Title 01 .ENDOCRINOLOGY MCQs.pdf ✅

A 23-year-old woman presents for review. She has not had a normal period for around 8 months now. A recent pregnancy test was negative. Blood tests are ordered: FSH 2.2 IU/L (0-20 IU/L) Oestradiol 84 pmol/l (100-500 pmol/l) Thyroid stimulating hormone 3.1 mIU/L Prolactin 2 ng/ml (0-10 ng/ml) Free androgen index 3 ( < 7 ) What is the most likely cause of her symptoms? A. Prolactinoma B. Premature ovarian failure C. Polycystic ovarian syndrome D. Addison's disease E. Excessive exercise ANSWER: E. Excessive exercise EXPLANATION: The bloods show a hypothalamic amenorrhoea which may be caused by stress or excessive exercise. The FSH would be raised in premature ovarian failure. NOTES Amenorrhoea Amenorrhoea may be divided into primary (failure to start menses by the age of 16 years) or secondary (cessation of established, regular menstruation for 6 months or longer). Causes of primary amenorrhoea • Turner's syndrome • testicular feminisation • congenital adrenal hyperplasia • congenital malformations of the genital tract Secondary amenorrhoea is defined as when menstruation has previously occurred but has now stopped for at least 6 months. Causes of secondary amenorrhoea (after excluding pregnancy) • hypothalamic amenorrhoea (e.g. Stress, excessive exercise) • polycystic ovarian syndrome (PCOS) • hyperprolactinaemia • premature ovarian failure • thyrotoxicosis* • Sheehan's syndrome • Asherman's syndrome (intrauterine adhesions) Initial investigations • exclude pregnancy with urinary or serum bHCG • gonadotrophins: low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure) • prolactin • androgen levels: raised levels may be seen in PCOS • oestradiol • thyroid function tests *hypothyroidism may also cause amenorrhoea. ed, regular menstruation for 6 months or Q-2 A 55-year-old taxi driver with type 2 diabetes mellitus comes for review. When he was diagnosed 12 months ago he was started on metformin and the dose was titrated up. His IFCC- HbA1c one year ago was 75 mmol/mol (DCCT-HbA1c 9%) and is now 69 mmol/mol (8.5%). His body mass index is 33 kg/m2. What is the most appropriate next step in management? A. Add exenatide B. Add sitagliptin C. Add glipizide D. Make no changes to his medication E. Add insulin ANSWER: B. Add sitagliptin EXPLANATION: His HbA1c is still significantly above target so some change to the medication is indicated. The NICE type 2 diabetes mellitus guidelines would generally advocate the use of a sulfonylurea in this situation. Q-1 ENDOCRINOLOGY MCQs
However. the patient is a taxi driver and overweight. A DPP-4 inhibitor such as sitagliptin would be ideal in this situation. There is no risk of hypoglycaemia and they DPP-4 inhibitors are weight neutral. NOTES: Diabetes mellitus: management of type 2 NICE updated its guidance on the management of type 2 diabetes mellitus (T2DM) in 2015. Key points are listed below: HbA1c targets have changed. They are now dependent on what antidiabetic drugs a patient is receiving and other factors such as frailty there is more flexibility in the second stage of treating patients (i.e. after metformin has been started) - you now have a choice of 4 oral antidiabetic agents It's worthwhile thinking of the average patient who is taking metformin for T2DM, you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%) Dietary advice: encourage high fibre, low glycaemic index sources of carbohydrates include low-fat dairy products and oily fish control the intake of foods containing saturated fats and trans fatty acids limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake discourage use of foods marketed specifically at people with diabetes initial target weight loss in an overweight person is 5-10% HbA1c targets: This is area which has changed in 2015 individual targets should be agreed with patients to encourage motivation HbA1c should be checked every 3-6 months until stable, then 6 monthly NICE encourage us to consider relaxing targets on 'a case-by- case basis, with particular consideration for people who are older or frail, for adults with type 2 diabetes' in 2015 the guidelines changed so HbA1c targets are now dependent on treatment: Lifestyle or single drug treatment Practical examples: a patient is newly diagnosed with HbA1c and wants to try lifestyle treatment first. You agree a target of 48 mmol/mol (6.5%) you review a patient 6 months after starting metformin. His HbA1c is 51 mmol/mol (6.8%). You increase his metformin from 500mg bd to 500mg tds and reinforce lifestyle factors Patient already on treatment: Drug treatment: The 2015 NICE guidelines introduced some changes into the management of type 2 diabetes. There are essentially two pathways, one for patients who can tolerate metformin, and one for those who can't: Tolerates metformin: metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added from the following list: → sulfonylurea → gliptin → pioglitazone → SGLT-2 inhibitor Management of T2DM HbA1c target Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%) 53 mmol/mol (7.0%) Management of T2DM HbA1c target Lifestyle 48 mmol/mol (6.5%) Lifestyle + metformin 48 mmol/mol (6.5%) Includes any drug which may cause hypoglycaemia (e.g. lifestyle + sulfonylurea) 53 mmol/mol (7.0%)
if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy with one of the following combinations should be offered: → metformin + gliptin + sulfonylurea → metformin + pioglitazone + sulfonylurea → metformin + sulfonylurea + SGLT-2 inhibitor → metformin + pioglitazone + SGLT-2 inhibitor → OR insulin therapy should be considered Criteria for glucagon-like peptide1 (GLP1) mimetic (e.g. exenatide) if triple therapy is not effective, not tolerated or contraindicated then NICE advise that we consider combination therapy with metformin, a sulfonylurea and a glucagonlike peptide1 (GLP1) mimetic if: → BMI >= 35 kg/m2 and specific psychological or other medical problems associated with obesity or → BMI < 35 kg/m2 and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesityrelated comorbidities only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months Practical examples you review an established type 2 diabetic on maximum dose metformin. Her HbA1c is 55 mmol/mol (7.2%). You do not add another drug as she has not reached the threshold of 58 mmol/mol (7.5%) a type 2 diabetic is found to have a HbA1c of 62 mmol/mol (7.8%) at annual review. They are currently on maximum dose metformin. You elect to add a sulfonylurea Cannot tolerate metformin or contraindicated if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions, consider one of the following: → sulfonylurea → gliptin → pioglitazone if the HbA1c has risen to 58 mmol/mol (7.5%) then a one of the following combinations should be used: → gliptin + pioglitazone → gliptin + sulfonylurea → pioglitazone + sulfonylurea if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy Starting insulin metformin should be continued. In terms of other drugs NICE advice: 'Review the continued need for other blood glucose lowering therapies' NICE recommend starting with human NPH insulin (isophane, intermediate acting) taken at bed-time or twice daily according to need Risk factor modification Blood pressure target is < 140/80 mmHg (or < 130/80 mmHg if end-organ damage is present) ACE inhibitors are first-line Antiplatelets should not be offered unless a patient has existing cardiovascular disease Lipids following the 2014 NICE lipid modification guidelines only patients with a 10-year cardiovascular risk > 10% (using QRISK2) should be offered a statin. The first-line statin of choice is atorvastatin 20mg on Graphic showing choice of statin. *this is a bit confusing because isn't the diagnostic criteria for T2DM HbA1c 48 mmol/mol (6.5%)? So shouldn't all patients be offered metformin at diagnosis? Our interpretation of this is that some patients upon diagnosis will elect to try lifestyle measures, which may reduce their HbA1c below this level. If it then rises to the diagnostic threshold again metformin should be offered Q-3 A 41-year-old woman is investigated for hot flushes and night sweats. Bloods show a significantly raised FSH level and her symptoms are attributed to the menopause. Following discussions with the patient she elects to have hormone replacement treatment. What is the most significant risk of prescribing an oestrogen-only preparation rather than a combined oestrogen-progestogen preparation? A. Increased risk of venous thromboembolism B. Increased risk of ovarian cancer C. Increased risk of endometrial cancer D. Increased risk of breast cancer E. Increased risk of colorectal cancer ANSWER: C. Increased risk of endometrial cancer
EXPLANATION: HRT: unopposed oestrogen increases risk of endometrial cancer NOTES: Hormone replacement therapy: adverse effects Hormone replacement therapy (HRT) involves the use of a small dose of oestrogen (combined with a progestogen in women with a uterus) to help alleviate menopausal symptoms. Side-effects nausea breast tenderness fluid retention and weight gain Potential complications increased risk of breast cancer: increased by the addition of a progestogen increased risk of endometrial cancer: reduced by the addition of a progestogen but not eliminated completely. The BNF states that the additional risk is eliminated if a progestogen is given continuously increased risk of venous thromboembolism: increased by the addition of a progestogen increased risk of stroke increased risk of ischaemic heart disease if taken more than 10 years after menopause Breast cancer in the Women's Health Initiative (WHI) study there was a relative risk of 1.26 at 5 years of developing breast cancer the increased risk relates to duration of use breast cancer incidence is higher in women using combined preparations compared to oestrogen-only preparations the risk of breast cancer begins to decline when HRT is stopped and by 5 years it reaches the same level as in women who have never taken HRT Q-4 Which one of the following unwanted effects is most likely to occur in patients taking gliclazide? A. Peripheral neuropathy B. Cholestasis C. Photosensitivity D. Syndrome of inappropriate ADH secretion E. Weight gain ANSWER: E. Weight gain EXPLANATION: All of the above side-effects may be seen in patients taking sulfonylureas but weight gain is the most common. NOTES: Sulfonylureas Sulfonylureas are oral hypoglycaemic drugs used in the management of type 2 diabetes mellitus. They work by increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells. Common adverse effects hypoglycaemic episodes (more common with long-acting preparations such as chlorpropamide) weight gain Rarer adverse effects syndrome of inappropriate ADH secretion bone marrow suppression liver damage (cholestatic) peripheral neuropathy Sulfonylureas should be avoided in breastfeeding and pregnancy Q-5 A 27-year-old female develops eye pain and reduced visual acuity following the initiation of treatment for her recently diagnosed Grave's disease. Which one of the following treatments is likely to have been started? A. Radioiodine treatment B. Thyroidectomy C. Propylthiouracil D. Carbimazole and thyroxine E. Carbimazole ANSWER: A. Radioiodine treatment EXPLANATION: Radioiodine treatment may lead to the development / worsening of thyroid eye disease in up to 15% of patients with Grave's disease NOTES: Thyroid eye disease Thyroid eye disease affects between 25-50% of patients with Graves' disease. Pathophysiology: • it is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation • the inflammation results in glycosaminoglycan and collagen deposition in the muscles