endocrine emergencies Flashcards
7 endocrine emergencies
- acute adrenal insufficency
- pituitary apoplexy
- myxoedema coma
- thyroid storm
- hypercalcaemia
- hypoglycaemia
- DKA
what might be seen in the social aspect of a pt’s life if they have low oxytocin levels
problems with relationships and bonding
3 types of adrenal insufficency
- primary (problem w the adrenal glands)
- central (problem w pit or hypothal)
- steroid-induced
causes of hypopituitarism (9, surgical sieve)
- isolated deficency (e.g. kallmans)
- infection
- vascular e.g. apoplexy, sheehan’s syndrome
- immunological e.g. immune checkpoint inhibitors
- neoplastic
- traumatic e.g. skull fracture through base, surgery
- inflitrations e.g. sarcoidosis
- radiation damage
9.empty sella syndrome
what drug history is important to take when possible addisonian presentation
steroid and opioid history
what is pituitary apoplexy
an acute clinical syndrome cause by either haemorrhagic or non-haemorrhagic (i.e. ischaemic) necrosis of the pituitary gland
2 causes of pituitary apoplexy
- large macro-adenoma
- Sheehan’s syndrome
when should thyroxine be given in relation to steroids in an acute setting
after steroids - never give thyroxine prior to steroids as this can precipitate the crisis
symptoms of pituitary apoplexy (9)
- headache
- vomiting
- visual disturbance
- meningism
- CN palsy
- decreased consciousness
- hypopituitarism
- addisonian crisis
- subarachnoid irritation (if haemorrhagic)
pituitary apoplexy acute mgx (6)
- ABCDE, ensure haemodynamic stability, assess fluid/electrolyte imbalance
- consider hydrocortisone replacement
- urgent biochemical and endocrine assessment
- urgent MRI or pituitary CT (if MRI is contraindicated) to confirm diagnosis
- liaise with the regional endocrine and neurosurgical teams
- if severely reduced visual acuity, deteriorating VF defect or deteriorating consciousness then consider surgery, otherwise monitor and treat conservatively
pituitary apoplexy long term mgx
- follow up by endocrine and neurosurgery teams
- require repeat assessment of pituitary and visual function at 4-6 weeks
- 6-12 monthly follow up to optimise hormonal replacement and monitor tumour progression/recurrence
what is thyroid storm
an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis
symptoms/signs of thyroid storm (9)
- fever >38C
- tachycardia >110 (and poss AF)
- cardiac failure
- agitation/restlessness, emotional swings, confusion
- dehydration, confusion
- weight loss, tremor, diarrhoea, vomiting
- heat intolerance
- SOB (+ poss bilateral creps)
- dry/uncomfortable eyes
what is burch-wartofsky scoring
determines likelihood of thyrotoxicosis independent of thyroid hormone levels
what are the parameters for burch wartofsky scoring
- thermoregulatory dysfunction
- CNS effects
- gastrointestinal-hepatic dysfunction
- tachycardia
- congestive heart failure
- AF
- precipitating event identified
4 precipitants for thyroid storm
- acute infection
- thyroid surgery
- radioiodine
- untreated thyrotoxicosis
thyroid storm mgx - specific (7)
- carbimazole (10mg TDS)
- prednisolone (30mg OD)
- Lithium (250mg TDS)
- propanolol (80mg TDS)
- cholesytramine 95mg TDS)
- lugol’s iodine (5 drops TDS)
- iapanoic acid (0.5g BD -> only in desperate measures as lab grade is the only kind available)
carbimazole MOA (3)
- inhibits TPO mediated iodinatino of thyroglobulin
- decreases type 1 deiodinase activity, reducing conversion of T4 to T3
- reduced TSI titre with possible immunosuppressive effects
how does prednisolone treat a thyroid storm (MOA)
prevents peripheral conversion of T4 to T3
how does lithium treat a thyroid storm (MOA -2)
- inhibits iodine uptake into folliculaar cells
- inhibits thyroid hormone secretion
how does propanolol treat a thyroid storm (MOA -2)
- improved peripheral effects of thyrotoxicosis
- inhibits T4 to T3 conversion (mild)
how does cholesytramine treat a thyroid storm (MOA)
blocks enterohepatic circulation of thyroid hormones so increases clearance
how does Lugol’s iodine treat a thyroid storm (MOA -3)
- inihibits thyroid hormone synthesis and release
- blocks peripheral conversion of T4 to T3
- decreases thyroid blood flow and vascularity (reduces intra-op blood loss)
how does iopanoic acid treat a thyroid storm (MOA)
inhibit conversion of T4 to T3
thyroid storm mgx - supportive (6)
- monitoring -> poss admitt to ITU/HDU
- chlorpromazine IM (agitation)
- anti-arrhythmic drugs e.g. digoxin
- cooling and IV fluids
- antibiotics (if appropriate)
- cholestyramine (aids clearance of thyroid hormones from enterohepatic circulation)
what is myxoedema coma
severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs - EMERGENCY
5 precipitating factors ox myxoedema coma
- cold exposure
- trauma
- infection
- phenothiazines
- cerebrovascular accident
clinical features of myxoedema coma (5)
- hypothermia
- bradycardia (+ hypotension -> low cardiac output)
- decreased/LOC
- respiratory depression
- slow relaxing reflexes
myxoedema coma investigations (4)
- venous blood (low T4, high TSH, low Na+, low glucose, raised MCV, high CK)
- ABG (T2 resp failure may be present - due to hypoventilation and respiratory acidosis)
- septic screen (CXR, blood and urine cultures)
- ECG (bradycardia, small complexes, evidence of acute ischaemia, J waves if hypothermic)
myxoedema coma mgx (8)
- IV access and send bloods for TSH, T4,T3 U&E, FBC, cortisol etc.)
- perform septic screen
- inform endocrine team and HDU
- give hydrocortisone 100mg IM (then 6hrly)
- give liothyronine (T3) 5-10mcg (DONT GIVE IV)
- slow re-warming with cardiac monitoring
- continue liothyronine and increase dose after 3 days
- start levothyroxine 25mcg (after 3 days)
why should liothyronine (T3) not be given IV
risk of arrhythmia
3 key points to the myxoedema coma mgx
- treat underlying illness
- warm up
- give steroids prior to TH
hypercalcaemia symptoms (4)
bones, groans, stones and psychic moans
- bone pain
- abdominal pain, vomiting, anorexia, constipation
- renal stones, polyuria, polydipsia
- depression, lethargy, confusion
5 causes of hypercalcaemia
- hyperparathyroidism (primary and tertiary, PTH is raised)
- malignancy - myeloma (PTH will be surpressed)
- vit D intoxication
- granulomatous disease e.g. sarcoidosis
- familial benign hypercalcaemia
6 treatments for hypercalcaemia
- if emergency - IV saline
- bisphosphonates IV,
- steroids
- cinacalcet
- denusomab
- treat underlying cause
2 signs to look for in hypocalcaemia
- Trousseau’s sign - involuntary contractions of hand and wrist after a bp cuff has been inflated for 3min;
- Chvostek sign -a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear
why does Chvostek’s sign occur
low levels of calcium in an individual’s blood, decreases the threshold needed for the neuron to transmit a signal to the muscle - hyperexcitability of neurons and spontaneous depol occurs
why does Trousseau’s sign occur
Ca2+ helps stabilise the normal resting membrane potential of neurons => neurons are less stable and more likely to fire spontaneously, which can trigger tetany
what other electrolyte imbalance occurs alongside hypocalcaemia
hypomagnesia
what ECG sign may be seen with hypocalcaemia
long QT
what does hypercalcaemia with low PTH and normal albumin indicate
non-parathyroid cause of hypercalcaemia -> check TFTS, ACE and do a CXR
what does hypercalcaemia with low PTH and low albumin indicate
cancer associated hypercalcaemia -> bone scan, CXR, other imaging to identify primary tumour
what does hypercalcaemia with high PTH and normal/high calcium indicate
primary hyperparathyroidism -> image parathyroidism
what does hypercalcaemia with high PTH and low urinary calcium indicate
familial hypocalciuric hypercalcaeima -> screen other family members and obtain a molecular diagnosis
what percentage of primary hyperparathyroidism is single gland disease
85%
what is the role of PTH in calcium homeostasis
- When the body’s levels of extracellular calcium change, it’s detected by a surface receptor in parathyroid cells called the calcium-sensing receptor;
- decreased calcium levels results in PTH release
- PTH causes the bones to release calcium, and gets the kidneys to reabsorb more calcium so it’s not lost in the urine and synthesize calcitriol (active vit D)
- then goes on to increase calcium absorption in the gastrointestinal tract
normal calcium range
8.5 to 10 mg/dl
what other factors (not PTH) affect the Ca2+ conc in the blood
- pH
- albumin levels
why does acidosis result in hypercalcemia
in acidic conditions, albumin becomes +vely charged (due to carboxylic acid groups not donating H+) -> stops Ca2+ binding (bc also +vely charged) -> increase Ca2+ levels
what is pseudohypercalcemia
an elevation in the serum total calcium concentration without any rise in the serum ionized calcium concentration
what causes pseudohypercalcaemia
hyperalbuminemia -> higher concentration of protein-bound calcium, while free ionized calcium concentrations stay essentially the same due to hormonal regulation
emergency mgx of hypercalcemia (4)
- fluid management -> 3-6L IV 0.9%NaCl /24hrs
- give bisphosphonates if appropriate
- definative therapy if indicated e.g. parathyroidectomy, steroids, chemo
- second line therapies if indicated
bisphosphonate doses to give in hypercalcaemia
- if Ca <3.4 mmol/L -> give pamidronate 60mg in 250ml NaCl/2hrs
- if Ca >3.4 mmol/L -> give pamidronate 90mg in 500ml NaCl/2hrs
- Zoledronate 4mg IVin 5L/15mins
how does denosumab treat hypercalcaemia
monoclonal antibody to inhibit RANK-ligand signalling
who is denosumab indicated in to treat hypercalcaemia
those with postmenopausal osteoporosis
what is cinacalcet and what is it used for
a calcimimetic that works by allosteric activation of the calcium-sensing receptor;
used for primary (if surgery not an option) and secondary hyperparathyroidism
when are steroids effective in hyperparathyroidism
- where 1α hydroxylation dependent mechanism is suspected
- sarcoidosis
- lymphoma
7 indications for surgical management of primary hyperparathyroidism (asymptomatic)
- serum adjusted calcium 0.25mmol/L above the upper reference
limit - DEXA T score <-2.5 at lumbar spine, hip, femoral neck or distal 1/3 radius
- vertebral fractures
- eGFR <60ml/min
- > 10mmol/day Ca excretion via urine
- presence of nephrolithiasis or nephrocalcinosis
- age <50 yrs
mutations in how many genes are implicated in primary hyperparathyroidism
9
10 causes of hypocalcaemia
- hypoparathyroidism
- vit D deficency/ insufficency
- altered vit D metabolism (medication overuse)
- kidney/liver disease
- pseudohypoparathyroidism
- hypomagnesemia or hypermafnesemia
- hungry bone syndrome
- infusion of phosphate
- rapid citrated blood transfusion
- medication
hypocalaemia mgx (2)
- in severe cases, for rapid control (minutes-hours) -> IV calcium gluconate 10ml of 10% solution over 10mins
- for control over days-weeks -> vit D treatment
2a. if PTH deficent give vit D analogue (e.g. calcitriol)
2b. if PTH intact give cholecalficerol
what are the 2 types of diabetes insipidus
cranial and nephrogenic
what is cranial diabetes insipidus
not enough ADH is produced=> excessive amounts of water are lost in large amounts of urine
what is nephrogenic diabetes insipidus
ADH is produced correctly but the kidneys do not respond in the correct way
