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Year 5 Histopathology > 4s: Endocrine Disease > Flashcards

4s: Endocrine Disease Flashcards

1
Q

Anatomy of the pituitary

A

Anterior (epithelial cells)

  • blood supply from portal system
  • secrete hormones that are under influence of control factors released by hypothalamus

Posterior (nerve cells)

  • nerves from supraoptic and paraventricular nuclei
  • release ADH and oxytocin
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2
Q

Symptoms of pituitary disease (3)

A

Hyperpituitarism

  • excess secretion of trophic hormones
  • usually due to functional adenoma

Hypopituitarism

  • hormone deficiency

Local mass defect

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3
Q

Hypothalamic factor, effect, and pituitary hormone

A
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4
Q

Types of adenoma in hyperpituiarism

A
  • 30% prolactinoma, 15% ACTH-oma, 15% GH-oma
  • 20% non-functioning adenoma
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5
Q

How do we describe pituitary adenomas and frequency of cells

A
  • Pituitary adenomas = ~10% overt intracranial tumours
  • Discovered incidentally in up to 25% of autopsies
  • Age: 30-50 years
  • Defined as a ‘microadenoma’ if <1 cm
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6
Q

Clinical effects of functioning pituitary adenomas (3)

A

Prolactinomas

  • amenorrhoea, galactorrhea, loss of libido, infertility
  • diagnosed quicker in females of reproductive age

GH adenomas

  • prepubertal children → gigantism
  • adult → acromegaly
  • diabetes, muscle weakness, HTN, congestive cardiac failure

Corticotroph Cell adenomas

  • Cushing’s disease
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6
Q

Clinical effects of functioning pituitary adenomas (3)

A

Prolactinomas

  • amenorrhoea, galactorrhea, loss of libido, infertility
  • diagnosed quicker in females of reproductive age

GH adenomas

  • prepubertal children → gigantism
  • adult → acromegaly
  • diabetes, muscle weakness, HTN, congestive cardiac failure

Corticotroph Cell adenomas

  • Cushing’s disease
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7
Q

3 causes of hypopituitarism

A

Non-secreting pituitary adenoma

Ischaemic necrosis → MOST COMMONLY post-partum (Sheehan’s syndrome)

  • pituitary enlarges during pregnancy and more susceptible to ischaemia
  • you get PPH (Sheehan syndrome) → ischaemia
  • other causes = DIC, sickle cell anaemia, elevated ICP, shock

Iatrogenic = ablation of pituitary by surgery or irradiation

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8
Q

Clinical features of anterior pituitary hypogunction

A

Children = growth failure (pituitary dwarfism)

GnRH deficiency

  • amenorrhoea and infertility in women
  • decreased libido and impotence in men

TSH and ACTH deficiency = 2o hypthyroidism and 2o hypoandrenalism

Prolactin deficiency = failure of post partum lactation

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9
Q

Posterior pituitary syndromes = 2 peptides released by the posterior pituitary

A

ADH → deficiency, insensitivity, excess → DI or SIADH

Oxytocin

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10
Q

Local mass effect of pituitary tumours

A
  • Compression of optic chiasm gives rise to bitemporal hemianopia
  • As the tumour gets larger, you may get features of raised ICP (e.g. headaches)
    • In severe cases, you may get obstructive hydrocephalus
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11
Q

Thyroid gland histology

A
  • The follicles have a small amount of stromal tissue in between them
  • Follicles lined by epithelial cells and have lots of colloid in the middle
  • Parafollicular cells are found in between the follicles
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12
Q

Thyroid physiology

A
  • In response to TSH, follicular epithelial cells pinocytose the colloid and convert thyroglobulin into T4 and T3
  • T4 and T3 are released into the circulation and they increase basal metabolic rate
  • Parafollicular cells (C cells) produce calcitonin which promotes the absorption of calcium by the skeletal system
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13
Q

Non-toxic goitre = enlargement without overproduction of thyroid hormones

A

Common if there is impaired synthesis of thyroid hormones (most often due to iodine deficiency)

There are certain parts of the world where iodine intake is low (developing countries)

  • May be seen during puberty in girls
  • Ingestion of some substances that interfere with thyroid hormone synthesis can cause it (e.g. brassicas)
  • May be due to hereditary enzyme deficiency
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14
Q

Multinodular goitre

A
  • With time, simple thyroid enlargement may be transformed to multinodular pattern
  • May become massive and cause mechanical effects such as dysphagia and airway obstruction
  • A hyperfunctioning nodule may develop → hyperthyroidism
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15
Q

Thyrotoxicosis/high T3, primary and secondary causes

A

Graves’ Disease

MOST COMMON cause of endogenous hyperthyroidism; mostly in FEMALES (7x)

Triad presentation: Thyrotoxicosis, Exophthalmos, Pretibial myxoedema

Autoimmune disorder associated with a variety of antibodies to the TSH-R and thyroglobulin

  • They stimulate thyroid hormone release and increases proliferation of the epithelium

Associated with other AI diseases (SLE, pernicious anaemia, T1DM and Addison’s disease)

NOTE: autoimmune diseases of the thyroid gland are a SPECTRUM (from Graves to Hashimoto’s)

  • Antibodies against thyroid antigens are common to both conditions but they differ in function
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16
Q

Causes of hyperthyroidism that are NOT associated with the thyroid gland

A
  • Struma ovarii (ovarian teratoma with ectopic thyroid)
  • Factitious thyrotoxicosis (exogenous thyroid intake)
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17
Q

Hypothyroidism/Low T4 primary and secondary causes

A
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18
Q

Hypothyroidism/Low T4 primary and secondary causes

A
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19
Q

Adenoma vs carcinoma

A
  • Adenomas – benign neoplasms of the follicular epithelium
  • Carcinomas – uncommon and account for <1% of solitary thyroid nodules
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19
Q

Adenoma vs carcinoma

A
  • Adenomas – benign neoplasms of the follicular epithelium
  • Carcinomas – uncommon and account for <1% of solitary thyroid nodules
20
Q

Features suggestive of neoplasia

how do we get a definitive answer

A
  • solitary rather than multiple
  • solid rather than cystic
  • younger patients
  • nodules NOT take up radioiodine (cold nodule)

Answer = FNA, histology

21
Q

Adenomas of the thyroid gland description

A
  • usually solitary
  • well-formed capsule
  • well-circumscribed and compress surrounding parenchyma
  • small proportion will be functional and cause thyrotoxicosis
  • important to examine the capsule for invasion to exclude follicular carcinoma
22
Q

4 types of carcinoma of the thyroid gland: PFMA

A
  • Papillary = psammoma bodies (calcifications), Orphan’s Annie Eyes (clear nuclei)
  • Follicular
  • Medullar = amyloid in thyroid (Congo red stain)
  • Anaplastic
23
Q

Risk factors for thyroid gland carcinoma

A
  • genetic factors e.g. MEN
  • Ionisign radiation (mainly papillary carcinoma)
24
Q

Papillary carcinoma

A
  • any age
  • papillary architecture

nuclear features = diagnosis

  • optically clear nuclei (Orphan Annie Eyes)
  • intranuclear inclusions
  • may have psammoma bodies (calcification)

non-functional and painless mass in neck

cervical lymph node metastasis

10-year survival 90%

25
Q

Follicular carcinoma

A
  • middle age
  • follicular
  • well-demarcated or show invasion
  • usually metastasise via bloodstream to lungs, bone, liver
26
Q

Medullary carcinoma

A

Neuroendocrine neoplasm from parafollicular C-cells

80% sporadic (40-50 yo) 20% familial (MEN - younger patients → 2A, 2B)

Characteristic feature = calcitonin produced by tumour cells broken down and deposited as amyloid within thyroid → visualised using Congo Red and looking at it under polarised light

27
Q

Anaplastic carcinoma

A
  • elderly
  • very aggressive
  • metastases COMMON → most patients die within 1 year due to local invasion
28
Q

How many parathyroid glands

A

four (can be located in thymus or anterior mediastinum)

29
Q

Physiology of parathyroid tissue

A

decreased Ca stimulates PTH release → PTH actions:

  • 1a-OHase activation → calcidiol to calcitriol → gut effects
  • osteoclast activation → Ca2+ liberation
  • direct renal Ca resorption
  • direct renal phosphate excretion
30
Q

Causes of hyperparathyroidism

A

80-90% are due to a solitary adenoma

10-20% are due to hyperplasia of ALL four glands

  • Sporadic OR a component of MEN T1, 2a
    • <1% are due to carcinoma
31
Q

Parathyroid adenoma histology

A

normal parathyroids are 50% fat (seen in image) however there is ~0% fat in oedematous parathyroid

32
Q

Clinical features of hyperparathyroidism: BONES,S TONES, GROANS, PSYCHIC MOANS

A

Hypercalcaemia

  • bone resorption with thinning of the cortex and cyst formation (osteitis fibrosa cystic)
  • normal PTH with a high calcium

Renal stones and obstructive uropathy = STONES

GI disturbance (constipation, pancreatitis, gallstones) = GROANS

CNS alterations (depression, lethargy, seizures) = PSYCHIC MOANS

Neuromuscular abnormalities (weakness)

Polyuria and polydipsia

33
Q

Causes of secondary hyperparathyroidism

A
  • any conditions (usually low Vit D) → chronically low Ca
  • Vit D deficiency MOST COMMON cause (i.e. renal failure → low vitamin D)
  • parathyroid glands enlarged (may be asymmetrical)
  • leads to bone changes (as in primary disease)
34
Q

Parathyroid = condition and (intact PTH, Ca)

A
35
Q

Causes of hypoparathyroidism

A
  • Surgical ablation
  • Congenital absence (DiGeorge syndrome)
  • Autoimmune
36
Q

Hypoparathyroidism features

A
  • neuromuscular irritability (tingling, muscle spasms, tetany)
  • cardiac arrhythmias
  • fits
  • cataracts

MNEMONIC: CATS go numb (convulsions, arrhythmia, tetany, spasm, numbness)

37
Q

Anatomy of the adrenal medulla (GFR, sweet sugar sex)

A

Glomerulosa → aldosterone [OUTER]

Fasciculata → glucocorticoids

Reticularis → androgens and glucocorticoids

  • Cortex = epithelial cells

Medulla → noradrenaline/adrenaline [INNER]

  • Medulla = neural cells
38
Q

Adrenocortical hyperfunction (3)

A

Hyperaldosteronism

Cushing’s syndrome = excess glucocorticoids

Virilising syndromes = excess androgens

39
Q

Adrenocortical hyperfunction (3)

A

Hyperaldosteronism

Cushing’s syndrome = excess glucocorticoids

Virilising syndromes = excess androgens

40
Q

4 causes of Cushing’s syndrome

A
  • Pituitary (CUSHING’S DISEASE) = tumour in anterior pituitary → adrenal hyperplasia
  • Adrenal = tumour in adrenal, nodular hyperplasia
  • Paraneoplastic = lung cancer (or other nonendocrene cancer) → adrenal hyperplasia
  • Iatrogenic = steroids → adrenal atrophy/Cushing’s syndrome
41
Q

Cushing’s syndrome features

A
  • HTN
  • Weight gain
  • Trunca obesity
  • Moon face
  • Buffalo hump
  • Cutaneous striae
42
Q

Exogenous and endogenous cause of Cushing’s syndrome

A

Administration of glucocorticoids aka iatrogenic (adrenal glands are atrophic) = highest exogenous cause

  • other exogenous cases due to ectopic ACTH (i.e. SCLC)
  • adrenals show bilateral hyperplasia

Primary hypothalamic or pituitary disease with high ACTH (Cushing’s disease) = highest endogenous cause

  • 30% are primary adrenal disorders
  • most will be due to a solitary neoplasm (either adenoma or carcinoma)
  • can sometimes be due to bilateral hyperplasia
43
Q

Cause of hyperaldosteronism

A

60% Bilateral adrenal hyperplasia

60% adenoma (Conn’s syndrome)

44
Q

Clinical features of hyperaldosteronism

A

HTN = small % of causes

Hypokalaemia

45
Q

Virilising syndromes = excess androgens (e.g. CAH)

A

May be associated with neoplasms (more commonly carcinoma than adenoma)

Congenital Adrenal Hyperplasia – most common = 21-OH deficiency

  • Autosomal recessive
  • Caused by hereditary defects in enzymes involved in cortisol biosynthesis
  • Reduced cortisol production → increased ACTH, adrenal stimulation and increased androgen synthesis
  • More commonly presents in childhood (more obvious in females)
46
Q

Causes of adrenal insufficiency

A

Primary

Secondary to reduced ACTH

  • non-functioning pituitary adenoma
  • another lesion of pituitary or hypothalamus (inc. infarction)
47
Q

Primary adrenal insufficiency: acute and chronic

A

ACUTE

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

CHRONIC (Addison’s Disease)

  • Autoimmune (90%), TB, HIV
  • Metastatic tumour (in particular, lung and breast)
  • RARE: amyloidosis, fungal infections, haemochromatosis, sarcoidosis
48
Q

2 types of adrenocortical neoplasms

A

Adenomas

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

Carcinomas

  • RARE; usually LARGE
  • Most commonly associated with virilising syndromes than adenomas
49
Q

Adrenal Medulla: diseases

A
  • Secretes catecholamines in response to signals from the CNS

Diseases:

Phaeochromocytoma = secretes catecholamines → 2nd HTN; rule of 10s

  • 10% associated with syndromes (MEN, vHL, Sturge-Weber)
  • 10% bilateral
  • 10% malignant occur outside the adrenal glands (paragangliomas)

Neuroblastoma

50
Q

Multiple Endocrine Neoplasia (MEN) Syndromes

A

a group of inherited conditions resulting in proliferative lesions (hyperplasia, adenomas and carcinomas) of multiple endocrine organs

  • Tumours occur at a younger age than sporadic tumours
  • Arise in more than one endocrine organ or may be multifocal within one endocrine organ
  • Tumours are often preceded by hyperplasia
  • Tumours are usually more aggressive than sporadic tumours and harder to treat

Year 5 Histopathology (10 decks)

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