Endocrinology Flashcards
Define hypothyroidism
Inadequate production of thyroid hormones by the thyroid gland
What is the most common cause of hypothyroidism in the developed world?
Hashimoto’s thyroiditis
What is Hashimoto’s thyroiditis?
Cased by autoimmune inflammation of the thyroid gland.
Associated with anti-TPO and anti thyroglobulin antibodies
Initially it causes a goitre after which there is atrophy of the thyroid gland
What is the most common cause of hypothyroidism in the developing world?
Iodine deficiency
What are the causes of hypothyroidism?
Hashimoto's thyroiditis Iodine deficiency Primary atrophic hypothyroidism Post-thyroidectomy (thyroid surgery) Subacute thyroiditis Drug induced -> Antithyroid drugs (carbimazole), amiodarone, radio-iodine, lithium
What is secondary hypothyroidism?
When the pituitary gland fails to produce enough TSH.
Known as hypopituitism
Symptoms of hypothyroidism
Tired Sleepy/lethargic Intolerant to cold Weight gain/decreased appetite Constipation Menorrhagia Reduced memory/cognition/concentration Hoarse voice Depression
Signs of hypothyroidism
BRADYCARDIC
Bradycardia Reflexes relax slowly Ataxia (cerebellar) Dry thin skin/hair Yawning/drowsy/coma Cold hands Ascites Round puffy face/double chin/obese (myxoedema) Defeated demeanour Immobile +/- ileus CHF
Associations of hypothyroidism
Type 1 diabetes mellitus Addison's disease Pernicious anaemia CF Turner's and Down syndrome Primary biliary cirrhosis
Investigations for hypothyroidism
Thyroid function tests (TFT’s):
Primary hypothyroidism = High TSH, Low T3/T4
Secondary hypothyroidism = Low TSH, Low T3/T4
Thyroid antibodies = anti-TPO and anti-Tg
Treatment for hypothyroidism
Oral levothyroxine (T4)
What is sick euthyroid?
Low TSH, T3 and T4 in any systemic illness
What is hyperthyroidism?
Over production of the thyroid hormones by the thyroid gland
What is thyrotoxicosis?
Abnormal and excessive quantity of thyroid hormone in the body
What is primary hyperthyroidism?
Due to thyroid pathology
The thyroid itself is behaving abnormally and producing excessive thyroid hormone
What is secondary hyperthyroidism?
Overstimulation of TSH.
Pathology is in the hypothalamus or pituitary
What is the most common cause of hyperthyroidism?
Grave’s disease
What are the causes of hyperthyroidism?
Grave’s disease
Toxic multinodular goitre
Toxic adenoma
De Quercain’s thyroiditis
Drugs (amiodarone and lithium - more common for hypothyroidism)
Ectopic thyroid tissue
Exogenous - iodine excess, levothyroxine excess
How does Grave’s disease present
Most common, in 75% of cases
Autoimmune condition
Abnormal TSH receptor anti bodies
Signs: Exopthalmos - protruding eyes bilaterally, Pretibial myxoedema, Grave’s eye disease - diplopia, photophobia, grittiness. Diffuse goitre (without nodules)
Describe toxic multinodular goitre
Nodules develop on thyroid gland and continuously produce excessive thyroid hormone
Seen in elderly and iodine excess
2nd most common cause
Goitre with firm nodules
Describe toxic adenoma
Single abnormal thyroid nodule releasing thyroid hormone (T3 & T4)
Treated with surgical removal of nodule
Describe De Quervain’s thyroiditis
Viral infection
Fever, neck pain, tenderness, dysphagia
Hyperthyroid phase then hypothyroid (due to negative feedback)
Raised ESR
Self-limiting - treat with NSAIDs (aspirin) and beta blockers
Risk factors for hyperthyroidism
High iodine intake
Smoking
Symptoms of hyperthyroidism
Diarrhoea Weight loss/increased appetite Sweating Heat intolerance Tremor Irritable Oligomenorrhoea Anxiety
Signs of hyperthyroidism
Fine tremor Tachycardia Thin hair Lid lag + lid retraction Goitre Palmar erythema Pretibial myxoedema
Investigations in hyperthyroidism
TFT’s: TSH Low, T3/T4 High
Anti-TSHR and anti-thyroglobulin elevated in Grave’s
ESR raised
Visual acuity
Treatment for hyperthyroidism
Carbimazole - 1st line Propylthiouracil - 2nd line Beta blockers - propanolol Radioactive iodine Thyroidectomy
What is a thyrotoxic crisis
Severe hyperthyroidism
Occurs in Grave’s or toxic multinodular goitre
Signs of a thyrotoxic crisis
Pyrexia Tachycardia Confusion Delirium AF Diarrhoea Vomiting Abdominal pain Heart failure
Precipitants to a thyrotoxic crisis
Infection
Recent thyroid surgery
Radioiodine
Treatment for a thyrotoxic crisis
Oxygen + fluid
Beta blockers - propanolol
Digoxin - slow the heart
Antithyroid drugs - carbimazole, Lugol’s solution - aqueous iodine
Define myxoedema coma
The ultimate hypothyroid state before death
May have had radioiodine, thyroidectomy or pituitary surgery
Symptoms and signs of a myxoedema coma
Symptoms: Hypothermia, hyporeflexia, bradycardia, coma, seizures
Signs: Goitre, cyanosis, low BP, heart failure
Treatment for a myxoedema coma
ICU Give T3 slowly High flow oxygen if cyanosed Hydrocortisone if pituitary hypothyroidism suspected Antiobiotics (cefuroxime) if infection
Differential diagnosis of diffuse goitre
Grave’s
Hashimoto’s
Differential diagnosis of nodular goitre
Multinodular goitre
Adenoma
Carcinoma
Differential diagnosis of painful goitre
De Quervain’s
Define hypercalcaemia
High levels of calcium in the blood
Causes of hypercalcaemia
Primary hyperparathyroidism (if high PTH) Malignancy (if low PTH)(from bone metastases, myeloma, PTHrP -> from squamous cell lung cancer)
TB Sarcoidosis Vitamin D intoxication Thyrotoxicosis Mikk-alkali syndrome Familial hypocalciuric hypercalcaemia Lithium Thiazides Acromegaly Dehydration Zolinger-Ellison syndrome
Symptoms of hypercalcaemia
Groans, stones, moans
Abdominal pain Vomiting Constipation Anorexia Polyuria Polydipsia Dehydration Renal stones Depression Dementia Confusion Muscle weakness Fatigue
What are the ranges for normal, mild, moderate and severe hypercalcaemia?
Normal = 2.25 - 2.5 mmol/L Mild = < 2.8 mmol/L - Polyuria, polydipsia, depression, mild cognition Moderate = < 3.5 mmol/L - Muscle weakness, fatigue, constipation, anorexia Severe = > 3.5 mmol/L - Abdominal pain, vomiting, dehydration, short QT, coma
Investigations for hypercalcaemia
Hyperparathyroidism = High PTH
Malignancy = Low albumin, low chloride, alkalosis, high phosphate, high alkaline phosphate
Treatment for hyerpcalcaemia
Correct dehydration - IV 0.9% Saline
Bisphosphonates - Pamidronate or zoledronic acid
Calcitonin - acts similar to bisphosphonates
Steroids (e.g. prednisolone) in sarcoidosis
Causes of hypocalcaemia
High PTH: Chronic kidney disease Vitamin D deficiency Hypoparathyroidism (post thyroid surgery) Pseudohypoparathyroidism Rhabdomyolysis Hypomagnesaemia
Low PTH: Acute pancreatitis
Over hydration
Osteomalacia
Respiratory alkalosis
Symptoms of hypocalcaemia
SPASMODIC
Spasms (carpopedal spasm) = Trousseau's sign Perioral paraesthesia Anxious, irritable, irrational Seizures Muscle tone increased in smooth muscle Orientation impaired and confusion Dermatitis (e.g. atopic) Impetigo herpetiformis Cataracts Cardiomyopathy (long QT on ECG) Choreoathetosis Chvostek's sign - tapping facial nerve causes face spasms
Investigations for hypocalcaemia
Calcium
PTH
Treatment for hypocalcaemia
Mild = oral calcium
Alfacalcidol (in CKD or still mild after calcium)
Acute onset = IV calcium gluconate when severe/medical emergency
Define hyperkalaemia
High serum potassium
It is an emergency and can lead to ventricular fibrillation and cardiac arrest
Causes of hyperkalaemia
Acute kidney injury Chronic kidney disease Rhabdomyolysis Adrenal insufficiency Tumour lysis syndrome Medications: ACE inhibitors, NSAIDs, ARB's, Spirolactone, cyclosporin, heparin Burns/excretion Haemolysis Type 4 renal tubular acidosis
What are the ranges for mild, moderate and severe hyperkalaemia?
Mild = 5.5 - 5.9 mmol/L Moderate = 6.0 - 6.4 mmol/L Severe = > 6.5 mmol/L
Symptoms of hyperkalaemia
Palpitations
Chest pain
Weakness
Fast irregular pulse
Investigations for hyperkalaemia
ECG= Tall tented T waves,
Loss of P waves
Wide QRS complex
Ventricular fibrillation
U&E’s
What are the ECG findings in hyperkalaemia?
Tall tented T waves (occurs first)
Loss of P waves
Wide QRS complex
Ventricular fibrillation
Management of hyperkalaemia
Insulin and dextrose
Calcium gluconate
Oral calcium resonium - removes K via stools
Causes of hypokalaemia
Diuretics Vomiting + diarrhoea Pyloric stenosis Conn's syndrome Cushing's syndrome Renal tubular acidosis
Give the ranges for mild, moderate and severe hypokalaemia
Mild = 3.1 - 3.5 mmol/L Moderate = 2.5 - 3.0 mmol/L Severe = < 2.5 mmol/L
Symptoms of hypokalaemia
Mild = asymptomatic Moderate = Muscle weakness, muscle pain, constipation Severe = Hypotonia, paralysis and weakness, ileus
Investigations for hypokalaemia
ECG: Long PR interval, ST depression, small or inverted T waves, prominent U waves, Long QT
U&E’s
Serum magnesium
ECG findings in hypokalaemia
Long PR interval ST depression Small or inverted T waves Prominent U waves Long QT
Management for hypokalaemia
Mild = Potassium supplementation - Sando-K Severe = IV potassium
Define hypernatraemia
Usually due to water loss in excess of sodium loss
Water deficit
Causes of hypernatraemia
Diarrhoea Burns Vomiting Diabetes insipidus Incorrect IV fluid replacement
Symptoms of hypernatraemia
Nausea and vomiting Confusion Polydipsia Polyuria Dehydration Convulsions
Investigations for hypernatraemia
High sodium
High urea
High albumin
Management for hypernatraemia
Water orally
IV glucose
Define hyponatraemia
May be caused by water excess or sodium depletion
High water in blood -> water moves into brain and causes cerebral oedema
Causes of hyponatraemia
Urinary sodium >20mmol/L: Hypovolaemic - Diuretics, renal failure, Addison’s disease
Euvolaemic - SIADH, Hypothyroidism, Desmopressin, ACE-i, oxytocin, Antidepressants, omeprazole
<20mmol/L: Hypovolaemic - Vomiting, diarrhoea, burns
Hypervolaemic - Heart failure, liver failure/cirrhosis, nephrotic syndrome/renal failure
Symptoms of hyponatraemia
Mild: Anorexia Nausea and vomiting Malaise Headache Irritability Weakness/muscle cramps
Severe: Confusion
Seizures/coma
Reduced GCS
Increased risk of falls in the elderly
What are the ranges for mild, moderate and severe hyponatraemia
Mild = 130 - 134 mmol/L Moderate = 120 - 129 mmol/L Severe = < 120 mmol/L
Define acute hyponatraemia
Develops within 48 hours
Usually from excessive fluid intake
Define chronic hyponatraemia
Occurs after 48 hours
Symptoms are usually less severe than acute
Management of hyponatraemia
Mild = Fluid restriction, Diuretics
Moderate = Hypertonic 3% saline in first 3-4 hours
Severe = Bolus of hypertonic saline, Vasopresser receptor antagonists e.g. Conivaptan
What is a complication of hyponatraemia?
Central pontine myelinosis/Osmotic demyelination syndrome/locked-in syndrome
Define Central pontine myelinosis
Overcorrection of severe hyponatraemia (>8mmol/L per day)
Occurs after 48-72 hours
Symptoms: Dysarthria - mutism, dysphagia, paraparesis, seizures, confusion, neurological deficit
Define Cushing’s syndrome
Refers to the signs and symptoms that develop after prolonged abnormal elevation of cortisol -> prolonged exposure to glucocorticoids
What is the different between Cushing’s syndrome and Cushing’s disease?
Cushing’s disease is where a pituitary adenoma (tumour) secretes excessive ATCH -> can cause Cushing’s syndrome
Causes of Cushing’s syndrome
ACTH dependent (Increased ACTH):
Cushing’s disease - 80% - pituitary adenoma
Ectopic ACTH production (due to small cell lung cancer) - 20%
ACTH independent (Low ACTH due to negative feedback):
Adrenal adenoma
Adrenal nodular hyperplasia
Exogenous steroids
Symptoms of Cushing’s syndrome
Central obesity Round moon face Buffalo neck Proximal limb wasting Hypertension Abdominal striae Type 2 diabetes mellitus Depression Lethargy Psychosis Insomnia Bruises Osteoporosis - curved spine Infection prone Amenorrhoea/ED
Investigations for Cushing’s syndrome
Overnight dexamethasone suppression test - 1st line:
1mg dexamethasone overnight, do serum cortisol at 8am. Dexamethasone acts by suppressing the release of cortisol by negative feedback on the hypothalamus and pituitary. This causes ACTH output to be reduced. No suppression in Cushing’s syndrome
48 hour dexamethasone suppression test - 2nd line:
Performed after abnormal first test. Measure cortisol at 0 and 48 hours.
In Cushing’s disease both cortisol and ACTH are suppressed.
In adrenal adenoma, ACTH is suppressed, cortisol isn’t/
In ectopic ACTH, both ACTH and cortisol are not suppressed
24 hour urinary free cortisol FBC - raised WCC Chest CT - small cell lung cancer Abdominal CT - adrenal tumour MRI brain - pituitary adenoma
Treatment for Cushing’s syndrome
Cushing’s disease = trans-sphenoidal removal of pituitary adenoma
Adrenal adenoma = removal of adrenal tumour
Ectopic ACTH = removal of tumour
Define Addison’s disease
Destruction of adrenal cortex and subsequent reduction in output of adrenal hormones: glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
What is primary adrenal insufficiency? (Addison’s disease)
Inability of adrenal glands to produce steroid
High ACTH as no negative feedback
Causes of primary adrenal insufficiency
Autoimmune
TB
Congenital adrenal hyperplasia
Adrenal metastases
Define secondary adrenal insufficiency
Inadequate ACTH stimulating adrenal glands resulting in low cortisol release
Causes of secondary adrenal insufficiency
Exogenous steroids (long term steroids) -> these should be tapered off slowly Damage to pituitary gland - surgery to remove tumour/infection
Define tertiary adrenal insufficiency
Inadequate CRH release by hypothalamus
Symptoms of Addison’s disease
Muscle cramps Fatigue and weakness Anorexia Nausea and vomiting Abdominal pain Weight loss Faints Depression
Signs of Addison’s disease
Postural hypotension
Pigmented palmar creases (and abdomen) and buccal mucosa (ACTH stimulates melanocytes to produce melanin)
Dry mucous membranes
Investigations for Addison’s disease
Low sodium (hyponatraemia) - due to lower mineralocorticoid
High potassium (hyperkalaemia) - due to lower mineralocorticoid
Low cortisol
Low glucose
Short ACTH stimulation test (Synacthen):
Take cortisol level. Give 250 mg Synacthen IM, after 30 mins retake cortisol. If cortisol rises >550mmol/L -> exclude Addison’s.
ACTH high in primary
ACTH low in secondary
21-hydroxylase adrenal autoantibodies in >80%
CT/MRI adrenals - tumour
Renin and aldosterone
High urea
Treatment for Addison’s
Replace steroids - Hydrocortisone (replaces cortisol)
Fludrocortisone (mineralocorticoid) - replaces aldosterone
Give steroid card
Double steroids in acute/febrile illness
What is an Addisonian crisis
Acute presentation of severe Addison’s. Absence of steroid hormones (glucocorticoids and mineralocorticoids) leads to life threatening presentation.
Biggest risk factor is withdrawal of long-term steroids
Other triggers: Infection, trauma, surgery
Symptoms of Addisonian crisis
Reduced consciousness Hypotension Hyponatraemia Hyperkalaemia Hypoglycaemia Shock
Management of an Addisonian crisis
IV hydrocortisone
IV fluid bolus - rehydration
Glucose IV if hypoglycaemic
Define Conn’s syndrome
Primary hyperaldosteronism
Excess production of aldosterone (mineralcorticoid) from adrenal glands.
Aldosterone acts on kidney to increase sodium reabsorption and increase potassium secretion.
Causes of Conn’s syndrome
Adrenal adenoma (secreting aldosterone) - most common 80%
Bilateral adrenal hyperplasia 20%
Adrenal carcinoma
Familial hyperaldosteronism
What is secondary hyperaldosteronism
Where excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.
Occurs in: Renal artery stenosis, heart failure, renal artery obstruction, Bartter’s syndrome
Symptoms of Conn’s syndrome
Oedema
Hypertension
Hypokalaemic symptoms -> weakness, cramps, paraesthesia, polyuria, polydipsia
Metabolic alkalosis
Investigations for Conn’s syndrome
Renin/aldosterone ratio
High aldosterone + low renin = primary hyperaldosteronism
High aldosterone + high renin = secondary hyperaldosteronism
U&E’s - hypernatraemia & hypokalaemia
CT/MRI adrenals - for adrenal adenoma
BP - high
Blood gas analysis (alkalosis)
Treatment for Conn’s syndrome
Laparoscopic adrenalectomy
Spironlactone (4 weeks) = controls BP and K
BAH = Spironolactone - blocks aldosterone
Aldosterone antagonists e.g. Eplerenone
Define Acromegaly
Excessive growth hormone secretion
Causes of acromegaly
Pituitary adenoma
Cancer - lung or pancreatic
Signs and symptoms of acromegaly
Headaches Bitemporal hemianopia - pituitary tumour presses on optic chiasm Spadelike hands Growth of jaw and feet Fontal bossing (prominent forehead and brow) Large nose Large tongue (macroglossia) Widely spaced teeth Increased sweating Snoring Arthralgia Osteoarthritis Dark, thick oily skin Bilateral carpal tunnel Hypertension Type 2 diabetes mellitus Amenorrhoea Loss of libido
Investigations for acromegaly
Raised serum IGF-1
Oral glucose tolerance test to confirm a raised IGF
MRI brain - pituitary tumour
Visual fields and acuity
Treatment for acromegaly
First line = Trans-sphenoidal surgery
Second line = Somatostatin analogues e.g. Octreotide/lanreotide
GH antagonist e.g. Pegvisomant
Dopamine agonists e.g. bromocriptine
What is phaeochromocytoma?
Excessive production of adrenaline
Where are the chromaffin cells located?
Adrenal glands - adrenal medulla
What is phaeochromocytoma a tumour of?
Chromaffin cells
What is the 10% rule in phaeochromocytoma?
10% are malignant
10% are extra adrenal (outside the adrenal gland)
10% are bilateral
Symptoms of phaeochromocytoma
Headache
Sweating
Tachycardia
Anxiety
Palpitations
Tremor
Hypertension
Investigations for phaeochromocytoma
24 hour urine catecholamines
Plasma free metanephrines
Abdominal CT/MRI - for extra adrenal tumours
Treatment for phaeochromocytoma
Adrenalectomy to remove tumour is definitive management
Pre-surgery alpha blocker (phenoxbenzamine) then beta blocker (propanolol)
What is a phaeochromocytoma emergency?
Hypertensive crisis
What causes a phaeochromocytoma emergency?
Anesthesia Contrast imaging Childbirth Stress Opiates
Symptoms of a phaeochromocytoma emergency
Pallor Pulsating headache Hypertension Feels 'about to die' Pyrexial
Treatment for a phaeochromocytoma emergency
ICU
IV alpha blocker e.g. phentolamine
Then phenoxybenzamine when BP controlled
What is carcinoid syndrome?
Tumours of enterchromaffin cells
What are the common locations for carcinoid syndrome?
Appendix 45%
Ileum 30%
Rectum 20%
Symptoms of carcinoid syndrome
Triad: Flushing
Diarrhoea
Cardiac failure
Wheeze
Palpitations
Abdominal pain
Investigations for carcinoid syndrome
24 hour urine 5H1AA
Chest x-ray/chest/pelvis MRI/CT
Plasma chromogranin A
Treatment for carcinoid syndrome
Octreotide (somatostatin analogue) -> to prevent carcinoid crisis
Surgical resection - tumours are intense yellow
What causes primary hyperparathyroidism?
Tumour of the parathyroid glands
Symptoms of primary hyperparathyroidism
Leads to hypercalcaemia: Abdominal pain Vomiting Constipation Dehydration Depressed Renal stones Fatigue Weakness Muscle pain Osteoporosis
Investigations for primary hyperparathyroidism
Increased PTH
Increased Ca
Decreased Phosphate
Treatment for primary hyperparathyroidism
Mild = increase fluid intake, avoid thiazides
Excision of the adenoma
Bisphosphonates - alendronate
Cinacalcet
What is secondary hyperparathyroidism?
Insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones
Parathyroid gland reacts to low serum calcium by excreting more PTH -> number of cells in parathyroid gland increase = hyperplasia
Causes hypocalcaemia
Investigations for secondary hyperparathyroidism
Increased PTH
Low Calcium
Increased Phosphate
Low vitamin D
Treatment for secondary hyperparathyroidism
Correct vitamin D deficiency
What is tertiary hyperparathyroidism?
Occurs after prolonged secondary hyperparathyroidism.
Leads to hyperplasia of the glands
High level of PTH causes high absorption of Calcum
Investigations for tertiary hyperparathyroidism
Increased PTH
Increased calcium
Increased phosphate
Treatment for tertiary hyperparathyroidism
Surgical removal of part of the parathyroid tissue
Define primary hypoparathyroidism
Low PTH secretion due to gland failure
Hypocalcaemia
Causes of primary hypoparathyroidism
Di George syndrome
Neck surgery
Wilson’s disease
Alcohol
Symptoms of primary hypoparathyroidism
Symptoms of hypocalcaemia
‘SPASMODIC’
Investigations for primary hypoparathyroidism
Low Calcium
High Phosphate
Low PTH
Treatment for primary hypoparathyroidism
Calcium supplements
Calcitriol
Causes of secondary hypoparathyroidism
Radiation
Surgery (thyroidectomy, parathyroidectomy)
Hypomagnesaemia
Define pseudohypoparathyroidism
Failure of target cell response to PTH - end-organ resistance to PTH
Signs of pseudohypoparathyroidism
Low IQ
Short 4th and 5th metacarpels
Short stature
Round face
Investigations for pseudohypoparathyroidism
Low Calcium
High PTH
Treatment for pseudohypoparathyroidism
Calcium
Define hypopituitarism
Decreased secretion of anterior pituitary hormones: GH FSH LH Prolactin TSH ACTH
Causes of hypopituitarism
Hypothalamus: Kallman’s syndrome, Tumour, inflammation, TB, meningitis
Pituitary stalk: Trauma, surgery, mass lesion, meningioma, carotid artery aneurysm
Pituitary: Tumour, irradiation, inflammation, ischaemic (pituitary apoplexy, DIC, Sheehan’s syndrome), autoimmunity
Features of hypopituitarism
GH lack: Central obesity, atherosclerosis, dry skin, reduced cardiac output, osteoporosis, reduced balance, reduced exercise ability, reduced wellbeing
FSH/LH lack: Oligo/amenorrhoea, reduced fertility, reduced libido, osteoporosis, ED, hypogonadism
Thyroid lack: Hypothyroidism signs - BRADYCARDIC
ACTH lack: Adrenal insufficiency signs
Prolactin lack: Absent lactation
Investigations for hypopituitarism
Low LH, FSH. Testosterone, T4. Cortisol, IGF-1
Short synacthen test - assess adrenal axis
Insulin tolerance test - assess adrenal and GH axes
MRI scan - look for hypothalamic/pituitary lesion
Treatment for hypopituitarism
Hormone replacement and treat underlying causes
Hydrocortisone for secondary adrenal failure
Thyroxine if hypothyroid
Somatotropin for GH
What are the types of pituitary tumours?
Chromophobe - 70%
Eosinophil/Acidophil - 15%
Basophil - 15%
Features of a chromophobe pituitary tumour
Many are non-secretory
Half produce prolactin, a few ACTH or GH
Local pressure effect in 30% - often visual loss
What hormone is most commonly produced from pituitary tumours?
Prolactin
Features of an eosinophil/acidophil tumour
Secrete GH or prolactin
Features of a basophil tumour
Secrete ACTH - presents with Cushing’s
May enlarge post adrenalectomy (Nelson’s syndrome)
Features of local pressure due to pituitary tumour
Headaches - bilateral Visual field defects (bilateral temporal hemianopia) Palsy of cranial nerves 3, 4 and 6 Squint Diabetes insipidus
Investigations for pituitary tumours
MRI
Visual fields
Pituitary function tests: PRL, IGF-1, ACTH, Cortisol, TFT’S, FSH/LH
Glucose tolerance test if acromegaly suspected
Water deprivation if DI suspected
Treatment for pituitary tumours
Start hormone replacement
Steroids given before levothyroxine to prevent adrenal crisis
Prolactinoma = bromocriptine
GH = somatostatin analogues - Octreotide
Surgery - trans-sphenoidal -> give hydrocortisone pre-op
Radiotherapy
Define pituitary apoplexy
Rapid pituitary enlargement due to a bleed into tumour
Causes mass effect, CV collapse, acute hypopituitarism
Symptoms of pituitary apoplexy
Acute onset headache
Meningism
Reduced GCS
Visual field defect/double vision
Treatment for pituitary apoplexy
IV hydrocortisone
IV saline fluid balance
Surgery
What is craniopharyngioma?
Tumour from Rathke's pouch. Between pituitary and 3rd ventricle floor Commonest childhood intracranial tumour Adults present with: Amenorrhoea and DI Investigations: CT/MRI Treatment: Surgery
Define prolactinaemia
Commonest hormonal disturbance of the pituitary
Hyperprolactinaemia is raised prolactin in the blood
Prolactin is secreted from anterior pituitary and release is inhibited by dopamine
How does hyperprolactinaemia present in women?
Inhibits GNRH -> reduced FSH/LH -> menstrual dysfunction and galactorrhoea -> low oestrogen
Amenorrhoea/oligomenorrhoea Infertility Loss of libido Weight gain Hirsutism
How does hyperprolactinaemia present in men?
Decreased libido and ED
Reduced facial hair
Causes of hyperprolactinaemia
Excess production from the pituitary e.g. Prolactinoma
Compression of pituitary stalk - reducing dopamine levels
Dopamine antagonists - Metoclopramide, domperidone, neuroleptics
Pregnancy, breastfeeding, stress
Other drugs: Haloperidol, antipsychotics (TCA, MAOI, SRI’s)
Head injury - trauma
Craniopharyngioma
Pituitary adenomas
Hypothyroidism
Hypothalamic tumours
What are the two types of prolactinomas?
Microadenoma = <1cm 90% Macroadenoma = >1cm 10% - Presents with headache, reduced acuity, diplopia, bitemporal hemianopia, upper temporal quadrantanopia
Investigations for hyperprolactinaemia
PRL= Normal <400, Mild 400-1000, True prolactinoma >5000
TFT’s
Exclude pregnancy
MRI pituitary
Treatment for hyperprolactinaemia
Dopamine agonist - 1st line
E.g. Bromocriptine/cabergoline
Trans-sphenoidal surgery - 2nd line
Complications of hyperprolactinaemia
Headache
Visual loss
Both as a result of pituitary apoplexy
Define diabetes insipidus
The passage of large volumes (>3L/day) of dilute urine due to impaired water resorption by the kidney
Can be due to reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response of the kidney to ADH (nephrogenic DI)
Define cranial DI
Reduced secretion of ADH from the posterior pituitary due to damage to the hypothalamus
Causes of cranial DI
Idiopathic Brain tumours Trauma Infection - TB, meningitis, encephalitis Sarcoidosis Brain surgery Congenital - Wolfram's syndrome, defects in ADH gene
Define nephrogenic DI
When the collecting ducts of the kidneys do not respond to ADH
Causes of nephrogenic DI
Drugs - lithium, demeclocycline Hypokalaemia Hypercalcaemia Chronic renal disease Mutations on AVPR2 gene on X chromosome that codes for the ADH receptor
Symptoms of DI
Polyuria
Polydipsia
Dehydration
Hypernatraemia -> lethargy, weakness, confusion
Investigations for DI
Low urine osmolality - diluted
High serum osmolality
Water deprivation test (desmopressin stimulation test)
Urine dipstick - negative for glucose (Exclude DM)
MRI pituitary/hypothalamus
How does the water deprivation test work?
Tests the ability of the kidneys to concentrate urine
Patient avoid fluids for 8 hours
Urine osmolality is measured
Desmopressin is given (synthetic ADH)
8 hours later urine osmolality is measured again
What are the findings from the water deprivation test?
Cranial DI= Low urine osmolality after deprivation and high after ADH
Nephrogenic DI= Low urine osmolality after deprivation and low after ADH
Primary polydipsia = High urine osmolality after deprivation and high after ADH
Treatment for DI
Cranial DI = Desmopressin -> overdose = hyponatraemia
Nephrogenic DI = treat underlying cause, NSAIDs, bendroflumethazide
Define SIADH
Large amounts of ADH
Results in excessive water reabsorption in the collecting ducts -> the water dilutes the sodium in the blood causing hyponatraemia
Where is ADH secreted from?
Produced in the hypothalamus and secreted by the posterior pituitary gland
Causes of SIADH
Malignancy - small cell lung cancer, pancreas, prostate, lymphoma
CNS disorders - meningitis, stroke, SAH, trauma, abscess
Chest disease - TB, pneumonia, small-cell lung cancer, lung abscess
Endocrine disorders - Hypothyroidism
Drugs - SSRI’s, NSAIDs, thiazide diuretics, opiates, cyclophosphamide
Symptoms of SIADH
Confusion Nausea and vomiting Fatigue Muscle aches Seizures/coma -> from hyponatraemia
Investigations for SIADH
U&E’s = Na low <135mmol/L = hyponatraemia
Urine osmolality high
Urine sodium high
Normal renin and adrenal function
Management for SIADH
Stop causative medication
Correct sodium slowly to prevent central pontine myelinolysis
Fluid restriction
ADH receptor blockers ‘vaptans’ e.g. Tolvaptan
Demeclocycline
