyperglycaemia
DKA
What are some long term complications of T1DM
Coronary artery disease Peripheral ischaemia - ulcers, diabetic foot Stroke HTN Peripheral neuropathy Retinopathy Glomerulosclerosis UTI, pneumonia, candida
What monitoring is done in T1DM
HbA1c - glycated Hb - how much glucose attached to the Hb - average glucose level over past 3 months. Measured every 3-6months to see their long term control
Capillary blood glucose
Flash glucose monitoring - sensor on skin measuring glucose level of interstitial fluid, lag time of 5mins
Describe the pathophysiology of T2DM
Repeated exposure to glucose and insulin makes the cells more resistant to the effects of insulin - more and more insulin to produce a response from the cells and get them to take up and use glucose
Overtime the pancreas becomes fatigues and damaged so produce less insulin
Chronic hyperglycaemia and micro/macrovascular complications
List some risk factors of T2DM
Old age
Ethnicity - black, chinese, south asian
FH
Modifiable - obesity, sedentary lifestyle, high carbohydrates
Describe the presentation of T2DM
Fatigue Polyuria and polydipsia Unintentional weight loss Opportunistic infection Slow healing Glucose in urine
Describe the oral glucose tolerance test
Performed in morning prior to breakfast - fasting plasma glucose result, give 75g glucose drink then measure plasma glucose 2hrs later
What is pre-diabetes
Indication the patient is heading towards diabetes
HbA1c 42-47 mmol/mol
Impaired fasting glucose (6.1-6.9)
Impaired glucose tolerance 7.8-11.1 on an OHGTT
Describe T2DM diagnostic criteria
HbA1C >48
Random glucose >11
Fasting glucose >7
OGTT 2hr result >11
Describe the management of T2DM
Dietary modification - veg and oily fish, low glycaemic index food, high fibre, low carbohydrate
Exercise and weight loss
Stop smoking
Optimise treatment for other illness
Monitor for complications - diabetic retinopathy, kidney disease, diabetic foot
Describe the medical management of T2DM
Metformin - 1st line
2nd line - add sulphonyurea, pioglitazone, DPP-4i or SGLT2i
3rd line - triple therapy with metformin and 2 second line drugs combined or metformin plus insulin
List some notable side effects of metformin
Diarrhoea and abdominal pain
Lactic acidosis
How does metformin work
Increases sensitivity to insulin and decreases liver production of glucose
How does pioglitazone work
Increases insulin sensitivity and decreases liver production of glucose
List some notable side effects of pioglitazone
Weight gain Fluid retention Anaemia Heart failure Extended use may increase risk of bladder cancer
How does sulfonylurea work
Stimulate insulin release from pancreas
List some notable side effects of sulfonylureas
Weight gain
Hypoglycaemia
Increased risk of CVD and MI as a monotherapy
List some rapid acting insulins
Novorapid
Humalog
Apidra
List some short acting insulins
Actrapid
Humulin S
Insuman rapid
List the intermediate acting insulins
Insulatard
Humalin I
Insuman basal
List some long acting insulins
Lantus
Levemir
Degludec
What are incretins
Hormones normally secreted by GI tract after eating a large meal
Increase insulin secretion
Inhibit glucagon production
Slow absorption by GI tract
What are some symptoms of Sitagliptin (DPP-4 inhibitors)
GI tract upset
Symptoms of URTI
Pancreatitis
What is acromegaly
Excessive growth hormone
What causes acromegaly
Pituitary adenoma
Secondary to other cancer - ectopic growth hormone releasing hormone or growth hormone
What visual disturbance is associated with pituitary tumours
Bitemporal hemianopia - loss of the outer half of vision of both eyes
Describe the presentation of acromegaly
Headaches Visual field defect Prominent forehead and brow Large nose, tongue, hands and feet, protruding jaw Arthritis from imbalanced growth of joints Hypertrophic heart Hypertension T2DM Colorectal cancer Development of new skin tags Profuse sweating
List the investigations for acromegaly
Insulin like growth factor 1 (IGF-1) - initial screening test (raised)
Oral glucose tolerance test whilst measuring growth hormone (high glucose normally suppresses growth hormone)
MRI brain for the pituitary tumour
Refer to ophthalmology for formal visual field testing
Describe the treatment of acromegaly
Trans-spehnoidal removal of pituitary tumour
If ectopic hormones from pancreatic or lung cancer - surgical removal of these cancers
Medication
- Pegvisomant (GH antagonist given SC and daily)
- Somatostatin analogues (block GH release) - ocreotide
- Dopamine agonists - block GH release (bromocriptine)
- Somatostatin - growth hormone inhibiting hormone - normally secreted in the brain, GI tract, pancreas - blocks GGH release from pituitary
- Dopamine also has inhibitory effect on GH release
How does parathyroid hormone raise blood calcium
Increase osteoclast activity in bone (reabsorbing Ca from bones)
Increasing calcium absorption from the gut
Increasing calcium absorption from the kidney
Increasing vitamin D activity - increase calcium absorption from intestines
What are the symptoms of hypercalcaemia
Renal stones
Painful bones
Abdominal groans - constipation, nausea, vomiting
Psychiatric moans - fatigue, depression and psychosis
What is primary hyperparathyroidism caused by
Uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands
What does primary hyperparathyroidism lead to
hypercalcaemia - abnormally high level of calcium in the blood
How is primary hyperparathyroidism treated
Surgically removing the tumour
What is secondary hyperparathyroidism
Where insufficient vitamin D or chronic renal failure leads to low absoprtion of calcium from intestine, kidneys and bones and causes hypocalcaemia, the parathyroid glands react to the low serum calcium by excreting more parathyroid hormone. Hyperplasia occurs in the parathyroid glands. The serum calcium begins to become low or normal but parathyroid hormone will be high
How is secondary hyperparathyroidism treated
Vitamin D
Renal transplant
What is tertiary hyperparathyroidism
When secondary hyperparathyroidism occurs for a long time. Hyperplasia of the glands. The baseline parathyroid hormone increases dramatically. High absorption of calcium and causes hypercalcaemia
How is tertiary hyperparathyroidism treated
Surgically remove some of the parathyroid tissue
Describe the renin, angiotensin aldosterone system
Juxtaglomerular cells in afferent arteriole in the kidney sense blood pressure in these vessels. When they sense a low blood pressure in the arteriole they secrete a hormone called renin. This liver secretes a protein called angiotensinogen which is converted to angiotensin 1 by renin. Angiotensin 1 becomes angiotensin 2 when converted by ACE in the lungs. Angiotensin 2 causes release of aldosterone in adrenal glands
What does aldosterone do to the kidney
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting duct
What is primary hyperaldosteronism
Conn’s syndrome
Too much aldosterone produced from the adrenal glands
Serum renin will be low as it is suppressed by the high blood pressure
Adrenal adenoma - secreting aldosterone
Bilateral adrenal hyperplasia
Familial hyperaldosteronism type 1 and 2
Adrenal carcinoma
Describe secondary hyperaldosteronism
Excessive renin stimulating adrenal glands to produce more aldosterone - serum renin will be high
Several causes of high renin levels and they occur when the blood pressure in the kidneys is disproportionately lower than the blood pressure in the rest of the body
List some causes of secondary hyperaldosteronism
- renal artery stenosis
- Renal artery obstruction
- Heart failure
Describe renal artery stenosis
Narrowing of the artery suppling the kidney
Usually found in patients with atherosclerosis as an atherosclerotic plaque causes narrowing of this vessel similar to the narrowing of the coronary arteries found in angina. Confirm with Doppler US, CT angiogram or magnetic resonance angiography
List the investigations for hyperaldosteronism
Renin/aldosterone ratio
BP
Serum electrolytes (hypokalaemia)
Blood gas analysis (alkalosis)
CT/MRI
Renal doppler US, CT angiogram or MRA for renal artery stenosis or obstruction
Describe the management of hyperaldosteronism
Eplerenone
Spironolactone
Remove the adenoma
Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis
What does a high aldosterone and low renin indicate
Primary hyperaldosteronism
What does a high aldosterone and high renin indicate
Secondary hyperaldosteronism
What does ADH normally do
Stimulate water reabsorption in the collecting duct
What electrolyte imbalance occurs in SIADH
Hyponatraemia
What happens to the fluid balance in SIADH
Euvolaemic
What happens to the urine in SIADH
High urine osmolarity
High urine sodium
More concentrated
List the symptoms of SIADh
Headache Fatigue Muscle aches and cramps Confusion Severe - seizure and reduced GCS
List some causes of SIADh
Post op
Infection - atypical pneumonia and lung abscess
Head injury
Medication - thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs
Malignancy
Meningitis
How do you diagnose SIADH
Dianosis of exclusion
Euvolaemic hyponatraemia
Exclude excessive water intake
No history of diuretic use
Negative synacthen test to exclude adrenal insufficiecny
No diarrhoea, vomiting, burns, fistula or excessive sweating
No CKD or AKI
How do you establish the cause of SIADH
Medications
CXR - pneumonia or lung cancer
Malignancy - CT CAP and MRI brain
How is SIADH managed
Treat the cause
Fluid restriction - concentrates blood and increases sodium concentration
Tolvaptans - ADH receptor blockers and cause rapid rise in sodium
Demeclocycline - rarely used now - ADH inhibitotion
Why is sodium corrected slowkly
Prevent central pontine myelinosis
How fast should sodium be corrected in hyponatraemia
<10mmol/L per 24hrs
What is central pontine myelinolysis
Osmotic demylination
Comliation of severe hyponatraemia being treated too quickly
Brain cells swell
1st phase - encephalopathic and confused and headache or nausea and vomiting
Second phase - spastic quadriparesis, pseudobulbar palsy, cognitive behavioural changes, risk of death
What is diabetes inspidus
Lack of ADH
What are the two types of DI
Nephrogenic
Cranial
What is an important differential for DI
Primary polydipsia
Describe nephrogenic diabetes insipidus
Collecting ducts not responding to ADH
What can casue nephrogenic DI
Drugs - lithium
Mutations in AVPR2 gene on X chromosome coding for ADH receptor
Intrinsic kidney disease
Electrolyte disturbance - hypokalaemia and hypercalcaemia
Describe cranial diabetes insipidus
Hypothalamus does not produce ADH for the pituitary gland to secrete
What can cause cranial DI
Brain tumour Head injury Brain malformation Brain infection Brain surgery or radiotherapy
Describe the presentation of diabetes insipidus
Polyuria Polydipsia Dehydration Postural hypotension Hypernatremia
How is diabetes insipidus investigated
Low urine osmolarity - low concentration of solute in urine
High serum osmolarity
Water deprivation test
Describe the water deprivation test/desmopressin stimulation test
Avoid fluid for 8hrs before
Measure urine osmolarity and synthetic ADH (desmopressin) is given
8 hrs later urine osmolarity measured again
Cranial DI - urine osmolarity will be high as kidney able to respond to the fake ADH
Nephrogenic DI - urine osmolarity will be low initially and remain low
Primary polydipsia - high urine osmolarity before and after desmopressin
Describe the management of diabetes insipidus
Cranial - replace ADH - desmopressin
Nephrogenic diabetes insipidus - higher doses desmopressin under close monitoring
Where is adrenaline produced
Adrenal medulla chromaffin cells
What is a pheochromocytoma
Tumour of chromaffin cells secreting lots of adrenaline
What are the signs and symptoms of pheochromocytoma
Bursts of adrenaline - more settled periods
Which genetic condition is associated with pheochromocytoma
MEN2
Describe the 10% rule in pheochromocytoma
10% cancerous
10% bilateral
10% outside adrenal gland
How is phaeochromocytoma diagnosed
24hr urine catecholamines
Plasma free metanepherines longer half life than adrenaline which varies in the response due to the bursts of adrenaline
Describe the presentation of phaeochromocytoma
Anxiety Sweating Headache HTN Palpitations, tachycardia, paroxysmal AF
Describe the management of phaeochromocytoma
Alpha blockers
Beta blockers once established on alpha blockers
Adrenalectomy - control symptoms before surgery
