Which of these causes hypercalcaemia?
b) Addison's disease
B. “Pam P. Schmidt” Mnemonic
P – Parathyroid hormone
A – Addison’s disease
M – Milk-alkali syndrome
P – Paget’s disease
S – Sarcoidosis
C – Cancer (most common cause)
H – Hyperthyroidism
M – Multiple myeloma
I – Immobilization
D – Hypervitaminosis D
T – Thiazide diuretics
Which of these is a clinical sign of hypercalcaemia?
“Stones, bones, groans, thrones, and psychiatric overtones”
Stones – nephrolithiasis, ectopic calcification
Bones – bone pain
Groans – lethargy, fatigue, weakness, headache Thrones – polyuria, polydipsia, oliguria (later)
Moans – ileus, abdominal pain, nausea and vomiting, pancreatitis
Psychiatric overtones – confusion, depression, AMS Watch for bradycardia and hypotension (volume depletion)
Bonus Pearl: hypercalcemia and hypermagnesemia cause HYPOreflexia, while hypocalcemia and hypomagnesemia produce HYPERrelexia!
Which of the following can precipitate DKA?
b) Sulphonylurea OD
c) Calorie counting
d) Hospital admission
The 5 I's
What is the definitiion of imparied glucose tolerance or impaired fasting glucose? (mmol/L)
a) Impaired fasting glucose of 7.1 - 7.9
b) Imparied fasting glucose of 8.1 - 8.9
c) Impaired glucose test of 6.1 - 6.9
d) Impaired glucose test of 11.1 - 11.9
e) HbA1c 6.0 - 6.4%
Impaired fasting glucose is 6.1 - 6.9 mmol/L
Impaired glucose tolerance is 7.8 - 11.0 mmol/L
HbA1c = 6.0 - 6.4%
Levels higher than stated are diagnostic criteria for diabetes.
What are the diagnostic criteria for diabetes?
a) Fasting plasma glucose >/= 8.0 mmol/L
b) 2 hours 75g oral glucose tolerance test >/= 11.1 mmol/L
c) Random plasma glucose >/= 10.0 mmol/L
d) HbA1c >6.5% in a child
e) HbA1c >6.5% in an adolescent
Fasting glucose >/= 7.0 mmol/L (no intake for 8 hours)
2h 75g OGTT >/= 11.1 mmol/L
Random plasma glucose >/= 11.1 mmol/L
HbAic >6.5% (not for the diangosis of type 1, children, adolecscents or pregnant women)
Patients with hyperglycaemic symptoms (polyuria, polydipsia, polyphagia, weight loss and blurry vision)
Which of the following can cause diabetes?
b) Down's syndrome
c) Klinefelter's syndrome
d) Turner's syndrome
Type 1 DM is caused by immune mediated beta cell destruction usually leading to absolute insulin deficiency.
Type 2 DM ranges from predominantly insulin resistance with relative insulin deficiciency to a predominantly insulin secretory defect with insulin resistance secondary to beta cell dysfunction.
Other specific causes of DM:
Genetic defect of beta cell function (Maturity onset diabetes of the young)
Pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, haemochromatosis (bronze diabetes)
Endocrinopathies: Acromegly, Cushing's syndrome, glucagonoma, phaeochromocystoma, hyperthyroidis,.
Drug induced: Glucocorticosteroids, thyroid hormone, beta-adrenergic agonists, thiazides, phenytoin, clozapine.
Infections: Congenital rubella, CMV, coxsackie.
Down's, Klinefelter's and Turner's syndrome are only associated with DM and not the cause.
Which of the following is a risk factor for type 1 diabetes?
b) First degree relative with DM
d) Myasthenia gravis
e) Black race
Personal or family history of autoimmune disease increases risk. Grave's, myasthenia gravis, autoimmune thyroid disease, coeliac disease and pernicious anaemia.
Type 2 risk factors include:
Age > 40, abdominal obesity, fatty liver, first-degree relative with DM, hyperuricaemia, race/ethnicity (Black or aboriginal, hispanic, Asian-American, Pacific Islander). History of insulin intolerance, HTN, dyslipidaemia, medications (2nd generation antipsychotics), PCOS and Hx of genestational DM or macrosomic baby.
Which of the following is correct when dosing insulin for diabetes?
a) In type 2 diabetes if insulin is required a nighttime basal dose fo 20 is a good starting dose.
b) In type 2 diabetes the fasting morning glucose should be <7.0 mmol/L. If not titrate up by 2 units until the target is achieved.
c) For type 1 DM the estimated total insulin requirement is 0.5 - 1.0 U/kg.
d) For type 1 DM the total insulin requirement is split to 40% basal at bedtime and 20% for breakfast, lunch and dinner.
e) For type 1 DM is premixed insulin is being used 1/3rd is given before breakfast and 2/3rds before dinner.
T2DM: Start with 10 units of basal insulin at bedtime and titrate up by 1 unit until fasting glucose is <7.0 mmol/L.
T1DM: Estimated requirements is 0.5 - 0.7 U/kg. 40% is given as basal insulin at bedtime and 20% is given as bolus insulin before breakfast, lunch and dinner. If using a premixed insulin give 2/3 dose before breakfast and 1/3 dose before dinner.
Which of the following statements are true:
a) Exogenous insulin use causes increased c-peptide
b) Neuroglycopenic symptoms occur before adrenergic symptoms in hypoglycaemia
c) C-peptide is released into the circulation when proinsulin is cleaved to insulin.
d) Hypoglycaemic unawareness is prominant in type 2 diabetes.
e) Hypoglycaemic unawareness can be caused from an increased glucagon/epinephrine response.
C-peptide is released into the circulation when proinsulin is cleaved to insulin.
Exogenous insulin causes decreased or normal c-peptide levels.
In hypoglycaemia adrenergic symptoms (palpitations, sweating, anxiety, tremor and tachycardia) occur before neuroglycopenic symptoms (dizziness, headache, clouding of vision, confusion, seizures and coma).
Hypoglycaemia unawarness is worse in type 1 diabetics and is caused by repeated low glucose and HbA1c levels, autonomic neuropathy and decreased glucagon/epinephrine response.
Which of the following statements are correct:
a) Pancreatic islet tumours can secrete ectopic GHRH
b) Growth Hormone excess in adults results in gigantism
c) In acromegaly there is decreased insulin-like growth factor-1
d) A glucose test of 75g will cause raised GH levels in healthy individuals.
e) Surgery is the only treatment option for a tumour in the sella turcica.
Growth hormone excess in children causes gigantism but acromegaly in adults (i.e. once the epiphyseal plates have closed).
In GH excess there will be elevated serum insulin-like growth factor and a glucose suppression test will show normal or elevated levels of growth hormone. Normally glucose suppresses GH.
There are many treatment options including surgery, octreotide (somatostatin analogue), dopamine agonist (bromocriptine/cabergoline), GH receptor antagonist (pegvisomant), radiation.
Which of the following is correct?
a) A prolactinoma is a rare pituitary adenoma
b) Hyperprolactnaemia is common in pregnancy
c) Dopamine stimulates prolactin release
d) Prolactin-secreting tumours are fast growing
e) Prolactin is metabolised by the liver and excreted by the kidneys
Hyperprolactinaemia is common in pregnancy and breastfeeding. It is the commonest pituitary adenomas and dopamine inhibits prolactin release. The tumours are usually slow growing. Prolactin is metabolised in both the liver and the kidneys.
Which of the following statement is true regarding diabetes insipidus (DI)?
a) Central DI can be caused by lithium
b) Nephrogenic DI can be caused by hyperkalaemia
c) A test dose of DDAVP will concentrate the urine in central DI
d) Fluid deprivation will not help with psychogenic polydipsia
e) Hyponatraemia is the classic laboratory finding
Central DI is due to insufficent ADH from either pituitary surgery, tumours, idiopathi/autoimmune, stalk lesions, hydrocephalus, histocytosis X, trauma, familiar central DI.
Nephrogenic DI is due to an ineefective response from the kidneys to ADH caused by; drugs (lithium), hypercalacaemia, hypokalaemia, chronic renal disease and hereditary nephrogenic DI.
Osmotic diuresis and psychogenic polydipsia must be ruled out. A fliud deprevation test will rule out psychogenic DI as urine output will reduce and urine osmolality will increase (the oppposite occurs in true DI).
Hypernatraemia can develop with inadequate water consumption or secondary to impaired thirst mechnism while passages of large dilute urine are occuring.
DDAVP = desmopressin which is the synthetic version of vasopressin. A DDAVP test will concentrate the urine in a central cause (central = concentrated urine). However, in nephrogenic there is no effect.
Treatment is DDAVP for central DI
Nephrogenic requires solute restriction, NSAIDs and thiazide diuretics. DDAVP can be used is there is partial response.
Which is of the following is true of the SIADH definition?
a) Hypo-osmolar hyopnatraemia must be present
b) Urine sodium >40mmol/L
c) Thyroid function can be abnormal but pituitary and adrenal function must be normal.
d) The patient can be hypotensive.
e) Hyponatraemia corrects with 3% saline
Urine osmolality greater than plasma osmolality
Urine sodium excretion greater than 20mmol/L
Normal renal, hepatic, cardiac, pituitary, adrenal and thyroid function
Absence of hypotension, hypovolemia, oedema and ADH-influencing drugs
Hyponatremia corrects with water restriction
Which of the following SIADH treatment is cheap and effective?
Tolvaptan and Conivaptan are very effective with minimal side effects but are very expensive. Urea is as effective and cheap (just tastes bad). Demeclocycline (antibiotic with anti-ADH properties) is now an old form of treatment and response is variable. Frusemide and 3% saline while cheap do often overshoot or cause electrolyte imbalances that are hard to monitor consistently. Fludrocortisone can also be used.
In which order do the pituitary hormones disappear when compressed by a tumour?
a) PRL, TSH, GH, LH, FSH, ACTH
b) TSH, ACTH, GH, LH, FSH, PRL
c) FSH, LH, TSH, ACTH, GH, PRL
d) GH, LH, FSH, TSH, ACTH, PRL
e) GH, LH, FSH, PRL, TSH, ACTH
Go, Look For The Adenoma Please
GH, LH, FSH, TSH, ACTH, PRL + posterior pituitary hotmones (ADH and oxytocin)
Which of the following results are correct for the diagnosis if secondary hypothyroidism?
a) Low TSH, High T3, T4
b) High TSH, High T3, T4
c) High TSH, Low T3, T4
d) Low TSH, normal T3, T4
e) Low TSH, Low T3, T4
Primary hyper (from the thyroid gland) has a low TSH and high T3 and T4
Secondary hyper (outside the thyroid gland) has a high TSH and thus a high T3 and T4
Primary hypo high TSH but no response from the thyroid gland hence low T3 and T4
Secondary hypo has low TSH and thus a low T3 and T4
If a patient with thyroid disease had thyroglobulin antiboties, anti-thyroid peroxidase antibodies and TSH receptor antibodies what disease would they most likely have?
a) Hashimoto's disease
b) Graves disease
c) Toxic adenoma
d) Subacute thyroiditis
e) Toxic multinodular goitre
Hashimoto's disease is an autoimmune disease causing slow destruction of the thyroid function.
Graves disease can have TSH receptor antibodies both blocking and stimulating. The classic finding is a positive thyroid stimulating immunoglobulin test.
Plasma thyrogobulin can be used to monitor for recurrent cancer to see if any thyroid tissue is gorwing post resection.
Ultrasound us used to measure the size of the gland and look for nodules to guide FNA. A radioisotope scan is used in hyperthroidism. If it shows a 'hot nodule' i.e. one that takes up die, the chance of malignancy is low. If there are cold nodules these need ultrasound and FNA.
Radioactive iodine uptake measures the patients turnover of iodine. High uptake = hyperthroid and low (i.e. not incorporated) means the gland is leaking thyroid hormone (thyroiditis), exogenous thyroid hormone or excess iodine uptake (amiodarone or contrast dye).
In regards to thyroiditis which of the following is true?
a) There are 3 types
b) De Quervain's is painless
c) Post-partum occurs in 5-10% of mothers
d) Has an elevated T3 and T4 throughout the disease
e) Most cases result in permanent hypothyroidism
There are two types: painless which occurs in post-partum/autoimmune and painful (De Quervains or post viral).
Disruption of thyroid follicles by an inflammatory process results in the release of stored hormone rather than excessive production. Typically results will initially reflect hyperthyroidism before hypothyroidism. ESR can be elevated in the painful subset. Radioactive iodine uptake will be reduced (as there is no turnover of thyroxine production). Most patients recover but 10% will be left hypothyroid. If it occurred during pregnancy then there is a future risk it will occur with other pregnancies.
Which of the following blood tests would you see in a thyroid storm?
c) Normal to Low TSH
d) Elevated LFTs
In a thyroid storm there is increased T3 and T4, undetectable TSH, anaemia, leuckocytosis, hyperglycaemia, hypercalcaemia and elevated LFTs.
Pt's will be hyperthermic, tachycardic, confused and may lead to coma, CHF and shock. Profuse vomiting and diarrhoea may also be a component.
Which of the following would not be in your treatment algorithm for a thyroid storm?
a) Methimazole 40 mg oral
b) PTU 1000mg oral
c) Propranolol 2mg IV
d) Lugol solution 8-10 drops as first line
e) Demamethasone 2mg IV
Dosing varies slightly among text books but essentially, provide oxygen, coll, give fluids and manage electrolytes. Acetominphen is okay but NSAIDs including aspirin are contraindicated.
1st give propranolol 1-2mg IV q10-15 mins or an esmolol infusion 50-200 mcg/kg/min
2nd block the thyroid hormone synthesis with methimazole 40mg PO loading and then 25mg q4h (avoid 1st trimester) or PTU 600-1000mg loading and then 200-250 mg q4h. Methimazole is preferred (no liver toxicity)
3rd block thyroid hormone release (1hr after 2nd step). You can give Lugol solution 8-10 drops q6h or potassium iodine 5 drops, or lithium 300mg q6h
4th decrease peripheral conversion of T4 to T3, hydrocortisone 100mg IV TID or dexamethasone 2mg IV q6h
Final step admit to ICU.
Which of these is a symptom of hyperthyroidism?
a) Muscle wasting
Heart rate up
Intolerance to heat
Muscle wasting/weight loss
Which of these are a symptom of hypothyroidism?
HIS FIRM CAP
Intolerance to cold
Which of the following would you find in a myxoedema coma?
Myxoedema coma is due to severe hypothyroidism, complicated by trauma, sepsis, cold exposure, MI or inadvertent administration of hypnotics or narcotics.
Hallmark of symptoms is of a decreased mental status with hypothermia, hyponatraemia, hypotension, hypoglycaemia, bradycardia, hypoventilation and sometimes generalised oedema is present.
Decreased T4, increased TSH and decreased glucose. It is important to check ACTH and cortisol for evidence of adrenal insufficiency.
Treatment is with corticosteroids (hydrocortisone 100mg q8h ) and levothyroxine 0.2 - 0.5mg IV loading then 0.1mg IV once daily until oral therapy is tolerated.
Patients often require a lot of invasive supportive care. Monitor temp, electrolytes, glucose levels.
Which of the following is true of aldosterone?
a) It lowers sodium levels
b) It inhibits ADH release
c) It vasodilates
d) It is produced in the Zona Fasciculata
e) It lowers potassium levels
It is produced in the Zona Glomerulosa, The zona fasciculata produces glucocorticoids (cortisol) and the final inner layer of the adrenals the Zona Reticularis produces the sex hormones.
Aldosterone is eventually acitvated from the renin-angiotensin system in response to low sodium, reduced arterial pressure, reduced volume, prostaglandins or sympathetic stimulation. As a result it retains sodium (and thus water), excretes potassium, vasoconstricts and promotes ADH release.
In Conn's syndrome where there is a aldosterone producing adrenal adenoma the patient will have HTN and mild hypokalaemia.
Which of the following is true in regards to Cushing's?
a) Cushing's disease is from excess glucocorticoid either endogenous or exogenous.
b) The most common causes are ACTH-dependent.
c) Radom cortisol testing is recommended.
d) Distal muscle wasting is present.
e) Hypopigmentation is present.
Cushing's syndrome is the result of chronic glucocorticoid excess either endogenous or exogenous. Cushing's disease is from an ACTH-secreting pituitary adenoma. 85% of cases are ACTH-dependent (e.g. bilateral adrenal hyperplasia due to an ACTH secreting pituitary adenoma (80%) or an ectopic ACTH secreteing tumour (usually small cell lung carcinoma). The ACTH independent causes are long term glucocorticoid therapy, primary adrenocortical tumour or bilateral adrenal nodular hyperplasia.
CLinical features involve weakness, insomnia, mood disorders, imapired cognition, easy bruising, hirsuitism, acne and oligomenorrhoea. Obesity, round face, facial plethora, fat pads, proximal muscle wasting, abdominal striae, skin atrophy, acanthosis nigrans, HTN, hyperglycaemia, osteoporosis, pathological fractures and hyperpigmentation.
Testin involves 24h urine free cortisol or a dexamethasone suppression test or a late night salivary cortisol.
Which of the following can be found in primary adrenal insufficiency (Addison's)?
a) Pale skin
b) Normal potassium level
c) Metabolic acidosis
d) Normal sodium level
Addison's has many aetiologies but is essentially an adrenal insufficiency with raised ACTH. This causes dark skin in the palmar creases, high potassium and low sodium (as aldosterone works to increase sodium and excrete potassium). A metabolic acidosis is present along with weakness, fatigue, weight loss, hypotension, salt craving, postural dizziness, myalgia, arthralgia, N+V, abdominal pain and diarrhoea.
Secondary adrenal insufficiency is due to a failing pituitary and hence low ACTH. Skin is not affected along with any blood abnormalities. Symptoms can be the same along with signs of other pituitary insufficiency (hypogonadism, hypothyroidism, GH deficiency, DI, headaches and visual abnormalities).
Synathen tests and morning plasma ACTH can differentiate the two entities.
Which of the following cancers is found in MEN 1?
a) Medullary thyroid cancer
b) Anterior pituitary adenoma
d) Intestinal ganglioneuromas
e) Mucosal neuroma
MEN syndromes are autosomal dominant and involve multiple endocrine glands.
MEN I think 3 Ps
Pituitary, Parathyroid and Pancreas
(Entero-pancreatic tumours include - pancreatic islet cell, gastrinoma, insulinoma, VIP-omas, Glucagonoma and carcinod syndrome).
MEN IIa Type 1
Thyroid (medullary thyroid cancer), adrenal medulla (pheochromocytoma), parathyroid and cutaneous lichen amyloidosis.
MEN IIa Type 2 just has a familial medullary thyroid Ca along with the above.
Thyoid MTC, Adrenal medulla (pheochromocytoma) and neurons (muscosal neuroma, intesintal gangioneuromas).