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MCQ knowledge > Endocrine > Flashcards

Endocrine Flashcards

1
Q

True/False: insulin inhibits ketogenesis

A

True

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2
Q

What are PPAR (peroxisome proliferator activated receptor) gamma?

A

PPAR gamma is an intra-cellular receptor that is activated by free fatty acids (natural endogenous ligands)

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3
Q

What is the clinical significance of PPAR (peroxisome proliferator activated receptor) gamma?

Give an example of a drug that is a PPAR gamma agonist.

A
  • Implicated in the pathology of obesity, diabetes, atherosclerosis and cancer.
  • PPAR gamma agonists used in the treatment of hyperlipidaemia and hyperglycaemia.
  • Thiazolidinediones (e.g. pioglitazone) are PPAR gamma AGONISTS that are insulin sensitising drugs used in DM.
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4
Q

A drug is described as insulin-sensitising. What does this mean? Give an example.

A

Lowers serum glucose level without increasing pancreatic insulin secretion.

Thiazolidinediones (e.g. pioglitazone)

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5
Q

What diuretic may be useful in the treatment of acute hypercalcaemia?

A

Frusemide.

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6
Q

Patient has tertiary hyperparathyroidism and is unfit for surgery. What drug may be offered?

A

Cinacalcet - calcimimetic that stimulates the calcium sensing receptor to reduce PTH secretion.

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7
Q

Patient has secondary hyperparathyroidism from CKD with elevated PTH. What drug may be offered?

A

Cinacalcet - calcimimetic that stimulates the calcium sensing receptor to reduce PTH secretion.

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8
Q

When should a patient with primary hyperparathyroidism be offered parathyroidectomy surgery (4 conditions)?

A
  1. Significant hypercalcaemia/hypercalciuria
  2. Impaired renal function
  3. Osteoporosis
  4. Age less than 50 years
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9
Q

What is the MOA of dapaglifozin?

Common SE of this drug?

A

Sodium-glucose-cotransporter 2 inhibitor.

SE: glycosuria

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10
Q

Give an example of:

  1. PPAR-alpha agonist
  2. PPAR-gamma agonist
A
  1. PPAR-alpha agonist = fibrates

2. PPAR-gamma agonist = thiozolidinediones

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11
Q

Name one fibrate class drugs ‘without’ fibrate in the name.

The rest will contain ‘fibrate’ somewhere in name

A

Gemfibrozil

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12
Q

Patient with DM on long-term metformin is noted to have mild anaemia that is macrocytic. What is the problem?

A

Metformin induced B12-deficiency associated with raised homocyteine levels.

Occurs in 30% of patients on Metformin and often misdiagnosed as DM neuropathy.

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13
Q

What has happened to the incidence of type 1 DM in the 20 years.

A

Doubled - reason unclear.

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14
Q

What is the typical histology of Grave’s disease?

A
  • follicular hyperplasia
  • intracellular colloid droplets
  • lymphocytic infiltration
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15
Q

An immobile long-stay patient in hospital for epilepsy treated with phenytoin and carbamazepine with a background of RA on prednisone is placed on heparin DYT prophylaxis.

What condition is the patient at-risk of developing?

A

Osteoporosis.

Phenytoin, carbamazepine, prednisone and heparin can ALL cause osteoporosis.

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16
Q

What are the 5 effects of GH?

Clue: growth PILES

A

PILES:

  • Protein synthesis
  • Insulin sensitivity decreased (ANTI-insulin)
  • Lipolysis
  • Epiphyseal growth
  • Sodium retention
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17
Q

T/F: Subacute thryroiditis does NOT cause increased uptake in a radiouptake iodine scan.

A

True.

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18
Q

SIADH has what findings in the following parameters:

Serum osmolality
Urine osmolality
Urine sodium
Fluid status
Fractional sodium excretion
A

Serum osmolality - decreased
Urine osmolality - greater than 100 mOsm/kg
Urine sodium - greater than 30
Fluid status - euvolemia
Fractional sodium excretion greater than 1%

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19
Q

What is carbergoline?

A

D2-receptor agonist - treatment of prolactinomas

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20
Q

T/F: Paget’s disease is usually symptomatic.

A

False.

Most cases o Paget’s disease is asymptomatic.

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21
Q

Which cell line is abnormal in the pathophysiology of Paget’s disease?

What is the consequence of this abnormality.

A

Osteoclast - accelerated bone turnover and abnormal bone remodelling.

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22
Q

What is a rare but fatal complication of Paget’s disease?

A

Osteosarcoma.

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23
Q

What is a benign complication of Paget’s disease?

A

Giant cell tumours.

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24
Q

Which of the following are elevated in Paget’s Disease:

  1. serum ALP
  2. bone-specific ALP
  3. serum calcium
  4. serum phosphate
A
  1. serum ALP - normal or raised
  2. bone-specific ALP - RAISED
  3. serum calcium - often normal
  4. serum phosphate - often normal
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25
Q

What type of imaging is useful in Paget’s Disease?

A

Plain XR - to reveal impending fractures

Radionucleotide bone scan - reveals active disease, more useful in early disease.

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26
Q

Which cytokines promote osteoclast differentiation (2)?

Which cytokine inhibits osteoclast differentiation (1)?

A

Promotors of osteoclast differentiation:

  • RANKL (Receptor activator of nuclear factor kappa-B ligand)
  • mCSF (macrophage colony-stimulating factor)

Inhibitors of osteoclast differentiation:
- OPG (osteoprotegerin)

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27
Q

What is osteoprotegerin (OPG)?

A
  • Soluble decoy receptor for RANKL

- Inhibits osteoclast differentiation

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28
Q

When is treatment of Paget’s Disease indicated?

A
  1. Symptomatic patients with elevated ALP should be treated.
  2. Asymptomatic patients:
    - elevated ALP requires treatment
    - normal ALP should be treated if bone scan suggests active disease
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29
Q

What treatment of Paget’s Disease in the following scenarios?

  1. Young patient with less extensive disease (1st line therapy)
  2. Elderly patients with extensive disease
  3. Intolerant of 1st line therapy (i.e. 2nd line therapy)
A
  1. Young patient with less extensive disease
    - nitrogen-based bisphosphanate (IV or PO)
  2. Elderly patients with extensive disease
    - zolendronic acid
  3. Intolerant of 1st line therapy (i.e. 2nd line therapy)
    - calcitonin
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30
Q

In patients treated with Paget’s Disease with nitrogen-based bisphosphonate, what should be tested and supplemented to avoid hypocalcaemia?

A
  • Test normal serum levels of calcium and 25-hydroxy vitamin D (calcidiol)
  • Supplement with vitamin D (800 international units daily) and calcium supplements (1200 mg/day of elemental calcium)
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31
Q

Comment about the following in MODY (Mature-Onset Diabetes of the Young) due to a glucokinase mutation (MODY 2):

  1. Fasting glucose level
  2. Insuline secretion
  3. Risk of macrovascular complications
  4. Treatment
A
  1. Fasting glucose level - high BSL
  2. Insuline secretion - decreased
  3. Risk of macrovascular complications - low risk
  4. Treatment - diet-controlled
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32
Q

MODY 3 is the most common type of MODY, comment on the following:

  1. What is the frequency within the MODY population?
  2. Which gene is involved?
  3. What is the pathophysiology?
  4. Other associated features?
  5. Treatment?
A

MODY 3:

  1. Frequency: 30-50%
  2. Gene: HNF1A (hepatic nuclear factor 1 alpha)
  3. Pathophysiology: Beta-cell dysfunction
  4. Associated feature: glycosuria
  5. Treatment: sulfonylurea
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33
Q

MODY 2 is the SECOND most common type of MODY, comment on the following:

  1. What is the frequency within the MODY population?
  2. Which gene is involved?
  3. What is the pathophysiology?
  4. Other associated features?
  5. Treatment?
A

MODY 2:

  1. Frequency: 15-20%
  2. Gene: Glucokinase
  3. Pathophysiology: Beta-cell SENSING dysfunction
  4. Associated feature: fasting hypergycaemia
  5. Treatment: diet control
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34
Q

Regarding sulfonylureas:

  1. Give MOA
  2. Give 4 examples
A
  1. Increase insulin secretion

2. gliclazide, glipizide, glibenclamide, glimepiride

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35
Q

Sulfonylureas can cause hypoglycaemia, especially in the elderly.

Which 2 are more prone to causing hypoglycaemia and hence which 2 are preferable in treating the elderly T2DM patient?

A
  • Avoid (long-acting) glibenclamide or glimepiride
  • Consider (shorter-acting) gliclazide or glipizide

NB: long-acting have more syllables (4 vs 3)!

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36
Q

T/F: the pathophysiology of the 4 most common types of MODY involve Beta-cell dysfunction.

A

True.

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37
Q

T2DM is a common condition.

What are the treatment targets for the following parameters in a T2DM patient:

  1. HDL cholesterol
  2. Total cholesterol
  3. Triglycerides
  4. BP target
A
  1. HDL cholesterol - greater than 1 mmol/L
  2. Total cholesterol - less than 4 mmol/L
  3. Triglycerides - less than 2 mmol/L
  4. BP target - less than 130/80 mmHg
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38
Q

T2DM is a common condition.

What are the treatment targets for the following parameters in a T2DM patient prone to HYPOGLYCAEMIA:

  1. HbA1c
  2. fBSL
A
  1. HbA1c - less than 8%
  2. fBSL - 6-8 mmol/L

NB: more relaxed ranges.

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39
Q

T2DM is a common condition.

What are the treatment targets for the following parameters in a T2DM patient NOT prone to hypoglycaemia:

  1. HbA1c
  2. fBSL
A
  1. HbA1c - less than 7%
  2. fBSL - 4-6 mmol/L

NB: more aggressive ranges.

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40
Q

T2DM is a common condition.

What is the LDL-C treatment targets for a T2DM patient also diagnosed with hypercholesterolaemia.

A

SECONDARY prevention: LDL-C less than 1.8 mmol/L (more strict)

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41
Q

T2DM is a common condition.

What is the LDL-C treatment targets for a T2DM patient WITHOUT a diagnosis of hypercholesterolaemia.

A

PRIMARY prevention: LDL-C less than 2 mmol/L (less strict)

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42
Q

What are the 2 main pathophysiological mechanisms for diabetes.

A
  1. Insulin insufficiency (Type 1)
  2. Insulin resistance (Type 2)

NB: may be a combination of the above

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43
Q

PCOS is a diagnosis of exclusion.

Which 6 conditions should be excluded prior to considering a diagnosis of PCOS?

A

C-C-CAP T:

Cancer (androgen secreting tumours)
Cushing's syndrome
Congenital adrenal hyperplasia
Acromegaly
Prolactinaemia (hyperprolactinaemia)
Thyroid dysfunction
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44
Q

What is the Rotterdam criteria for diagnosis of PCOS?

A

Need 2 out of 3 of the following:

  1. Oligo/anovulation (menstrual disturbance)
  2. Hyperandrogenism (clinical or biochemical)
  3. Polycystic ovaries (on ultrasound)

Hyperandrogenism:
Clinically: hirsutism
Biochemically: raised FAI or free testosterone

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45
Q

What are the 2 biochemical features of hyperandrogenism?

Which of these is more useful in PCOS?

A

Raised FAI (free androgen index) or free testosterone

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46
Q

What is the free androgen index (FAI) ratio?

How does obesity affect this ratio?

A

FAI = 100 x [total testosterone / SHBG]

SHBG is reduced in obesity leading to increased FAI. FAI correlated more with obesity than PCOS.

NB: SHBG = sex hormone binding globulin

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47
Q

What are the DDx of Cushing’s syndrome?

A

Endogenous:

  • Pituitary tumour (secrete ACTH) - 70%
  • Adrenal tumour (secrete cortisol) - 15%
  • Ectopic (secrete ACTH) - 15%

Exogenous glucocorticoids

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48
Q

Pituitary tumours that cause Cushing’s syndrome are referred to as Cushing’s disease. What are the 3 DDx?

A
  • Microadenoma
  • Macroadenoma
  • Hyperplasia
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49
Q

What are 2 DDx for ectopic causes of Cushing’s syndrome?

A

Paraneoplastic Cushing’s syndrome:

  • Carcinoid tumour
  • Small cell lung cancer (SCLC)
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50
Q

What endogenous source of Cushing’s syndrome (i.e. pituitary, adrenal or ectopic) is suggested with a low or undetectable DHEA-S (dehydroepiandrosterone sulphate)

A

Adrenal Cushing’s Syndrome.

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51
Q

You suspect a patient may have Cushing’s syndrome.

What 3 tests (and their positive results) may be useful to elucidate?

A
  1. Evening salivary cortisol (11pm)
  2. 24h urinary free cortisol
  3. Overnight 1mg DST (dexamethasone suppression test)
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52
Q

For the ‘overnight 1mg DST’ used to confirm Cushings disease, give the values for:

  1. Negative test
  2. Equivocal test
  3. Positive test
A
  1. Negative test - less than 1.8 ug/dL
  2. Equivocal test - 1.8-7.5 ug/dL
  3. Positive test - greater than 7.5 ug/dL
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53
Q

A patient suspected of Cushing’s syndrome has initial tests that are equivocal for Cushing’s syndrome, with repetition of several tests suggesting the same equivocal results.

Which 2 furthers tests may be used to elucidate?

A
  1. Overnight 2mg DST (high dose)

2. DST-CRH (dexamathasone-corticotrophin-releasing hormone test)

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54
Q

Empaglifozin is used in the treatment of T2DM.

What is the MOA?

May it be used as a monotherapy or only an add-on OHG?

A

MOA:

  • SGLT2 inhibition (sodium-glucose cotransporter 2)
  • Leads to glycosuria

May be used as a monotherapy OR an add-on OHG.

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55
Q

Where is SGLT2 located in the nephron and what is it’s responsibility?

A

SGLT2 is in the PT and is responsible for 60% of renal glucose reabsorption.

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56
Q

Regarding Empagliflozin, comment on the following:

  1. Does is cause weight loss?
  2. Does it reduce BP?
  3. Does it cause hypoglycaemia when used as monotherapy?
A
  1. may cause 2-3kg weight loss that plateaus at 6m
  2. Reduces BP modestly by 1-5mm Hg
  3. Does NOT cause hypoglycaemia
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57
Q

What complication should be considered when using Empagliflozin for women with T2DM that are post-menopausal?

A

8x risk of genitourinary infections due to glycosuria.

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58
Q

Which of the new OHG decreases both cardiovascular mortality AND slow nephropathy progression?

A

Empagliflozin

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59
Q

The ‘Gliptins’ or DPP4 inhibitors (Dipeptidyl peptidase-4 inhibitors) are used in the treatment of T2DM.

What is the MOA?

A
  • DPP-4 enzyme INACTIVATES incretins (GLP-1, GIP)
  • Incretins usually have 2 effects:
  1. Stimulate insulin release
  2. Inhibit glucagon release
  • This leads to lowering of blood glucose
  • DDP-4 inhibition therefore leads to the prolonged effects of incretins.
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60
Q

The endocrine pancreas has the following 5 cells within the islet of Langerhans, what proportion of this parenchyma do they occupy and what do they secrete?

  1. Alpha-cell
  2. Beta-cells
  3. Delta-cells
  4. Epsilon-cells
  5. Gamma-cells
A
  1. Alpha-cell (20%) secrete glucagon
  2. Beta-cells (70%) secrete insulin (and amylin)
  3. Delta-cells (5%) secrete somatostatin
  4. Epsilon-cells (4%) secrete ghrelin
  5. Gamma-cells (1%) secrete pancreatic polypeptide
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61
Q

What are the 3 functions of incretins?

A

Post-prandial hormones that:

  1. Stimulate insulin release from pancreatic beta-cells
  2. Inhibit glucagon release from pancreatic alpha-cells
  3. Reduce gastric emptying and slows rate of nutrient absorption
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62
Q

Name 2 incretins and which cells secrete them.

A

Incretins are secreted by gut cells:

K-cells secrete GIP (gastric inhibitory peptide)
L-cells secerete GLP-1 (glucagon-like peptide-1)

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63
Q

Which 4 OHGs used in T2DM are beneficial (or neutral) with respect to CV outcomes?

A

MAPS:

Metformin
Acarbose
Pioglitazone (thiazolidinedione)
SGLT2 inhibitor

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64
Q

Which 3 OHGs used in T2DM are unfavourable with respect to CV outcomes?

A

Rosiglitazone

Sulfonylureas

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65
Q

Which class of OHGs are unfavourable in a T2DM with CCF?

A

Thiazolidinediones

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66
Q

What are 6 features of a thyroid nodule that suggests malignancy?

A
  1. Hypoechoic
  2. Calcification (microcalcification or interrupted rim)
  3. Irregular margins
  4. Tall than wide
  5. Extrathyroid extension
  6. High vascularity
67
Q

A thyroid is noted incidentally on clinical examination or imaging. What should be the next test?

A

TSH

68
Q

Incidental thyroid nodule is associated with a suppressed TSH.

What should be the next test?

What is the treatment if this test is positive?

A
  • Radionuclide thyroid scan to assess for hyperfunctioning nodule
  • Hyperfunctioning nodules should undergo surgical excision or radioiodine ablation.
69
Q

Incidental thyroid nodule is associated with a normal or elevated TSH. An ultrasound is done to determine the number and size of the nodules.

What is the next step for the following scenarios:

  1. Solitary solid nodule (any size) with malignant feature on US.
  2. Multiple nodules greater than 1 cm
  3. Multiple nodules less than or equal to 1 cm
  4. Palpable nodule not demonstrated on imaging
A
  1. Solitary solid nodule (any size) with malignant features
    - US-guided FNA
  2. Multiple nodules greater than 1 cm
    - US-guided FNA
  3. Multiple nodules less than or equal to 1 cm
    - Follow-up
  4. Palpable nodule not demonstrated on imaging
    - Follow-up
70
Q

Incidental thyroid nodule is associated with a normal or elevated TSH. Ultrasound findings suggest need for FNA.

What intervention should be considered with the following results:

  1. Confirmed or suspicious of malignancy
  2. Benign
  3. Unsatisfactory specimen
A
  1. Confirmed or suspicious of malignancy
    - Thyroid surgery
  2. Benign
    - Follow-up in 6m or earlier if symptomatic
  3. Unsatisfactory specimen
    - Repeat FNA in 1-4 weeks
71
Q

T/F: Hyponatraemia is a disorder of water balance NOT sodium.

A

True.

72
Q

What is the general 3 step approach to working up a patient with Hyponatraemia?

A
  1. Exclude pseudohypernatraemia - high glucose
  2. If hypernatraemia with symptoms - treat with hypertonic saline.
  3. Evaluate 3 things:

a. History - medication review
b. Clinical - volume status
c. Investigations - paires serum/urine sodium/osmolality

73
Q

Give 3 DDx for a patient with hyponatraemia and fluid OVERLOAD.

A
  • CCF
  • Nephrotic syndrome
  • Liver failure
74
Q

Give 3 DDx for a patient with hyponatraemia and EUVOLEMIA.

A
  • SIADH (most likely)

Exclude:

  • Secondary adrenal insufficiency
  • Hypothyroidism

NB: SIADH = Syndrome of Inappropriate ADH

75
Q

Give 3 DDx for a patient with hyponatraemia and HYPOVOLEMIA.

A

SAADH:

  • Nausea and vomiting
  • Diarrhoea
  • Primary adrenal insufficiency

NB: SAADH = Syndrome of Appropriate ADH

76
Q

Hyponatraemic patient is EUVOLEMIC and thought to have SIADH.

What serum/urine sodium and osmolality is consistent with this diagnosis?

A

Excessive ADH = increased water in serum and less water in urine.

Serum osmolality = LOW (less than 280 mmol/kg)
Serum sodium = LOW (less than 135 mmol/L)

Urine osmolality = HIGH
Urine sodium = HIGH (greater than 30 mEq/L)

77
Q

Hyponatraemic patient is HYPOVOLEMIC and thought to have SAADH.

What serum/urine sodium and osmolality is consistent with this diagnosis?

A

Serum osmolality = LOW (less than 280 mmol/kg)
Serum sodium = LOW (less than 135 mmol/L)

Urine osmolality = VARIABLE
Urine sodium = HIGH (less than 30 mEq/L)

78
Q

Which 2 cell types within bone marrow secrete RANKL?

A

Osteoblasts and Stromal cells

79
Q

What does RANKL bind to?

What is the effect of this binding?

A
  • RANKL binds to RANK receptors found on osteoclast precursors and osteoclasts.
  • RANKL binding promotes osteoclast differentiation and activity.
80
Q

What is the MOA of Denosumab?

A

Denosumab is a humanised mAb that binds to RANKL and prevents osteoclast activation.

81
Q

What is the MOA of Bisphosphonates (e.g. zolendronic acid)?

Why do bisphosphonates have such a long half-life?

A
  • Bisphosphonates binds to bone and prevent entry and bone absorption by osteoclasts.
  • Bisphosphonates accumulate in bone leading to a long half-life (e.g. zolendronic acid t/12 = 146h)
82
Q

T/F: the clearance of Denosumab is dependent upon renal function.

A

False.

Like other mAb, the clearance is through the reticuloendothelial system and independent of renal clearance.

83
Q

What is the difference between ‘Classic’ and ‘Late-onset’ Hypogonadism?

A

Classic hypogonadism: proven HPT-axis pathology

Late-onset hypogonadism: NO proven HPT-axis pathology (typically greater than 60yo)

84
Q

Give 2 examples of Classic Hypogonadism.

A
  • Pituitary tumour

- Klinefelter’s syndrome

85
Q

What is the genetic abnormality in Klinefelter’s syndrome?

A

47, XXY karyotype

86
Q

What is the difference in clinical features and testosterone levels in patients with ‘Classic’ and ‘Late-onset’ Hypogonadism?

A

Classic hypogonadism:

  • Specific symptoms: low libido, small testes, gynecomastia
  • LOW testosterone

Late-onset hypogonadism:

  • Non-specific symptoms: erectile dysfunction, low energy and mood
  • Borderline and fluctuating testosterone
87
Q

What is the treatment of ‘Classic’ and ‘Late-onset’ Hypogonadism?

A

Classic hypogonadism:
- Testosterone replacement

Late-onset hypogonadism:

  • Weight loss
  • Optimise comorbidities
  • Stop opioids
88
Q

What is the effect of Testosterone replacement on the following physiological domains:

  1. Sexual function
  2. Body composition
  3. Bone
A
  1. Sexual function
    - Improves ERECTIONS with baseline total testosterone less than 10 nmol/L
    - Improves libido if baseline total testosterone less than 12 nmol/L
  2. Body composition
    - increase of lean mass and decrease in fat mass
  3. Bone
    - improves BMD
89
Q

What is the effect of Testosterone replacement on the following psychological domains:

  1. QoL / Mood
  2. Cognition
A
  1. QoL / Mood
    - inconsistent improvement
  2. Cognition
    - unclear
90
Q

T/F: Testosterone replacement in the elderly male is beneficial in DM.

A

False - no proven benefit.

91
Q

T/F: Testosterone replacement causes erythrocytosis.

A

True - common.

92
Q

There is an inverse relationship between cardiovascular event and total testosterone levels in men.

Does testosterone replacement in older men therefore result in decreased cardiovascular events?

A

No.

TOM trial (NEJM 2010) suggested increased cardiovascular events with testosterone treatment in older men.

93
Q

Patient has LOW free T4 and normal TSH. What is the diagnosis?

A

LOW free T4 should be coupled with a high TSH (to compensate) - hence the normal TSH is INAPPROPRIATELY low.

Diagnosis: secondary hypothyroidism

94
Q

Patient has HIGH calcium and normal PTH. What is the diagnosis?

A

HIGH calcium should be coupled with a LOW PTH (to compensate) - the normal PTH is INAPPROPRIATELY high.

Diagnosis: hyperparathyroidism

95
Q

Patient has LOW testosterone and normal gonadotrophins. What is the diagnosis?

A

LOW testosterone should be coupled with a HIGH gonadotropin (to compensate) - the normal gonadotropin is INAPPROPRIATELY low.

Diagnosis: secondary hypogonadism

96
Q

Patient has LOW glucose and normal insulin. What is the diagnosis?

A

LOW glucose should be coupled with a LOW insulin (to compensate) - the normal normal is INAPPROPRIATELY high.

Diagnosis: insulinoma

97
Q

Patient has HIGH urinary cortisol and normal ACTH. What is the diagnosis?

A

HIGH urinary cortisol should be coupled with a LOW ACTH (to compensate) - the normal ACTH is INAPPROPRIATELY high.

Diagnosis: ACTH-dependent Cushing’s syndrome (Pituitary tumour or Ectopic ACTH producing tumour)

98
Q

Patient is suspected of Cushing’s syndrome, comment on the diagnosis for the following results:

  • Low/undetectable ACTH
  • cortisol NOT suppressed by either high or low dose dexamethasone supression test
A

ACTH-independent Cushing’s syndrome - primary hypercortisolism

99
Q

Patient is suspected of Cushing’s syndrome, comment on the diagnosis for the following results:

  • Elevated ACTH in the hundreds
  • DST: cortisol NOT suppressed by either high or low dose dexamethasone suppression test
A

Ectopic ACTH syndrome (adrenal / chest source)

100
Q

Patient is suspected of Cushing’s syndrome, comment on the diagnosis for the following results:

  • Normal or elevated ACTH (but not in the hundreds)
  • DST: cortisol NOT suppressed by low dose but is suppressed by high dexamethasone suppression test
A

Cushing’s disease (pituitary tumour with some residual feedback control)

101
Q

Patient is diagnosed with sick euthyroid on TFTs. Should thyroid hormone treatment be commenced?

A

No.

102
Q

Patient has low/undetectable TSH, very high fT4 and high T4/T3 ratio.

No giotre / nodules / exophthalmos
Negative TPO / TSHR Ab
Low/undetecable thyroglobulins

What is the diagnosis?

A

Factitious thyrotoxicosis (likely thyroxine ingestion)

Appropiately LOW TSH and thyroglobulin in the context of very high fT4.

103
Q

T/F: Biotin (vitamin B7) may be used at high doses in the treatment of MS and mitochondrial disorders.

A

True

104
Q

T/F: High-dose biotin can mimic the biochemistry of Grave’s disease with a patient that is clinically euthyroid.

A

True

105
Q

What occurs to the following parameters in Grave’s disease?

A
  • Suppressed TSH
  • High fT4/T3
  • High TSH-R Abs
106
Q

What are the 3 types of bariatric surgery?

Which of the following mechanism do they employ:

  1. Malabsorptive
  2. Restrictive
A
  1. Rouz-En-Y gastric bypass = malabsorptive + restrictive
  2. Adjustable gastric band = restrictive
  3. Vertical sleeve gastrectomy = restrictive
107
Q

What is the function of leptin and ghrelin?

Where do they both act?

A

Leptin (satiety hormone): secreted by adipocytes and inhibits hunger

Ghrelin (hunger hormone): secreted by ghrelinergic cells in the GIT.

Both act upon the arcuate nucleus of the hypothalamus to regulate energy homeostasis.

HUNGER / SATIETY - Ghrelin with G for hunGer.

108
Q

What is the most common karyotype of Klinefelters syndrome?

A

47 XXY

109
Q

Klinefelters is one of the most common chromosomal disorders affecting live male births (1 in 500-1000).

What are the effects of Klinefelter’s syndrome on the following parts of the body:

  1. Shoulders
  2. Breasts
  3. Body hair
  4. Body habitus
  5. Pubis and testicular volume
  6. Leg length
  7. Peripheral veins
A
  1. Shoulders - narrow shoulders
  2. Breasts - gynaecomastia
  3. Body hair - reduced
  4. Body habitus - central adiposity
  5. Pubis and testicular volume - horizontal pubic hairline and small testicular volume
  6. Leg length - long legs
  7. Peripheral veins - varicose veins
110
Q

What size are the testes in Klinefelter’s syndrome?

A

pea-like

111
Q

Klinefelter’s syndrome is at increased risk of which 3 common disorders?

A
  • Osteoporosis
  • T2DM
  • Metabolic syndrome
112
Q

Which 3 types of cancers are more likely in Klinefelter’s syndrome?

A
  • Mediastinal germ-cell tumour (500x)

- Breast tumour (50x)

113
Q

What happens to the following parameters in Klinfelter’s Syndrome:

  1. Total testosterone
  2. LH
A
  1. Total testosterone - low/normal

2. LH - high

114
Q

Regarding sclerostin:

  1. Which gene encodes this glycoprotein?
  2. Which cell secretes sclerostin?
  3. How is sclerostin implicated in bone mass?
A
  • SOST-gene encodes sclerostin
  • Sclerostin is secreted by osteocytes
  • Sclerostin inhibits osteoblast proliferation (reduced bone mass)
115
Q

Loss of function in the SOST gene (that encode Sclerostin) results in what rare condition?

A

van Buchem Disease - autosomal recessive disease causing bone overgrowth and high bone mass

116
Q

Which pathway mediates osteoblast proliferation?

Which glycoprotein inhibits this pathway?

A
  • [wnt - Ipr5/6 - beta-catenin] pathway mediated osteoblast proliferation
  • Sclerostin (seccreted by osteocytes) is the endogenous inhibitor of this pathway.
117
Q

What is Romosozumab?

A
  • humanised mAb that target Sclerostin - increases bone formation and decreases resorption
  • possible benefit in postmenopausal women with osteoporosis
118
Q

What is the difference between the T-score and Z-score in BMD studies?

A

T-score: compares with young healthy adults of same sex

Z-score: compares with adults of same age and same sex

NB: Both score measure number of standard deviations above or below

119
Q

In a patient over 50yrs, which 5 endocrine co-morbidities would warrant a DXA scan to assess BMD?

A
  • Early menopause
  • Androgen deprivation therapy
  • Hypogondadism
  • Hyperthyroidism
  • Hyperparathyroidism
120
Q

In a patient over 50yrs, which gastroenterological co-morbidity would warrant a DXA scan to assess BMD?

A

Coeliac disease / Malabsorptive disorder

121
Q

In a patient over 50yrs, which 2 chronic co-morbidities would warrant a DXA scan to assess BMD?

A
  • Chronic liver disease

- Chronic kidney disease

122
Q

In a patient over 50yrs, which rheumatological co-morbidity would warrant a DXA scan to assess BMD?

A

RA

123
Q

In a patient over 50yrs ingestion long-term congestion of what dose of steroids over what period of time would warrant a DXA scan to assess BMD?

A

Greater than 7.5mg Prednisone over more than 3 months.

124
Q

In a patient over 50yrs, which type of fractures would warrant a DXA scan to assess BMD?

A
  • Minimal trauma fracture

- Vertebral fracture

125
Q

In a patient over 70yrs, which co-morbidities would warrant a DXA scan to assess BMD?

A

None.

All patients over 70yrs may have BMD assessed on virtue of age alone.

126
Q

On the T-score, what should NORMAL bone be?

A

T-score = -1 or above

Interpretation: BMD not more than 1.0 SD
below young adult mean

127
Q

On the T-score, what would suggest OSTEOPENIA?

A

T-score = -1.0 and -2.5

Interpretation: BMD between 1.0 and 2.5
SDs below young adult mean

128
Q

On the T-score, what would OSTEOPOROSIS?

A

T-score = -2.5 or below

Interpretation: BMD 2.5 or more SDs below
young adult mean

129
Q

What is the Z-score useful for in BMD assessment?

A
  • Z-score is a useful indicator of possible secondary
    osteoporosis.
  • Z-score = -2.0 or below triggers need to investigate for underlying diseases.
130
Q

For which of the following scenarios is commencement of osteoporosis treatment indicated:

  1. T-score less than or equal to -2.5 + risk factors + minimal trauma fracture
  2. T-score less than or equal to -2.5 + risk factors WITHOUT minimal trauma fracture
  3. T-score is -1 to -2.5 + risk factors + minimal trauma fracture
  4. T-score is -1 to -2.5 + risk factors WITHOUT minimal trauma fracture
  5. T-score less than -1.5 WITHOUT minimal trauma fracture but intending to take 7.5mg prednisone for greater than 3 months.
  6. T-score less than -1.0
A
  1. T-score less than or equal to -2.5 + risk factors + minimal trauma fracture - TREAT
  2. T-score less than or equal to -2.5 + risk factors WITHOUT minimal trauma fracture - TREAT
  3. T-score is -1 to -2.5 + risk factors + minimal trauma fracture - TREAT
  4. T-score is -1 to -2.5 + risk factors WITHOUT minimal trauma fracture - NO treatment
  5. T-score less than -1.5 WITHOUT minimal trauma fracture but intending to take 7.5mg prednisone for greater than 3 months - TREAT
  6. T-score less than -1.0 - NO treatment
131
Q

Patient has had a transphenoidal resection of a non-functioning pituitary adenoma. A short synacthen test is performed post-op to assess ACTH sufficiency.

When should this be done ideally to avoid a false negative (i.e. allow time for the adrenals to atrophy)?

A

4-6 weeks post-op

Unreliable within 2 weeks post-op.

132
Q

The short synacthen test is used to assess adrenal insufficiency. What does it involve?

A
  • Baseline cortisol is measures followed by administration of synthetic ACTH
  • Serum cortisol measured at 1h post-administration (normal greater than 500 nmol/L)
133
Q

What is the utility of the insulin tolerance test?

A
  • Assessment of GH and ACTH/cortisol reserve.

- Differentiation of Cushing’s syndrome from pseudo-Cushing’s syndromes (eg depression, alcohol excess)

134
Q

What are 5 contraindications of the insulin tolerance test in the adult population?

A
  1. Age > 60 years
  2. IHD
  3. Epilepsy
  4. Severe panhypopituitarism, hypoadrenalism (0900 cortisol < 100 nmol/L)
  5. Hypothyroidism impairs the GH and cortisol response.
135
Q

Patient with newly diagnosed hypothyroidism requires an insulin tolerance test to differentiate Cushing’s syndrome from pseudo-Cushing’s syndrome.

When should the insulin tolerance test (ITT) be ideally conducted?

A
  • Patients should have corticosteroid replacement commenced prior to thyroxine as the latter has been reported to precipitate an Addisonian crisis with dual deficiency.
  • If adrenal insufficiency is confirmed, the need for a repeat ITT may need to be reconsidered after 3 months thyroxine therapy.
136
Q

Describe the insulin tolerance test used to differentiate Cushing’s syndrome from pseudo-Cushing’s syndrome.

A
  • ACTH and growth hormone are both released as a part of the stress mechanism triggered by hypoglycaemia.
  • Test cannot be interpreted unless hypoglycaemia (< 2.2 mmol/L) is achieved.

Hypopituitarism:

  • An adequate cortisol response is defined as a rise to greater than 550 nmol/L.
  • Patients with impaired cortisol responses i.e. 400 - 550 nmol/L may only need steroid cover for major illnesses or stresses.
  • An adequate GH response occurs with an absolute response > 20 mU/L (7µg/L).

Cushing’s syndrome:
There will be a rise of less than 170 nmol/L above the fluctuations of basal levels of cortisol.

137
Q

What is the indication for a Glucagon stumulation test?

A

Assessing growth hormone deficiency

138
Q

You suspect an Addisonian crisis, what are the anticipated biochemical findings with the following:

  1. K
  2. Na
  3. Ca
A

Hyperkalaemia
Hyponatraemia
Hyperclacaemia

139
Q

Patient is hypokalaemic.

What urinary K+ would suggest that this is RENAL cause of K+ loss?

A

24h Urinary K+ > 20 mmol/day suggests RENAL loss

24h Urinary K+ < 20 mmol/day suggest extra-RENAL loss (i.e GIT - diarrhoea and vomiting)

140
Q

Patient is hypokalaemia.
24h Urinary K+ is 44mmol/day.
Serum HCO3- is normal/high.
Patient has LOW/NORMAL BP.

What are your DDx (3)?

A

Hypokalaemic metabolic alkalosis with hypotension/normotension.

DDx (BMD):

  • Barrter (loop) or Gitelman (thiazide) syndromes
  • Mg depletion
  • Diuretics (loops / thiazides)
141
Q

Patient is hypokalaemia.
24h Urinary K+ is 44mmol/day.
Serum HCO3- is normal/high.
Patient has HIGH BP.

What should be checked?

A

Hypokalaemic metabolic alkalosis with hypertension.

Check Renin / Aldosterone ratio.

142
Q

What is Liddle syndrome?

A

AD genetic disorder with increased activity of ENaC channel.

Hypokalaemic metabolic alkalosis with hypertension with
low renin / low aldosterone.

143
Q

Hypokalaemic metabolic alkalosis with hypertension.

What is the urinary Cl likely to be?

A

Urinary Cl- > 10mEq/L

144
Q

Hypokalaemic metabolic alkalosis with hypertension.

Patient has HIGH aldosterone and LOW renin.

Dx?

A

Primary hyperaldosteronism.

145
Q

Hypokalaemic metabolic alkalosis with hypertension.

Patient has HIGH aldosterone and HIGH renin.

DDx (4)?

A

Secondary Hyperaldosteronism:

  • Renovascular HTN
  • Increased Beta-adrenergic receptor activity (hyperthyroidism, phaeochromocytoma, beta-agonists)
  • Malignant hypertension
  • Renin-secreting tumour
146
Q

Hypokalaemic metabolic alkalosis with hypertension.

Patient has NORMAL aldosterone and NORMAL renin.

Dx?

A

Cushing’s syndrome

147
Q

Hypokalaemic metabolic alkalosis with hypertension.

Patient has LOW aldosterone and LOW renin.

DDx (4)?

A

Pseudo-hyperaldosteronism:

  • Apparent mineralocorticoid excess
  • Liddle syndrome
  • CKD
  • Congenital adrenal hyperplasia
148
Q

Patient is noted to have pituitary macroadenoma, with elevated prolactin levels and visual field defects.

What is the appropriate next step?

A

Dopamine agonist therapy (e.g. bromocriptine)

If symptoms/size of tumour are refractory to treatment or treatment intolerance is noted after 4m, THEN consider surgery (transsphenoidal hypophysectomy).

149
Q

Patient has hypercalcaemia, high PTH and LOW urinary calcium.

Dx?

A

FHH - familial hypocalciuric hypercalcaemia.

150
Q

Patient has a solitary thyroid nodule, so you suspect a malignancy.

What TSH level would be consistent with malignancy?

A

Any (low/normal/high)

151
Q

Patient has a solitary thyroid nodule with NORMAL/HIGH TSH. You order a thyroid US.

What 5 ultrasound features of the nodule suggest a thyroid maignancy?

What is the next step if malignancy is suspected?

A

VICES:

Vascularity
Irregular border
Calcification 
Echogenicity decreased (hypo-echogenicity)
Size > 3cm

FNA biopsy indicated with malignancy suspected.

152
Q

Patient has a solitary thyroid nodule with LOW TSH. A thyroid ultrasound is pending. A radioactive iodine scan is arranged, what do the following findings suggest?

  1. Hot lesion
  2. Cold lesion
A
  1. Hot lesion - rarely malignant

2. Cold lesion - consistent with malignant, proceed to FNA biopsy.

153
Q

Patient has multiple thyroid nodules and is noted to be hyperthyroid on TFT (high T4 / low TSH). Technectium scan reveals multiple hot spots.

Dx?

A

Toxic multinodular goitre

154
Q

ENDO - CA - Q6

A

ENDO - CA - Q6

155
Q

What is the class of drug and MOA for Metformin?

A

Class of drug: biguanide

MOA: reduces hepatic glucose production; increases peripheral utilisation of glucose.

156
Q

What is the class of drug and MOA for Gliclazide?

A

Class of drug: sulfonylurea

MOA: increases pancreatic insulin secretion; may decrease insulin resistance.

157
Q

Hypothyroidism is associated with which of the following:

A. Hyponatraemia
B. Hyperprolactinaemia
C. Elevated CK
D. Elevated LDH
E. All the above
A

E. All the above

158
Q

How does hypothyroidism cause hyperprolactinaemia?

A

hypothyroidism –> decreased T4 feedback to hypothalamus –> increased TRH secretion (secondary pituitary enlargement) –> TRH with weak effect on lactotrophs in pituitary –> hyperprolactinaemia

159
Q

Elderly lady with low vitamin D is prescribed a megadose of vit D. What happens to the following:

  1. Serum calcium levels
  2. Urinary calcium levels
  3. Risk of falls and fracture
A

Patient will have hypercalcaemia, hypercalciuria and have have paradoxical increase in risk of falls and fractures.

160
Q

A mother with adrenal insufficiency presents to hospital. Which synthetic corticosteroid is most appropriate in the following scenarios:

  1. Mother with a normal foetus that want not wants the corticosteroid to cross the placenta
  2. Mother is a foetus with immature lung that wants the corticosteroid to cross the placenta.
A
  1. Mother with a normal foetus that want not wants the corticosteroid to cross the placenta
    - Hydrocortisone does not cross the placenta
  2. Mother is a foetus with immature lung that wants the corticosteroid to cross the placenta.
    - Dexamethasome crosses the placenta
161
Q

What is the Rotterdam Criteria for PCOS diagnosis (3 criteria, needs 2/3 for diagnosis)

A
  1. Oligo/Ano-ovulation
  2. Hyperandrogenism (Clinical or Biochemical)
  3. Polycystic ovaries
162
Q

For PCOS - what are the biochemical values of the following that qualify for hyperandrogenism:

  1. Testosterone
  2. Androstenedione
  3. DHEAS
A
  1. Testosterone > 70
  2. Androstenedione > 245
  3. DHEAS > 248
163
Q

For PCOS - what are the 2 criteria required on US to qualify as polycystic oavries?

A

Either:

  1. 12 or more follicles in in each ovary
  2. > 10cc size of ovary

MCQ knowledge (22 decks)

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