Diabetes & Endocrinology

Question 1

Renal tubular acidosis

Answer 1

clinical syndrome characterised by hyperchloraemic metabolic acidosis with a normal anion gap

Question 2

RTA 1

Answer 2

hypokalaemia,
recurrent renal stones nephrocalcinosis
Distal
Linked to RA, Sjogrens, SLE

Question 3

RTA 2

Answer 3

Proximal
Hypokalaemia
Linked to Wilson’s disease, cystinosis, Fanconi’s syndrome

Question 4

RTA 3

Answer 4

Mixed
rare and caused by carbonic anhydrase II deficiency

Question 5

RTA 4

Answer 5

Hyperkalaemia
Linked with diabetes mellitus and hypoaldosteronism

Question 6

Thyrotoxicosis with tender goitre

Answer 6

Subacute (De Quervain’s) thyroiditis (post-viral illness)
- manage with NSAIDs and supportive measures, should self resolve
-will have raised ESR

Question 7

Hypercalcaemia with suppressed PTH

Answer 7

Suspicious for malignancy

Question 8

Water deprivation test in nephrogenic DI

Answer 8

urine osmolality after fluid deprivation: low
urine osmolality after desmopressin: low
- tubules unrespsonsive to ADH

Question 9

Water deprivation test in cranial DI

Answer 9

After fluid deprivation: osmolality low
After desmopressin: osmolality high
- tubules still able to respond to ADH so concentrate urine when exogenous source of ADH provided

Question 10

Phaeochromocytoma antihypertensive

Answer 10

Phenoxybenzamine

Question 11

Impaired glucose tolerance

Answer 11

fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l

Question 12

Diagnosis of type 2 DM

Answer 12

fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

Question 13

HbA1c threshold for T2DM

Answer 13

48

Question 14

SGLT-2 inhibitor mechanism and SEs

Answer 14

reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.
- UTI, Fourniers
-Euglycaemic ketoacidosis

Question 15

Primary hyperaldosteronism findings

Answer 15

hypertension, hypernatraemia, and hypokalemia

Question 16

Primary hyperaldosteronism causes

Answer 16

Bilateral adrenocortical hyperplasia - MOST COMMON
Adenoma (Conn’s)
Carcinoma

Question 17

Aldosterone actions

Answer 17

Sodium reabsorption
Potassium excretion

Question 18

Stress incontinence management

Answer 18

1st - pelvic floor exercise
2nd - surgical intervention or duloxetine

Question 19

Urge incontinence management

Answer 19

1st - bladder retraining
Mirabegron - preferred in older ladies
Oxybutynin - avoid if risk of falls
Tolterodine
Botulinum if pharmacological management ineffective

Question 20

DDP-4 inhibitors

Answer 20

• Gliptins
• inhibits degradation of incretin hormones, leading to increased insulin secretion, decreased glucagon release and therefore lower blood glucose level
• do not cause weight gain

Question 21

GLP-1 mimetic

Answer 21

Exenatide, liraglutide
-increase insulin secretion and inhibit glucagon secretion
- weight loss

Question 22

Galactosaemia

Answer 22

Autosomal recessive
Absence of galactose-1-phosphate uridyl transferase. Intracellular accumulation of galactose-1-phosphate
- jaundice, cataracts, failure to thrive hepatomegaly, hypoglycaemia after galactose, Fanconi syndrome

Question 23

Pseudohyperkalaemia

Answer 23

High cell counts and high potassium

Question 24

1st line treatment for painful diabetic neuropathy

Answer 24

Duloxetine

Question 25

Drug induced gynaecomastia

Answer 25

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids
more rarely: heroin, isoniazid, tricyclics

Question 26

Sulfonylureas

Answer 26

Gliclazide
Weight gain
Hypos
K-ATP channels

Question 27

Hypokalaemic alkalosis

Answer 27

Vomiting
Cushing’s
Conn’s
Thiazide and loop diuretics

Question 28

Hyperkalaemic acidosis

Answer 28

Diarrhoea
Acetazolamide
Renal tubular acidosis

Question 29

Carbimazole mechanism

Answer 29

blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production