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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
Risk factors for thyroid gland carcinoma
* genetic factors e.g. MEN * Ionisign radiation (mainly papillary carcinoma)
24
Papillary carcinoma
* 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
Follicular carcinoma
* middle age * follicular * well-demarcated or show invasion * usually **metastasise** via bloodstream to lungs, bone, liver
26
Medullary carcinoma
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
Anaplastic carcinoma
* elderly * very aggressive * **metastases COMMON** → most patients die within 1 year due to local invasion
28
How many parathyroid glands
**four** (can be located in thymus or anterior mediastinum)
29
Physiology of parathyroid tissue
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
Causes of hyperparathyroidism
80-90% are due to a **solitary adenoma** 10-20% are due to **hyperplasia of ALL four glands** * S*poradic OR a component of MEN T1, 2a* * \<1% are due to carcinoma
31
Parathyroid adenoma histology
normal parathyroids are 50% fat (seen in image) however there is ~**0% fat** in oedematous parathyroid
32
Clinical features of hyperparathyroidism: BONES,S TONES, GROANS, PSYCHIC MOANS
**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
Causes of secondary hyperparathyroidism
* 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
Parathyroid = condition and (intact PTH, Ca)
35
Causes of hypoparathyroidism
* Surgical ablation * Congenital absence (DiGeorge syndrome) * Autoimmune
36
Hypoparathyroidism features
* neuromuscular irritability (tingling, muscle spasms, tetany) * cardiac arrhythmias * fits * cataracts MNEMONIC: CATS go numb (convulsions, arrhythmia, tetany, spasm, numbness)
37
Anatomy of the adrenal medulla (GFR, sweet sugar sex)
Glomerulosa → aldosterone [OUTER] Fasciculata → glucocorticoids Reticularis → androgens and glucocorticoids * Cortex = **epithelial cells** Medulla → noradrenaline/adrenaline [INNER] * Medulla = **neural cells**
38
Adrenocortical hyperfunction (3)
Hyperaldosteronism Cushing's syndrome = excess glucocorticoids Virilising syndromes = excess androgens
39
Adrenocortical hyperfunction (3)
Hyperaldosteronism Cushing's syndrome = excess glucocorticoids Virilising syndromes = excess androgens
40
4 causes of Cushing's syndrome
* 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
Cushing's syndrome features
* HTN * Weight gain * Trunca obesity * Moon face * Buffalo hump * Cutaneous striae
42
Exogenous and endogenous cause of Cushing's syndrome
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
Cause of hyperaldosteronism
60% Bilateral adrenal hyperplasia 60% adenoma **(Conn's syndrome)**
44
Clinical features of hyperaldosteronism
**HTN** = small % of causes ## Footnote **Hypokalaemia**
45
Virilising syndromes = excess androgens (e.g. CAH)
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
Causes of adrenal insufficiency
Primary Secondary to reduced ACTH * non-functioning pituitary adenoma * another lesion of pituitary or hypothalamus (inc. infarction)
47
Primary adrenal insufficiency: acute and chronic
**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
2 types of adrenocortical neoplasms
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
Adrenal Medulla: diseases
* 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
Multiple Endocrine Neoplasia (MEN) Syndromes
*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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