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Year 5 - Pathology > HISTO: Endocrine disease > Flashcards

HISTO: Endocrine disease Flashcards

1
Q

What cells does the anterior vs posterior pituitary consist of?

A

Anterior – epithelial cells, supplied by blood from pituitary portal system (hypothalamus –> pituitary)

Posterior – nerve cells, supplied by nerves from the supraoptic nucelus and paraventricular nucelus

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2
Q

What are anterior pituitary cells derived from? What do they secrete and under what control?

A

Epithelial cells derived from developing oral cavity

Secrete trophic hormones under the control of factors released by the hypothalamus

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3
Q

List the hormones produced by the anterior pituitary and their stimulus.

A
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4
Q

Define hyperpituitarism and name the most common cause.

A

Excess secretion of trophic hormones

Usually due to functional adenoma

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5
Q

How are pituitary adenomas classified?

A

Now classified on the basis of the hormones produced - detected by immunohistochemistry

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6
Q

What cell type is most common in pituitary adenomas?

A

Prolactin cells are found in ~20% of pituitary adenomas

Sometimes none of these cells are present and sometimes there is a mix of several different ones

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7
Q

What % of intracranial tumours do pituitary adenomas make up?

When do pituitary adenomas usually occur?

What is a microadenoma?

A

10% of intracranial tumours - discovered incidentally in of autopsies 25%

Peak in 4th - 6th decade

Microadenomas = < 1cm

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8
Q

What are the clinical features associated with different pituitary adenomas? (e.g. prolactinomas, GH adenomas, CRH adenomas)

A

Prolactinomas

  • Amenorrhea, galactorrhea, loss of libido, infertility
  • Usually diagnosed earlier in females of reproductive age

Growth hormone adenomas

  • Prepubertal children - gigantism
  • Adults - acromegaly
  • Diabetes mellitus, muscle weakness, hypertension, congestive cardiac failure

Corticotroph cell adenomas = Cushing’s syndrome

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9
Q

Name 3 causes of hypopituitarism.

A
  • Nonsecretory pituitary adenomas
  • Ischaemic necrosis
  • Ablation of pituitary by surgery or irradiation
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10
Q

What are some causes of ischaemic necrosis of the pituitary leading to hypopituitarism?

A

Most commonly post-partum (Sheehan’s syndrome) – pituitary enlarges during pregnancy and so is susceptible to ischaemia especially in PPH

DIC, sickle cell anaemia, elevated ICP, shock

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11
Q

What are the manifestations of anterior pituitary hypofunction in children vs adults?

A

Children: growth failure (pituitary dwarfism)

Adults:

  • Gonadotrophin deficiency - amenorrhea and infertility in women. Decreased libido and impotence in men
  • TSH and ACTH deficiency - hypothyroidism and hypoadrenalism
  • Prolactin deficiency - failure of post-partum lactation
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12
Q

What hormones are produced by the posterior pituitary?

A

Posterior pituitary releases two peptides - antidiuretic hormone (ADH) and oxytocin

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13
Q

What is a common clinical defects of the posterior pituitary?

A

Clinically important posterior pituitary syndromes involve ADH

  • diabetes insipidus
  • Inappropriately high ADH
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14
Q

What are 3 complications of large pituitary tumours?

A
  • Compression of optic chiasm - bitemporal hemianopia
  • Elevated ICP and its symptoms
  • Obstructive hydrocephalus
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15
Q

Describe the main functions of the thyroid.

A

BMR

  • TSH from anterior pituitary
  • –> follicular epithelial cells take up (pinocytose) colloid
  • –> convert thyroglobulin into T4 and T3
  • –> released into circulation
  • –> Increased in BMR

Calcium regulation

  • Thyroid also contains parafollicular/‘C’ cells that synthesize calcitonin
  • Promotes absorption of calcium by the skeletal system
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16
Q

What is the difference between toxic and non-toxic goitre?

A

Non toxic = no production of hormones.

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17
Q

What is the most common cause of non-toxic goitre? What are some other causes?

A
  • Iodine deficiency - endemic in areas where iodine in soil and water is low
  • Puberty in females
  • Ingestion of brassicas or other substances interfering with TH synthesis
  • Hereditary enzyme defects
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18
Q

What are the complications of multinodular goitres (which can become large)?

A
  • dysphagia and airways obstruction
  • hyperthyroidism if hyperfunctioning nodule present
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19
Q

What is thyrotoxicosis?

A

Hypermetabolic state caused by elevated circulating levels of free T3 and T4

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20
Q

What are the causes of thyrotoxicosis? What is the most common cause?

A

Graves disease is the most common cause

Primary

  • Grave’s disease
  • Hyperfunctioning multinodular goitre
  • Hyperfunctioning adenoma
  • Thyroiditis

Secondary

  • TSH secreting pituitary adenoma (rare, <1%)
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21
Q

What are some rare causes of thyrotoxicosis not associated with thyroid disease?

A
  • Struma ovarii (ovarian teratoma with ectopic thyroid)
  • Factitious thyrotoxicosis (exogenous thyroid intake)
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22
Q

What is the triad of Grave’s disease?

A
  1. Thyrotoxicosis
  2. Infiltrative ophthalmopathy with exophthalmos in up to 40%
  3. Infiltrative dermopathy (pretibibial myxoedema) in a minority of cases
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23
Q

Who is most affected by Grave’s disease?

A

Primarily younger adults. F:M, 7:1

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24
Q

What is the pathogenesis of Grave’s disease? What other conditions is it associated with?

A

Autoimmune - variety of antibodies including antibodies to TSHr and thyroglobulin (TG)

Antibodies to TSH receptor most important in pathogenesis - may stimulate release of thyroid hormones and increased proliferation of epithelium

Associated with other autoimmune diseases such as:

  • SLE,
  • pernicious anaemia,
  • type 1 diabetes
  • Addison’s disease
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25
Q

What is the ‘opposite’ of Grave’s disease?

A

Hashimoto’s disease manifested by hypothyroidism

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26
Q

What are the primary and secondary causes of hypothyroidism?

A

Primary

  • Postablative (after surgery or radioiodine therapy)
  • Autoimmune - Hashimoto’s thyroiditis
  • Iodine deficiency
  • Congenital biosynthetic defect

Secondary

  • Pituitary or hypothalamic failure (uncommon)
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27
Q

How does Hashimoto’s present?

A
  • Hypothyroidism
  • Painless enlargement of the thyroid
  • Females 15:1 ages 45-65 years
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28
Q

What is a histopathological feature of Hashimoto’s seen here?

A

Epithelial cells become enlarged with eosinophilic cytoplasm - Hürthle cells

There is also usually:

  • Infiltration of lymphoid cells
  • Presence of germinal centres within the thyroid showing that it is AI disease
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29
Q

What are the types of neoplasms of the thyroid split into?

A
  1. Adenomas –Benign neoplasms of follicular epithelium
  2. Carcinomas - Uncommon and account for less than 1% of solitary thyroid nodules

NB: neoplasms of the thyroid are uncommon in general

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30
Q

What characteristics suggest that a thyroid nodule may be neoplastic?

A
  • Solitary rather than multiple
  • Solid rather than cystic
  • Younger patient
  • Male
  • Cold nodule (does not take up iodine)
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31
Q

What is the most important investigation for diagnosing a neoplastic thyroid nodule?

A

Ultimately it is the morphology that provides the answer

  • Fine needle aspiration cytology
  • Histology
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32
Q

What are the characteristics of thyroid adenomas?

A
  • Solitary
  • Well circumscribed + compresses the surrounding parenchyma
  • Well formed capsule
  • May rarely cause thyrotoxicosis

*Important to examine the capsule for invasion to exclude follicular carcinoma*

33
Q

What are the types of thyroid carcinomas? Which is the most common?

A
  • Papillary (75-85%)
  • Follicular (10-20%)
  • Medullary (5%)
  • Anaplastic (<5%)

Usually occur in adults and make up <1% of cancer deaths.

34
Q

What are the risk factors for thyroid carcinomas?

A

Genetic factors - inc. MEN

Ionizing radiation - papillary carcinomas

35
Q

What type of thyroid tumour does ionizing radiation most commonly cause?

A

Primarily papillary carcinomas

36
Q

What is diagnosis of papillary carcinomas based on?

A

They don’t all have papillary features (as the name may suggest) so diagnosis is based on NUCLEAR FEATURES:

  • Optically clear nuclei
  • Intranuclear inclusions

They may also contain psammoma bodies

37
Q

When do papillary carcinomas occur in terms of age?

A

Any age

38
Q

How do papillary carcinomas present?

A
  • May present with metastases in cervical nodes
  • Painless neck mass
  • Nonfunctional
39
Q

What is seen on this slide of papillary carcinoma?

A
  • Psammoma body seen in the middle (focus of calcification)
  • Nuclei look empty
40
Q

What is the prognosis with papillary carcinomas?

A
  • 10 year survival up to 90%
41
Q

Where do follicular carcinomas metastasise to?

A
  1. Lung
  2. Bone – lung, breast and adrenal also characteristically metastasise to bone
  3. Liver
42
Q

What are the features of follicular carcinomas? When do they occur?

A
  • Follicular morphology
  • May be well demarcated with minimal invasion or clearly infiltrative

Peak incidence in middle age

43
Q

What are medullary carcinomas?

A

Neuroendocrine neoplasm derived from parafollicular C cells

44
Q

What is the aetiology of most medullary carcinomas?

A
  • 80% sporadic - adults 5-6th decade
  • 20% familial - MEN - younger patients
45
Q

What feature of medullary carcinomas is seen here?

A

Calcitonin that they produce is broken down and deposited in the tumour like amyloid

Congo red stain under polarised light allows its detection (as seen in green)

46
Q

What is the causes of death in most anaplastic carcinomas of the thyroid?

A

Most cases death within one year due to local invasion

Features:

  • Occur in elderly patients
  • Very aggressive
  • Metastases common
47
Q

Where can the parathyroid glands be located?

A

Usually close to upper and lower poles of thyroid but may be in the thymus or anterior mediastinum

48
Q

What are the functions of the parathyroid glands?

A

Paarthyroid activity is controlled by level of free calcium in blood whereby decreased calcium stimulates release of PTH

PTH

  • Activates osteoclasts
  • Increases renal tubular reabsorption of calcium
  • Increases conversion of vitamin D to its active form
  • Increases urinary phosphate excretion
  • Increases intestinal calcium absorption
49
Q

What are the most common causes of hyperparathyroidism?

A
  • 80-90% - solitary adenoma
  • 10-20% hyperplasia of all 4 glands - sporadic or component of MEN type 1
  • <1% carcinoma
50
Q

What are the features seen in this parathyroid adenoma?

A
  • Thin capsule
  • Normal parathyroid at the bottom
  • Normal parathyroid is about 50% fat whereas the adenoma has very little fat
51
Q

What are the laboratory features of hyperparathyroidism?

A
  • High serum ionised calcium
  • PTH is high in parathyroid causes of hypercalcaemia
52
Q

What are the clinical features of 1o hyperparathyroidism?

A
  • Bone resorption with thinning of cortex and cyst formation - osteitis fibrosa cystica - may lead to fractures
  • Renal stones and obstructive uropathy
  • GI disturbances - constipation, pancreatitis and gallstones
  • CNS alterations - depression, lethargy and fits
  • Neuromuscular abnormalities - weakness
  • Polyuria and polydipsia
53
Q

What is the pathophysiology of secondary hyperparathyroidism?

A

Caused by any condition associated with chronic depression of serum calcium e.g. renal failure which is the most common cause

Parathyroid glands become enlarged - may be asymmetrical

Leads to bone changes as with primary disease

54
Q

What are the causes of hypoparathyroidism?

A
  • Surgical ablation (most common) – usually surgeons aim to remove 3 and a half of the glands to treat hyperparathyroidism due to hyperplasia. In adenoma you just remove the adenoma.
  • Congenital absence
  • Autoimmune
55
Q

What are the clinical manifestations of hypoparathyroidism?

A
  • Neuromuscular irritability - tingling, muscle spasms, tetany
  • Cardiac arrhythmias
  • Fits
  • Cataracts
56
Q

What types of cells does the adrenal cortex vs medulla consist of?

A

Cortex = epithelial

Medulla = neural cells

57
Q

What are the layers of the adrenal gland? What does each layer produce?

A
  • Zona glomerulosa – secretes aldosterone
  • Zona fasciculata – secretes glucocorticoids
  • Zona reticularis – secretes androgens and glucocorticoids
  • Medulla – noradrenaline and adrenaline
58
Q

What are the main three clinical manifestations of arenocortical hyperfunction?

A
  • Cushing’s syndrome – excess glucocorticoids
  • Hyperaldosteronism
  • Virilising syndromes – excess androgens
59
Q

What are the clinical features of Cushing’s syndrome?

A
  • Hypertension and weight gain
  • Truncal obesity
  • ‘moon’ facies
  • ‘buffalo hump’
  • Cutaneous striae
60
Q

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

A

Administration of exogenous glucocorticoids - adrenal glands become atrophic

61
Q

What are the endogenous causes of Cushing’s syndrome?

A

(1) >50% caused by Cushing’s disease (high ACTH)

  • Pituitary adenoma - producing ACTH
  • Pituitary hyperplasia -of ACTH secreting cells
  • Adrenal glands show nodular cortical hyperplasia

(2) 30% are primary adrenal disease due to:

  • Solitary neoplasm:
    • Adenoma
    • Carcinoma
  • Bilateral hyperplasia (uncommon)
62
Q

What are the exogenous causes of Cushing’s syndrome?

A

Secretion of ectopic ACTH by non-endocrine tumours - most commonly small cell carcinoma of the lung

Adrenals show bilateral hyperplasia

63
Q

What is a serious consequence of stopping steroids suddenly?

A

Addisonian crisis.

64
Q

What is the most common cause of primary hyperaldosteronism?

A

Conn’s syndrome in 35% = aldosterone secreting adenoma

60 % have bilateral adrenal hyperplasia

65
Q

What are the clinical manifestations of primary hyperaldosteronism?

A

HTN and hypokalaemia

NB accounts for <1% of causes of hypertension but important to recognise as surgically correctable

66
Q

What are adrenogenital syndromes? What is a common cause?

A

Syndromes due to excess androgens

Causes:

  • Commonly from neoplasms (usually carcinomas rather than adenomas)
  • May be caused by congenital adrenal hyperplasias
67
Q

What is the cause of congenital adrenal hyperplasia? What is the pathophysiology?

A

AR inheritance

Enzymes of cortisol biosynthesis are defective

Decreased cortisol –> high ACTH –> adrenal stimulation –> increased androgen synthesis

Usually presents in childhood

68
Q

What are the primary causes of adrenal insufficiency?

A

Acute

  • Sudden withdrawal of corticosteroid therapy
  • Haemorrhage (neonates)
  • Sepsis with DIC (Waterhouse-Friderichson syndrome)

Chronic (Addison’s disease)

  • Autoimmune (75-90%)
  • TB
  • HIV
  • Metastatic tumour (lung and breast particularly)
  • Rarely amyloid, fungal infections, haemochromatosis, sarcoidosis
69
Q

What are the secondary causes of adrenal insufficiency?

A

Secondary to reduced ACTH

  1. Non-functional pituitary adenomas
  2. Other lesions of pituitary or hypothalamus including infarction
70
Q

What are the main features of adrenocortical neoplasms?

A

Adenomas - most non-functional but may be associated with Cushing’s syndrome or Conn’s syndrome

Carcinomas – rare, usually large and more commonly associated with virilizing syndrome than adenoma

71
Q

What stimulates release of catecholamines from the adrenal medulla?

A

sympathetic nervous system

72
Q

What 2 neoplasms may occur in the adrenal medulla?

A
  • Phaeochromocytoma
  • Neuroblastoma
73
Q

What is the rule of 10s in phaeochromocytomas?

A
  • 10% familial - arise in association with a familial syndrome inc. MEN 2A and 2B, von Hippel-Lindau disease and Sturge-Weber syndrome
  • 10% bilateral
  • 10% malignant
  • 10% outisde - arise outside the adrenal (paragangliomas)
74
Q

What is the name given to phaeochromocytomas that occur outside of the adrenals?

A

Paragangliomas – usually occur along sympathetic chain along the sides of the spine or in the neck

75
Q

Define MEN syndrome.

A

Group of inherited diseases resulting in proliferative lesions (hyperplasias, adenomas and carcinomas) of multiple endocrine organs

76
Q

What is the pattern of tumours occurring in MEN syndromes?

A
  • Younger age
  • Multiple endocrine organs affected
  • Often multifocal
  • Preceded by hyperplasia
  • Aggressive and harder to treat
77
Q

What is the most common form of thyroid cancer?

A

Papillary carcinoma

78
Q

What type of thyroid carcinoma arises from the parafollicular or C cells of the thyroid?

A

Medullary carcinoma of the thyroid

79
Q

What syndrome is caused by adrenal adenoma that secretes aldosterone?

A

Conn’s syndrome

Year 5 - Pathology (89 decks)

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