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MSRA > Endocrine > Flashcards

Endocrine Flashcards

1
Q

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?)

A

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

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2
Q

What are the criteria for pre diabetes?

A

HbA1c 42-47
Fasting glucose 6.1-6.9

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3
Q

What’s the criteria for impaired fasting glucose?

A

6.1-7

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4
Q

What’s the criteria for impaired glucose tolerance?

A

Fasting glucose <7

2 hour tolerance 7.8-11.1

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5
Q

What is the most likely adverse effect from radioiodine therapy?

A

Hypothyroidism

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6
Q

What is the mainstay of treatment for Addison’s?

A

Hydrocortisone (glucocorticoid replacement) and fludrocortisone (mineralocorticoid)

In intercurrent illness > double the hydrocortisone but leave the fludrocortisone the same

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7
Q

What conditions can give a falsely low HbA1c reading and why?

A

Sickle cell anaemia and haemoglobinopathies

Due to decreased FBC lifespan

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8
Q

What condition can cause a falsely high HbA1c reading and why?

A

Splenectomy - increased RBC lifespan

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9
Q

What test is used to diagnose Addison’s?

A

Short synacthen test

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10
Q

How do you manage De Quervain’s thyroiditis?

A

Conservative management with ibuprofen, sometimes steroids in more severe cases

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11
Q

What are the causes of primary hyperaldosteronism?

A

Adrenal adenoma in 20-30% of cases
Bilateral adrenal hyperplasia in 60-70% of cases

Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

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12
Q

How does primary hyperaldosteronism present?

A

Hypertension

Hypokalaemia

Metabolic alkalosis

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13
Q

What would the aldosterone/ renin ratio show in primary hyperaldosteronism?

A

High aldosterone levels
Low renin levels

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14
Q

How is primary hyperaldosteronism managed?

A

Adrenal adenoma > surgery
Bilateral hyperplasia > spironolactone (aldosterone antagonist)

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15
Q

What are the TFT results in sick euthyroid syndrome?

A

Low T3/4, normal TSH

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16
Q

What is toxic multinodular goitre and how is it investigated and treated?

A

Thyroid gland contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.

Nuclear scintigraphy reveals patchy uptake.

Treatment is with radioiodine.

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17
Q

How does phaeochromocytoma present and how is it investigated?

A

Headache, sweating, palpitations, hypertension

Urinary metanephrines

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18
Q

How are prolactinomas treated?

A

Dopamine agonists - bromocriptine. Surgery if it doesn’t respond > trans sphenoidal approach.

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19
Q

What blood gas pattern do you see in cushings?

A

Hypokalaemic metabolic alkaosis

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20
Q

What is the main serious adverse effect of carbimazole to be aware of?

A

Agranulocytosis

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21
Q

What is the difference between cushing’s disease and cushing’s syndrome?

What is cushing’s triad?

A

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.

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22
Q

When should you start thyroxine when TFT results show a picture of subclinical hypothyroidism?

A

TSH high on 2 occasions 3 months apart and they are symptomatic
- Do a 6 mnonth trial of thyroxine

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23
Q

How do you interpret C-peptide levels?

A

Low - T1DM
Normal/ high - T2DM

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24
Q

What are the causes of a raised prolactin?

A

pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metoclopramide, domperidone, prochlorperazine

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25
Q

What medications can reduce hypoglycaemic awareness in diabetics?

A

B-blockers

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26
Q

How does primary hyperaldosteronism present?

A

High BP
Low potassium, high sodium

Causes:
Bilateral idiopathic adrenal hyperplasia
Or conn’s if there is an adrenal adenoma

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27
Q

Which condition is associated with a tender goitre?

A

De Quervain’s thyroiditis aka subacute thyroiditis

Can present with either hyper or hypothyroidism (hyper initially before developing into hypo)

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28
Q

What heart condition is acromegaly associated with?

A

Cardiomyopathy, hypertension, arrhythmias and LVH

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29
Q

How is acromegaly treated?

A

Ocreotide (somatostatin analogue) or trans-sphenoidal surgery

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30
Q

Hypercalcaemia is a side effect of which drug class?

A

Thiazide diuretics

31
Q

What are the investigations for acromegaly?

A

IGF-1 levels, OGTT, serial GH measurements

32
Q

How do you treat phaeochromocytoma?

A

Alpha blocker eg phenoxybenzamine 1st line, b-blocker 2nd line

33
Q

What are the diagnostic criteria for diabetes?

A

Fasting glucose >7
Random glucose >11.1
HbA1c >48
2 hr glucose OGTT >11.1

Repeat testing or in combination with positive symptoms

34
Q

Describe LADA?

A

Positive auto-antiodies
May not require insulin at time of diagnosis
Occurs in adults

35
Q

Describe MODY?

A

Negative autoantibodies =

36
Q

Describe the principle of carbohydrate counting?

A

1 unit of insulin per 10g of carbohydrate

37
Q

What is the mechanism of action of metformin?

A

Decreases hepatic gluconeogenesis and increases peripheral glucose uptake

38
Q

What is the mechanism of action of the sulphonylureas?
Gliclazide, glimepiride

A

Increases insulin secretion
By blocking B cell kATP channels
So needs functioning B cells to be effective

39
Q

What is the mechanism of action of the SGLT2 inhibitors?

A

Blocks SGLT2 in the proximal tubules - reducing glucose reabsortpion

40
Q

What is the mechanism of action of the thiazidenides?
Pioglitazone

A

PPARy agonists - enhance the action of insulin (but don’t affect its secretion)

41
Q

What is the mechanism of action of the DPP-IV inhibitors (aka gliptins)?

A

Prolong the action of GLP-1 (incretin) / reduce its breakdown
This promotes insulin secretion

42
Q

What is the mechanism of action of the GLP receptor agonists (dulaglutide, semaglutide, exenatide)?

A

Stimulate insulin secretion, delay gastric emptying, decrease appetite and suppress glucagon

43
Q

Which diabetic drugs cause: weight loss/ weight gain or are weight neutral?

A

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

44
Q

Which diabetic drugs can cause hypos?

A

Sulphonylureas - gliclazide, glimepiride

45
Q

Which diabetic drugs are good and bad in renal disease?

A

Sulphonylureas (gliclazide, glimepiride)- BAD

SGLT2 inhibitors - GOOD

46
Q

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?

A

TZDs - pioglitazone

47
Q

Which class of diabetes drugs has a link to pancreatitis?

A

GLP receptor agonists - dulaglutide, semaglutide, exenatide

48
Q

What are the biochemical diagnostic criteria for DKA?

A

Ketones > 3
BG > 11
Bicarb <15 / pH <7.3

49
Q

What biochemical resutls would you expect in HHS?

A

Very high glucose
Hyperosmolar (>320)
Significant renal impairment
Na may be raised
Less acidotic/ ketotic than in DKA

50
Q

Papillary thyroid cancer is the most common type. How does it spread?

A

Mostly lymphatic spread, also haematogenous
Usually spreads to the lungs
Reasonable survival rate

51
Q

How does follicular carcinoma spread?

A

Haematogenous spread to bones, liver, lung

52
Q

What syndrome / group of disorders is medullary thyroid carcinoma associated with?

A

Familial MEN

53
Q

Which type of thyroid cancer is very aggressive?

A

Anaplastic carcinoma

54
Q

What is the surgery of choice for thyroid cancers and why?

A

Subtotal thyroidectomy - total thyroidectomy risks damage to adjacent structures fc

55
Q

What biochemical results would you expect in cushing’s?

A

High ACTH (pituitary or ectopic causes)
Low ACTH in adrenal causes
High cortisol

56
Q

What investigations are used in cushing’s?

A

Dexamethasone suppression test
24hr urine cortisol
Pituitary MRI
Pituitary surgery

57
Q

What are the treatment options for cushing’s?

A

Metyrapone

Surgery

58
Q

How do prolactinomas present, what are the investigation and treatment options?

A

Amenorrhoea, infertility, impotence
Headaches
Abnormal visual fields

Pituitary MRI
Pituitary hormones

Cabergoline - dopamine agonist

59
Q

Acromegaly is usually caused by a macroadenoma. How is it investigated and treated?

A

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

60
Q

What is the difference between cranial and nephrogenic DI?

A

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

60
Q

What are the investigation and treatment options for DI?

A

Water deprivation test
(urine will remain dilute due to lack of ADH)

61
Q

How do you treat DI?

A

Desmopressin ( only in cranial DI - in nephrogenic DI in the kidneys are resistant so no use)

62
Q

What is conn’s syndrome?
What biochemical results do you see?

A

Primary hyperaldosteronism due to an adrenal adenoma or carcinoma
Increased cortisol
High sodium, Low potassium
Alkalosis

63
Q

Investigation and management of primary hyperaldosteronism (conn’s)?

A

Raised aldosterone to renin ratio
Adrenal CT
Adrenal vein sampling

Management - adrenalectomy or spironolactone if bilateral

64
Q

What is addison’s, what biochemical results do you see?

A

Primary adrenal deficiency

Low cortisol
Low sodium, High potassium
Low glucose
Anti-adrenal autoantibodies

65
Q

What are the investigation and management options of addison’s?

A

Synacthen test
Raised renin to aldosterone ratio (opposite to conn’s)

Management - hydrocortisone and fludrocortisone

66
Q

What is congenital adrenal hyperplasia?

A

Primary adrenal deficiency

Autosomal recessive inheritance

Low cortisol, high testosterone

Managed with glucocorticoid and mineralocorticoid replacement

67
Q

What is phaeochromocytoma?

A

Catecholamine secreting tumour in the adrenal medulla

68
Q

What biochemical results do you see in phaeochromocytoma and how do you investigate for it?
How is it treated?

A

High glucose
High calcium
Lactic acidosis

24 hour catecholamines and metanephrins
MRI
PET scan

Alpha blockers then b-blockers

69
Q

What are the zones of the adrenal gland and what is secreted form each?

A

Zona glomerulosa
- Mineralocorticoids (aldosterone)

Zona fasciculata
- Glucocorticoids (cortisol)

Zone reticularis
- Androgens

Medulla
- Catecholamines (epinephrine/ norepinephrine)

70
Q

What biochemical results do you see in the different types of hyperparathyroidism?

A

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

71
Q

What is osteomalacia/ Ricketts?

A

Vitamin D deficiency

See a picture of secondary hyperparathyroidism with raised PTH to try and compensate for poor calcium absorption

72
Q

What is paget’s disease?

A

Increased bone turnover

Raised ALP
Managed wit bisphosphonantes

73
Q

What is osteogenesis imperfecta?

A

Genetic disorder with mutations in collagen genes

Fractures and blue sclera

MSRA (13 decks)

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