Endocrine 2

12/3/2018 Endocrine - FRCEM Success
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Question
Endocrine Navigator
Question 1 of 11
1 Current Question
A 45 year old woman, with known thyroid disease, presents
to AED complaining of agitation, palpitations and feeling hot and 2 ...
ushed. These symptoms started 2 days earlier. Her observations
3 ...
are: BP 180/150, HR 120, RR 20, sats 98% OA, and temperature
38.5°C. A picture of the patient is shown below: 4 ...
5 ...
6 ...
7 ...
8 ...
9 ...
10 ...
11 ...
Courtesy of Jonathan Trobe, M.D. – University of Michigan Kellogg Eye

Center (The Eyes Have It) [CC BY 3.0
(http://creativecommons.org/licenses/by/3.0)], via Wikimedia
Commons
a. Give two abnormalities seen in the image and give her

underlying diagnosis. (1 mark)
b. Outline what thyroid function test abnormalities (T3, T4,
TSH) you would expect in this patient. (1 mark)
c. You are concerned about the possibility of thyrotoxic crisis.
Give three drugs that could be used to manage this condition.
(1 mark)
You did not answer this question
https://intermediate.frcemsuccess.com/rev/endocrine/ 1/3
Answer
a. Lid retraction and proptosis – Graves’ disease
b. Elevated T3 and T4 and inappropriately low TSH
c. Any three of:
Carbimazole
Propylthiouracil
Iodine oral solution
Beta-blockers
Notes
Hyperthyroidism occurs when an excess of circulating thyroid hormones
(thyrotoxicosis) is produced by an overactive thyroid gland.
Causes:
Primary (high T3 & T4, low TSH)

Graves’ disease (most common cause – accounts for 75% of cases):
autoimmune antibodies stimulate the TSH receptor leading to
excessive secretion of thyroid hormones and hyperplasia of thyroid
follicular cells, causing a toxic diffuse goitre
Toxic multinodular goitre
Toxic thyroid adenoma
Drugs e.g. amiodarone, IV contrast media, lithium
Secondary (high T3 & T4, high TSH)
Pregnancy
Pituitary adenoma
Graves’ orbitopathy:
Eye irritation, photophobia, redness or excessive lacrimation

Eyelid retraction (sclera is visible above the superior corneal limbus)
Lid lag (delay in moving the eyelid as the eye moves downward)
Proptosis with inability to close the eyes – high risk of corneal
ulceration
Diplopia (typically when looking upwards and outwards)
Restricted eye movements
Orbital aching
Visual disturbance
Thyrotoxic crisis:
Thyroid storm (thyrotoxic crisis) is a rare and potentially life-threatening

complication of hyperthyroidism, and may occur after trauma, childbirth,
surgery, infection, or stroke, for example (in people with untreated or
suboptimally treated hyperthyroidism).
Clinical features:
Tachycardia
Fever
Atrial brillation
Heart failure
Diarrhoea
Vomiting
Dehydration
Jaundice
Agitation
Delirium
Coma
Management:
Treat underlying cause e.g. infection

IV access and uid resuscitation
Monitor blood glucose
Antipyretics and cooling techniques
Antithyroid treatment:
Carbimazole
Propylthiouracil
Iodine oral solution (at least 1 hour after oral treatment, to prevent
new hormone synthesis)
Beta-blockers (initially IV propranolol 5 mg, than orally)
Hydrocortisone (treats possible adrenal insuf ciency and
reduces T4 to T3 conversion)
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Question
Endocrine Navigator
Question 2 of 11
1 Unanswered
A 19 year old girl, known to have type 1 diabetes mellitus, is
brought to AED by ambulance. She has been unwell with vomiting 2 Current Question
over the past couple of days with a tummy bug. She has cut down
3 ...
on her insulin as she was concerned about becoming
hypoglycaemic. She is drowsy and dehydrated. You suspect 4 ...
diabetic ketoacidosis. Her venous blood gas is shown below:
5 ...
pH 7.25 (7.35 – 7.45) 6 ...

PaCO 3.2 kPa (4.7 – 6.0) 7 ...
HCO3 11 mmol/L (22 – 28)
K+ 4.5 mmol/L (3.5 – 5.3) 8 ...
Na+ 135 mmol/L (135 – 145)
9 ...
Cl- 100 mmol/L (5 – 105)
10 ...
a. Describe the abnormalities seen on this arterial blood gas. (1
mark) 11 ...
b. Calculate this patient’s anion gap, giving your working. (1
mark)
c. Give three alternative causes for the nding in part b. (1
mark)
Answer
a. Metabolic acidosis with partial respiratory compensation
b. Anion gap = (Na+ + K+) – (Cl– + HCO3–) = (135 + 4.5) – (100 + 11) =
28.5 mmol/L (N.B. normal range: 7 – 16)
c. Causes of raised anion gap acidosis (any three of the following):
C: Cyanide/carbon monoxide
A: Alcoholic ketoacidosis
T: Toluene
M: Methanol/metformin
U: Uraemia
D: Diabetic ketoacidosis
P: Paracetamol/paraldehyde/propylene glycol
I: Iron/isoniazid
L: Lactate
E: Ethanol/ethylene glycol
S: Salicylate
Notes
Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1
diabetes mellitus characterised by ketonaemia (ketosis), hyperglycaemia and
acidosis. DKA usually occurs as a consequence of absolute or relative insulin
de ciency that is accompanied by an increase in counter-regulatory hormones
(i.e. glucagon, cortisol, growth hormone, catecholamines). This hormonal
imbalance enhances hepatic gluconeogenesis and glycogenolysis resulting in
severe hyperglycaemia. Enhanced lipolysis increases serum free fatty acids that
are then metabolised as an alternative energy source in the process of
ketogenesis. This results in accumulation of large quantities of ketone bodies
and subsequent metabolic acidosis.
Clinical features of DKA:
Thirst, polyuria, polydipsia

Dehydration
Hypotension and tachycardia
Abdominal pain, nausea, vomiting, diarrhoea
Kussmaul breathing (respiratory compensation for metabolic acidosis)
Ketotic breath
Altered conscious level, confusion, coma
Complications of DKA:
Cerebral oedema (more common in children)

Pulmonary oedema
Severe hypokalaemia (as a consequence of treatment)
Hyperkalaemia
Hypoglycaemia (as a consequence of treatment)
Adult respiratory distress syndrome (ARDs)
Aspiration pneumonia
Comorbid states e.g. pneumonia, acute myocardial infarction, sepsis
Diagnosis:
Ketonaemia > 3.0 mmol/L or signi cant ketonuria (more than 2+ on

standard urine sticks)
Blood glucose > 11.0 mmol/L or known diabetes mellitus
Bicarbonate (HCO3-) < 15.0 mmol/L and/or venous pH < 7.3
Investigations:
Blood and urine ketones

Capillary blood and venous plasma glucose
U&Es
Venous blood gas
ECG and continuous cardiac monitoring
Infection screen
FBC, CRP
CXR if indicated
Urine dipstick and culture if indicated
Blood cultures if indicated
Pregnancy test
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Question
Endocrine Navigator
Question 3 of 11
1 Unanswered
brought to AED by ambulance. She has been unwell with vomiting 2 Unanswered
3 Current Question
hypoglycaemic. She is drowsy and dehydrated. Her observations 4 ...
are: temperature 37.5°C, HR 100 bpm, BP 105/65, RR 24, sats
5 ...
92% OA. Her capillary blood glucose level is 30 mmol/L, and her
urine shows +++ ketones. 6 ...
7 ...
a. Outline the insulin regimen (including dose and rate) that
should be started immediately in this patient. (1 mark) 8 ...
b. Outline when and how glucose should be given in the 9 ...
treatment of diabetic ketoacidosis. (1 mark)
c. Outline how treatment should be monitored and what 10 ...
treatment targets aimed for. (1 mark) 11 ...
Answer
a. Intravenous human soluble insulin (e.g. Actrapid) infusion at a
concentration of 1 unit/mL, at a xed rate of 0.1 units/kg/hour – and
rate than adjusted accordingly
b. Once blood-glucose concentration falls below 14 mmol/L – IV dextrose
10% should be given at a rate of 125 mL/hour, together with 0.9% saline
and insulin infusions
c. Check blood ketone and blood glucose concentrations hourly – Blood
ketone concentration should fall by at least 0.5 mmol/litre/hour and
blood glucose concentration should fall by at least 3 mmol/litre/hour
Notes
f
Management of DKA:
ABCDE assessment
Large bore IV access
Assess uid status, consider catheterisation (aim for urine output > 0.5
ml/kg/hr)
Fluid resuscitation
If Systolic BP < 90 mmHg (adjusted for age, sex, and medication as
appropriate), 500 mL sodium chloride 0.9% should be given by
intravenous infusion over 10 – 15 minutes, and repeated if SBP still
< 90 mmHg. If there is no clinical improvement, seek immediate
senior assessment and consider ITU involvement
When systolic BP > 90 mmHg, IV sodium chloride infusion should
be continued at a rate that replaces de cit and provides
maintenance
Potassium chloride (40 mmol/L) should be included in the uids (as
long as the serum potassium level < 5.5 mmol/L and the patient is
passing urine), and the plasma potassium concentration maintained
between 3.5 – 5.5 mmol/L (measured at 60 minutes, 2 hours, and 2
hourly thereafter; and hourly if outside the normal range)
Insulin
An intravenous human soluble insulin infusion should be started at
a concentration of 1 unit/mL, at a xed rate of 0.1 units/kg/hour
Established subcutaneous long-acting insulin therapy should be
continued concomitantly
Blood ketone and blood glucose concentrations should be checked
hourly and the insulin infusion rate adjusted accordingly. Blood
ketone concentration should fall by at least 0.5 mmol/litre/hour
and blood glucose concentration should fall by at least 3
mmol/litre/hour
The insulin infusion should be continued until blood ketone
concentration is below 0.6 mmol/litre, blood pH is above 7.3 and
the patient is able to eat and drink; ideally the insulin infusion
should be stopped about an hour after giving subcutaneous fast-
acting insulin and a meal
Glucose
Once blood-glucose concentration falls below 14 mmol/litre,
glucose 10% should be given by intravenous infusion (into a large
vein through a large-gauge needle) at a rate of 125 mL/hour, in
addition to the sodium chloride 0.9% infusion

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Question
Endocrine Navigator
Question 4 of 11
1 Unanswered
A 71 year old female patient with known type 2 diabetes, for
which she takes metformin and a sulphonylurea, is brought to AED 2 Unanswered
by her carer, with drowsiness and confusion. Her BM is tested by
3 Unanswered
the triage nurse and found to be 2.5 mmol/L.
4 Current Question
a. How could you initially manage this patient non-invasively 5 ...

(including dose and route)? (1 mark)
6 ...
b. Before you can enact your management plan, the patient
becomes more drowsy and unresponsive. Give two treatment 7 ...
options (including dose and route) available to you now. (1
8 ...
mark)
c. Give two factors that may precipitate hypoglycaemia in type 1 9 ...
or 2 diabetes mellitus. (1 mark)
10 ...
11 ...
Answer
a. Give 15 – 20 g oral quick acting carbohydrate of the patient’s choice
where possible e.g. 90 – 120 mL of Lucozade or 5 – 7 Dextrosol tablets
or 1.5 – 2 tubes of Glucogel
b. Any two of:
Glucagon 1 mg intramuscularly
75 – 100 ml of 20% glucose intravenously
150 – 200 ml of 10% glucose intravenously
c. Any two of:
Overly strict glycaemic control
Impaired hypoglycaemic awareness
Severe hepatic dysfunction
Impaired renal function
Increased exercise
Missed/delayed meal
ssed/de ayed ea
Alcohol
Pregnancy
Drugs
Addison’s disease
Overdose of insulin/oral hypoglycaemic agents (e.g. prescription
error)
Notes
Hypoglycaemia is a medical emergency; any blood glucose less than 4.0 mmol/L
should be treated. Autonomic symptoms are generated by the activation of the
sympathoadrenal system and neuroglycopenic symptoms are the result of
cerebral glucose deprivation. Hypoglycaemia should be excluded in any person
with diabetes who is acutely unwell, drowsy, unconscious, unable to co-operate,
presenting with aggressive behaviour or seizures.
Clinical features:
Sweating
Palpitations
Shaking
Hunger
Headache
Nausea
Confusion
Drowsiness
Odd behaviour
Speech disturbance
Incoordination
Seizures
Management
In adults who are conscious and cooperative:

Give 15 – 20 g quick acting carbohydrate of the patient’s choice
where possible e.g. 90 – 120 mL of Lucozade or 5 – 7 Dextrosol
tablets
Repeat capillary blood glucose 10 – 15 minutes later
If blood glucose is still < 4.0 mmol/L, repeat step 1 (no more than 3
treatments in total)
If blood glucose remains < 4.0 mmol/L after 30 – 45 minutes or 3
cycles, consider
1 mg glucagon IM
150 – 200 mL of 10% glucose IV over 15 minutes
Once blood glucose is > 4.0 mmol/L and the patient recovered, give
a long acting carbohydrate of the patient’s choice where possible
e.g. two biscuits, one slice of bread
In adults who are conscious but uncooperative:
Give either 1.5 – 2 tubes Glucogel/Dextrogel (may repeat up to 3
times) or if this is ineffective give glucagon 1 mg IM (may only give
times) or if this is ineffective give glucagon 1 mg IM (may only give
once)
In adults who are unconscious:
Give either:
75 – 100 ml of 20% glucose intravenously over 15 minutes
150 – 200 ml of 10% glucose intravenously over 15 minutes
1 mg glucagon intramuscularly (less effective in alcoholics,
prolonged starvation, severe liver disease, and sulphonylurea
therapy)
If the hypoglycaemia was due to sulfonylurea or long acting insulin therapy then
be aware that the risk of hypoglycaemia may persist for up to 24 – 36 hours
following the last dose, especially if there is concurrent renal impairment.

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Question
Endocrine Navigator
Question 5 of 11
1 Unanswered
A 69 year old lady with a history of type 2 diabetes mellitus
for which she takes metformin, is brought to AED by ambulance. 2 Unanswered
She has been in bed for the last couple of days with a u-like
3 Unanswered
illness. She is drowsy, confused and dehydrated. Her blood results
are shown below: 4 Unanswered
5 Current Question
K+ 4.5 mmol/L (3.5 – 5.3)
Na+ 145 mmol/L (135 – 145) 6 ...
Urea 25 mmol/L (2.5 – 6.7) 7 ...
Creatinine 170 umol/L (50 – 150)
Glucose 32 mmol/L 8 ...
a. Hyperosmolar hyperglycaemic state (HHS) is characterised 9 ...
by which three features? (1 mark) 10 ...

b. Calculate this patient’s osmolality, showing your workings. (1
mark) 11 ...
c. If the measured serum osmolality is 360 mOsm/kg, calculate

the osmolal gap and give two possible causes for this nding.
(1 mark)
Answer
a. Hypovolaemia, marked hyperglycaemia and raised serum
osmolality (without signi cant hyperketonaemia and acidosis)
b. Calculated osmolality = [2Na+ + Glucose + Urea] =[(2 x 145) + 32 + 25]

= 347 mOsm/kg (N.B. normal serum osmolality is 275 – 295 mOsm/kg)
c. Osmolal gap = [Serum osmolality – Calculated osmolality] = [360 – 347]
= 13 mmol/kg Causes of raised osmolal gap:
Alcohol e.g. ethanol, methanol, ethylene glycol, isopropyl alcohol
Mannitol
Lorazepam infusion
Notes
HHS usually develops gradually in patients with type II diabetes mellitus due to
a combination of illness, dehydration and relative insulin de ciency.
HHS is characterised by:
Hypovolaemia
Marked hyperglycaemia (30 mmol/L or more) without signi cant
hyperketonaemia (< 3 mmol/L) or acidosis (pH > 7.3, bicarbonate > 15
mmol/L)
Osmolality usually 320 mOsmol/kg or more
Complications:
Hypothermia
Myocardial infarction
Stroke
Peripheral arterial thrombosis
Seizures
Cerebral oedema
Central pontine myelinolysis (CPM)
Venous thromboembolism
Foot ulceration
Management:
Fluid and electrolyte replacement

Use 0.9% sodium chloride as the principle uid
Measurement or calculation of osmolality should be undertaken
every hour initially and the rate of uid replacement adjusted to
ensure a positive uid balance suf cient to promote a gradual
decline in osmolality
Fluid replacement alone (without insulin) will lower blood glucose
which will reduce osmolality causing a shift of water into the
intracellular space
This inevitably results in a rise in serum sodium (a fall in blood
glucose of 5.5 mmol/L will result in a 2.4 mmol/L rise in sodium).
Rising sodium is only a concern if the osmolality is NOT declining
concurrently. Rapid changes must be avoided – a safe rate of fall of
plasma glucose of between 4 and 6 mmol/hr is recommended
(thereafter, the rate of fall of plasma sodium should not exceed 10
mmol/L in 24 hours)
A target blood glucose of between 10 and 15 mmol/L is a
reasonable goal. Complete normalisation of electrolytes and
osmolality may take up to 72 hours
Monitor and replace potassium as required
Insulin
Sh ld l b t t d i i iti l it ti if th i i i t
Should only be started in initial resuscitation if there is signi cant
ketonaemia on initial assessment (as xed rate intravenous insulin
infusion given at 0.05 units/kg/hr)
A fall of glucose at a rate of up to 5 mmol/L per hour is ideal
Otherwise, insulin may be started if blood glucose has ceased to
fall following appropriate uid resuscitation, or if already in place,
the infusion rate may be increased by 1 unit/hr
Anticoagulation
Start prophylactic dose LMWH

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Question
Endocrine Navigator
Question 6 of 11
1 Unanswered
A 59 year old patient, awaiting surgery for
pheochromocytoma, presents to AED with a headache. His 2 Unanswered
observations are: BP 230/125, HR 105, RR 16, sats 98% OA.
3 Unanswered
4 Unanswered
a. Outline the basic pathophysiology of a pheochromocytoma.
(1 mark) 5 Unanswered
b. What class of drug should be used to treat his hypertension?
6 Current Question
(1 mark)
c. Give two further endocrine causes of secondary 7 ...
hypertension? (1 mark)
8 ...
9 ...
10 ...
11 ...
Answer
a. Tumour of the adrenal medulla that secretes excess catecholamines
b. Alpha-blocker (e.g. phentolamine)
c. Any two of:
Cushing’s syndrome
Conn’s syndrome
Pheochromocytoma
Acromegaly
Hyperparathyroidism
Notes
A pheochromocytoma is a rare tumour of the adrenal medulla that secretes
catecholamines.
Clinical features (often paroxysmal):
Headache
Profuse sweating
Profuse sweating
Palpitations
Tremor
Flushing
Hypertension
Postural hypotension
Hyperglycaemia
Management:
Long-term management of pheochromocytoma involves surgery. However,

surgery should not take place until there is adequate blockade of both alpha-
and beta-adrenoceptors; the optimal choice of drug therapy remains unclear.
Alpha-blockers are used in the short-term management of hypertensive
episodes in pheochromocytoma. Once alpha blockade is established,
tachycardia can be controlled by the cautious addition of a beta-blocker; a
cardioselective beta-blocker is preferred.
Phenoxybenzamine hydrochloride, a powerful alpha-blocker, is effective in the

management of pheochromocytoma but it has many side-effects. Phentolamine
mesylate is a short-acting alpha-blocker used mainly during surgery of
pheochromocytoma; its use for the diagnosis of pheochromocytoma has been
superseded by measurement of catecholamines in blood and urine.

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Endocrine Navigator
Question 7 of 11
1 Unanswered
A 45 year old man is brought into AED feeling dizzy,
nauseous and lethargic. The paramedics have noted an alert 2 Unanswered
bracelet which identi es the patient as having Addison’s disease.
3 Unanswered
His observations are: temp 37.1°C, BP 90/55, HR 105, RR 16, sats
98% OA. 4 Unanswered
5 Unanswered
a. Outline the basic pathophysiology of Addison’s disease. (1
6 Unanswered
mark)
b. Give two typical electrolyte abnormalities you would expect 7 Current Question
in Addison’s disease. (1 mark)
8 ...
c. Give two factors which may have precipitated an Addisonian
crisis. (1 mark) 9 ...
10 ...
11 ...
Answer
a. Destruction of the adrenal cortex resulting in de ciency of
corticosteroid
b. Any two of:
Hyponatraemia
Hyperkalaemia
Hypercalcaemia
c. Any two of:
Trauma
Infection
Myocardial infarction
Stroke
Asthma
Alcohol
Surgery
Pregnancy
g y
Allergic reaction
Notes
Addison’s disease is a result of destruction of the adrenal cortex resulting in
reduced production of glucocorticoids, mineralocorticoids and adrenal
androgens.
Causes of Addison’s disease:
Tuberculosis (commonest cause worldwide)

Autoimmune disease
Adrenal metastases
Adrenal haemorrhage
Infection
Amyloidosis
Haemochromatosis
Congenital adrenal hyperplasia
Clinical features of Addison’s disease:
Hyperpigmentation
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Hypercalcaemia
Low cortisol, raised ACTH
Addisonian crisis occurs when a person with Addison’s disease experiences

severe physical stress. The adrenal glands cannot supply the extra
corticosteroids needed to cope with the stress, and life-threatening symptoms
develop.
Clinical features of Addisonian crisis:
Acute abdominal pain

Low-grade fever
Nausea and vomiting
Dehydration
Hypotension
Tachycardia
Hypoglycaemia
Hypovolaemic shock
Altered consciousness
Seizures
Stroke
Cardiac arrest
Management of suspected adrenal crisis:

Give immediate hydrocortisone intramuscularly or intravenously

Adults: 100 mg
Children > 6 years: 50 – 100 mg
Children 1 – 5 years: 50 mg
Children up to 1 year: 25 mg
IV uid resuscitation
Monitor and treat hypoglycaemia and other electrolyte imbalance
Treat underlying cause

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Question
Endocrine Navigator
Question 8 of 11
1 Unanswered
3 Unanswered
hypoglycaemic. She is drowsy and dehydrated. You suspect 4 Unanswered
diabetic ketoacidosis. Her observations are: temperature 37.5°C,
5 Unanswered
HR 100 bpm, BP 105/65, RR 24, sats 92% OA.
6 Unanswered
a. Give two biochemical or clinical features that indicate severe 7 Unanswered

diabetic ketoacidosis. (1 mark)
b. Brie y outline the pathophysiology of hypokalaemia in 8 Current Question
treatment of diabetic ketoacidosis and how this can be 9 ...

avoided. (1 mark)
c. Give two possible complications of diabetic ketoacidosis. (1 10 ...
mark) 11 ...
Answer
a. Any two of:
Blood ketones over 6 mmol/L
Bicarbonate level below 5 mmol/L
Venous/arterial pH below 7.0
Hypokalaemia on admission (under 3.5 mmol/L)
GCS less than 12 or abnormal AVPU scale
Oxygen saturation below 92% on air (assuming normal baseline
respiratory function)
Systolic BP below 90 mmHg
Pulse over 100 or below 60 bpm
Anion gap above 16
b. Insulin causes a transcellular shift of potassium from extracellular uid
to intracellular uid – potassium should be added to the bags of uid as

long as K+ level remains < 5.5 mmol/L and the patient is passing urine
c. Any two of:
Cerebral oedema
Pulmonary oedema
Adult respiratory distress syndrome (ARDS)
Venous thromboembolism
Acute kidney injury
Notes

Dehydration
Ketotic breath

Pulmonary oedema
Severe hypokalaemia
Hyperkalaemia (as a consequence of treatment)
Diagnosis:

ca bo ate ( CO3 ) 5.0 o / a d/o e ous p .3
Investigations:

U&Es
Venous blood gas
Infection screen
FBC, CRP
CXR if indicated
Pregnancy test

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Endocrine Navigator
Question 9 of 11
1 Unanswered
3 Unanswered
hypoglycaemic. She is drowsy and dehydrated. 4 Unanswered
5 Unanswered
a. Give two speci c clinical features on examination that you
6 Unanswered
might see in a patient with diabetic ketoacidosis. (1 mark).
b. Give two immediate bedside investigations you 7 Unanswered
would request in this patient. (1 mark)
8 Unanswered
c. Give three criteria for the diagnosis of diabetic ketoacidosis,
with values. (1 mark) 9 Current Question
10 ...
11 ...
Answer
a. Kussmaul’s breathing and peardrop (ketotic) breath
b. Capillary blood glucose test and capillary blood ketone test (or urine
dipstick for ketones if this is not available)
c. All three of:
Notes
(i l ti l th h t h l i ) Thi h l

Dehydration
Ketotic breath

Pulmonary oedema
Severe hypokalaemia (as a consequence of treatment)
Hyperkalaemia
Diagnosis:

Investigations:

U&Es
Venous blood gas
Infection screen
FBC, CRP
CXR if indicated
Pregnancy test

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Endocrine Navigator
Question 10 of 11
1 Unanswered
An 81 year old patient is brought to AED by her carer with
worsening confusion and lethargy. Blood tests are performed 2 Unanswered
which show low levels of thyroid hormones and elevated TSH.
3 Unanswered
4 Unanswered
a. Give two possible causes of primary hypothyroidism. (1 mark)
b. Give two clinical features you may expect on examination of 5 Unanswered
this patient. (1 mark)
6 Unanswered
c. Give two factors that may precipitate myxoedema crisis in a
patient with hypothyroidism. (1 mark) 7 Unanswered
8 Unanswered
9 Unanswered
10
Current Question
Answer
11 ...
a. Any two of:
Iodine de ciency
Autoimmune thyroiditis (e.g. Hashimoto’s thyroiditis)
Post-ablative therapy or surgery
Drugs e.g. antithyroid drugs, iodine, amiodarone, lithium
Transient thyroiditis e.g. postpartum
Thyroid in ltrative disease e.g. sarcoidosis, amyloidosis,
tuberculosis
Congenital hypothyroidism
b. Any two of:
Hypothermia
Facial swelling and puf ness
Coarse, sparse hair
Dry, cool skin
Bradycardia
Non-pitting oedema of hands/feet
Hypore exia
c. Any two of:
c. Any two of:
Hypothermia
Infection
Drugs e.g. amiodarone, beta-blockers, lithium
Hypoglycaemia
Stroke
GI bleed
Heart failure
Surgery
Trauma
Notes
Hypothyroidism is the clinical result of impaired production of the thyroid
hormones, thyroxine (T4) and tri-iodothyronine (T3), which are essential for
normal growth, development, and metabolism.
Causes:
Primary:
Iodine de ciency
Autoimmune thyroiditis (e.g. Hashimoto’s thyroiditis)
Post-ablative therapy or surgery
Drugs e.g. antithyroid drugs, iodine, amiodarone, lithium
Transient thyroiditis e.g. postpartum
Thyroid in ltrative disease e.g. sarcoidosis, amyloidosis,
tuberculosis
Congenital hypothyroidism
Secondary
Pituitary dysfunction
Hypothalamic dysfunction
Myxoedema coma:
Affected people are typically older and have previously undiagnosed

hypothyroidism or are poorly compliant with medication. The precipitant is
usually onset of another condition such as heart failure, sepsis, or stroke.
Patients present with hypothermia (as low as 23°C), coma and seizures.
Clinical features:
Altered mental state

Weight gain
Hypothermia
Facial swelling and puf ness
Coarse, sparse hair
Dry, cool skin
Non-pitting oedema of hands and feet
Bradycardia
Constipation
Management:
Thyroid hormone replacement

Intravenous hydrocortisone 100 mg
Supportive therapy
Therapeutic warming

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Question
Endocrine Navigator
Question 11 of 11
1 Unanswered
A 45 year old man is brought into AED feeling dizzy,
nauseous and lethargic. The paramedics have noted an alert 2 Unanswered
bracelet which identi es the patient as having Addison’s disease.
3 Unanswered
His observations are: temp 37.1°C, BP 90/55, HR 105, RR 16, sats
98% OA. 4 Unanswered
5 Unanswered
a. Give two possible causes of Addison’s disease. (1 mark)
6 Unanswered
b. What drug (including dose and route) should be given
immediately to this patient? (1 mark) 7 Unanswered
c. What biochemical endocrine abnormality would be expected
8 Unanswered
in Addison’s disease? (1 mark)
9 Unanswered
You did not answer this question 10 Unanswered
11
Current Question
Answer
a. Any two of:
Autoimmune disease
Adrenal metastases
Adrenal haemorrhage
Infection
Amyloidosis
Haemochromatosis
b. Hydrocortisone intramuscularly or intravenously – 100 mg in adults
c. Low cortisol and elevated ACTH
Notes
Addison’s disease is a result of destruction of the adrenal cortex resulting in
reduced production of glucocorticoids, mineralocorticoids and adrenal
androgens.
Causes of Addison’s disease:

Autoimmune disease
Adrenal metastases
Adrenal haemorrhage
Infection
Amyloidosis
Haemochromatosis
Clinical features of Addison’s disease:
Hyperpigmentation
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Hypercalcaemia
Low cortisol, raised ACTH
Addisonian crisis occurs when a person with Addison’s disease experiences

severe physical stress. The adrenal glands cannot supply the extra
corticosteroids needed to cope with the stress, and life-threatening symptoms
develop.
Clinical features of Addisonian crisis:
Acute abdominal pain

Low-grade fever
Nausea and vomiting
Dehydration
Hypotension
Tachycardia
Hypoglycaemia
Hypovolaemic shock
Altered consciousness
Seizures
Stroke
Cardiac arrest
Management of suspected adrenal crisis:
Give immediate hydrocortisone intramuscularly or intravenously

Adults: 100 mg
Children > 6 years: 50 – 100 mg
Children 1 – 5 years: 50 mg
Children up to 1 year: 25 mg
Monitor and treat hypoglycaemia and other electrolyte imbalance
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12/3/2018 Endocrine - FRCEM Success

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Causes of Addison’s disease:

Tuberculosis (commonest cause worldwide)

Clinical features of Addison’s disease: