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YEAR 5: Histopathology > Histo: Endocrine disease > Flashcards

Histo: Endocrine disease Flashcards

1
Q

What types of cell are the anterior and posterior pituitary made up of?

A

Anterior = epithelial cells

Posterior = nerve cells

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2
Q

What is the blood supply to the anterior pituitary?

A

Pituitary portal system

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3
Q

Where do the nerves that make up the posterior pituitary originate?

A

Supraoptic nucleus and paraventricular nucleus

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4
Q

Describe the histology of the anterior pituitary.

A

Made up of epithelial cells derived from the developing oral cavity

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5
Q

How is hyperpituitarism classified?

A

Based on the hormone produced (this is detected by immunohistochemistry)

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6
Q

What is the most common type of pituitary adenoma?

A

Prolactinoma

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7
Q

What is a microadenoma?

A

A pituitary adenoma with a diameter < 1 cm

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8
Q

Outline the clinical features of prolactinoma.

A
  • Amenorrhoea
  • Galactorrhoea
  • Loss of libido
  • Infertility
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9
Q

What are the clinical manifestations of growth hormone adenomas?

A
  • Gigantism (in prepubertal children)
  • Acromegaly (in adults)
  • Diabetes, Muscle weakness, Congestive HF, HTN
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10
Q

What disease is caused by corticotroph cell adenomas?

A

Cushing’s disease

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11
Q

List some causes of hypopituitarism.

A
  • Non-secreting pituitary adenoma
  • Ischaemia
  • Iatrogenic (e.g. surgery, radiotherapy)
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12
Q

What is the most common cause of ischaemic necrosis of the pituitary gland?

A

Sheehan’s syndrome - the pituitary enlarges during pregnancy and is more susceptible to ischaemia. A post-partum haemorrhage may induce ischaemia.

Other causes: DIC, sickle cell anaemia, shock

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13
Q

List some clinical features of hypopituitarism.

A
  • Pituitary dwarfism
  • Gonadotrophin deficiency - amenorrhoea, infertility, impotence, loss of libido
  • Hypothyroidism and hypoadrenalism
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14
Q

Which hormones are produced by the posterior pituitary?

A

ADH and oxytocin

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15
Q

Which clinical syndrome involves ADH?

A

Diabetes insipidus

SIADH

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16
Q

List some consequences of the local mass effet of pituitary tumours.

A
  • Bitemporal hemianopia (optic chiasm)
  • Headaches (raised ICP)
  • Obstructive hydrocephalus
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17
Q

Describe the histological appearance of the thyroid gland.

A
  • Arranged into follicles with a small amount of stromal tissue between them
  • They are lined by epithelial cells and have a large amount of colloid in the middle
  • Parafollicular cells are found between the follicles
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18
Q

Describe the physiological response of the thyroid gland to TSH.

A
  • Stimulating of TSH receptors leads to pinocytosis of the colloid by the thyroid follicular cells and promotes the conversion of thyroglobulin into T3 and T4
  • Release of thyroid hormones into the circulation results in a rise in basal metabolic rate
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19
Q

Which hormone do parafollicular cells produce?

A

Calcitonin - this promotes the absorption of calcium by the skeletal system

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20
Q

What is a non-toxic goitre?

A

Enlargement of the thyroid gland without overproduction of thyroid hormones

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21
Q

What is the most common cause of non-toxic goitre?

A
  • Iodine deficiency
  • NOTE: bassicas (e.g. cabbages) interfere with thyroid hormone synthesis
  • It may also be caused by a hereditary enzyme deficiency
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22
Q

List some primary causes of thyrotoxicosis.

A
  • Graves’ disease
  • Hyperfunctioning multinodular goitre/adenoma
  • Thyroiditis
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23
Q

List some causes of thyrotoxicosis that are not associated with the thyroid gland.

A
  • Struma ovarii - ovarian teratoma with ectopic thyroid hormone production
  • Factitious thyrotoxicosis - exogenous thyroid hormone intake
  • Hyatidiform mole (high hCG levels mimic TSH)
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24
Q

Which antibodies are often seen in Graves’ disease?

A

Antibodies to the TSH receptor and thyroglobulin

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25
Q

Describe the effect of TSH receptor-stimulating antibodies.

A

They stimulate thyroid hormone release and increase proliferation of the thyroid epithelium.

26
Q

List some primary causes of hypothyroidism.

A
  • Post-ablative
  • Autoimmune (Hashimoto’s)
  • Iodine deficiency
  • Congenital biosynthetic defect
27
Q

Describe the presentation of Hashimoto’s thyroiditis.

A

Painless enlargement of the thyroid gland with symptoms of hypothyroidism.

28
Q

Describe the histology of Hashimoto’s thyroiditis.

A
  • There are lots of lymphoid cells with germinal centres
  • The epithelial cells become large with lots of eosinophilic cytoplasm (Hurthle cells)
29
Q

List some features of a thyroid lump that would be suggestive of neoplasia.

A
  • Solitary rather than multiple
  • Solid rather than cystic
  • Younger patients
  • Male more than female
  • Less likely to take up radioiodine
30
Q

List some features of adenomas of the thyroid gland.

A
  • Usually solitary
  • Well circumscribed
  • Well-formed capsule
  • Small proportion will be functional
31
Q

List the four types of thyroid cancer in order of decreasing prevalence.

A
  • Papillary (80%)
  • Follicular (15%)
  • Medullary (5%)
  • Anaplastic
32
Q

What are some risk factors for thyroid cancer?

A
  • Genetic factors (e.g. MEN)
  • Ionisation radiation (mainly papillary)
33
Q

What is the diagnosis of papillary thyroid cancer based on?

A
  • Nuclear features
    • Optically clear nuclei
    • Intranuclear inclusions (Orphan Annie Eye)
  • There may also be psammoma bodies (little foci of calcification)
  • Usually non-functional
  • On histology, they have a papillary structure (central connective tissue stalk with surrounding epithelium)
34
Q

Where does papillary thyroid cancer tend to metastasise to?

A

Cervical lymph nodes

35
Q

Where does follicular thyroid cancer tend to metastasise?

A

Lungs, bone and liver (via the bloodstream)

36
Q

Which cells are medullary thyroid cancers derived from?

A

Parafollicular C cells

NOTE: 80% are spoardic, 20% are familial

37
Q

What tends to happen to the calcitonin produced by tumour cells in medullary thyroid cancer?

A
  • It is broken down and deposited as amyloid within the thyroid
38
Q

What are the parathyroid glands derived from?

A

Developing pharyngeal pouches

39
Q

List the actions of PTH.

A
  • Activates osteoclasts
  • Increased renal absorption of calcium
  • Increases activation of vitamin D
  • Increases urinary phosphate exretion
  • Increases intestinal calcium absorption
40
Q

What is hyperparathyroidism usually caused by?

A
  • 80% solitay adenoma
  • 20% due to hyperplasia of all four glands (sporadic or part of MEN1)
41
Q

Describe the histological appearance of a parathyroid adenoma.

A

Very cellular tissue with no fat (whereas the normal parathyroid gland is quite fatty)

42
Q

What bone change is seen in hyperparathyroidism?

A

Osteitis fibrosa cystica - caused by bone resorption with thinning of the cortex

43
Q

What is the most common cause of secondary hyperparathyroidism?

A

Renal failure

44
Q

List some causes of hypoparathyroidism.

A
  • Surgical ablation
  • Congenital absence
  • Autoimmune
45
Q

List some clinical features of hypoparathyroidism.

A
  • Neuromuscular irritability
  • Cardiac arrhythmias
  • Fits
  • Cataracts

CATs go NUMB

46
Q

Which cell types constitute the cortex and medulla of the adrenal gland?

A

Cortex = epithelial

Medulla = neural

47
Q

What are the layers of the adrenal cortex and which hormones do they produce?

A
  • Glomerulosa - aldosterone
  • Fasciculata - glucocorticoids
  • Reticularis - sex steroids
48
Q

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

A

Administration of exogenous corticosteroids (leads to adrenal atrophy)

49
Q

What happens to the adrenal glands in Cushing’s disease?

A

Undergo nodular hyperplasia of the cortex

50
Q

List some other causes of Cushing’s syndrome.

A
  • Cushing’s disease
  • Adernal adenoma/carcinoma
  • Adrenal hyperplasia
51
Q

What are the causes of hyperaldosteronism?

A
  • 35% adenoma (Conn’s syndrome)
  • 60% bilateral adrenal hyperplasia
52
Q

List the two main clinical features of hyperaldosteronism.

A

Hypertension

Hypokalaemia

53
Q

What causes virilising syndromes?

A
  • May be associated with neoplasms (more commonly carcinoma than adenoma)
  • Congenital adrenal hyperplasia
54
Q

Describe the pathophysiology of congenital adrenal hyperplasia.

A
  • Autosomal recessive
  • Hereditary defect in an enzyme involved in cortisol synthesis leads to cortisol deficiency
  • This leads to increased ACTH release from the pituitary gland
  • ACTH stimulates androgen synthesis from the adrenal gland
55
Q

List three causes of acute primary adrenal failure.

A
  • Haemorrhage
  • DIC associated with sepsis (Waterhouse-Friderichson syndrome)
  • Sudden withdrawal of corticosteroid treatment
56
Q

List some causes of chronic primary adrenal failure.

A
  • Autoimmune (90%)
  • TB
  • HIV
  • Metastic tumour
57
Q

What are the two types of adrenocortical neoplasm?

A
  • Adenomas - mostly functional, may be associated with Cushing’s syndrome or Conn’s syndrome
  • Carcinomas - rare, more commonly associated with virilisng syndromes than adenomas
58
Q

What are the two types of tumours of the adrenal medulla?

A
  • Phaeochromocytoma
  • Neuroblastoma
59
Q

What is the rule of 10s regarding phaeochromocytomas?

A
  • 10% associated with a syndrome
  • 10% bilateral
  • 10% malignant
  • 10% oustide the adrenal gland (paraganglioma)
60
Q

Define multiple endocrine neoplasia.

A

A group of inherited conditions resulting in proliferative lesions of multiple endocrine organs

61
Q

Outline the features of MEN.

A
  • Tumours tend to occur at a younger age
  • Tumours tend to arise in multiple endocrine organs or may be multifocal within one organ
  • Tumours are often preceded by hyperplasia
  • Tumours are usually more aggressive than sporadic tumours

YEAR 5: Histopathology (20 decks)

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