Diabetes & Endocrinology Flashcards
Renal tubular acidosis
clinical syndrome characterised by hyperchloraemic metabolic acidosis with a normal anion gap
RTA 1
hypokalaemia,
recurrent renal stones nephrocalcinosis
Distal
Linked to RA, Sjogrens, SLE
RTA 2
Proximal
Hypokalaemia
Linked to Wilson’s disease, cystinosis, Fanconi’s syndrome
RTA 3
Mixed
rare and caused by carbonic anhydrase II deficiency
RTA 4
Hyperkalaemia
Linked with diabetes mellitus and hypoaldosteronism
Thyrotoxicosis with tender goitre
Subacute (De Quervain’s) thyroiditis (post-viral illness)
- manage with NSAIDs and supportive measures, should self resolve
-will have raised ESR
Hypercalcaemia with suppressed PTH
Suspicious for malignancy
Water deprivation test in nephrogenic DI
urine osmolality after fluid deprivation: low
urine osmolality after desmopressin: low
- tubules unrespsonsive to ADH
Water deprivation test in cranial DI
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
Phaeochromocytoma antihypertensive
Phenoxybenzamine
Impaired glucose tolerance
fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l
Diagnosis of type 2 DM
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)
HbA1c threshold for T2DM
48
SGLT-2 inhibitor mechanism and SEs
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
Primary hyperaldosteronism findings
hypertension, hypernatraemia, and hypokalemia
Primary hyperaldosteronism causes
Bilateral adrenocortical hyperplasia - MOST COMMON
Adenoma (Conn’s)
Carcinoma
Aldosterone actions
Sodium reabsorption
Potassium excretion
Stress incontinence management
1st - pelvic floor exercise
2nd - surgical intervention or duloxetine
Urge incontinence management
1st - bladder retraining
Mirabegron - preferred in older ladies
Oxybutynin - avoid if risk of falls
Tolterodine
Botulinum if pharmacological management ineffective
DDP-4 inhibitors
- 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
GLP-1 mimetic
Exenatide, liraglutide
-increase insulin secretion and inhibit glucagon secretion
- weight loss
Galactosaemia
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
Pseudohyperkalaemia
High cell counts and high potassium
1st line treatment for painful diabetic neuropathy
Duloxetine
Drug induced gynaecomastia
spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids
more rarely: heroin, isoniazid, tricyclics
Sulfonylureas
Gliclazide
Weight gain
Hypos
K-ATP channels
Hypokalaemic alkalosis
Vomiting
Cushing’s
Conn’s
Thiazide and loop diuretics
Hyperkalaemic acidosis
Diarrhoea
Acetazolamide
Renal tubular acidosis
Carbimazole mechanism
blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production
