Endocrine Flashcards
At what HbA1c should you add in another agent to treat diabetes?
What is the target range? And what is the target range if you’re on a drug which can cause hypos (e.g sulphonylureas?)
HbA1c >58
Or add an SLGT2 inhibitor to metformin if there are established cardiovascular risk factors
Note HbA1c 48 is the target
53 if you’re on a drug that can cause hypos
What are the criteria for pre diabetes?
HbA1c 42-47
Fasting glucose 6.1-6.9
What’s the criteria for impaired fasting glucose?
6.1-7
What’s the criteria for impaired glucose tolerance?
Fasting glucose <7
2 hour tolerance 7.8-11.1
What is the most likely adverse effect from radioiodine therapy?
Hypothyroidism
What is the mainstay of treatment for Addison’s?
Hydrocortisone (glucocorticoid replacement) and fludrocortisone (mineralocorticoid)
In intercurrent illness > double the hydrocortisone but leave the fludrocortisone the same
What conditions can give a falsely low HbA1c reading and why?
Sickle cell anaemia and haemoglobinopathies
Due to decreased FBC lifespan
What condition can cause a falsely high HbA1c reading and why?
Splenectomy - increased RBC lifespan
What test is used to diagnose Addison’s?
Short synacthen test
How do you manage De Quervain’s thyroiditis?
Conservative management with ibuprofen, sometimes steroids in more severe cases
What are the causes of primary hyperaldosteronism?
Adrenal adenoma in 20-30% of cases
Bilateral adrenal hyperplasia in 60-70% of cases
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma
How does primary hyperaldosteronism present?
Hypertension
Hypokalaemia
Metabolic alkalosis
What would the aldosterone/ renin ratio show in primary hyperaldosteronism?
High aldosterone levels
Low renin levels
How is primary hyperaldosteronism managed?
Adrenal adenoma > surgery
Bilateral hyperplasia > spironolactone (aldosterone antagonist)
What are the TFT results in sick euthyroid syndrome?
Low T3/4, normal TSH
What is toxic multinodular goitre and how is it investigated and treated?
Thyroid gland contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.
Nuclear scintigraphy reveals patchy uptake.
Treatment is with radioiodine.
How does phaeochromocytoma present and how is it investigated?
Headache, sweating, palpitations, hypertension
Urinary metanephrines
How are prolactinomas treated?
Dopamine agonists - bromocriptine. Surgery if it doesn’t respond > trans sphenoidal approach.
What blood gas pattern do you see in cushings?
Hypokalaemic metabolic alkaosis
What is the main serious adverse effect of carbimazole to be aware of?
Agranulocytosis
What is the difference between cushing’s disease and cushing’s syndrome?
What is cushing’s triad?
Cushing’s disease - increased ACTH production from the pituitary, usually due to an adenoma
Cushing’s syndrome - due to prolonged exposure to cortisol. E.g steroids or adrenal causes.
Cushing’s triad - irregular respirations, bradycardia and systolic hypertension resulting from raised intracranial pressure.
When should you start thyroxine when TFT results show a picture of subclinical hypothyroidism?
TSH high on 2 occasions 3 months apart and they are symptomatic
- Do a 6 mnonth trial of thyroxine
How do you interpret C-peptide levels?
Low - T1DM
Normal/ high - T2DM
What are the causes of a raised prolactin?
pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metoclopramide, domperidone, prochlorperazine
What medications can reduce hypoglycaemic awareness in diabetics?
B-blockers
How does primary hyperaldosteronism present?
High BP
Low potassium, high sodium
Causes:
Bilateral idiopathic adrenal hyperplasia
Or conn’s if there is an adrenal adenoma
Which condition is associated with a tender goitre?
De Quervain’s thyroiditis aka subacute thyroiditis
Can present with either hyper or hypothyroidism (hyper initially before developing into hypo)
What heart condition is acromegaly associated with?
Cardiomyopathy, hypertension, arrhythmias and LVH
How is acromegaly treated?
Ocreotide (somatostatin analogue) or trans-sphenoidal surgery
Hypercalcaemia is a side effect of which drug class?
Thiazide diuretics
What are the investigations for acromegaly?
IGF-1 levels, OGTT, serial GH measurements
How do you treat phaeochromocytoma?
Alpha blocker eg phenoxybenzamine 1st line, b-blocker 2nd line
What are the diagnostic criteria for diabetes?
Fasting glucose >7
Random glucose >11.1
HbA1c >48
2 hr glucose OGTT >11.1
Repeat testing or in combination with positive symptoms
Describe LADA?
Positive auto-antiodies
May not require insulin at time of diagnosis
Occurs in adults
Describe MODY?
Negative autoantibodies =
Describe the principle of carbohydrate counting?
1 unit of insulin per 10g of carbohydrate
What is the mechanism of action of metformin?
Decreases hepatic gluconeogenesis and increases peripheral glucose uptake
What is the mechanism of action of the sulphonylureas?
Gliclazide, glimepiride
Increases insulin secretion
By blocking B cell kATP channels
So needs functioning B cells to be effective
What is the mechanism of action of the SGLT2 inhibitors?
Blocks SGLT2 in the proximal tubules - reducing glucose reabsortpion
What is the mechanism of action of the thiazidenides?
Pioglitazone
PPARy agonists - enhance the action of insulin (but don’t affect its secretion)
What is the mechanism of action of the DPP-IV inhibitors (aka gliptins)?
Prolong the action of GLP-1 (incretin) / reduce its breakdown
This promotes insulin secretion
What is the mechanism of action of the GLP receptor agonists (dulaglutide, semaglutide, exenatide)?
Stimulate insulin secretion, delay gastric emptying, decrease appetite and suppress glucagon
Which diabetic drugs cause: weight loss/ weight gain or are weight neutral?
Weight gain:
Sulphonylureas - gliclazide, glimeprimide
TZDs - related to fluid retention and weight gain is subcut not visceral
Weight loss:
SGLT2 inhibitors - the flozins
GLP receptor agonists - dulaglutide, emaglutide, exenatide
Weight neutral:
Metformin/ maybe slight weight loss
DPP-IV inhibitors - the gliptins
Which diabetic drugs can cause hypos?
Sulphonylureas - gliclazide, glimepiride
Which diabetic drugs are good and bad in renal disease?
Sulphonylureas (gliclazide, glimepiride)- BAD
SGLT2 inhibitors - GOOD
Which class of diabetes drugs is linked to increased risk of fractures (therefore avoid in the elderly), hepatotoxicity, fluid retention (avoid in HF) and bladder cancer?
TZDs - pioglitazone
Which class of diabetes drugs has a link to pancreatitis?
GLP receptor agonists - dulaglutide, semaglutide, exenatide
What are the biochemical diagnostic criteria for DKA?
Ketones > 3
BG > 11
Bicarb <15 / pH <7.3
What biochemical resutls would you expect in HHS?
Very high glucose
Hyperosmolar (>320)
Significant renal impairment
Na may be raised
Less acidotic/ ketotic than in DKA
Papillary thyroid cancer is the most common type. How does it spread?
Mostly lymphatic spread, also haematogenous
Usually spreads to the lungs
Reasonable survival rate
How does follicular carcinoma spread?
Haematogenous spread to bones, liver, lung
What syndrome / group of disorders is medullary thyroid carcinoma associated with?
Familial MEN
Which type of thyroid cancer is very aggressive?
Anaplastic carcinoma
What is the surgery of choice for thyroid cancers and why?
Subtotal thyroidectomy - total thyroidectomy risks damage to adjacent structures fc
What biochemical results would you expect in cushing’s?
High ACTH (pituitary or ectopic causes)
Low ACTH in adrenal causes
High cortisol
What investigations are used in cushing’s?
Dexamethasone suppression test
24hr urine cortisol
Pituitary MRI
Pituitary surgery
What are the treatment options for cushing’s?
Metyrapone
Surgery
How do prolactinomas present, what are the investigation and treatment options?
Amenorrhoea, infertility, impotence
Headaches
Abnormal visual fields
Pituitary MRI
Pituitary hormones
Cabergoline - dopamine agonist
Acromegaly is usually caused by a macroadenoma. How is it investigated and treated?
Glucose tolerance test
- Elevated IGF1 and hyperglycaemia
CT/ MRI pituitary
Pituitary hormones
Treated with surgery
Radiotherapy
Ocreotide - somatostain analogue
Carbegoline - dopamine agonist
Pegvisomant - GH antagonist
What is the difference between cranial and nephrogenic DI?
In cranial DI there is not enough ADH
(often idiopathic)
In nephrogenic DI there is enough ADH but the kidneys are resistant to it
Both cause polyuria and polydipsia
What are the investigation and treatment options for DI?
Water deprivation test
(urine will remain dilute due to lack of ADH)
How do you treat DI?
Desmopressin ( only in cranial DI - in nephrogenic DI in the kidneys are resistant so no use)
What is conn’s syndrome?
What biochemical results do you see?
Primary hyperaldosteronism due to an adrenal adenoma or carcinoma
Increased cortisol
High sodium, Low potassium
Alkalosis
Investigation and management of primary hyperaldosteronism (conn’s)?
Raised aldosterone to renin ratio
Adrenal CT
Adrenal vein sampling
Management - adrenalectomy or spironolactone if bilateral
What is addison’s, what biochemical results do you see?
Primary adrenal deficiency
Low cortisol
Low sodium, High potassium
Low glucose
Anti-adrenal autoantibodies
What are the investigation and management options of addison’s?
Synacthen test
Raised renin to aldosterone ratio (opposite to conn’s)
Management - hydrocortisone and fludrocortisone
What is congenital adrenal hyperplasia?
Primary adrenal deficiency
Autosomal recessive inheritance
Low cortisol, high testosterone
Managed with glucocorticoid and mineralocorticoid replacement
What is phaeochromocytoma?
Catecholamine secreting tumour in the adrenal medulla
What biochemical results do you see in phaeochromocytoma and how do you investigate for it?
How is it treated?
High glucose
High calcium
Lactic acidosis
24 hour catecholamines and metanephrins
MRI
PET scan
Alpha blockers then b-blockers
What are the zones of the adrenal gland and what is secreted form each?
Zona glomerulosa
- Mineralocorticoids (aldosterone)
Zona fasciculata
- Glucocorticoids (cortisol)
Zone reticularis
- Androgens
Medulla
- Catecholamines (epinephrine/ norepinephrine)
What biochemical results do you see in the different types of hyperparathyroidism?
Primary hyperparathyroidism
(adenomas/ carcinomas)
High PTH, high calcium, low phosphate
Secondary hyperparathyroidism
(most commonly due to renal failure - parathyroid gland hyperplasia develops)
High PTH, low calcium, high phosphate
Tertiary hyperparathyroidism
(occurs after many years of secondary
High PTH, high calcium, low or normal phosphate
What is osteomalacia/ Ricketts?
Vitamin D deficiency
See a picture of secondary hyperparathyroidism with raised PTH to try and compensate for poor calcium absorption
What is paget’s disease?
Increased bone turnover
Raised ALP
Managed wit bisphosphonantes
What is osteogenesis imperfecta?
Genetic disorder with mutations in collagen genes
Fractures and blue sclera
