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Endocrinology / Renal Medicine > Endocrine Conditions > Flashcards

Endocrine Conditions Flashcards

1
Q

Describe the glucocorticoid axis

A

Adrenal cortex = Cortisol, aldosterone, gonadotrophins
Adrenal medulla = Catecholamines

CRH (corticotrophin releasing hormone) from hypothalamus –> ACTH from anterior pituitary –> Cortisol from adrenal cortex

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2
Q

Why might one-off serum cortisol measurements be misleading in the diagnosis of hypoadrenalism or Cushing’s syndrome?

A

Cortisol is produced in a circadian rhythm so levels will vary throughout the day

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3
Q

What is Waterhouse-Friderichsen’s Syndrome?

A

Adrenal haemorrhage as a result of meningococcal septicaemia. Causes widespread purpura, meningitis, coma, DIC. Normal vascular tone requires cortisol to stimulate alpha and beta adrenoceptors so there is shock when this is defective. Treatment is with antibiotics e.g. ceftriaxone and hydrocortisone for adrenal support.

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4
Q

List some causes of primary hypoadrenalism i.e. adrenal insufficiency (Addison’s Disease)

A

Over 80% of cases are autoimmune and associated with other autoimmune conditions e.g. autoimmune thyroid disease, TIDM, etc.
Other causes: Adrenal TB, adrenal haemorrhage (Waterhouse-Fridrichsen syndrome due to meningococcal sepsis), surgical removal, opportunistic infection, adrenal metastases, etc.

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5
Q

What is the key test for diagnosis of hypoadrenalism?

A

Short Synacthen Test (ACTH stimulation): Measure cortisol levels before and 30mins after administration of tetracosactide (Synacthen) - Addison excluded if cortisol rises >550nmol/L on second measurement

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6
Q

Does the short Synacthen test allow differentiation between primary and secondary adrenal insufficiency?

A

No

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7
Q

Which autoantibodies may be present in 80% of patients with primary hypoadrenalism?

A

21-hydroxylase adrenal autoantibodies

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8
Q

What will be the abnormalities of sodium and potassium in primary hypoadrenalism? Why?

A

Low sodium, high potassium - caused by decreased mineralocorticoid

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9
Q

Why is it important to educate a patient with primary hypoadrenalism about their condition?

A

Very important for them to understand potential consequences of stopping steroids abruptly (i.e. Addisonian Crisis). Advise they need to increase hydrocortisone dose if unwell, injured, before strenuous exercise etc. Teach how to inject IM hydrocortisone in case oral intake not possible e.g. vomiting.

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10
Q

What is the management for a patient with primary hypoadrenalism?

A

Steroids e.g. hydrocortisone

Mineralocorticoids e.g. fludrocortisone

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11
Q

How might a patient with Addison’s Disease present?

A

Insidious onset of non-specific symptoms: lethargy, weight loss, anorexia, dizziness
Postural hypotension
Hyperpigmentation - buccal mucosa, skin creases
GI symptoms: Abdominal pain, vomiting etc.
May present with acute crisis

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12
Q

How might a patient with an Addisonian Crisis present?

A

Hypovolaemic shock: Raised HR, postural hypotension, oligouria, vasoconstriction, confusion, comatose

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13
Q

What is the immediate management for a patient with an Addisonian Crisis?

A

Bloods for cortisol and ACTH sent immediately to laboratory…also U&E to check K+ and Na+
Hydrocortisone 100mg IV stat
Fluid bolus - crystalloid or colloid to maintain BP
Monitor blood glucose as risk of hypoglycaemia
Look for underlying cause e.g. blood and urine culture for infection

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14
Q

What is the further management (after initial treatment) of a patient with Addisonian Crisis?

A

IV glucose if hypoglycaemia
IV fluids as clinical state determines
Continue hydrocortisone e.g. 100mg/8hr IV or IM
Switch to oral steroids after 72 hours if patient’s condition allows

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15
Q

What is the commonest cause of Cushing’s Syndrome?

A

Exogenous i.e. synthetic steroid use

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16
Q

What is Cushing’s DISEASE?

A

Cushing’s caused by pituitary ACTH-secreting tumour

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17
Q

What symptoms may be seen in a patient with Cushing’s Syndrome?

A

Weight gain: Central distribution of fat e.g. trunk, neck (buffalo hump)
Mood changes: Depression, irritability
Hirtuism
Acne

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18
Q

What signs might be present on a patient with Cushing’s Syndrome?

A 
Redistribution of fat: Central deposition, buffalo hump, moon face
Skin and muscle atrophy
High blood pressure
Osteoporosis
Recurrent infections
Poor wound healing
Bruises
Purple abdominal striae
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19
Q

What test would you do to investigate Cushing’s Syndrome?

A

Dexamethasone Suppression Test

24 hour urinary cortisol

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20
Q

What is the main hormonal role of ADH?

A

Water reabsorption in the collecting tubules in the kidney

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21
Q

What stimulates ADH secretion?

A

High plasma osmolality
Fall in BP
Fall in blood volume

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22
Q

What is diabetes insipidus and what are the two types?

A

Dysfunction of ADH

Cranial diabetes insipidus = Impaired production of ADH
Nephrogenic diabetes insipidus = Resistance to the action of ADH

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23
Q

What are the clinical features of diabetes insipidus?

A

Polyuria
Dilute urine
Nocturia
Polydipsia

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24
Q

List the causes of nephrogenic diabetes insipidus

A 
Hypokalaemia
Hypercalcaemia
Drugs: Lithium, certain antibiotics
Prolonged polyuria
Familial (mutation in ADH receptor)
Renal tubular acidosis
Sickle cell disease
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25
Q

At what level of polyuria would you suspect diabetes insipidus?

A

Urine volume >3L/24hr

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26
Q

What is a water deprivation test?

A

Investigates diabetes insipidus and it’s cause: Serum and urine osmolality, urine volume and body weight tested every hour for up to 8 hours while the patient abstains from all food and drink.

If body weight falls by >3%, stop the test and measure urgent serum osmolality
If serum osmolality remains within normal levels and urine concentration increases, this is a normal result.
If serum osmolality rises without adequate rise of urine osmolality, this suggests diabetes insidious and a test to establish a cranial or nephrogenic cause should be done.

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27
Q

How you do you distinguish between cranial and nephrotic diabetes insipidus after doing a water deprivation test?

A

Administer desmopressin…

Cranial diabetes insipidus - Urine osmolality will rise after desmopressin administration
Nephrogenic diabetes insipidus - Urine osmolality will not change after desmopressin

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28
Q

What is SIADH?

A

Syndrome of Inappropriate ADH Secretion

Production of ADH despite low plasma osmolality and normal plasma volume

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29
Q

What causes SIADH?

A

Cancer e.g. small cell lung cancer, pancreatic, prostate
Brain - Meningitis, tumour, brain abscess
Drugs - Opiates, carbamazepine
Lungs - Pneumonia, lung abscess

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30
Q

What is the treatment for SIADH?

A
  • Treat the underlying cause
  • Fluid restriction e.g. 500-1000mL in 24 hours
  • Hypertonic (high sodium) saline with loop diuretic to prevent fluid overload
  • Demeclocycline - a vasopressin inhibitor
  • Vasopressin antagonists
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31
Q

Give 2 key effects of angiotensin II

A

Vasoconstriction

Stimulates production of aldosterone

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32
Q

What is Conn’s Syndrome?

A

Primary hyperaldosteronism

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33
Q

What effect does aldosterone have on sodium, potassium, blood presure and renin?

A

Sodium retention
Potassium loss in the urine
Increases blood pressure
Inhibits renin production (due to the retention of sodium)

34
Q

What tests would you do if you suspect primary hyperaldosteronism?

A

U&E - Hypokalaemia (but not always!)

Raised aldosterone:renin ratio

35
Q

List some signs of hypokalaemia

A 
Weakness
Cramps
Parasthesia
Polyuria
Polydipsia
36
Q

What are the causes of primary hyperaldosteronism?

A

Aldosterone producing adenoma

Bilateral adrenocortical hyperplasia

37
Q

Describe the pathogenesis causing diabetic ketoacidosis

A

Absence of insulin causes unrestrained glucose production by the liver, causing dramatic hyperglycaemia. There is osmotic diuresis in the kidney which causes water loss and dehydration. Fatty acids released by the breakdown of fat are converted to acidic ketones which causes metabolic acidosis.

38
Q

Give the diagnostic criteria for diabetic ketoacidosis

A

Hyperglycaemia i.e. blood glucose >11 mol/L
Ketonaemia i.e. blood ketones >3.0 mmol/L (or +++ measurement in the urine)
Acidosis i.e. blood pH

39
Q

What is the WHO criteria for diagnosis of diabetes?

A
  • Evidence of hyperglycaemia (polyuria, polydipsia, thrush, lethargy, weight loss) and raised glucose detected once - fasting >7mmol/L or random >11.1mmol/L
    OR
  • Raised glucose detected on 2 separate occasions (values above) OR oral glucose tolerance test 2 hour value >11.1mmol/L
    OR
  • HbA1c >48mmol/L (6.5%)
40
Q

What are the values for diagnosing impaired glucose tolerance?

A

Fasting glucose >7mmol/L
AND
OGTT 2 hour result >7.8mmol/L but

41
Q

What is the value for diagnosing impaired fasting glucose?

A

Fasting glucose >6.1mmol/L but

42
Q

What is the target HbA1c for patients with otherwise uncomplicated diabetes?

A

7.5% (48mmol/L)

43
Q

What type of substance does a phaeochromocytoma produce?

A

Catecholamines

44
Q

How might you investigate suspected pheochromocytoma?

A

Bloods - Raised WCC
24 hour urine x 3 - look for metadrenaline and normetadrenaline
Imaging e.g. CT/MRI abdomen
Isotope scanning to localise extra-medullary tumours

45
Q

What is the treatment for phaeochromocytoma?

A

Surgery to excise the tumour, with alpha and beta blockade using phenoxybenzamine and propranolol respectively before the procedure

46
Q

Which thyroid cancer may produce calcitonin?

A

Medullary carcinoma - acts as a useful tumour marker

47
Q

What are the 3 syndromes associated with congenital adrenal hyperplasia?

A

Salt-wasting adrenogenitalism
Simple virilising adrenogenital syndrome
Nonclassic adrenal virulism

48
Q

What is the most common enzyme deficiency in congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

49
Q

How would you screen a family member of a patient with MEN Type 1? Why?

A

Serum calcium levels - there is a high penetrance of hyperparathyroidism in MEN 1

50
Q

What type of tumours are associated with MEN Type 1?

A

All the ‘P’s!

  • Parathyroid hyperplasia/adenomas
  • Pancreatic endocrine tumours e.g. gastrinoma, VIPoma, insulinoma, glucagonoma, somatostatinoma
  • Pituitary prolactinoma
  • Pituitary GH producing tumour
51
Q

What type of tumours are associated with MEN Type 2?

A

Thyroid - medullary thyroid carcinoma
Adrenals - phaeochromocytoma
Parathyroid hyperplasia

52
Q

What is the serum glucose definition of hypoglycaemia?

A
53
Q

List some causes of hypoglycaemia

A
  • Exogenous drugs e.g. insulin, sulphonylureas, alcohol, aspirin overdose, ACE inhibitors, beta blockers
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Islet cell malignancy (insulinoma), Immune hypoglycaemia (due to autoantibodies to the insulin receptor)
  • Non-pancreatic tumours
54
Q

What stimulates the release of parathyroid hormone?

A

Fall in free ionised calcium

Rise in plasma phosphate

55
Q

What effects does parathyroid hormone have on calcium and phosphate levels, and how does it achieve this?

A

Increases calcium by:

  • Increased renal tubular reabsorption
  • Stimulates osteoclasts to breakdown bone and release calcium
  • Indirectly increases GI absorption of calcium by activating Vitamin D in the kidneys

Reduces phosphate by reducing renal tubular reabsorption

56
Q

In which 2 organs is Vitamin D activated? Which stages of activation does it undergo in each?

A 
Liver = 25-hydroxylase
Kidney = 1-alpha hydroxylase
57
Q

What is the most common cause of hypercalcaemia?

A

Hyperparathyroidism

58
Q

What differentials would you suggest in a patient with high calcium and normal (or low) parathyroid hormone?

A

Non-PTH cause of the hyperparathyroidism e.g. malignancy, sarcoidosis, Vitamin D excess

59
Q

Why might a malignancy cause hypercalcaemia?

A
  • If it has metastasised to bone

- The tumour may produce PTH-related peptide (PTHrP) which increases calcium levels

60
Q

What differentials would you suggest in a patient with low calcium and raised parathyroid hormone?

A

Non-PTH cause of the hypoparathyroidism e.g. Vitamin D deficiency, renal failure

61
Q

What are the symptoms of hypercalcaemia?

A

Fractures
Renal stones
Abdominal discomfort e.g. pain, constipation, diarrhoea
Psychiatric symptoms e.g. depression

62
Q

What is the treatment for acute severe hypercalcaemia?

A
  • Rehydrate with IV 0.9% saline
  • Bisphosphonatesafter rehydration e.g. pamindromate 30mg in 300mL 0.9% saline over 3 hours (dose depends on serum calcium level)
  • Chemotherapy if malignancy the cause
  • Steroids if sarcoidosis the cause
63
Q

What is the most common cause of hypocalcaemia?

A

Chronic kidney disease

64
Q

What are the characteristics of the metabolic syndrome?

A 
Central obesity (BMI > 30 or raised waist circumference)
AND 2 of the following:
- BP 130/85
- Triglycerides >1.7mmol/L
- HDL 5.6mmol/L or known diabetic
65
Q

What is the hormone abnormality in acromegaly?

A

Excess growth hormone production

66
Q

List some complications of acromegaly

A

Impaired glucose tolerance or diabetes mellitus
Vascular problems: HTN, increased risk of IHD and stroke, left ventricular hypertrophy, cardiomyopathy, arrhythmias
Increased risk of colon cancer

67
Q

Why is a glucose tolerance test useful in acromegaly?

A

Confirms diagnosis - Normally growth hormone is suppressed by high glucose levels, but in acromegaly this suppression does not occur

68
Q

What is the most common cause of acromegaly?

A

Benign growth hormone secreting pituitary adenoma

69
Q

What is the most common hormonal disturbance of the pituitary gland?

A

Hyperprolactinaemia

70
Q

What inhibits prolactin release?

A

Dopamine

71
Q

List some drugs which may cause hyperprolactinaemia

A 
Metoclopramide
Haloperidol
Alpha-methyldopa
Oestrogens
Ecstasy / MDMA
Anti-psychotics
72
Q

List some symptoms of hyperprolactinaemia in females

A 
Amenorrhoea / oligomenorrhoea
Infertility
Galactorrhoea
Weight gain
Decreased libido
Dry vagina
73
Q

What is the main treatment for hyperprolactinaemia?

A

Dopamine agonist e.g. bromocriptine

74
Q

What emergency is associated with pheochromocytoma?

A

Hypertensive crisis

75
Q

What is the most common type of pituitary tumour?

A

Benign pituitary adenoma

76
Q

What is a common visual field defect caused by a pituitary tumour?

A

Bilateral temporal hemianopia

77
Q

List some local pressure effects which might be seen due to growth of a pituitary tumour

A
  • Headache
  • Visual field defects e.g. bilateral temporal hemianopia due to compression of the optic chiasm
  • Cranial nerve palsy (III, IV, VI)
  • Diabetes insipidus
  • Disturbance of temperature, sleep and appetite centres
  • CSF rhinorrhoea
78
Q

In hypopituitarism, what order are the pituitary hormones lost in?

A

Growth hormone, gonadotrophins, FSH/LH, prolactin, TSH, ACTH

79
Q

What is the most common cause of hypopituitarism?

A

Hypothalamic or pituitary tumour, surgical removal or radiotherapy

80
Q

What are the 3 main causes of erectile dysfunction?

A

Smoking
Alcohol
Diabetes

81
Q

What is the classic triad of symptoms in pheochromocytoma?

A

Headache
Sweating
Tachycardia

(Features of the sympathetic nervous system)

82
Q

Where are phaeochromocytomas normally found?

A

Adrenal medulla

Endocrinology / Renal Medicine (6 decks)

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