Endocrine Flashcards

1
Q

How long is the treatment regime for Grave’s disease?

A

12-18 months

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2
Q

what electrolyte abnormality is seen in Cushing’s?

A

hypokalaemic metabolic alkalosis

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3
Q

what two tests are commonly used to confirm Cushing’s syndrome?

A

overnight dexamethasone suppression test
24hr urinary free cortisol

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4
Q

what is the most common cause for childhood hypothyroidism?

A

autoimmune thyroiditis

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5
Q

what is sick euthyroid syndrome?

A

changes in thyroid function tests when a patient is in hospital
often everything is low
In the majority of cases however the TSH level is within the normal range
Changes are reversible upon recovery from the systemic illness hence no treatment is usually needed

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6
Q

what is subacute thyroiditis?

A

occurs following viral infection and typically presents with hyperthyroidism
usually self-limiting

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7
Q

What diabetic medications cause weight loss?

A

canagliflozin - sglt2 inhibitor
exenatide - glp1 mimetic

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8
Q

How is HHS diagnosed?

A
  1. hypovolaemia
  2. marker hyperglycaemia&raquo_space; 30mmol/l without significant ketonaemia or acidosis
  3. significantly raised serum osmolality (>320 mosmol/kg)
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9
Q

what is the main cause of primary hyperaldosteronism?

A

bilateral idiopathic adrenal hyperplasia

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10
Q

what are the features of primary hyperaldosteronism?

A

hypertension
hypokalaemia e.g. muscle weakness
alkalosis

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11
Q

What is carcinoid syndrome?

A

Group of symptoms that occur due to release of hormones by neuroendocrine tumours
Occurs when metastases are present in the liver and release serotonin into the systemic circulation
May also occur with lung carcinoid as mediators are not ‘cleared’ by the liver

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12
Q

What are the features of carcinoid syndrome?

A

flushing - often the earliest symptom
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis

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13
Q

What is the treatment of Graves’ disease?

A

Carbimazole

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14
Q

what is the most common pituitary tumour?

A

pituitary adenoma - benign, non-secreting tumoue

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15
Q

which are the symptoms of a pituitary tumour?

A

headache
visual field defects

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16
Q

how is a pituitary tumour diagnosed?

A

MRI brain
screening tests for visual field defects
hormone tests as appropriate

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17
Q

what is the most common pituitary secreting tumour?

A

prolactin

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18
Q

what is the clinical presentation of prolactinoma?

A

women: oligomenorrhoea/amenorrhoea, galactorrhoea, infertility, vaginal dryness
men: reduced facial hair, erectile dysfunction
in both sexes: mass effects from tumour - headache, visual field defects

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19
Q

what are investigations for prolactinoma?

A

MRI brain: microadenoma appears as lesions in the pituitary, macroadenoma appears as space-occupying tumour
serum prolactin

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20
Q

how are prolactinomas managed?

A

pharmacological:
- dopamine agonist e.g. cabergoline - decrease in serum prolactin
- hormone replacement therapy
surgery:
- trans-sphenoidal resection indicated if failure of medical treatment
- radiotherapy

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21
Q

what are the causes of low magnesiumm?

A

drugs: diuretics, PPIs
total parenteral nutrition
diarrhoea: may occur with acute or chronic diarrhoea
alcohol
hypokalaemia
hypercalcaemia e.g. 2ndary to hyperparathyroidism
metabolic disorders

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22
Q

what are the features of low magnesium?

A

similar to hypocalcaemia:
- paraesthesia
- tetany
- seizures
- arrhythmias
- decreased PTH secretion
- ECG features similar to those of hypokalaemia
- exacerbates digoxin toxicity

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23
Q

What is the mechanism of action of ADH?

A

ADH stimulates synthesis of aquaporin-2 in the apical membrane of the collecting duct which promotes water reabsorption

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23
Q

What is the mechanism of action of ADH?

A

ADH stimulates synthesis of aquaporin-2 in the apical membrane of the collecting duct which promotes water reabsorption

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24
Q

how is primary hyperaldosteronism diagnosed?

A

plasma aldosterone/renin ratio is the first-line investigation
it should show high aldosterone levels alongside low renin levels
following this a high-res CT abdomen and adrenal vein sampling is used to differentiate between unilateral adenoma and bilateral sources of aldosterone excess

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25
Q

what is the management of primary hyperaldosternism?

A

adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

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26
Q

When is SGLT-2 monotherapy indicated in a diabetic patient?

A

if metformin is contraindicated and the patient has a risk of CVD, established CVD or chronic heart failure

26
Q

When is SGLT-2 monotherapy indicated in a diabetic patient?

A

if metformin is contraindicated and the patient has a risk of CVD, established CVD or chronic heart failure

27
Q

what pharmacological management can be provided to diabetic patients where metformin is contraindicated?

A

DDP-4 inhibitor of pioglitazone or sulfonylurea
SGLT-2 may be used if certain criteria are met

28
Q

what are the features of carcinoid syndrome?

A

flushing
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis

29
Q

how should carcinoid syndrome be investigated?

A

urinary 5-HIAA
plasma chromogranin A y

30
Q

how is carcinoid syndrome managed?

A

somatostatin analogues e.g. octreotide

31
Q

What are the causes of nephrogenic diabetes insipidus?

A

drugs e.g. lithium
intrinsic kidney disease
electrolyte disturbances i.e. hypokalaemia/hypercalcaemia

32
Q

what are the causes of cranial diabetes insipidus?

A

brain tumours
head injury
brain malformations
brain infections e.g. meningitis, encephalitis, tuberculosis
brain surgery or radiotherapy

33
Q

what happens before and after giving desmopressin and nephrogenic DI?

A

urine osmolality is low before and after giving desmopressin
because the kidneys do not respond to ADH

34
Q

What happens before and after giving desmopressin in cranial DI?

A

urine osmolality is low before
after desmopressin it is high
kidneys respond to the ADH leading to water reabsorption and more concentrated urine

35
Q

what is the most common thyroid cancer?

A

papillary - 70%
often in young females, has an excellent prognosis

36
Q

When should a GLP-1 mimetic be considered in a diabetic patient?

A

if triple therapy is not effective or tolerated and:
- BMI >/= 35 and specific psychological or other medical problems associated with obesity or
- BMI </= 35 and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significantly obesity-related comorbidities

37
Q

What can cause a lower than expected HbA1c level?

A

anything that reduces red blood cell life span:
- sickle cell
- GP6D deficiency
- hereditary spherocytosis
- haemodialysis

38
Q

What can cause a higher than expected HbA1c level?

A
  • vit b12/folic acid deficiency
  • iron deficiency anaemia
  • splenectomy
39
Q

What are the possible paraneoplastic features of small cell lung cancer?

A

ADH
ACTH
Lambert-Eaton syndrome

40
Q

What are the possible paraneoplastic features of squamous cell carcinoma?

A

PTH secretion causing hypercalcaemia
clubbing
hyperthyroidism to ectopic TSH

41
Q

what are the possible paraneoplastic features of adenocarcinoma?

A

gynaecomastia

42
Q

How does myxoedema coma usually present?

A

confusion and hypothermia

43
Q

How is myxoedema coma treated?

A

IV thyroid replacement
IV fluid
IV corticosteroids - until possibility of co-existing adrenal insufficiency has been excluded
electrolyte imbalance correct
sometimes rewarming

44
Q

What are the features and causes of primary hyperparathyroidism?

A

Parathyroid hormone is making too much PTH
elevated PTH and Ca2+
low phosphate
may be asymptomatic if mild
recurrent abdominal pain: renal colic, pancreatitis
changes to emotional or cognitive state
most cases are due to a solitary adenoma (80%), multifocal disease occurs in 10-15%

45
Q

What are the features and causes of secondary hyperparathyroidism?

A

parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure
elevated PTH
low ca2+
elevated phosphate
low Vit D
may have few symptoms
eventually may develop bone disease

46
Q

What are the features and causes of tertiary hyperparathyroidism?

A

occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause
Ca2+ is normal or high
Elevated PTH
decreased or normal phosphate levels
vit D normal or decreased
ALP levels elevated
features: metastatic calcification, bone pain and/or fracture, nephrolithiasis, pancreatitis

47
Q

what is the definitive treatment of primary hyperparathryoidism?

A

total parathyroidectomy

48
Q

what is primary adrenal insufficiency and what are some of the causes?

A

addisons disease - damage to adrenal glands resulting in reduction in secretion of cortisol and aldosterone - most common cause is autoimmune - others are tuberculosis, metastases, meningococcal septicaemia, HIV, antiphospholipid syndrome

49
Q

what is 2ndary adrenal insufficiency and what are the causes?

A

inadequate ACTH stimulating adrenal glands resulting in low cortisol release - result of loss or damage to pituitary gland - can be due to surgery, infection, loss of blood flow or radiotherapy

50
Q

what is tertiary adrenal insufficiency and what causes it?

A

inadequate CRH release by the hypothalamus - usually the result of patients being on long term oral steroids i.e. more than 3 weeks causing suppression of the hypothalamus - when exogenous steroids are suddenly withdrawn the hypothalamus does not wake up fast enough and endogenous steroids are not adequately produced - long term steroids should be tapered slowly to allow time for adrenal axis to regain normal function

51
Q

what is the short synacthen test?

A

first choice test for adrenal insufficiency:
giving synacthen - synthetic ACTH - blood cortisol is measured at baseline, 30 and 60 minutes after administration - synthetic ACTH will stimulate healthy adrenal glands to produce cortisol and the cortisol levels should rise at least double - a failure of cortisol to rise indicates primary adrenal insufficiency

52
Q

what is the treatment of adrenal insufficiency?

A

replacement steroids
hydrocortisone is a glucocorticoid hormone to replace cortisol
fludrocortisone is a mineralocorticoid to replace aldosterone if needed
steroid car d- doses should be doubled in acute illness

53
Q

how is addisonian crisis treated?

A

intensive monitoring if unwell
parenteral steroids - IV hydrocortisone 100mg stat then every 6 hrs
iv fluid resus
correct hypoglycaemia
careful monitoring of electrolytes and fluid balance

54
Q

what is sheehans syndrome?

A

injury to pituitary gland following extreme blood loss during child birth

55
Q

what is the most common endogenous cause of Cushing’s?

A

pituitary adenoma

56
Q

what are the 4 phases of thyroiditis?

A

phase 1 - lasts 3-6 weeks - hyperthyroidism, painful goitre, raised ESR
phase 2 - 1-3 weeks - euthyroid
phase 3 -weeks-months - hypothyroidism
phase 4 - thyroid structure and function goes back to normal

57
Q

what is a phaeochromocytoma?

A

rare catecholamine secreting tumour - about 10% are familial and may be associated with MEN type II, neurofibromatosis etc.

58
Q

how would you investigate a carcinoid tumour?

A

urinary 5-hIAA
plasma chromogranin A y

59
Q

how would you manage a carcinoid tumour?

A

somatostatin analogues e.g. octreotide
diarrhoea - cyproheptadine may help

60
Q

what is the first-line test for acromegaly?

A

serum IGF-1

61
Q

what are the features of phaeochromocytoma?

A

hypertension
headaches
palpitations
sweating
anxiety

62
Q

what are the tests for investigating phaechromoctyoma?

A

24hr urinary collection of metanephrines

63
Q

what is the management of phaeochromocytoma?

A

surgery is definitive management
patient must first however be stabilized with medical management
alpha blocker e.g. phenoxybenzamine given before a
beta blocker e.g. propranolol

64
Q

what is the most common cause of Addisons in the UK?

A

auto-immunity

65
Q

what glucose level indicates impaired fasting glucose?

A

fasting glucose of greater than or equal to 6.1 but less than 7