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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is type 1 diabetes mellitus?

A

Autoimmune destruction of pancreatic beta cells within the Islets of Langerhans resulting in insulin deficiency

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2
Q

What is type 2 diabetes mellitus?

A

Insulin resistance

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3
Q

Give some risk factors for type 2 diabetes.

A
  • Older
  • Central obesity
  • Sedentary lifestyle
  • Hypertension and/or hyperlipidaemia
  • African/Caribbean ancestry
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4
Q

Describe the clinical presentation of diabetes.

A
  • Polyuria
  • Polydipsia
  • Weight loss
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5
Q

How is type 2 diabetes diagnosed?

A

Symptomatic individual:
ONE glucose result in diabetic range (fasting/random)

Asymptomatic individual:
TWO separate glucose results in diabetic range (fasting/random/2 hr postprandial)

Symptomatic/asymptomatic individual:
ONE HbA1c result in diabetic range

Diabetic values:

  • Fasting > 7 mmol/L
  • Random or 2 hr postprandial > 11.1 mmol/L
  • HbA1c > 48 mmol/L
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6
Q

Describe the conservative management of type 2 diabetes.

A

Lifestyle advice, e.g. weight loss, take regular exercise etc.

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7
Q

Describe the pharmacological management of type 2 diabetes.

A
  • 1st line = Metformin (Biguanide)
  • 2nd line = Metformin + Gliclazide (Sulfonylurea)
  • 3rd line = Metformin + Gliclazide + Sitagliptin (DPP4i)
  • 4th line = insulin therapy
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8
Q

Side effects of pharmacological therapies for type 2 diabetes.. which cause weight gain/loss?

A
  • Biguanides = weight LOSS (also cause GI disturbance: nausea, anorexia)
  • Sulfonylureas/glitazones = weight GAIN
  • DPP4 inhibitors = no change
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9
Q

How is type 1 diabetes diagnosed?

A

Signs of hyperglycaemia (polydipsia, polyuria) AND ONE of the following:

  • Ketosis
  • Rapid weight loss
  • Age of onset <50 years
  • BMI <25 kg/m2
  • Personal/family history of autoimmune disease
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10
Q

Describe the management of type 1 diabetes.

A

Insulin

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11
Q

What are the microvascular and macrovascular complications of diabetes mellitus?

A

Microvascular =
Diabetic neuropathy, retinopathy, nephropathy

Macrovascular =
CVD

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12
Q

What is hyperthyroidism?

A

Excess thyroid hormone

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13
Q

What are the causes of hyperthyroidism?

A
  • 2/3 cases = GRAVES DISEASE
  • Toxic multinodular goitre
  • Toxic thyroid adenoma
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14
Q

What are the symptoms and signs of hyperthyroidism?

A

Symptoms:

  • Weight loss
  • Diarrhoea
  • Sweating, palpitations, tremor (anxiety)
  • Amenorrhoea

Signs:

  • Tachycardia
  • Lid lag/retraction
  • Exophthalmos
  • Onycholysis
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15
Q

How is hyperthyroidism investigated?

A

Thyroid function tests:

  • Primary = low TSH and high T3/T4
  • Secondary = high TSH and high T3/T4

Thyroid autoantibodies:

  • Thyroid peroxidase
  • Thyroglobulin
  • TSH receptor antibody

Radioactive iodine isotope uptake scan

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16
Q

Describe the pharmacological management of hyperthyroidism.

A
  • Beta blockers for rapid symptom control

- Carbimazole (antithyroid drug)

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17
Q

Describe the interventional management of hyperthyroidism.

A

Thyroidectomy

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18
Q

What is Graves’ disease? Extra signs present with Graves’ disease?

A

Autoimmune induced excess production of thyroid hormone (via TSH receptor antibody)

Signs - Graves’ ophthalmology:

  • Extraocular muscle swelling
  • Eye discomfort
  • Excessive lacrimation
  • Diplopia
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19
Q

What is hypothyroidism?

A

Too little thyroid hormone

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20
Q

What are the causes of hypothyroidism?

A
  • Hashimoto’s thyroiditis

- Iodine deficiency

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21
Q

What are the symptoms and signs of hypothyroidism?

A

Symptoms:

  • Weight gain
  • Constipation
  • Fatigue, myalgia
  • Menorrhagia

Signs:

  • Bradycardia
  • Reflexes relax slowly
  • Ataxia
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22
Q

Describe the pharmacological management of hypothyroidism.

A

Synthetic thyroid hormone (levothyroxine)

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23
Q

What is acromegaly? What is gigantism?

A

Acromegaly = Increased production of growth hormone occurring in adults (after fusion of epiphyseal growth plates)

Gigantism = Increased production of growth hormone occurring in children

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24
Q

What is the main cause of acromegaly?

A

Pituitary adenoma

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25
Q

What are the symptoms and signs of acromegaly?

A

Symptoms:

  • Acroparasthesia
  • Arthralgia
  • Sweating
  • Headache

Signs:

  • Massive growth of hands, feet and jaw
  • Widely spaced teeth
  • Puffy lips, eyelids and skin
  • Deep voice
26
Q

How is acromegaly investigated?

A

NOT random growth hormone test - GH is a pulsatile protein and levels vary throughout day

Administer glucose:

  • Normally glucose suppresses GH levels
  • If given glucose and GH levels still high, this is diagnostic for acromegaly

MRI pituitary fossa for adenoma

27
Q

Describe the pharmacological/interventional management of acromegaly.

A
  • Transsphenoidal surgery to remove adenoma

- GH antagonist, e.g. pegvisomant

28
Q

What is hyperaldosteronism?

A

Excess aldosterone production, independent of RAAS

Aldosterone works in kidney to cause potassium loss- excess causes hypokalaemia and sodium + water retention

29
Q

What are the causes of hyperaldosteronism?

A
  • 2/3 cases = CONN’S SYNDROME (a solitary, benign adrenocortical adenoma)
  • Bilateral adrenocortical hyperplasia
30
Q

What are the symptoms of hyperaldosteronism?

A

Symptoms of hypokalaemia =

  • Cramps
  • Constipation
  • Paraesthesia
  • Arrhythmias
31
Q

How is hyperaldosteronism investigated?

A

U+E = hypokalaemia

ECG - signs of hypokalaemia:
No POT and no T, but a long PR and a long QT

ADRENAL CT is diagnostic

32
Q

Describe the pharmacological/interventional management of hyperaldosteronism.

A

Depends on cause…

  • Treat hypokalaemia (give K+)
  • Pharmacological = spironolactone (aldosterone antagonist)
  • Interventional: laparoscopic adrenalectomy
33
Q

What is Cushing’s syndrome? What is Cushing’s disease?

A

Cushing’s syndrome = excess cortisol + loss of hypothalamic pituitary axis feedback + loss of circadian rhythm

Cushing’s disease = all of above + CAUSED by pituitary adenoma

34
Q

What are the causes of Cushing’s syndrome?

A

ACTH independent causes:

  • Iatrogenic - STEROIDS!!
  • Adrenal adenoma

ACTH dependent causes:
- Cushing’s disease (pituitary adenoma)

35
Q

Describe the symptoms of Cushing’s syndrome.

A
  • Weight gain/truncal obesity
  • Hirsuitism
  • Acne
  • Moon face/buffalo hump
  • Striae
36
Q

How is Cushing’s syndrome investigated?

A

Dexamethasone suppression test:

  • Dexamethasone usually suppresses cortisol levels
  • Failure of dexamethasone to suppress cortisol levels over 24 hr period is diagnostic of Cushing’s syndrome

MRI for pituitary adenoma

37
Q

Describe the management of Cushing’s syndrome.

A

Depends on cause:

  • If iatrogenic then stop steroids
  • Adrenal adenoma = adrenalectomy, radiotherapy
  • Cushing’s disease (pituitary adenoma) = transsphenoidal removal of pituitary adenoma
38
Q

What is Addison’s disease?

A
  • Autoimmune destruction of the adrenal cortex resulting in primary adrenal insufficiency (adrenal impairment resulting in low cortisol and low aldosterone levels)
39
Q

What are the leading causes of primary adrenal insufficiency in the UK and worldwide?

A
  • Worldwide = TB

- UK = Addison’s disease

40
Q

Describe the symptoms of Addison’s disease.

A
  • Hyperpigmentation of the skin
  • Depression
  • Abdominal pain, nausea and vomiting
41
Q

Describe the investigation of Addison’s disease.

A

ACTH stimulation test:

  • Give ACTH (synacthen) and measure cortisol levels
  • Normally, ACTH would cause a rise in cortisol levels; in Addison’s, cortisol remains low after giving ACTH

Test for 21-hydroxylase adrenal autoantibodies

U+E: hyperkalaemia and hyponatraemia (due to low levels of aldosterone)

42
Q

Addison’s disease can result in hyperkalaemia…

a) Describe the ECG changes you would see with hyperkalaemia
b) Describe the non-urgent and urgent management of hyperkalaemia

A

a) Small P waves, tall T waves, wide QRS complex
b) Non-urgent = polystyrene sulfonate resin
Urgent = calcium gluconate, insulin

43
Q

Describe the pharmacological management of Addison’s disease.

A
  • Hydrocortisone to replace cortisol

- Fludrocortisone to replace aldosterone

44
Q

What is diabetes insipidus?

A

EITHER

  • Too little ADH secretion from posterior pituitary (cranial DI)
  • OR kidney not responding to ADH (nephrogenic DI)
45
Q

What are the causes of diabetes insipidus?

A

Cranial DI:

  • Head trauma
  • Pituitary adenoma

Nephrogenic DI:
- Drugs, e.g. Lithium

46
Q

What are the symptoms of diabetes insipidus?

A
  • Polyuria
  • Polydipsia
  • Dehydration
47
Q

How is diabetes insipidus investigated?

A

Water deprivation test:

  • Restrict fluid
  • Measure urine osmolarity - +ve for DI if urine osmolarity remains low
  • Differentiate between cranial and nephrogenic DI by using desmopressin (ADH analogue)
48
Q

Describe the pharmacological management of diabetes insipidus.

A
  • Cranial DI - desmopressin

- Nephrogenic DI - bendroflumethiazide, NSAIDs

49
Q

What is SIADH?

A

SIADH stands for ‘syndrome of inappropriate secretion of ADH’
Too much ADH being secreted from posterior pituitary

50
Q

What are the causes of SIADH?

A
  • Malignancy
  • Drugs
  • CNS disorders
51
Q

What are the symptoms and signs of SIADH?

A

Symptoms:

  • Confusion
  • Nausea
  • Anorexia

Signs:
- Concentrated urine

52
Q

How is SIADH investigated?

A

Measure urine osmolarity (v high) and plasma osmolarity (v low)

53
Q

Describe the management of SIADH.

A
  • Treat underlying cause if possible
  • Restrict fluid intake
  • Vasopressin receptor antagonists (‘vaptans’)
54
Q

What is hyperparathyroidism? What are the types of hyperparathyroidism? Give examples of what causes each type

A

Too much PTH secreted from parathyroid glands into bloodstream

  • Primary, most commonly caused by parathyroid adenoma
  • Secondary - when a condition such as kidney failure or vitamin D deficiency lowers calcium levels, so parathyroid glands produce more parathyroid hormone
55
Q

Does PTH reduce/increase serum calcium levels? Describe the mechanisms by which it achieves this

A

PTH increases serum calcium levels by…

  • Stimulating osteoclasts to resorb bone to release calcium into blood
  • Stimulating kidneys to reabsorb more calcium from urine into blood
  • Stimulating gut to absorb more calcium
56
Q

Describe the serum PTH and calcium results for…

a) primary hyperparathyroidism
b) secondary hyperparathyroidism

A

a) high PTH, high calcium

b) high PTH, low calcium

57
Q

Describe the management of hyperparathyroidism

A 
Primary = surgery to remove parathyroid adenoma
Secondary = treat underlying condition, e.g. kidney disease, vit D deficiency
58
Q

What are the symptoms of hyperparathyroidism?

A

STONES, BONES, MOANS, GROANS

Kidney stones
Bone pain/tenderness
Depression/fatigue
Abdominal pain, constipation

59
Q

What is hypoparathyroidism?

What are the causes of hypoparathyroidism?

A

Too little PTH secreted from parathyroid glands into bloodstream

Causes:

  • Surgical (removal of parathyroid glands)
  • Autoimmune
60
Q

What are the symptoms and signs of hypoparathyroidism?

A

HYPOcalcaemia:

Symptoms:
- Paraesthesia (especially around mouth and lips)

Signs:

  • Chvostek’s sign (twitching of facial muscles when ficial nerve is tapped)
  • Trousseau’s sign (spasm caused by inflating BP cuff around upper arm)
  • Long QT interval
61
Q

Describe the management of hypoparathyroidism

A

Treat hypocalcaemia:

  • Urgent = IV calcium glucoronate
  • Maintenance = Adcal D3

Treat underlying cause, e.g. autoimmune with steroids

62
Q

Give some signs of DKA

A

Kussmaul’s breathing
Vomiting
Loss of consciousness
Pear drop breath

Phase 2a (16 decks)

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