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Paper 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is primary adrenal insufficiency commonly known as?

A

Addison’s disease

Addison’s disease is characterized by destruction of the adrenal cortex, leading to deficiencies in cortisol and aldosterone.

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2
Q

What leads to the hyperpigmentation seen in Addison’s disease?

A

Increased CRH and ACTH production due to reduced cortisol levels

The feedback mechanism causes elevated levels of ACTH, which can stimulate melanin production.

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3
Q

What is the incidence of Addison’s disease?

A

3-4 million per year

The prevalence of Addison’s disease is estimated to be between 40-60 million per year.

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4
Q

What is the most common cause of primary adrenal insufficiency in the western world?

A

Autoimmune destruction of the adrenal cortex

This condition is more common in women, with autoantibodies targeting steroid biosynthesis enzymes.

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5
Q

Name three causes of primary adrenal insufficiency.

A
  • Autoimmune destruction
  • Tuberculosis
  • Rare causes (e.g., adrenal hemorrhage, malignant metastasis)

Autoimmune destruction is the leading cause in the western world.

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6
Q

What are the clinical features of Addison’s disease?

A
  • Weight loss
  • Malaise
  • Weakness
  • Nausea and vomiting
  • Abdominal pain
  • Confusion
  • Fainting

Symptoms can vary widely, leading to late diagnosis.

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7
Q

What is an Addisonian crisis?

A

A life-threatening presentation of Addison’s disease

It often occurs due to the sudden withdrawal of exogenous steroids.

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8
Q

What are common symptoms of an Addisonian crisis?

A
  • Hypotension
  • Dehydration
  • Confusion
  • Hyponatraemia
  • Hypoglycaemia

These symptoms are critical and require immediate medical attention.

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9
Q

What are some signs of chronic Addison’s disease?

A
  • Loss of weight
  • General wasting
  • Pigmentation (palmar creases, buccal mucosa)
  • Postural hypotension
  • Dehydration

Signs can be very subtle and may overlap with other conditions.

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10
Q

What blood test results may indicate adrenal insufficiency?

A
  • Hyponatraemia
  • Hyperkalaemia
  • Elevated urea and creatinine

These abnormalities occur due to mineralocorticoid deficiency.

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11
Q

What is the purpose of the Synacthen test?

A

To assess adrenal function by measuring cortisol response to synthetic ACTH

A lack of cortisol response can indicate primary adrenal insufficiency.

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12
Q

What is the management for adrenal insufficiency?

A
  • Mineralocorticoid replacement (fludrocortisone)
  • Glucocorticoid replacement (hydrocortisone)
  • IV hydrocortisone and fluid rehydration during Addisonian crisis

Hormone replacement is crucial for managing adrenal insufficiency.

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13
Q

What is secondary adrenal insufficiency primarily caused by?

A

Iatrogenic causes from long-term steroid therapy

This leads to suppression of the pituitary-adrenal axis.

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14
Q

True or False: Secondary adrenal insufficiency results in hyperpigmentation.

A

False

In secondary adrenal insufficiency, ACTH is not produced, hence no hyperpigmentation occurs.

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15
Q

What is the definition of Cushing’s syndrome?

A

Chronic glucocorticoid excess + loss of the normal feedback mechanisms of the HPA axis and loss of circadian rhythm of cortisol secretion.

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16
Q

What is the most common cause of Cushing’s syndrome?

A

Exogenous administration of steroids.

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17
Q

What are the rare endogenous causes of Cushing’s syndrome?

A

Endogenous causes are rare.

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18
Q

What is the annual epidemiology rate of Cushing’s syndrome?

A

3 million per year.

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19
Q

What are the two classifications of Cushing’s syndrome?

A
  • ACTH-dependent
  • ACTH-independent
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20
Q

What is Cushing’s disease?

A

A pituitary adenoma resulting in corticotrophs releasing excess ACTH.

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21
Q

What is ectopic ACTH production?

A

It manifests as a paraneoplastic syndrome in a number of malignancies such as small-cell lung cancer.

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22
Q

What are the primary causes of ACTH-independent Cushing’s syndrome?

A
  • Primary cortisol secreting adrenal tumours (adenomas and carcinomas)
  • Hyperplasia
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23
Q

What are common symptoms of Cushing’s syndrome?

A
  • Tiredness
  • Depression
  • Weight gain (central)
  • Easy bruising
  • Back pain
  • Amenorrhoea
  • Reduced libido
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24
Q

What are the signs of Cushing’s syndrome?

A
  • Acne
  • Moon face (cushingoid facies)
  • ‘Buffalo hump’
  • Central obesity
  • Hyperpigmentation (in ACTH dependent)
  • Proximal muscle wasting
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25
Q

What is a key investigation for diagnosing Cushing’s syndrome?

A

24-hour urinary cortisol showing levels of 3 or 4 times normal.

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26
Q

What does a midnight cortisol test demonstrate?

A

The loss of the normal circadian pattern.

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27
Q

What is the purpose of the low-dose dexamethasone suppression test?

A

To demonstrate the loss of normal feedback on the pituitary gland and hypothalamus.

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28
Q

What should occur in a normal individual after administration of dexamethasone?

A

It should suppress the morning rise in serum cortisol.

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29
Q

What indicates a lack of suppression in patients with Cushing’s syndrome during the dexamethasone test?

A

A lack of suppression warrants further investigation.

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30
Q

What is a medical management option for Cushing’s syndrome?

A

Metyrapone, an inhibitor of 11-beta-hydroxylase.

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31
Q

What type of management is indicated when there is a tumor in Cushing’s syndrome?

A

Surgical management.

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32
Q

What is T1DM?

A

A condition caused by an inability to produce or secrete insulin.

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33
Q

In which age group does T1DM typically occur?

A

Children and adolescents.

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34
Q

How many adults in the UK are affected by T1DM?

A

About 370,000 adults.

35
Q

What is the main factor leading to the destruction of beta-cells in T1DM?

A

Autoimmunity.

36
Q

What triggers the development of autoantibodies in genetically susceptible individuals?

A

An external trigger, such as a viral infection.

37
Q

What percentage of T1DM patients have circulating autoantibodies?

A

Up to 85%.

38
Q

Which antibody is most commonly identified in T1DM patients?

A

Anti-glutamic acid decarboxylase (anti-GAD) antibody.

39
Q

What are counter-regulatory hormones to insulin?

A
  • Glucagon
  • Adrenaline
  • Growth hormone
  • Cortisol
40
Q

What are the symptoms of insulin deficiency in T1DM?

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Electrolyte derangement
  • Weight loss
41
Q

What is a significant consequence of insulin deficiency?

A

A profound catabolic state may occur.

42
Q

What happens to fatty acids in the absence of insulin?

A

They are converted into ketone bodies.

43
Q

What condition can develop due to high circulating ketones?

A

Diabetic ketoacidosis (DKA).

44
Q

What can severe acidosis lead to?

A

Failure of pH-dependent enzyme systems.

45
Q

What are common clinical features of T1DM?

A
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Glycosuria
  • Weight loss
46
Q

What signs may indicate dehydration in T1DM patients?

A
  • Dry skin
  • Dry mucous membranes
  • BMI < 25
47
Q

What are the potential presentations of diabetic ketoacidosis?

A
  • Confusion
  • Dehydration
  • Vomiting
  • Abdominal pain
  • Decreased urine output
  • Reduced GCS
  • Coma
  • Shock
  • Kussmaul breathing
  • Hyperkalaemia
48
Q

How is T1DM diagnosed?

A

When classical clinical features are found in the presence of a raised random blood glucose level.

49
Q

What is required for the management of T1DM?

A
  • Life-long exogenous insulin
  • Blood glucose monitoring at least 4 times a day
50
Q

What class of oral hypoglycaemics blocks ATP-dependent potassium channels?

A

Sulphonylureas.

51
Q

What is the mechanism of action of biguanides like metformin?

A

Increases peripheral uptake of glucose and decreases gluconeogenesis.

52
Q

What do DPP4 inhibitors do?

A

Increase incretin levels, inhibiting glucagon release and decreasing blood glucose levels.

53
Q

What is a common acute complication of T1DM?

A

Hypoglycaemia.

54
Q

What are symptoms of hypoglycaemia?

A
  • Sweating
  • Tremor
  • Anxiety
  • Altered consciousness
55
Q

What is hyperosmolar hyperglycaemic state (HHS)?

A

A state in which high blood sugar results in high osmolarity without significant ketoacidosis.

56
Q

What is diabetic retinopathy?

A

Persistent damage to the retina leading to areas of ischaemia and new vessel formation.

57
Q

What is the pathogenesis of diabetic nephropathy?

A

High blood glucose leads to hyaline deposits and thickening of the basement membrane.

58
Q

What does diabetic neuropathy refer to?

A

A collection of conditions resulting from glucose-related damage to neurones.

59
Q

What complications can arise from diabetic foot?

A
  • Ulcers
  • Secondary infection
  • Skin necrosis
  • Amputation
60
Q

What macrovascular complication is associated with diabetes?

A

Atherosclerosis.

61
Q

What is T2DM?

A

A condition caused by a combination of insulin resistance and deficiency.

62
Q

What is insulin resistance?

A

The inability of cells to respond adequately to normal levels of insulin, primarily occurring in muscles, liver, and fat tissue.

63
Q

What happens to glucose release in the liver during insulin resistance?

A

The liver inappropriately releases glucose into the blood.

64
Q

What percentage of the risk for developing T2DM is due to obesity?

A

About 80%.

65
Q

What is the genetic risk of developing T2DM if both parents have the condition?

A

As high as 75%.

66
Q

List three environmental risk factors for developing T2DM.

A
  • Obesity and inactivity
  • Poor dietary habits
  • Low birth weight
67
Q

Which populations have a higher prevalence of T2DM?

A
  • Asians
  • Men
  • Elderly (>40)
68
Q

What initiates the uptake of glucose into cells during normal glucose homeostasis?

A

The release of insulin following ingestion.

69
Q

What are the anabolic effects of insulin receptor activation?

A
  • Inhibit proteolysis and lipolysis
  • Inhibit hepatic gluconeogenesis
  • Promote hepatic glycogen synthesis
70
Q

What occurs during insulin resistance that leads to hyperglycaemia?

A

Failed uptake of glucose and catabolic effects on lipids, proteins, and hepatic tissue.

71
Q

What is impaired glucose tolerance (IGT)?

A

Abnormal regulation of glucose following a meal in the post-prandial state.

72
Q

What is impaired fasting glucose (IFG)?

A

High levels of glucose during the fasting state.

73
Q

What is glucotoxicity?

A

The toxic effect of high glucose levels on beta cells, leading to a depletion in their cellular mass.

74
Q

List three clinical features of T2DM.

A
  • Lethargy
  • Polyuria
  • Polydipsia (thirst)
75
Q

What is the major diagnostic tool for T2DM?

A

Measurement of glycated haemoglobin (HbA1c).

76
Q

What HbA1c level indicates diabetes?

A

HbA1c > 48 mmol/mol.

77
Q

What fasting plasma glucose level indicates diabetes?

A

> 7 mmol/L.

78
Q

What random plasma glucose level indicates diabetes?

A

> 11.1 mmol/L.

79
Q

What does an oral glucose tolerance test measure?

A

The ability of the body to deal with a glucose load over a two-hour period.

80
Q

What are the main steps in the management of T2DM?

A
  • Lifestyle modification
  • Monotherapy with metformin
  • Dual therapy if HbA1c rises
  • Triple therapy or insulin-based therapy if no effect
81
Q

What are the acute problems associated with T2DM?

A

Hypoglycaemia.

82
Q

List two microvascular complications of T2DM.

A
  • Retinopathy
  • Nephropathy
83
Q

What is a macrovascular complication of T2DM?

A

Atherosclerosis.

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