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Systems: Endocrine AB > Pathology of the Endocrine System > Flashcards

Pathology of the Endocrine System Flashcards

1
Q

What is the endocrine system?

A

Integrated network of glands that secrete chemical messengers (hormones) directly into bloodstream

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2
Q

What do hormones act on?

A

-Target cells distant from site of synthesis. -They bind to receptors the change cell activity

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3
Q

What is the endocrine system responsible for?

A

-Regulation of metabolism, growth and development, tissue function
Maintenance of functional balance

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4
Q

How can normal endocrine glands be described?

A

Packets of cells with secretory granules that are vascular and ductless

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5
Q

How is balance within the endocrine system maintained?

A

By feedback inhibition

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6
Q

What are the components of the classic endocrine system?

A
  • Pineal gland
  • Hypothalamus
  • Pituitary gland
  • Thyroid gland
  • Parathyroid gland
  • Adrenal glands
  • Pancreas
  • Other (organs such as ovaries, testes and kidneys) (diffuse endocrine cells)
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7
Q

How are endocrine organs linked?

A

Feedback axes

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8
Q

What do endocrine disease processes lead to?

A

Changes in function and/or structure

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9
Q

What can dysregulated hormone release lead to?

A
  • Hyperfunction

- Hypofunction

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10
Q

Hyperplasia

A

Increased number and secretory activity of cells

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11
Q

Atrophy

A

-Diminution of cells due to lack of stimulation

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12
Q

What can cause tissue damage?

A
  • Inflammation
  • Autoimmune disease
  • Compression
  • Trauma
  • Infection
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13
Q

Give example of disease processes of endocrine organs.

A
  • Hyperplasia
  • Atrophy
  • Tissue damage
  • Neoplasia
  • Congenital abnormality
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14
Q

Give 2 examples of neoplasia

A
  • Adenoma

- Carcinoma

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15
Q

How can adenomas be classified?

A
  • Functioning

- Non-functioning

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16
Q

How can carcinomas be classified?

A
  • Primary

- Metastatic

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17
Q

How can cause of endocrine disease be determined?

A
  • Morphologic findings

- Biochemical measurements of hormone levels, regulators and metabolites

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18
Q

What general considerations are there when it comes to endocrine disease?

A
  • Disease in one endocrine gland may have multiorgan clinical effects
  • Disease in one endocrine gland may lead to altered activity of another endocrine gland
  • Feedback effects may cause changes in endocrine gland
  • Endocrine organs have high reserve capacity
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19
Q

What is the main function of the thyroid gland?

A

Synthesis, storage and release of T4 and T3

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20
Q

What is the main function of T4 and T3?

A

Regulate basal metabolic rate

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21
Q

What is the main function of calcitonin?

A

Regulates calcium homeostasis

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22
Q

What are the main histological features of the thyroid gland?

A
  • Follicles
  • Colloid-contains thyroglobulin
  • Epithelial cells – TG synthesis, iodination, resorption & release of T4 and T3
  • C-cells – secrete calcitonin
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23
Q

How can hyperthyroidism manifest?

A

Thyroxicosis

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24
Q

How can hypothyroidism manifest?

A
  • Myxoedema
  • Cretinism
  • Subclinical
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25
Q

How can thyroid enlargement manifest?

A
  • Goitre

- Isolated nodule/mass

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26
Q

How can most thyroid diseases be classified?

A

Primary

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27
Q

Give examples of thyroid diseases.

A
  • Thyroiditis (autoimmune/others)
  • Gland destruction
  • Multinodular goitre
  • Tumours (benign/malignant)
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28
Q

What can cause hyperthyroidism?

A
  • Diffuse toxic hyperplasia (Graves disease) – 70%
  • Toxic multinodular goitre – 20%
  • Toxic adenoma
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29
Q

What is the pathophysiology of Grave’s disease?

A
  • Autoimmune production of anti- TSH receptor antibodies
  • Stimulate activity, growth, inhibit TSH binding
  • Ophthalmopathy immune mediated – ocular fibroblasts have TSH receptor
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30
Q

Who does Grave’s disease usually affect?

A
  • F>M
  • Peak 20-40 years
  • Genetic predisposition
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31
Q

How does the thyroid present in Grave’s disease?

A

Diffuse hyperplasia and hyperfunction

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32
Q

What changes are there in the histology of Grave’s disease?

A
  • Increased cell activity

- Increase in cell numbers

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33
Q

What can cause hypothyroidism?

A
  • Hashimoto’s thyroiditis (auto-immune destruction)
  • Iatrogenic (surgery drugs)
  • Iodine deficiency
  • Congenital hypothyroidism
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34
Q

Who does Hashimoto’s thyroiditis usually affect?

A
  • F>M

- 45-65years

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35
Q

What is the pathophysiology behind Hashimoto’s thyroiditis?

A

-Autoimmune destruction of thyroid epithelial cells
-Cytotoxic T cells, cytokine and antibody mediated destruction
-Circulating autoantibodies to
thyroglobulin, thyroid peroxidase

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36
Q

How does the thyroid present in Hashimoto’s thyroiditis?

A

Diffuse enlargement with gradual failure

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37
Q

What changes are there in the histology of Hashimoto’s thyroiditis?

A
  • Hurthle cell change

- Intense infiltrate of lymphocytes and plasma cells

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38
Q

How does iodine deficiency cause multinodular goitre?

A
  • Iodine deficiency, goitrogens
  • Impaired synthesis of T3 and T4
  • Increase in TSH
  • Hypertrophy and hyperplasia of epithelium
  • Simple goitre leads to multinodular
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39
Q

What changes are there in the histology of multinodular goitre?

A
  • Crowded follicles
  • Distended colloid filled follicles
  • Haemorrhage, fibrosis, cystic change
  • Nodular appearance
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40
Q

What may a thyroid nodular be?

A
  • Dominant nodule in multinodular goitre
  • Cyst
  • Follicular adenoma
  • Cracinoma
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41
Q

Give examples of different types of thyroid carcinomas.

A

-Differentiated thyroid carcinoma
-Papillary carcinoma (75-85%)
-Follicular
carcinoma (10-20%)
-Anaplastic carcinoma (5%)
-Medullary carcinoma (5%) (lymphoma)

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42
Q

How should thyroid nodules be investigated?

A
  • TFTs
  • Ultrasound
  • FNA and cytlogy
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43
Q

Describe the features of follicular adenomas.

A
  • Most non-functioning
  • Circumscribed, encapsulated tumour
  • Histology often small microfollicles
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44
Q

What are the featires of follicular carcinomas?

A
  • Rare, usually solitary
  • Malignant cells breach capsule
  • Metastases – blood, bones
  • RAS mutation of translocation
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45
Q

Who do papillary carcinomas usually affect?

A
  • <50years

- ~2000/year

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46
Q

What can cause papillary carcinomas?

A
  • BRAF mutation or RET/PTC gene rearrangement

- Exposure to ionising radiation

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47
Q

How do papillary carcinomas spread?

A

Lymphatics

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48
Q

What is the prognosis of papillary carcinomas?

A

Excellent prognosis - 95% survival (esp <45yrs 99% at 1yr)

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49
Q

What is the histology of papillary carcinomas?

A
  • Papillary projections
  • Empty nuclei
  • Psammoma bodies
  • May be cystic
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50
Q

What is a thyroid medullary carcinomas?

A

Malignant tumour of the C cells

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51
Q

What is produced by a thyroid medullary carcinoma?

A

Calcitonin (+/- other polypeptides)

52
Q

What can cause thyroid medullary carcinomas?

A
  • 70% sporadic

- 30% MEN2A, 2B, familial FMTC, mutations in RET proto-oncogene

53
Q

What can be seen on histology of thyroid medullary carcinomas?

A
  • Tumour cells

- Amyloid

54
Q

How many parathyroid glands do you have?

A

4

55
Q

How much do the parathyroid glands weigh?

A

120mg

56
Q

How does primary hyperparathyroidism usually present?

A

Often asymptomatic hypercalcaemia

57
Q

What can cause primary hyperparathyroidism?

A
  • Sporadic or familial (MEN-1)
    • Adenoma (85-95%
    • Hyperplasia (5-10%)
    • Carcinoma (rare)
58
Q

What causes secondary hyperparathyroidism?

A

Physiological response to decrease Ca renal failure

59
Q

What is the role of the hypothalamus?

A
  • Maintain homeostasis

- Govern emotional behaviour

60
Q

How is the nervous system linked to the endocrine system?

A

Via the pituitary gland

61
Q

What is the pituitary?

A

Small gland located in the sella turcica

62
Q

How is the pituitary connected to the hypothalamus?

A

By the pituitary stalk

63
Q

What does the pituitary play a critical role in?

A

Regulating other endocrine glands

64
Q

What does the anterior pituitary secrete?

A
  • ACTH
  • TSH
  • GH
  • Prolactin
  • FSH/LH
65
Q

How is the anterior pituitary controlled?

A

Controlled by release factors from hypothalamus

66
Q

Where does the anterior pituitary receive its blood supply from?

A

Hypothalamus

67
Q

What is the posterior pituitary?

A

Down growth of hypothalamus

68
Q

What does the posterior pituitary secrete?

A
  • ADH

- Oxytocin

69
Q

Describe the histology of the anterior pituitary.

A

3 major cell types

  • Pink acidophils which secrete GH and PRL
  • Dark purple basophils which secrete ACTH, TSH, FSH and LH
  • Pale chromophobes
70
Q

What is the most common cause of pituitary hyperfunction?

A

Pituitary adenoma

71
Q

Who is usually affected by pituitary adenomas?

A

-Adults aged 35-60 years

72
Q

What can cause pituitary adenomas?

A
  • Most sporadic

- 5% inherited e.g. MEN1

73
Q

How do pituitary adenomas appear macroscopically?

A
  • Soft, well-circumscribed lesion

- Small microadenomas may be incidental eg at post mortem

74
Q

What is the histological appearance of pituitary adenomas?

A
  • Cells of same appearance as normal gland

- Classified by hormone(s) produced by the neoplastic cells - detected by immunohistochemical stains

75
Q

If functioning, what is the effect of a pituitary adenoma on the pituitary?

A

Hormone excess

76
Q

What can a prolactinoma cause?

A
  • Galactorrhoea

- Menstrual disorders

77
Q

What does a GH secreting tumour lead to?

A
  • Acromegaly

- Gigantism

78
Q

What does a ACTH secreting tumour lead to?

A

-Cushing’s disease

79
Q

If a pituitary tumour is large and produces mass pressure effect what can happen?

A
  • Radiographic abnormalities
  • Visual field abnormalities
  • Elevated intracranial pressure
  • Compression damage (hypopituitarism)
80
Q

What can cause pituitary hypofunction?

A
  • Compression by tumours such as craniopharnygiomas or metastatic lesions
  • Trauma
  • Infections such as TB or sarcoidosis
  • Post partum ischaemic necrosis (Sheehan’s syndrome)
81
Q

How much must be loss to result in pituitary hypofunction?

A

75%

82
Q

What type of hormones does the adrenal cortex secrete?

A

Steroid hormones

83
Q

What does the zona glomerulosa secrete?

A

-Mineralocorticoids such as aldosterone

84
Q

What does the zona fasciculate secrete?

A

Glucocorticoids such as cortisol

85
Q

What does the zona reticularis secrete?

A

Sex steroids such as oestrogen and androgens

86
Q

What doe the neuroendocrine (chromaffin) cells of the adrenal medulla secrete?

A

Adrenaline/noradrenaline

87
Q

What does adrenal hyperfunction lead to?

A

Clinical syndromes which depend in which adrenal hormones are stimulated

88
Q

What 3 syndromes are associated with adrenal cortical hyperfunction?

A
  • Hypercortisolism(CUSHING’S SYNDROME)
  • Hyperaldosteronism (Conn’s syndrome)
  • Adrenoginital syndormes
89
Q

What is hypercortisolism called?

A

Cushing’s syndrome

90
Q

What is exogenous Cushing’s syndrome due to?

A

Iatrogenic steroids

91
Q

What can endogenous Cushing’s syndrome be classified as?

A
  • ACTH dependent

- ACTH independent

92
Q

Give examples of ACTH dependent causes of Cushing’s syndrome.

A
  • Pituitary adenoma Cushings disease – 70%

- Ectopic ACTH

93
Q

What can cause ACTH independent Cushing’s syndrome?

A

Functioning adrenal adenoma 10%

94
Q

What is hyperaldosteronism called?

A

Conn’s syndrome

95
Q

What can cause Conn’s syndrome?

A
  • Bilateral idiopathic hyperplasia

- Functioning adrenal adenoma

96
Q

What is secondary hyperaldosteronism due to?

A

Physiological due to decreased renal perfusion and increased renin-angiotension

97
Q

What can cause adrenogenital syndromes?

A
  • Functioning adrenal tumour
  • Pituitary tumour Cushings disease
  • Congenital adrenal hyperplasia (steroid enzyme deficiency)
98
Q

What can cause acute adrenal insufficiency destruction of glands?

A

Meningococcal septicaemia (Waterhouse friderichsen)

99
Q

What is primary chronic adrenal insufficiency destruction of glands caused by?

A

Addison’s disease

100
Q

What can cause Addison’s disease?

A
  • Autoimmune :(autoimmune polyendocrine syndromes – spare medulla)
  • Infections: (TB, fungus HIV-related infections)
  • Replacement: (metastatic carcinoma amyloidosis)
  • Atrophy: (prolonged steroid therapy)
  • Congenital hypoplasia
101
Q

What is secondary adrenal insufficiency destruction of glands caused by?

A

Pituitary failure

102
Q

What can functioning adrenocortical adenomas lead to?

A
  • Hyperadrenal syndromes

- Atrophy of adjacent cortex

103
Q

How are non-functioning adrenocortical adenomas often diagnosed?

A

Often incidental i.e. on imaging/autopsy

104
Q

How do adrenocortical adenomas appear?

A
  • Yellow-brown circumscribed

- Most 2-3cm <30g

105
Q

How do adrenocortical adenomas appear histologically?

A
  • Cells similar to those of normal cortex
  • Nuclei small
  • Some pleomorphism (“endocrine atypia”).
  • Cytoplasm eosinophilic to vacuolated, depends on lipid
  • Mitoses inconspicuous
106
Q

What carcinomas can affect the adrenal cortex?

A
  • Primary adrenocortical carcinoma

- Metastatic carcinoma

107
Q

How do primary adrenocortical carcinomas appear?

A
  • More likely functional- virilising

- Most large >20cm, haemorrhage and necrosis, cystic

108
Q

How do primary adrenocortical carcinomas metastasise?

A
  • By lymphatics and blood

- Invades adrenal vein

109
Q

Who do primary adrenocortical carcinomas usually affect?

A

Rare but can affect any age

110
Q

Where are metastatic adrenocortical carcinomas usually found?

A
  • Lung

- Breast

111
Q

What tumour affects the adrenal medulla?

A

Pheochromocytoma

112
Q

Why do pheochromocytomas cause hypertension?

A

Adrenal medulla corticoids cells secrete catecholamines which raises BP

113
Q

What can cause pheochromocytomas?

A
  • Sporadic

- Up to 25% inherited e.g. MEN2

114
Q

How do pheochromocytomas usually appear?

A

-Usually benign behaviour, can be bilateral

115
Q

What is the histological appearance of a pheochromocytoma?

A
  • Nests “Zellballen” of polygonal cells in vascular network

- Granular cytoplasm containing catecholamines

116
Q

Why are pheochromocytomas referred to as the 10% tumour?

A
  • 10% bilateral
  • 10% non-functioning
  • 10% malignant
  • 10% extra adrenal
117
Q

What is multiple endocrine neoplasia?

A
  • Inherited disorders with underlying genetic mutation
  • Hyperplasia/ neoplasms of endocrine organs (younger age, multifocal)
  • Several distinct syndromes
118
Q

What syndrome is MEN1 associated with?

A

Wermer syndrome

119
Q

What causes Wermer syndrome?

A

MEN 1 tumour suppressor gene mutation -defect in menin protein involved in regulating cell growth

120
Q

How does Wermer syndrome manifest?

A
  • Parathyroid hyperplasia and adenomas
  • Pancreatic and duodenal endocrine tumours (hypoglycaemia and ulcers)
  • Pituitary adenoma (prolactinoma)
121
Q

What is the genetic association with MEN2?

A

RET proto-oncogene mutations

122
Q

What tumours is MEN2 associated with?

A
  • Medullary carcinoma of thyroid

- Pheochromocytoma

123
Q

What syndrome is MEN2A associated with?

A

Sipple syndrome and parathyroid hyperplasia

124
Q

What causes MEN2A?

A

Extracellular domain auto dimerisation of RET receptor

125
Q

How does MEN2B manifest itself?

A
  • Neuromas of skin &mucous membrane

- Skeletal abnormalities

126
Q

Who does MEN2B affect?

A

Younger patients, agresisive

127
Q

What does MEN2B cause?

A

Autoactivation of tyrosine kinase pathway

Systems: Endocrine AB (25 decks)

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