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endocrine emergencies Flashcards

1
Q

describe primary hyperaldosteronism

A

XS production of aldosterone
independent of the RAAS
causing increased Na+ and water retention
and decreased renin release (JGA trying to compensate)
2/3 - Conn’s
1/3 - bilateral adrenocortical hyperplasia

GOOD WAY TO THINK ABOUT IT:
loads of aldosterone means that body holds on to all of it’s water and salt through reabsorption in kidneys

lose K+ as is co-transporter with Na+

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2
Q

what is the presentation of primary hyperaldosteronism? (and to an extent, secondary..)

A

often Asx
Signs of hypokalaemia - weakness / cramps / parasthesiae / polyuria / polydipsia
HTN sometimes

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3
Q

what investigations should you request for suspected 1y hyperaldosteronism, and what might be the findings?

A

U&E: Raised Na+, Low K+, alkalotic (excreting lots of H+)
LOOK FOR A SUPPRESSED RENIN AND HIGH ALDOSTERONE (aldo may be normal if severe hypokal)
Renin - low? (high would suggest 2y)
Aldosterone - raised

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4
Q

how would you treat:

  1. Conn’s syndrome
  2. Bilateral adrenocortical hyperplasia
A
  1. control BP and K+ for 4 weeks before laparoscopic adrenalectomy
  2. Treat medically with aldosterone antagonis: spiro / amiloride / eplerenone
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5
Q

will renin be raised or decreased in 2y hyperaldosteronism?

A

RAISED
2y is caused by decreased renal perfusion - eg. Renal artery stenosis / accelerated HTN / diuretics / CCF / hepatic failure

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6
Q

describe the presentation of a phaeochromocytoma (triad..)

A 
JUST THINK INCREASED ADRENALINE
Episodic headache
sweating 
tachycardia
(+/- BP changes - occasionally SIG HTN)
OFTEN EPISODIC AND OFTEN VAGUE!!
CNS: headache / dizziness 
Psych: anxiety / panic / hyperactivity
Gut: D&V /  abdo pain
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7
Q

what tests would you order if susp Phae

A

FBC - WWC increased
24 hr urinary collection of metanephrines
could do clonidine suppression test if borderline..
CT / MRI abdo

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8
Q

how would you prepare someone with a Phae for surgery?

A
  1. a-blocker (long acting) started eg. phenoxybenzamine
  2. b-blocker started AFTER eg. propranolol
    (need to start a first because if started b first would have crisis due to unopposed a-adrenergic stimulation (would result in increased TPR / CA vasoconstriction)
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9
Q

what are the rules of 10 for phaeos?

A

10% malignant
10% familial
10% extra-adrenal (often found by the aortic bifurcation)
10% bilateral

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10
Q

What syndrome might explain these three presentations?

  1. HTN associated with hypokalaemia
  2. refractory HTN, especially despite >=3 anti-HTN drugs
  3. HTN pre-40 (especially women..)
A

?pheao?

could also be 1y hyperaldosteronism

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11
Q

what can cause a hypertensive crisis in someone with a Phaeo?

A

stress / abdo palpation / parturition / GA / contrast media

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12
Q

what are the S&S of a phae emergency?

A

Pallor / pulsating headache / HTN / feels ‘about to die’ / pyrexial.

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13
Q

how should you manage an acute phaeo emergency?

A
  1. Get help - ICU
  2. combined a+B blockade - with a started irst otherwise HTN may worsen
    2a. Short acting a-blocker - phentolamine
    2b. long acting a-blocker - phenoxybenzamine
  3. B-blocker (control tachyarrythmias / myocardial ischaemia / / dysrythmias)
  4. Surgery after 4/6 weeks. Alpha blocker increased until level of significant postural hypotension..
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14
Q

29 year old male
very fit but recently taken up fell running
18 mile race with 2200m of ascent in morning of hottest day of the year
Regular water throughout race and all afternoon after - witnessed
That evening - found at home drowsy and confused, evidence of urinary incontinence
ambulance to A&E

O/E:
GCS 10, agitated
BP, P normal, not dehydrated
No focal neurology
CT head normal
ABG - no acid/base disturbance
02 sats on air 99%
Investigations
Na+ 			122 mmol/L (133 – 145)
K+			4.1 mmol/L (3.5 – 5.2)
Urea			2.6 mmol/L (2.5 – 7.8)
Creat			79 umol/L (44 – 80)
Glucose 		4.6 mmol/L (4.0 – 5.5)
Plasma osmol	249 mOsmol/kg (270 – 295)
Urine osmol        220 mOsmol/kg
Urine sodium	30 mmol/L

What is the diagnosis / causal mechanism?
How do you manage this?

A

Mechanism / Dx: high ADH (vasopressin) secretion because of intense exercise + XS hypotonic fluid intake

Pt has low GCS
hyponatraemic
fit and well, no real medical problems, sudden..

3.0% normal saline (hypertonic solution) 150ml bolus over 20 mins
May need to repeat bolus

Sx of severe hyponatraemia: Coma / seizures / confusion..

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15
Q

if your patient has been severely hyponatraemic for more than 48hrs (chronic hyponatraemia) - how fast can you correct this and what is the consequence if you correct too fast?

A

don’t bring up more than 10mmol in the first 24hrs
not more than 8mmol / day after that
Consequence: Osmotic demyelination (all the water rushes out of the CNS - CNS has adjusted to hyponatraemia)

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16
Q

38 year old African American – presented to A+E
7 day - feeling weak and unwell
2 months - Lethargic, nauseous, loss of appetite, weight loss 8kg
Dizzy, felt like lying down all day
GP started Thyroxine 8 days ago
Observed in A+E
Given anti-emetic - Home

Re-presented later that day – worse
Referred to medics
Thin, not well
Orientated and not confused
BP 110/58, lying, 90/60 standing 
P 100 reg
Medication history: levothyroxine 50ug OD only
Investigations:
Hyponatraemia
TSH raised
Urine Na raised
Potassium slightly raised

What is your choice of treatment?

A

ie. gp started on levothyroxine - got worse
- is still ill - so questioning initial choice of hypothyroid diagnosis

Suspected adrenal insufficiency -

Give 100mg Hydrocortisone + 0.9% Saline
(mineralocorticoid effect - holds Na in the circulation - prevents the potential imminent shock)

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17
Q

how should you split the assessment of causes of Hyponatraemia by fluid volume?

A

Fluid Overloaded
Normovolaemic
Dehydrated
(see ppt)

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18
Q

what is the gold standard test to Dx adrenal insufficiency?

A

Short synacthen test
(essentially giving ACTH)
measure plasma cortisol at 0 mins and 30 mins
should raise 500 nmol/L - if it doesn’t then it is primary adrenal insufficiency

19
Q

if there is a high ACTH in adrenal insufficiency - is it likely to be primary or secondary adrenal insufficiency?

A

primary - as Pituitary is making loads of ACTH o try and kick the adrenals into action..

20
Q

what is the effect of cortisol on TSH in the pituitary?

A

cortisol inhibitis TSH

thus in adrenal insufficiency - can often get raised TSH

21
Q

what can happen if a patient who has been on steroids for a long time?

A

they could be adrenally suppressed
If suspecting it - give hydrocortisone
DON’T BE SCARED TO DO THIS

22
Q

what is the acute management of adrenal insufficiency?

A
  1. samples for cortisol and ACTH
  2. IV Normal saline
  3. Hydrocortisone 100mg IM 6hourly until eating and drinking
    Tx precipitant (infection??)
    Hydrocortisone TDS to maintain
    (add fludrocortisone if primary adrenal insufficiency)
23
Q

What is the immediate management of a suspected (clinical diagnosis..) Phaeo

A

Start non-competitive short-acting alpha-blocker (phentolamine (phento - pronto) - then long - phenoxybenzamine)
(first because B-blocker may mean that all the circulating catecholamine is directed to the a-receptors - which will cause further vasoconstriction and may make things worse!! can actually trigger a Phaeo crisis..)
THEN - start B-blocker
Urine for metanephrines
Plasma metanephrines
MANGE ON HDU / ITU
Then image once biochem confirmed.. (to avoid diagnosing an ‘incidentaloma’

24
Q

what is HTN + TACHY until proven otherwise (especially in a younger pt)

A

PHAEO

25
Q 
24 year old woman
 sudden headache
 neck stiffness
 diplopia – VI nerve palsy on left
 photophobia
relatively common px until..
 Urgent CT - ? Mass in pituitary fossa

What is the Dx
What is the initial management?

A

Dx: likely Adrenal insufficiency - from Pituitary Apoplexy

Mx: IV hydrocortisone

26
Q

what is the presentation of pituitary apoplexy?

A

SIMILAR TO SAH + OCULAR SIGNS IN MOST + VISUAL FIELD DEFECTS

usually a history of pituitary tumour
or look Cushingoid / Acromegalic
May have circulatory collapse due to low ACTH and low cortisol

27
Q

how do you manage Pituitary Apoplexy?

A

Urgent neurosurgical referral, and surgery may be required
blood taken first for full pituitary screen:
LH,FSH,TSH,FT4,FT3,cortisol, Prolactin, ACTH (if possible)
IM/IV hydrocortisone as for adrenal failure - this MUST be given if any suspicion of apoplexy

28
Q 
54 year old woman
Confused and has had a low mood 
Suffers from constipation
Had been drinking “a lot”
She has recently been diagnosed with a peptic ulcer

Which blood test to carry out?

A

adjusted calcium

29
Q

give some causes of hypercalcaemia:

A
  1. 1y hyperparathyoidism
  2. malignancy
Everything else..:
Lithium, thiazides
Thyrotoxicosis
Adrenal insufficiency
Hypervitaminosis D
Granulomatous disease
Familial hypocaliuric hypercalcaemia
30
Q

Management of hypercalcaemia

A

check drugs / fam Hx / thorough symptom Hx
ECG - short QT
check PTH / phosph / alk phosph / renal fn
Rehydration with intravenous fluids – 0.9% saline 4-6 litres in 24 hours
Intravenous bisphosponates
Zoledronic acid 4mg over 15mins; Pamidronate 30 to 90mg at 20mg/hr
Glucocorticoids
Calcimimetics
Denosumab

31
Q

how would you manage mild hypocalcaemia?

A

Mild hypocalcaemia (Asymptomatic, >1.9mmol/L)
Commence oral calcium supplements (AdCal 3 tabs bd)
Post-thyroidectomy – Calcium supplements and consider adding 1-alphacalcidol (0.25mcg/day)
If Vitamin D deficiency, load with cholecalciferol for 12 weeks
If hypomagnesaemia, replace magnesium

32
Q

how would you manage severe hypocalcaemia?

A

Severe hypocalcaemia (Symptomatic, <1.9mmol/L)
10-20mls of 10% calcium gluconate over 10 mins (in 50-100mls of 5% dextrose)
Dilute 100mls of 10% calcium gluconate in 1L of Normal saline (at 50-100mls/hour)
Post-operative hypocalcaemia or hypoparathyroidism give 1-alphacalcidol 0.25mcg/day

33
Q 
32 year old lady
Agitated and tremulous
Palpitations 
Irritable
Vomiting
Temp: 39.8oC
Tachycardia and BP 170/110
Tremor

WHAT TEST??

A

Random cortisol

THYROTOXICOSIS

34
Q

how would you manage a Thyrotoxic Crisis?

A

Propythiouracil better than Carbimazole, 250 mg 4-6 hourly (po/NG/rectally) (prevents synthesis)
1 hour later 8 drops Lugol’s iodine qds (prevents release)
Propanolol 80-120 mg qds
Cholestyramine 4g qds (enterohepatic circulation)
Other general therapeutic measures e.g. fluids and treat any underlying illnesses

35
Q

what is the most common (non-idiopathic) treatable cause of HTN?

A

primary hyperaldosteronism

NB - most patients are NORMOKALAEMIC

36
Q

describe a typical presentation of 1y hyperaldosteronism

A 
htn
nocturia / polyuria
lethargy
mood disturbance
difficulty concentrating
37
Q

what is the commonest endocrine emeregency?

A

hypoglycaemia

ALWAYS CHECK THE BMS IN EVERYONE…

38
Q

define hypoglycaemia

A

plasma glucose =< 3 mmol/L

39
Q

list some Sx of hypoglycaemia

A

autonomic:
sweating / anxiety / hunger/ tremor / palp / dizziness

neuroglycopenic:
confused / drowsy / decreased GCS / vision changes / seizure / coma

40
Q

what are the causes of hypoglycaemia in

  1. a known diabetic
  2. a non-diabetic
A
  1. insulin / sulfonylurea Tx in a diabetic
    increased acitivty / missed meal / overdose
    (check circulating oral hypoglycaemics…)
  2. EXPLAIN the symptoms

Exogenous drugs - eg. insulin / alcohol / ACEi

Pituaitary insufficiency

Liver failure

Addisions!!

Iselt-cell tumours / immune hypoglycaemia (eg anti-insulin receptor antibodies in Hodgkin’s disease

Non-pancreatic neoplasms, eg fi brosarcomas and haem angiopericytomas.

41
Q

what is the management of DKA?

A

fluids first (0.9% saline)
then after 1hr add insulin (?0.1units/kg body weight…?)
monitor with vbgs - pH / lactate / ketonaemia
monitor potassium - hypokalaemia is a risk - may need to add K+ to saline bags (40mg if 3.5-5.5 - bt if <3.5 call HDU

reassess frequently to make sure not pushing fluid too fast - especially paeds / elderly / comorbidities

usually 1L over 1hr
1L over 2hrs
1L over 2hrs
1L over 4 hours
1L over 4hrs
1L over 8hrs

when plasma glucose <14mmol/l start 10% glucose at 125mL/hr to prevent hypoglycaemia…

DO NOT GIVE BICARB - acidaemia should correct itself - and bicarb increases the risk of cerebral oedema..

42
Q

if someone has ++ketonuria but normal blood glucose - what should you consider?

A

alcohol

as well as DKA obvs..

43
Q

how do you treat a hyperglycaemic hyperosmolar state?

A
  1. LMWH proph as occlusive events are a real danger
    unless CIed
  2. Rehydrate slowly with IVI 0.9% saline over 48hrs
  3. start to replace K+ when PUing
  4. ONLY use insulin if blood glucose not falling by 5mmol/hr
44
Q

describe a typical px of hhs

A

unwell patients with t2dm
longer hx - usually about 1wk
marked dehydration + glucose >30
no switch to ketone metabolism - so ketones normalish and pH ok
keep Blood glucose at 10-15 mmol/l for first 24hrs to avoid cerebral oedema

endocrine (3 decks)

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