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Histopathology > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

What is the anterior pituitary made of?

A

Epithelial cells derived from developing oral cavity

Supplied by blood from the pituitary portal system, hypothalamus to pituitary

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2
Q

What is the posterior pituitary made of?

A

It’s nervous in origin

Supplied by nerves, supra optic nucleus and paraventricular nucleus

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3
Q

What does the anterior pituitary do?

A

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

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4
Q

What are the symptoms of pituitary disease?

A

Hyperpituitarism- excess secretion of tropic hormones, usually due to functional adenoma
Hypopituitarism- deficiency of trophic hormones
Local mass effects of expanding lesions

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5
Q

What was hyperpituitarism classified on and what is it classified on now?

A

Orginally classified on morphological features of predominant cell type e.g acidophil, basophils, chromophobe adenomas
Now classified on the basis of the hormones produced, detected by immunohistochemistry

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6
Q

What is the commonest pituitary adenoma?

A

Prolactinoma 20-30%

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7
Q

What percentage of pituitary adenomas don’t secrete anything?

A

20%

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8
Q

What % of intracranial tumours come to clinical attention?

A

10%
But it is discovered incidentally in up to 25%of autopsies
Adults, peak 4-6th decade
Micro adenomas are less than 1cm

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9
Q

What are the clinical effects of prolactinomas?

A

Amenorrhea, galactorrhoea, loss of libido, infertility

Usually diagnosed earlier in females of reproductive age

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10
Q

What are the clinical effects of growth hormone adenomas?

A

Gigantism/acromegaly

DM, muscle weakness, hypertension, congestive cardiac failure

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11
Q

What are the clinical features of corticotroph cell adenomas?

A

Cushiness syndrome

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12
Q

What is hypopituiarism caused by?

A

Non secretory adenomas
Ischaemic necrosis, most commonly post partum Sheehans syndrome, or DIC, sickle cell anaemia, elevated intracranial pressure, shock
Ablation of pituitary by surgery or irradiation

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13
Q

What are the clinical manifestation of AP hypopituiarism?

A

Children- growth failure
Gonadotropin deficiency, amenorrhea and infertility in women. Decreased libido and impotence in men
Later many see effects of TSH and ACTH deficiency
Rarely, prolactin deficiency, failure of post partum lactation

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14
Q

What are the PP syndromes?

A

Releases 2 peptides, ADH and oxytocin

Important pp syndromes involve ADH, DI and SIADH

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15
Q

What are the local mass effects of pituitary tumours?

A

Compression of optic chiasm leading to bitemporal hemianopia
Signs and symptoms of raised intracranial pressure-headaches or papilloedma
Obstructive hydrocephalus

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16
Q

What is the mechanism of the thyroid gland?

A

In response to TSH from AP, follicular epithelial cells pinocytose colloid and convert thyroglobulin into T4 and T3.
T4 and T3 are released into circulation
Effect is to increase metabolic basal rate.
Parafollicular cells synthesise calcitonin, which promotes absorption of calcium by the skeletal system

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17
Q

What can happen to the thyroid?

A

Common presentation is enlargement of the thyroid
Non toxic goitre- common if there is impairment of synthesis of thyroid hormone, due to iodine deficiency
Endemic in areas where iodine in soil and water is low- Derbyshire neck
Common in puberty girls
Ingestion of stuff that interferes with thyroid hormone synthesis e.g brassicas
Hereditary enzymes defects

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18
Q

What can happen to a simple goitre?

A

With time, may be transformed to a multinodular pattern
May reach massive size
Lead to mechanical effects including dysphagia and airways obstruction
Hyperfunctioning nodule may develop leading to hyperthyroidism

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19
Q

What is thyrotoxicosis?

A

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

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20
Q

What are the primary causes if thyrotoxicosis?

A

Graves
Hyperfunctioning multinodular goitre
Hyperfunctioning adenoma
Thyroiditis

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21
Q

What are secondary causes of thyrotoxicosis?

A

TSH secreting pituitary adenoma

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22
Q

What are the causes of thyrotoxicosis that aren’t associated with the thyroid?

A 
Struma ovarii (ovarian teratoma with ectopic thyroid) 
Factitious thyrotoxicosis (exogenous thyroid intake)
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23
Q

What is Graves’ disease?

A

Most common cause of endogenous hyperthyroidism
Triad of thyrotoxicosis, infiltrative opthalmopathy with exophthalmos in up to 40%, and infiltrative dermopathy (pretibial myxodema) in minority of cases
Primarily younger adults f.M 7.1

24
Q

What is the pathogenesis of graves?

A

Autoimmune disorder
Variety of antibodies including antibodies to TSH receptor and thyroglobulin
TSH receptor antibodies most impt in pathogenesis, may stimulate release of thyroid hormones and increased proliferation of epithelium
Associated with SLE, pernicious anaemia, type 1 diabetes, and Addison’s disease

25
Q

How do autoimmune disorders of the thyroid span a continuum?

A

Graves at one end, hashimoto at the other.
Autoantibodies against thyroid antigens are common to both but their specifities differ leading to different functional consequences

26
Q

What are the primary causes of hypothyroidism?

A

Post ablative
Autoimmune hashimoto
Iodine deficiency
Congenital biosynthetic

27
Q

What is the secondary cause of hypothyroidism?

A

Pituitary or hypothalamic failure

28
Q

What is the commonest endogenous cause of hypothyroidism?

A

Hashimoto’s
45-65 years
F:M 15:1
Presents with painless enlargement

29
Q

What are the 2 sorts of neoplasms of the thyroid?

A

Adenomas- benign neoplasms of follicular epithelium

CarcinomasA- uncommon and account for less than 1% of solitary thyroid nodules

30
Q

What are the clues to the nature of thyroid nodules?

A

Solitary nodules more often neoplastic than multiple nodules and solid over cystic
More likely in younger, males
More likely in nodules that don’t take up radioactive iodine (cold)

31
Q

How do you ultimately distinguish neoplasm of thyroid?

A

fna

Histology

32
Q

What are adenomas of the thyroid like?

A

Usually solitary
Well circumscribed, compresses on surrounding parenchyma
Well formed capsule
Small proportion causes thyrotoxicosis
Impt to examine for invasion to exclude follicular carcinoma

33
Q

What is the epi for thyroid carcinoma?

A 
Less than 1% of cancer deaths 
Most cases in adults 
Papillary 75-85%
Follicular 10-20%
Medullary 5%
Anaplastic less than 5%
34
Q

Why are things that predispose to carcinoma of the thyroid?

A

MEN genetic

Ionising radiation, primarily papillary carcinoma

35
Q

What about papillary carcinoma?

A 
May occur at any age
May have papillary architecture 
Diagnosis based on nuclear features 
Optically clear nuclei
Intranuclear inclusions 
May be psammoma bodies (foci of calcification)
36
Q

How do papillary carcinomas present?

A

Non functional
Present as painless mass in neck
May present with metastasis in cervical lymph node
10 year survival up to 90%

37
Q

What about follicular carcinoma?

A

Tumours of middle age
Follicular morphology
Well demarcated with minimal invasion or clearly infiltrative
Usually metastasise via bloodstream to lungs bone and liver

38
Q

What about medullary carcinoma?

A

Neuroendocrine neoplasm derived from parafollicular C cells
80% sporadic adults 5-6th decade
20% familial MEN younger patients

39
Q

What is the least common thyroid carcinoma?

A

Anaplastic occur in elderly
Very aggressive
Metastases common
Most cases death within one year due to local invasion

40
Q

What is attached to the thyroid?

A

Parathyroid glands, derive from developing pharyngeal pouches
Usually 4, close to upper and lower poles of thyroid but may be in the thymus or anterior mediastinum

41
Q

What does PTH do?

A

Activates osteoclasts
Increases renal tubular re absorption of calcium
Increases conversion of vitamin D to its active form
Increases urinary phosphate excretion
Increases intestinal calcium absorption

42
Q

What are the causes of hyperparathyroidism?

A

80-90% solitary adenoma
10-20% hyperplasia of all 4 glands (sporadic or component of MEN type 1)
Less than1% carcinoma

43
Q

What are the effects of 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

44
Q

What causes hypoparathyroidism?

A

Surgical ablation
Congenital absence
Autoimmune

45
Q

What are the clinical manifestations of hypoparathyroidism?

A

Neuromuscular irritability, tingling muscle spasms, tetany
Cardiac arrhythmia
Fits
Cataracts

46
Q

What does adrenocortical hyper function lead to?

A

Cushings, excess glucocorticoids
Hyperaldosteronism
Virilising syndromes- excess androgens

47
Q

What is Cushings syndrome caused by?

A

Most cases, caused by administration of exogenous glucortioids (adrenal glands atrophic)
More than 50% due to pituitary disease, increased ACTH adenoma
(Some have hyperplasia of ACTH secreting cells in pituitary
Adrenal glands show nodular cortical hyperplasia)
30% cases primary adrenal
Most cases due to solitary neoplasm either adenoma or carcinoma
Less commonly due to bilateral hyperplasia

48
Q

What are the adrenals like when there is ectopic ACTH?

A

Bilateral hyperplasia

49
Q

What are the primary causes of hyperaldosteronism?

A

35% aldosterone secreting adenoma (conns)

60% bilateral adrenal hyperplasia

50
Q

What are the clinical manifestations of conns?

A

Hypertension and hypokalemia

Accounts for less than 1% of hypertension but important to recognise as surgically correctable

51
Q

What happens in adrenogential syndromes?

A

Excess of androgens
May be associated with neoplasm, more commonly carcinoma than adenoma
CAH- autosomal recessive, defects in enzymes, decreased cortisol, increased ACTH, increased androgen synthesis
May present in childhood, less commonly in adults

52
Q

What causes adrenal insufficiency?

A

Primary- acute, sudden withdrawal of corticosteroid therapy, haemorrhage in neonates, sepsis with DIC (Waterhouse friderichson syndrome)
Chronic- addisons, mets to adrenal,
Rarely amyloid, fungal infections, haemochromatosis, sarcoidosis

53
Q

What are the secondary causes of adrenal insufficiency?

A

Secondary to reduced ACTH, non functional pituitary adenomas, other lesions of pituitary or hypothalamus including infarction

54
Q

What are adrenocortical neoplasms?

A

Adenomas- mostly non functional, may be associated with Cushings or conns
Carcinomas- rare, usually large, commonly associated with virilising

55
Q

What is the adrenal medulla?

A

Secretes catecholamines in response to signals from sympathetic nervous system
Most important diseases are neoplasm- phaeo, neuroblastoma

56
Q

What is the rule of 10 in phaeo?

A

10% arise in association with a familial syndrome inc MEN 2a and b, vin hippel lindau, and sturge weber syndrome
10% bilateral
10% malignant
10% of catecholamines secreting tumours arise from outside the adrenal (paragangliomas)

57
Q

What can endocrine disease arise from?

A

Under or over production of lesions

Mass lesion in endocrine organs, causing local or metastatic problems

Histopathology (4 decks)

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