endocrine emergencies Flashcards

1
Q

7 endocrine emergencies

A
  1. acute adrenal insufficency
  2. pituitary apoplexy
  3. myxoedema coma
  4. thyroid storm
  5. hypercalcaemia
  6. hypoglycaemia
  7. DKA
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2
Q

what might be seen in the social aspect of a pt’s life if they have low oxytocin levels

A

problems with relationships and bonding

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3
Q

3 types of adrenal insufficency

A
  1. primary (problem w the adrenal glands)
  2. central (problem w pit or hypothal)
  3. steroid-induced
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4
Q

causes of hypopituitarism (9, surgical sieve)

A
  1. isolated deficency (e.g. kallmans)
  2. infection
  3. vascular e.g. apoplexy, sheehan’s syndrome
  4. immunological e.g. immune checkpoint inhibitors
  5. neoplastic
  6. traumatic e.g. skull fracture through base, surgery
  7. inflitrations e.g. sarcoidosis
  8. radiation damage
    9.empty sella syndrome
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5
Q

what drug history is important to take when possible addisonian presentation

A

steroid and opioid history

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6
Q

what is pituitary apoplexy

A

an acute clinical syndrome cause by either haemorrhagic or non-haemorrhagic (i.e. ischaemic) necrosis of the pituitary gland

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7
Q

2 causes of pituitary apoplexy

A
  1. large macro-adenoma
  2. Sheehan’s syndrome
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8
Q

when should thyroxine be given in relation to steroids in an acute setting

A

after steroids - never give thyroxine prior to steroids as this can precipitate the crisis

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9
Q

symptoms of pituitary apoplexy (9)

A
  1. headache
  2. vomiting
  3. visual disturbance
  4. meningism
  5. CN palsy
  6. decreased consciousness
  7. hypopituitarism
  8. addisonian crisis
  9. subarachnoid irritation (if haemorrhagic)
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10
Q

pituitary apoplexy acute mgx (6)

A
  1. ABCDE, ensure haemodynamic stability, assess fluid/electrolyte imbalance
  2. consider hydrocortisone replacement
  3. urgent biochemical and endocrine assessment
  4. urgent MRI or pituitary CT (if MRI is contraindicated) to confirm diagnosis
  5. liaise with the regional endocrine and neurosurgical teams
  6. if severely reduced visual acuity, deteriorating VF defect or deteriorating consciousness then consider surgery, otherwise monitor and treat conservatively
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11
Q

pituitary apoplexy long term mgx

A
  1. follow up by endocrine and neurosurgery teams
  2. require repeat assessment of pituitary and visual function at 4-6 weeks
  3. 6-12 monthly follow up to optimise hormonal replacement and monitor tumour progression/recurrence
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12
Q

what is thyroid storm

A

an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis

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13
Q

symptoms/signs of thyroid storm (9)

A
  1. fever >38C
  2. tachycardia >110 (and poss AF)
  3. cardiac failure
  4. agitation/restlessness, emotional swings, confusion
  5. dehydration, confusion
  6. weight loss, tremor, diarrhoea, vomiting
  7. heat intolerance
  8. SOB (+ poss bilateral creps)
  9. dry/uncomfortable eyes
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14
Q

what is burch-wartofsky scoring

A

determines likelihood of thyrotoxicosis independent of thyroid hormone levels

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15
Q

what are the parameters for burch wartofsky scoring

A
  1. thermoregulatory dysfunction
  2. CNS effects
  3. gastrointestinal-hepatic dysfunction
  4. tachycardia
  5. congestive heart failure
  6. AF
  7. precipitating event identified
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16
Q

4 precipitants for thyroid storm

A
  1. acute infection
  2. thyroid surgery
  3. radioiodine
  4. untreated thyrotoxicosis
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17
Q

thyroid storm mgx - specific (7)

A
  1. carbimazole (10mg TDS)
  2. prednisolone (30mg OD)
  3. Lithium (250mg TDS)
  4. propanolol (80mg TDS)
  5. cholesytramine 95mg TDS)
  6. lugol’s iodine (5 drops TDS)
  7. iapanoic acid (0.5g BD -> only in desperate measures as lab grade is the only kind available)
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18
Q

carbimazole MOA (3)

A
  1. inhibits TPO mediated iodinatino of thyroglobulin
  2. decreases type 1 deiodinase activity, reducing conversion of T4 to T3
  3. reduced TSI titre with possible immunosuppressive effects
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19
Q

how does prednisolone treat a thyroid storm (MOA)

A

prevents peripheral conversion of T4 to T3

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20
Q

how does lithium treat a thyroid storm (MOA -2)

A
  1. inhibits iodine uptake into folliculaar cells
  2. inhibits thyroid hormone secretion
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21
Q

how does propanolol treat a thyroid storm (MOA -2)

A
  1. improved peripheral effects of thyrotoxicosis
  2. inhibits T4 to T3 conversion (mild)
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22
Q

how does cholesytramine treat a thyroid storm (MOA)

A

blocks enterohepatic circulation of thyroid hormones so increases clearance

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23
Q

how does Lugol’s iodine treat a thyroid storm (MOA -3)

A
  1. inihibits thyroid hormone synthesis and release
  2. blocks peripheral conversion of T4 to T3
  3. decreases thyroid blood flow and vascularity (reduces intra-op blood loss)
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24
Q

how does iopanoic acid treat a thyroid storm (MOA)

A

inhibit conversion of T4 to T3

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25
Q

thyroid storm mgx - supportive (6)

A
  1. monitoring -> poss admitt to ITU/HDU
  2. chlorpromazine IM (agitation)
  3. anti-arrhythmic drugs e.g. digoxin
  4. cooling and IV fluids
  5. antibiotics (if appropriate)
  6. cholestyramine (aids clearance of thyroid hormones from enterohepatic circulation)
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26
Q

what is myxoedema coma

A

severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs - EMERGENCY

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27
Q

5 precipitating factors ox myxoedema coma

A
  1. cold exposure
  2. trauma
  3. infection
  4. phenothiazines
  5. cerebrovascular accident
28
Q

clinical features of myxoedema coma (5)

A
  1. hypothermia
  2. bradycardia (+ hypotension -> low cardiac output)
  3. decreased/LOC
  4. respiratory depression
  5. slow relaxing reflexes
29
Q

myxoedema coma investigations (4)

A
  1. venous blood (low T4, high TSH, low Na+, low glucose, raised MCV, high CK)
  2. ABG (T2 resp failure may be present - due to hypoventilation and respiratory acidosis)
  3. septic screen (CXR, blood and urine cultures)
  4. ECG (bradycardia, small complexes, evidence of acute ischaemia, J waves if hypothermic)
30
Q

myxoedema coma mgx (8)

A
  1. IV access and send bloods for TSH, T4,T3 U&E, FBC, cortisol etc.)
  2. perform septic screen
  3. inform endocrine team and HDU
  4. give hydrocortisone 100mg IM (then 6hrly)
  5. give liothyronine (T3) 5-10mcg (DONT GIVE IV)
  6. slow re-warming with cardiac monitoring
  7. continue liothyronine and increase dose after 3 days
  8. start levothyroxine 25mcg (after 3 days)
31
Q

why should liothyronine (T3) not be given IV

A

risk of arrhythmia

32
Q

3 key points to the myxoedema coma mgx

A
  1. treat underlying illness
  2. warm up
  3. give steroids prior to TH
33
Q

hypercalcaemia symptoms (4)

A

bones, groans, stones and psychic moans

  1. bone pain
  2. abdominal pain, vomiting, anorexia, constipation
  3. renal stones, polyuria, polydipsia
  4. depression, lethargy, confusion
34
Q

5 causes of hypercalcaemia

A
  1. hyperparathyroidism (primary and tertiary, PTH is raised)
  2. malignancy - myeloma (PTH will be surpressed)
  3. vit D intoxication
  4. granulomatous disease e.g. sarcoidosis
  5. familial benign hypercalcaemia
35
Q

6 treatments for hypercalcaemia

A
  1. if emergency - IV saline
  2. bisphosphonates IV,
  3. steroids
  4. cinacalcet
  5. denusomab
  6. treat underlying cause
36
Q

2 signs to look for in hypocalcaemia

A
  1. Trousseau’s sign - involuntary contractions of hand and wrist after a bp cuff has been inflated for 3min;
  2. Chvostek sign -a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear
37
Q

why does Chvostek’s sign occur

A

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

38
Q

why does Trousseau’s sign occur

A

Ca2+ helps stabilise the normal resting membrane potential of neurons => neurons are less stable and more likely to fire spontaneously, which can trigger tetany

39
Q

what other electrolyte imbalance occurs alongside hypocalcaemia

A

hypomagnesia

40
Q

what ECG sign may be seen with hypocalcaemia

A

long QT

41
Q

what does hypercalcaemia with low PTH and normal albumin indicate

A

non-parathyroid cause of hypercalcaemia -> check TFTS, ACE and do a CXR

42
Q

what does hypercalcaemia with low PTH and low albumin indicate

A

cancer associated hypercalcaemia -> bone scan, CXR, other imaging to identify primary tumour

43
Q

what does hypercalcaemia with high PTH and normal/high calcium indicate

A

primary hyperparathyroidism -> image parathyroidism

44
Q

what does hypercalcaemia with high PTH and low urinary calcium indicate

A

familial hypocalciuric hypercalcaeima -> screen other family members and obtain a molecular diagnosis

45
Q

what percentage of primary hyperparathyroidism is single gland disease

A

85%

46
Q

what is the role of PTH in calcium homeostasis

A
  1. When the body’s levels of extracellular calcium change, it’s detected by a surface receptor in parathyroid cells called the calcium-sensing receptor;
  2. decreased calcium levels results in PTH release
  3. 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)
  4. then goes on to increase calcium absorption in the gastrointestinal tract
47
Q

normal calcium range

A

8.5 to 10 mg/dl

48
Q

what other factors (not PTH) affect the Ca2+ conc in the blood

A
  1. pH
  2. albumin levels
49
Q

why does acidosis result in hypercalcemia

A

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

50
Q

what is pseudohypercalcemia

A

an elevation in the serum total calcium concentration without any rise in the serum ionized calcium concentration

51
Q

what causes pseudohypercalcaemia

A

hyperalbuminemia -> higher concentration of protein-bound calcium, while free ionized calcium concentrations stay essentially the same due to hormonal regulation

52
Q

emergency mgx of hypercalcemia (4)

A
  1. fluid management -> 3-6L IV 0.9%NaCl /24hrs
  2. give bisphosphonates if appropriate
  3. definative therapy if indicated e.g. parathyroidectomy, steroids, chemo
  4. second line therapies if indicated
53
Q

bisphosphonate doses to give in hypercalcaemia

A
  1. if Ca <3.4 mmol/L -> give pamidronate 60mg in 250ml NaCl/2hrs
  2. if Ca >3.4 mmol/L -> give pamidronate 90mg in 500ml NaCl/2hrs
  3. Zoledronate 4mg IVin 5L/15mins
54
Q

how does denosumab treat hypercalcaemia

A

monoclonal antibody to inhibit RANK-ligand signalling

55
Q

who is denosumab indicated in to treat hypercalcaemia

A

those with postmenopausal osteoporosis

56
Q

what is cinacalcet and what is it used for

A

a calcimimetic that works by allosteric activation of the calcium-sensing receptor;
used for primary (if surgery not an option) and secondary hyperparathyroidism

57
Q

when are steroids effective in hyperparathyroidism

A
  1. where 1α hydroxylation dependent mechanism is suspected
  2. sarcoidosis
  3. lymphoma
58
Q

7 indications for surgical management of primary hyperparathyroidism (asymptomatic)

A
  1. serum adjusted calcium 0.25mmol/L above the upper reference
    limit
  2. DEXA T score <-2.5 at lumbar spine, hip, femoral neck or distal 1/3 radius
  3. vertebral fractures
  4. eGFR <60ml/min
  5. > 10mmol/day Ca excretion via urine
  6. presence of nephrolithiasis or nephrocalcinosis
  7. age <50 yrs
59
Q

mutations in how many genes are implicated in primary hyperparathyroidism

A

9

60
Q

10 causes of hypocalcaemia

A
  1. hypoparathyroidism
  2. vit D deficency/ insufficency
  3. altered vit D metabolism (medication overuse)
  4. kidney/liver disease
  5. pseudohypoparathyroidism
  6. hypomagnesemia or hypermafnesemia
  7. hungry bone syndrome
  8. infusion of phosphate
  9. rapid citrated blood transfusion
  10. medication
61
Q

hypocalaemia mgx (2)

A
  1. in severe cases, for rapid control (minutes-hours) -> IV calcium gluconate 10ml of 10% solution over 10mins
  2. 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
62
Q

what are the 2 types of diabetes insipidus

A

cranial and nephrogenic

63
Q

what is cranial diabetes insipidus

A

not enough ADH is produced=> excessive amounts of water are lost in large amounts of urine

64
Q

what is nephrogenic diabetes insipidus

A

ADH is produced correctly but the kidneys do not respond in the correct way

65
Q
A