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Pathology eLearning - Y5 > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

What is the anterior pituitary?

A

Epithelial cells derived from developing oral cavity.

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

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2
Q

What are the hormones produced by the anterior pituitary?

A

FLAT PEG

  • FSH
  • LH
  • ACTH
  • Prolactin
  • Estogen
  • Growth Hormone
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3
Q

What are symptoms of pituitary disease?

A

Hyperpituitarism: Excess secretion of trophic hormones, usually due to functional adenoma.

Hypopituitarism: Deficiency of trophic hormones

Local mass effects

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4
Q

What is hyperpituitarism?

A

Usually due to functional adenoma.

Originally classified on the morphological character of the predominant cell type e.g acidophil, basophil or chromophobe adenomas.

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

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5
Q

What is the most common cause of anterior pituitary tumour?

A

Prolactinoma

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6
Q

What is the epidemiology of pituitary adenomas?

A

10% of intracranial tumours that come to clinical attention

Discovered incidentally in up to 25% of autopsies

Adults. Peak 4th - 6th decade

Microadenomas if < 1cm

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7
Q

What are clinical features of a prolactinoma?

A

Amenorrhea, galactorrhea, loss of libido, infertility

Usually diagnosed earlier in females of reproductive age

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8
Q

What are clinical features of growth hormone adenomas?

A

Prepubertal children: Gigantism

Adults: Acromegaly

Diabetes mellitus, muscle weakness, hypertension, congestive cardiac failure

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9
Q

What are clinical features of corticotroph adenomas?

A

Cushing’s syndrome

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10
Q

What are the most common causes of hypopituitarism?

A

Nonsecretory pituitary adenomas

Ischaemic necrosis:

  • Most commonly post-partum (Sheehan’s syndrome)
  • DIC, sickle cell anaemia, elevated intracranial pressure, shock

blation of pituitary by surgery or irradiation

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11
Q

What are clinical features of hypopituitarism?

A

Children: Growth failure (pituitary dwarfism)

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 are the hormones released by the posterior pituitary?

A

Posterior pituitary releases two peptides - antidiuretic hormone (ADH) and oxytocin. Clinically important posterior pituitary syndromes involve ADH:

  • Diabetes insipidus
  • Syndrome of inappropriately high ADH
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13
Q

What are signs and symtoms of a local mass?

A

Compression of optic chiasm leading to bitemporal hemianopia

Signs and symptoms of elevated intracranial pressure e.g. Obstructive hydrocephalus

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14
Q

What is this?

A

Thyroid

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15
Q

How does the thyroid function?

A

In response to TSH from anterior pituitary follicular epithelial cells pinocytose colloid and convert thyroglobulin into T4 and T3.

T4 and T3 released into circulation.

Effect is to increase the basal metabolic rate.

Thyroid also contains a population of parafollicular or ‘C’ cells that synthesize calcitonin - promotes absorption of calcium by the skeletal system.

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16
Q

What is a goitre?

A

Enlargement of the thyroid

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17
Q

What is a non-toxic goitre?

A

Goitre is enlargement of the thyroid. Common if there is impaired synthesis of thyroid hormone - most often due to iodine deficiency.

Endemic in areas where iodine in the soil and water is low (‘Derbyshire neck’). May be seen at puberty particularly in females.

May be due to ingestion of substances that interfere with thyroid hormone synthesis e.g. brassicas. May be due to hereditary enzyme defects.

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18
Q

What is a multinodular goitre?

A

With time simple thyroid enlargement may be transformed to a multinodular pattern.

May reach massive size.

May lead to mechanical effects including dysphagia and airways obstruction.

A hyperfunctioning nodule may develop leading to hyperthyroidism.

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19
Q

What is this?

A

Multinodular goitre

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20
Q

What is thyrotoxicosis?

A

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

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21
Q

What are primary causes of thyrotoxicosis?

A

Grave’s disease

Hyperfunctioning multinodular goitre

Hyperfunctioning adenoma

Thyroiditis

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22
Q

What are secondary causes of thyrotoxicosis?

A

TSH secreting pituitary adenoma (rare)

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23
Q

What are 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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24
Q

What is Grave’s Disease?

A

Most common cause of endogenous hyperthyroidism.

Triad of:

  • Thyrotoxicosis
  • Infiltrative ophtahalmopathy with exophthalmos in up to 40%
  • Infiltrative dermopathy (pretibibial myxoedema) in a minority of cases

Primarily younger adults. F:M, 7:1

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25
Q

What is the pathogenesis of Grave’s Disease?

A

Autoimmune disorder.

Variety of antibodies including antibodies to TSH receptor and thyroglobulin.

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 and Addison’s disease.

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26
Q

What is the association between autoantibodies and thyroid disease?

A

Autoimmune disorders of the thyroid span a continuum with Grave’s disease at one end and Hashimoto’s disease manifested by hypothyroidism at the other.

Autoantibodies against thyroid antigens are common to both but their specificities differ leading to different functional consequences.

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27
Q

What are primary causes of hypothyroidism?

A

Postablative (after surgery or radioiodine therapy)

Autoimmune - Hashimoto’s thyroiditis

Iodine deficiency

Congenital biosynthetic defect

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28
Q

What are secondary causes of hypothyroidism?

A

Pituitary or hypothalamic failure (uncommon)

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29
Q

What is Hashimoto’s thyroiditis?

A

Other end of the spectrum of autoimmune thyroid disease from Grave’s disease.

Common cause of hypothyroidism.

Most common from 45 - 65 years.

F:M 15:1.

Presents with painless enlargement.

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30
Q

What is this?

A

Hashimoto’s thyroiditis

31
Q

What are neoplasms of the thyroid?

A

Adenomas: Benign neoplasms of follicular epithelium.

Carcinomas: Uncommon and account for less than 1% of solitary thyroid nodules.

32
Q

What are clues which can be used to identify thyroid nodules?

A

Solitary nodules more often neoplastic than multiple nodules.

Solid nodules more likely to be neoplastic than cystic nodules.

Nodules in younger patients more likely to be neoplastic than in older patients.

Nodules in males more likely to be neoplastic than those in females.

Nodules that do not take up radioactive iodine (cold nodules) more commonly neoplastic than ‘hot’ nodules.

33
Q

What are techniques used to identify the nature of thyroid nodules?

A

Fine needle aspiration cytology

Histology

34
Q

Whatr are thyroid adenomas?

A

Usually solitary.

Well circumscribed lesion that compresses the surrounding parenchyma.

Well formed capsule.

Small proportion cause thyrotoxicosis.

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

35
Q

What are carcinomas of the thyroid?

A

<1% of cancer deaths

Most cases in adults

  • Papillary (75-85%)
  • Follicular (10-20%)
  • Medullary (5%)
  • Anaplastic (<5%)
36
Q

What is the pathogenesis of thyroid carcinomas?

A

Genetic factors - inc. MEN

Ionizing radiation –Primarily papillary carcinomas

37
Q

What is papillary carcinoma?

A

May occur at any age

May have papillary architecture

BUT diagnosis is based on nuclear features:

  • Optically clear nuclei
  • Intranuclear inclusions

May be psammoma bodies

38
Q

What is this?

A

Papillary carcinoma

39
Q

What is this?

A

Papillary carcinoma

40
Q

What are clinical features of papillary carcinoma?

A

Nonfunctional

Present as painless mass in neck

May present with metastasis in cervical lymph node

10 year survival up to 90%

41
Q

What is a follicular carcinoma?

A

Peak incidence in middle age

Follicular morphology

May be well demarcated with minimal invasion or clearly infiltrative

Usually metastasise via bloodstream to lungs bone and liver

42
Q

What is a medullary carcinoma?

A

Neuroendocrine neoplasm derived from parafollicular C cells

80% sporadic: Adults 5-6th decade

20% familial: MMEN - younger patients

43
Q

What is this?

A

Medullary carcinoma

44
Q

What is an anaplastic carcinoma?

A

Occur in elderly patients

Very aggressive

Metastases common

Most cases death within one year due to local invasion

45
Q

What are the parathyroid glands?

A

Derive from developing pharyngeal pouches

Usually 4

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

46
Q

What is this?

A

Parathyroid gland

47
Q

What is the function of the parathyroid glands?

A

Activity controlled by level of free calcium in blood.

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
48
Q

What are causes of hyperparathyroidism?

A

80-90% - solitary adenoma

10-20% hyperplasia of all 4 glands: Sporadic or component of MEN type 1.

<1% carcinoma

49
Q

What is this?

A

Parathyroid adenoma

50
Q

What is hyperparathyroidism?

A

Increased level of serum ionised calcium.

Most common cause of clinically silent hypercalcaemia.

PTH is high in comparison with hypercalcaemia due to non-parathyroid diseases.

51
Q

What is primary 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

52
Q

What are symptoms of primary hyperparathyroidism?

A

“Painful bones, renal stones, abdominal groans, psychic moans”

Less common now as hypercalcaemia more frequently picked up on routine blood tests.

53
Q

What is secondary hyperparathyroidism?

A

Caused by any condition associated with chronic depression of serum calcium.

Renal failure is by far the most common cause.

Parathyroid glands are enlarged - may be asymmetrical.

Leads to bone changes as with primary disease.

54
Q

What are causes of secondary hyperparathyroidism?

A

Surgical ablation

Congenital absence

Autoimmune

55
Q

What are the clinical manifestations of hyperparathyroidism?

A

Neuromuscular irritability - tingling, muscle spasms, tetany

Cardiac arrhythmias

Fits

Cataracts

56
Q

What are the layers of the adrenal glands?

A

Zona glomerulosa: Secretes aldosterone

Zona fasciculata: Secretes glucocorticoids

Zona reticularis: Secretes androgens and glucocorticoids

Medulla: Noradrenaline and adrenaline

57
Q

What is adrenocortical hyperfunction?

A

Cushing’s syndrome – excess glucocorticoids

Hyperaldosteronism

Virilising syndromes – excess androgens

58
Q

What are signs and symptoms of Cushing’s Syndrome?

A

Hypertension and weight gain

Truncal obesity

‘Moon’ facies

‘Buffalo hump’

Cutaneous striae

59
Q

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

A

Most cases caused by administration of exogenous glucocorticoids – Adrenal glands are atrophic.

60
Q

What is endogenous Cushing’s Syndrome?

A

>50% due to primary hypothalamic-pituitary disease with increased ACTH – Cushing’s disease.

Most associated with ACTH-producing adenoma in the pituitary.

Some have hyperplasia of ACTH secreting cells in pituitary.

Adrenal glands show nodular cortical hyperplasia.

61
Q

What are endogenous causes of Cushing’s Syndrome?

A

30% of cases – primary adrenal

Most cases are due to a solitary neoplasm

  • Adenoma
  • Carcinoma

Less commonly due to bilateral hyperplasia

62
Q

What are exogenous causes of Cushing’s Syndrome?

A

Remaining cases due to secretion of ectopic ACTH by non-endocrine tumours.

Most commonly small cell carcinoma of the lung.

Adrenals show bilateral hyperplasia.

63
Q

What is primary hyperaldosteronism?

A

35 % aldosterone secreting adenoma – Conn’s syndrome.

60 % bilateral adrenal hyperplasia.

Clinical manifestations are hypertension and hypokalaemia.

Accounts for <1% of causes of hypertension but important to recognise as surgically correctable.

64
Q

What are adrenogenital syndromes?

A

Excess of androgens. May be associated with neoplasms – more commonly carcinoma than adenoma.

65
Q

What is congenital adrenal hyperplasia?

A

Group of autosomal recessive disorders.

Hereditary defects in enzymes involved in cortisol biosynthesis.

Decreased cortisol results in increased ACTH, adrenal stimulation and increased androgen synthesis.

May present in childhood or less commonly in adults.

66
Q

What are causes of primary adrenal insufficiency?

A

Primary

Secondary to reduced ACTH:

  • Non-functional pituitary adenomas
  • Other lesions of pituitary or hypothalamus including infarction
67
Q

What are acute causes of primary adrenal insufficiency?

A

Sudden withdrawal of corticosteroid therapy

Haemorrhage (neonates)

Sepsis with DIC (Waterhouse-Friderichson syndrome)

68
Q

What are chronic cuases of primary adrenal sufficiency (Addison’s Disease)?

A

Autoimmune (75-90%)

TB

HIV

Metastatic tumour (lung and breast particularly)

Rarely amyloid, fungal infections, haemochromatosis, sarcoidosis

69
Q

What are adrenocortical neoplasms?

A

Adenomas:

  • Most non-functional
  • May be associated with Cushing’s syndrome or Conn’s syndrome

Carcinomas:

  • Rare
  • Usually large
  • More commonly associated with virilizing syndrome than adenoma
70
Q

What are neoplasms of the adrenal medulla?

A

Secretes catecholamines in response to signals from the sympathetic nervous system. Most important diseases are neoplasms:

  • Phaeochromocytoma
  • Neuroblastoma
71
Q

What are phaeochromocytomas?

A

Secrete catecholamines and give rise to a surgically correctable form of hypertension.

Rule of 10s:

  • 10% arise in association with a familial syndrome inc. MEN 2A and 2B, von Hippel-Lindau disease and Sturge-Weber syndrome.
  • 10% are bilateral.
  • 10% are malignant.
  • In addition 10% of catecholamine-secreting tumours arise outside the adrenal (paragangliomas).
72
Q

What is multiple endocrine neoplasia (MEN) syndrome?

A

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

73
Q

What are MEN tumours?

A

Occur at a younger age than sporadic tumours

Arise in multiple endocrine organs

Often multifocal in one organ

Often preceded by hyperplasia

Usually more aggressive than sporadic tumours

Pathology eLearning - Y5 (17 decks)

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