Y3 - Endo Flashcards
Describe the anatomy of the thyroid gland!
- left and right lobe joined by a central isthmus
- moves on swallowing
- supplied by the inferior and superior thyroid arteries
What do the thyroid hormones do?
- T4 is the main circulating hormone and gets converted peripherally to T3 too
- thyroid hormones basically increase basal metabolic rate, affecting growth in kids too.
How would hyperthyroidism present?
- AF/ tachycardia/ palpitations
- increased and loose bowel movements
- menorrhagia
- intolerance to heat
- Insomnia/ irritability
- weight loss, increased appetite
- anxious/ sweating/ resting tremor
- Graves = lid retraction, proptosis, pre-tibial myxoedema, thyroid acropachy on nails
What are some causes of hyperthyroidism? also known as thyrotoxicosis
- Graves = autoimmune most common
- singular toxic nodule
- toxic multinodular goitre
-
thyroiditis (inflammatino of thyroid) caused by viral infection/ meds (amiodarone)/ post partum
- typically followed by a hypothyroid phase
- this is because inflammation causes follicular cell breakdown so thyroid hormones are released
- but obviously once the store is released, the breakdown of cells means there is then underproduction
How would you investigate and manage hyperthyroidism?
- T3
- T4
- TSH
- TSH receptor stimulating antibodies = Graves
- Thyroid peroxidase antibodies (not that specific but indicative of autoimmune)
- US of thyroid shows nodules
- Iodine uptake isotope scan shows either localised increased uptake (nodule) or uniform increased uptake (Graves) or absent uptake (thyroiditis)
Management
- BBlockers for symptoms
-
Carbimozole
- se = _generalised ras_h. also agranulocytosis so do urgent fbc if unexplained fever/sore throat and stop if neutrophils are low
- definitive = Radioactive Iodine + Thyroidectomy
How would hypothyroidism present?
- weight gain
- constipation
- fatigue
- intolerance to cold
- bradycardia
What are some causes of hypothyroidism?
- damage from intentional treatment of thyroid disease eg surgical
- inadvertant damage from eg radiation to head and neck
- Hashimotos thyroiditis
- Iodine insufficiency
- Post partum
- Medications like amiodarone and lithium
How would you investigate and manage hypothyroidism?
- T3
- T4
- Thyroid peroxidase Antibodies
- TSH
Managment
Levothyroxine!!!
What hormones are produced by the adrenal glands? What do they do
Cortex
- Glucocorticoids = cortisol
-
Mineralcorticoids = aldosterone
- distal convoluted tubule to cause K+ loss and Na+ retention
- is regulated by Renin Angiotensin System (activated by low blood vol, low Na+ or high K+)
- Androgens
Medulla produces adrenaline and dopamine and their metabolites
How would Primary Adrenal Insufficiency (Addisons disease) present?
- Low Cortisol = fatigue, weight loss, nausea, abdo pain, anorexia, hypoglycaemia, hyperpigmentation from ACTH upregulation
- Low Aldosterone = postural hypotension, dizziness, Hyponatraemia, Hyperkalaemia
- Low androgens = loss of axillary and pubic hair, low libido
Why is there hyperpigmentation in addisons?
ACTH excess due to low cortisol.
Acth stimulates melaocyte stimulating hormones which results in hyperpigmentation
How would you investigate and manage Addisons?
- low 9am Cortisol while ACTH is raised
- Synacthen test for confirmation
- Hyperkalaemia, Hyponatraemia, Hypoglycaemia, Mild anaemia, Raised urea
Management
- Hydrocortisone for glucocorticoid replacement
- Fludrocortisone for mineralcorticoid replacement
- educate about steroid rules (double glucocorticoid during illness, ensure it is given in surgery/ nausea or vomiting)
- give steroid emergency card, medical alert jewellry, details of their endo team
How would you manage secondary adrenal insufficiency (ACTH deficiency)
- only replace Glucocorticoid = Hydrocortisone
- steroid card etc
- education etc inform them not to stop steroids suddenly = adrenal crisis
What is phaeochromocytoma and paragangliomas?
Phaeochromocytomas are catecholamine secreting tumours of the adrenal medulla.
Paraganglionomas are tumours of the extra adrenal chromaffin tissue
How would phaeochromocytomas present?
- panic attacks and anxiety
- headache, sweating, pallor, palpitations
How would you investigate and manage phaeochromocytomas?
- 24 hour urinary catecholamines and plasma metanephrines
- CT/MRI abdo for tumour
Management
- surgical excision
- alpha blockade first (as unregulated alpha = hypertensive crisis)
- then beta blockade to control reflex tachycardia
What are the 5 axes produced in the pituitary and what do they do?
Growth hormone (GH)
- secreted pulsatile
- acts on liver to produce IGF-1
- -ve feedback from somatostatin
ACTH
- secreted circadian rhythm
- stimulates cortisol release
Gonadal (FSH/LH)
- FSH and LH are inhibited by prolactin
Thyroid (TSH)
- stimulates T4 and T3
Prolactin
- causes lactation
- inhibits gonadal hormones
- itself is inhibited by dopamine
How would you assess the pituitary gland?
- MRI of pituitary for microadenomas (<1cm) or macroadenomas
- Synacthen test
- Insulin Tolerance Test for GH and ACTH reserve (not in ischaemic heart disease or epilepsy)
- Prolactin and TSH can be measured at any time
- FSH and LH in women measured in first 5 days of menstrual cycle
- FSH and LH and Testosterone in men measured at fasting 0900
- Measure GH and IGF-1
- Basal Cortisol at 0900
How would you investigate hyperprolactinaemia?
- MRI for microadenoma (<1cm) or macroadenoma
- rule out pregnancy
- medications review (dopamine antagonists like antipsychotics or antiemetics)
- prolactin levels typically >5000 in secreting prolactinoma
Microadenoma
- menstrual disturbance, galactorrhoea, infertility
- unlikely to be PCOS if no pituitary lesions on MRI, also prolactin is usually <1000
Macroadenoma
- prolactin typically >5000miU
How would you manage hyperprolactinaemia?
- give dopamine agonists like bromocriptine or cabergoline
- SE = nausea, postural hypotension, psychiatric disturbance
- They can cause the tumour to shrink really fast and cause CSF leak = meningitis risk
How would acromegaly present?
- large hands and feet
- puffy hands = carpal tunnel syndrome
- coarse facial features
- frontal bossing of forehead
- protrusion of chin
- wide spaced teeth
- Enlarged soft tissue = large soft palate and tongue
- Snoring and sleep apnoea
- Sweating, headaches, HTN
- Risk of CVS, bowel cancer, DM
How would you investigate and manage acromegaly?
- GH and IGF-1
- Oral Glucose Tolerance Test
- Pituitary MRI to show tumour
Management
-
Surgical excision
- repeat OGTT and follow up with GH/IGF-1 monitoring
- Stereotactic radiotherapy if it is away from optic chiasm
- somatostatin analogues can help
- Monitor for sleep apnoea, bowel cancer, CVS, DM
How would you manage hypopituitarism?
ACTH = hydrocortisone
GH = daily growth hormone subcut injections
FSH/LH = COCP/HRT in females or testosterone injections for males
Thyroid = levothyroxine
How would Cushings disease present?
Pituitary adenoma resulting in excess cortisol.
- dorso cervical fat pad
- facial roundness and plethora
- thin skin, striae, easy bruising
- osteoporosis of limbs
- central obesity
- HTN, DM
How would you investigate and manage Cushings disease?
- Screen for alcoholism and depression
- Elevated 24 hour urinary Cortisol
-
Overnight dexamethasone suppression test
- failure to suppress cortisol <50nmol/L after overnight Dexamethasone Suppression test
- Elevated late night salivary cortisol levels
- Hypokalaemic, Metabolic alkalosis
- MRI of pituitary
Management
- Metyrapone and ketoconazole
- Radiotherapy
- Transphenoidal removal of pituitary adenoma
- If it is adrenal = lap adrenalectomy
What are some symptoms of hyponatraemia?
- headache
- nausea, vomiting
- general malaise
- confusion, agitation, drowsiness later
How would you investigate hyponatraemia?
- Urine Osmolality
- Urine Sodium
- <30mmol/L = low effective arterial vol
- >30mmol/L and euvolaemic = SIADH once ACTH def is excluded
- >30mmol/L and dehdyrated = Addisons/ vomiting/ DI
How would you diagnose and manage SIADH?
- Diagnosis of exclusion as there isn’t really a test…
- Rule out other causes eg. adrenal insufficiency*** (-ve short synacthen), rule out diuretics, excess fluid intake, ckd, aki, etc.
- clinical examination shows euvolaemia
- low serum osmolality <275momol/kg
- high urine osmolality >100mosmol/kg
- urine Na >30mmol/l
Ensure to rule out ACTH deficiency as it also causes excretion of free water (cortisol deficiency causes increased vasopressin activity).***
Also look for any underlying malignancy eg. small cell lung cancer.
Management
(the goal is to correct sodium slowly to prevent central pontine myelinolysis)
- fluid restriction
-
tolvaptan (adh receptor blocker)
- monitor as it can cause rapid sodium increase
- demeclocycline (tetracycline antibiotic that inhibits adh)
How would you diagnose cranial/nephrogenic diabetes insipidus?
- >3L urine in 24 hours
- high serum osmolality >295mosmol/kg
- low urine osmolality <300mosmol/kg
- do water deprivation test (they should have unacceptable thirst and significant weight loss due to water loss. stop if symptoms get too severe!)
- then give a synthetic vasopressin like desmopressin.
- Cranial will get better, Nephrogenic no response
Management
- Desmopressin for cranial DI
- Nephrogenic = less salt, protein, nsaids, diuretics
How would you investigate hypercalcaemia?
- high PTH
- high PTH is usually primary hyperPTH due to a single parathyroid adenoma
- Parathyroid hyperplasia in more than one gland = Multiple Endocrine Neoplasia
- Very high calcium >3.5 could be parathyroid cancer (associated with jaw tumours)
- suppressed PTH
- malignancy unless proven otherwise!!!
- usually squamous cell carcinoma
- also could be benign granulomatous disease like tb/ sarcoidosis
- Parathyroid ultrasound for adenoma
How would hypercalcaemia present?
- renal stones
- abdominal pain, GI upset, constipation
- Depression, fatigue, psychiatric symptoms
- Bony aches and pains
- polydypsia and polyuria
How would you manage hypercalcaemia?
- Surgery if Ca>2.85
- parathyroidectomy
- Calcimimetics like cinacalcet for primary hyperparathyroidism
How would hypocalcaemia present?
- seizures
- tetany
- qt prolongation on ecg
- Chvosteks sign +ve = facial spasm when cheek is tapped gently with finger
- Trousseaus sign = carpo-pedal spasm induced after inflation of sphygmomanoometer
What are some causes of hypocalcaemia?
Ca<1.9
- Vit D deficiency = will have a low phosphate
- Hypomagnesaemia = GI loss, alcohol/drugs, PPIs
- Parathyroid gland damage from surgery etc.
How would you manage hypocalcaemia?
- Calcium replacement
- vitamin d supplements
- bisphospohonates
- stop offensive meds for hypomagnesaemia and give IV MgSO4 24mmol/24 hours
How would Conns present?
(primary hyperaldosteronism)
- Hypernatraemia, hypokalaemia
- polyuria, polydipsia
- HTN
- metabolic alkalosis
How would you investigate Conns?
-
Aldosterone:Renin ratio >800 confirms diagnosis
- false +ve with BBlockers
- False -ves with ACEI, ARBs, CCB
- ECG = hypokalaemia
- CT/MRI for adrenal mass/hyperplasia
-
Lying and standing aldosterone:renin
- adrenal hyperplasia = aldosterone >30% after standing over 4 hours
- adrenal adenoma = no change
How would you manage Conns?
adrenal adenoma (Conns)
- surgial removal of adenoma
- Spironolactone (aldosterone antagonist)
Bilateral adrenal hyperplasia
-
spironolactone
- SE = gynaecomastia and ED as also blocks testosterone receptors
-
Amiloride
- K+ sparing diuretic weaker than spironolactone
-
Eplerenone
- aldosterone antagonist that does not block testosterone receptors
What is the pathophysiology of SIADH?
- ADH is produced in the hypothalamus and secreted by the posterior pituitary
- ADH stimulates water reabsorption from collecting ducts in kidneys
- SIADH is when ADH is secreted excessively
- either due to posterior pituitary secreting too much
- or ADH coming from somewhere else like a Small cell lung cancer
- Results in excessive water, diluting sodium in the blood = hyponatraemia
- but the water is not significant enough to cause fluid overload = euvolaemic hyponatraemia
- Urine becomes more concentrated as water is retained = high urine osmolality and high urine sodium
What is central pontine myelinolysis?
(also known as osmotic demyelination syndrome)
a complication of rapidly correcting severe hyponatraemia (>10mmol/L increase in over 24 hours)
- as blood sodium falls, water moves from the level of low solute conc (blood) to high solute conc (brain)
- this causes the brain to swell
- the brain reduces its solutes so that water moves back down through the blood brain barrier and reduces oedema in the brain
- this adaptation takes a few days and so in people who have a chronically low sodium, their brain cells will have adapted to have a low osmolality.
- Therefore when we correct that low sodium rapidly, water rapidly shifts out of the brain cells into the blood.
Early First phase Presentation
- electrolyte imbalance = encephalopathic and confusion
- nausea, vomiting, headache
Second phase presentation
- Later on the demyelination of neurones starts, particularly in the pons
- spastic quadriparesis
- pseudobulbar palsy
- cognitive and behavioural changes
Management = supportive
