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Pathology of Endocrine Diseases Flashcards

1
Q

what is the endocrine system?

A

Integrated network of GLANDS - secrete chemical messengers – hormones - directly into bloodstream

HORMONES act on target cells distant from site of synthesis - bind to receptors – change cell activity

REGULATION of metabolism, growth and development, tissue function

maintain functional balance

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2
Q

where are hormones synthesised and stored?

A

glands

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3
Q

how are endocrine glands described?

A

packets of cells with secretory granules
vascular
ductless

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4
Q

how is balance of the endocrine system maintained?

A

negative feedback

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5
Q

what makes up the classical endocrine system?

A

Pineal gland
Hypothalamus
Pituitary gland

Thyroid gland
Parathyroid gland
Adrenal glands
Pancreas

but several organs eg ovary, testes, kidneys, produce hormones also endocrine type cells scattered throughout body lung, GI tract, paraganglia (under neuropeptide control)

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6
Q

what can dysregulated hormone release lead to?

A

HYPERFUNCTION
HYPOFUNCTION

effect of a mass lesion

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7
Q

what disease processes affects endocrine organs?

A

HYPERPLASIA
increased number and secretory activity of cells
ATROPHY
diminution of cells due to lack of stimulation
TISSUE DAMAGE
inflammation, autoimmune disease, compression, trauma, infarction
NEOPLASIA
Adenoma – functioning or non functioning
Carcinoma – 1ry or metastatic
CONGENITAL ABNORMALITY

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8
Q

what is a benign neoplasm?

A

Often circumscribed, localised, cannot invade, don’t usually transform

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9
Q

what is malignant neoplasm?

A

Synonymous with cancer, invades, metastasises, if untreated, will often prove fatal

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10
Q

what does the thyroid gland synthesise store and release?

A

thyroxine (T4), triiodothyronine (T3)
Regulates basal metabolic rate

calcitonin
Regulates calcium homeostasis

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11
Q

what is the role of thyroxine (T4), triiodothyronine (T3)?

A

Regulates basal metabolic rate

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12
Q

what is the role of calcitonin?

A

Regulates calcium homeostasis

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13
Q

what physiological effects do thyroxine (T4), triiodothyronine (T3) have?

A

Increases BMR; Accelerates protein synthesis in children; Enhances sympathetic tone (sympathomimetic effect on heart, brown fat) carbohydrate and lipid metabolism

stimulates protein synthesis

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14
Q

what are manifestations of thyroid diseases?

A

Hyperthyroidism
Thyrotoxicosis*

Hypothyroidism
Myxoedema, Cretinism
Subclinical

Thyroid enlargement
Goitre
Isolated nodule/mass

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15
Q

what are primary and secondary causes of thyroid diseases?

A

Thyroiditis
Autoimmune
Others

Gland destruction

Multinodular goitre
Tumours
Benign
Malignant

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16
Q

what are causes of hyperthyroidism?

A

Diffuse toxic hyperplasia (Graves disease) – 70%

Toxic multinodular goitre – 20%

Toxic adenoma

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17
Q

what is graves disease?

A

F>M, peak 20-40 yrs, genetic predisposition

Autoimmune production of anti- TSH receptor antibodies
stimulate activity, growth, inhibit TSH binding
ophthalmopathy immune mediated – ocular fibroblasts have TSH receptor

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18
Q

what affect does graves disease have on the thyroid?

A

diffuse hyperplasia and hyperfunction

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19
Q

how does graves disease affect the thyroid gland?

A

enlarged gland (meaty)

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20
Q

what are causes of hypothyroidism?

A

Hashimoto’s thyroiditis
(auto-immune destruction)

Iatrogenic – surgery, drugs

Iodine deficiency

Congenital hypothyroidism

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21
Q

what is hashimotos thyroiditis?

A

F>M , 45-65yrs

Autoimune destruction of thyroid epithelial cells
Cytotoxic T cells, cytokine and antibody mediated destruction
Circulating autoantibodies to
thyroglobulin ,
thyroid peroxidase

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22
Q

what effect does hashimotos thyroiditis have on the thyroid?

A

Diffuse enlargement gradual failure

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23
Q

describe the manifestation of a multinodular goitre?

A

Iodine deficiency, goitrogens
↓
Impaired synthesis of T3,T4
↓
↑TSH
↓
Hypertrophy and hyperplasia of thyroid epithelium

Simple → → multinodular

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24
Q

what are causes of multinodular goitre?

A

Iodine deficiency commonest cause – also goitrogens like cabbage brussels sprouts and cassava which contains thiocyanate
Endemic/Sporadic Endemic >10% population

Physiological
Puberty
Pregnancy
Autoimmune
Graves’ disease
Hashimoto’s disease
Thyroiditis
Acute (de Quervain’s )
Chronic fibrotic (Reidel’s)
Iodine deficiency (endemic goitre)
Dyshormogenesis
Goitrogens

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25
what can a thyroid nodule be?
Dominant nodule in multinodular goitre Cyst Follicular adenoma Carcinoma (5% of nodules) Differentiated thyroid carcinoma Papillary carcinoma 75-85% Follicular carcinoma 10-20% Anaplastic carcinoma <5% Medullary carcinoma 5% (lymphoma)
26
how should a thyroid nodule be investigated?
TFTs Ultrasound FNA - cytology
27
how are thyroid carcinomas often found?
inicdentally
28
what are risk factores for thyroid carcinoma?
Family Hx Chronic inflammatory conditions Radiation exposure Obesity
29
what is follicular adenoma?
Most non-functioning Circumscribed, encapsulated tumour Histology often small microfollicles
30
how would you describe follicular carcinoma?
Rare, usually solitary Malignant cells breach capsule Metastases – blood, bones invasion through thyroid capsule
31
how would you describe a papillary carcinoma?
Usually <50yrs BRAF mutation or RET/PTC gene rearrangement Associated with exposure to ionizing radiation Spreads via lymphatics... but Excellent prognosis - 85% survival 10 yrs (esp <55yrs)
32
how would you describe a thyroid medullary carcinoma?
Malignant tumour of C – cells produces calcitonin (+/- other polypeptides) 70% sporadic 30% MEN 2A, 2B, familial FMTC – mutations in RET proto-oncogene – prophylactic thyroidectomy
33
how are thyroid carcinomas treated?
Surgery Radioactive iodine External radiotherapy Chemotherapy
34
what are parathyroid glands?
4 small glands – 120mg Produce PTH – regulates plasma Ca2+
35
what is Primary hyperparathyroidism?
often asymptomatic hypercalcaemia Sporadic or familial (MEN-1) Adenoma (85-95%) Hyperplasia (5-10%) Carcinoma (rare)
36
what is Secondary hyperparathyroidism?
Physiological response to ↓ Ca2+ renal failure
37
describe the pitiutary gland?
Small gland, located in sella turcica Connected to hypothalamus by pituitary stalk Critical role in regulating other endocrine glands
38
what are the two distinct components of the pituiatary gland?
anterior pituitary posterior pituitary
39
describe the function of anterior pituitary?
adenohypophysis 80% secretes ACTH, TSH, GH, PROLACTIN, FSH/LH blood supply from hypothalamus controlled by release factors from hypothalamus
40
describe the function of the posterior pituitary?
neurohypophysis downgrowth of hypothalamus Secretes ADH, OXYTOCIN
41
what is the most common cause of pituitary hyperfunction?
pituitary adenoma (pituitary carcinomas v rare and some hypothalamic disorders)
42
what is the aetiology of pituitary adenoma?
usually adults, 35 to 60 yrs most sporadic; 5% inherited eg MEN1
43
how does a pituitary adenoma appear macroscopically?
soft, well-circumscribed lesion small microadenomas may be incidental eg at post mortem
44
what are the effects of pituitary adenoma?
If functioning - hormone excess Prolactinoma - 20-30% galactorrhoea, menstrual disorders GH secreting acromegaly, gigantism ACTH secreting Cushing’s disease Non-functioning - 25-30% of detected tumours immunohistochemical demonstration (mostly prolactin)
45
describe clinically some effects of a pituitary adenoma?
46
if the pituitary tumour is large what affect might this have?
Local mass effects: may be confined to the sella turcica but as adenoma expands, may lead to radiographic abnormalities of the sella turcica, including sellar expansion, bony erosion of sella turcica and anterior clinoid processes, and disruption of the diaphragma sella visual field abnormalities, classically in the form of defects in the lateral (temporal) visual fields, so-called bitemporal hemianopsia. – as tumour extend superiorly through the diaphragm sella into the suprasellar region, where they often compress the optic chiasm elevated intracranial pressure, including headache, nausea, and vomiting compression damage – hypopituitarism esp non functioning which present later
47
describe pituitary hypofunction?
75% needs to be lost Compression by tumours – craniopharyngioma. metastatic
48
what can be caused by pituitary hypofunction?
Trauma Infection (rare) TB Sarcoidosis
49
what syndrome is characterised by post partum ischaemic necrosis?
Sheehan’s syndrome
50
what is produced by the adrenal cortex?
Steroid hormones
51
what is produced by the adrenal medulla?
Neuroendocrine (chromaffin) cells Adrenaline/ noradrenaline response to stress maintain BP Extra adrenal paraganglia similar
52
what is the adrenal cortex made up of?
53
what are different adrenal pathologies?
Hyperfunction clinical syndromes depend on which adrenal hormones stimulated Hypofunction Mass lesion - effect late Effect on adrenal gland –hyperplasia (diffuse or nodular), atrophy, mass lesion
54
what three syndromes are characterised by adrenal cortical hyperfunction?
Hypercortisolism– CUSHING’S SYNDROME Hyperaldosteronism (Conn’s syndrome) Adrenogenital syndormes
55
what are different causes of cushings syndrome (hypercortisolism)
Exogenous -Iatrogenic steroids Endogenous ACTH dependent pituitary adenoma Cushings disease – 70% ectopic ACTH ACTH independent functioning adrenal adenoma 10%
56
what is ACTH independent hypercortisolism?
57
what is ACTH dependent hypercortisolism?
58
what is hyperaldosteronism (conns syndrome)?
Bilateral idiopathic hyperplasia Functioning adrenal adenoma (2ry hyperaldosteronism – physiological due to ↓renal perfusion ↑renin-angiotensin) Increases sodium retention in the nephron
59
what is adrenogenital syndrome?
Functioning adrenal tumour Pituitary tumour Cushings disease Congenital adrenal hyperplasia – steroid enzyme deficiency
60
what is acute adrenal insufficiency caused by?
destruction of the glands through: meningococcal septicaemia Waterhouse Friderichsen
61
what is chronic adrenal insufficiency caused by?
1ry - Addison’s disease Autoimmune : autoimmune polyendocrine syndromes – spare medulla Infections: TB, fungus HIV-related infections Replacement: metastatic carcinoma amyloidosis, Atrophy: prolonged steroid therapy Congenital hypoplasia 2ry - Pituitary failure [causing destruction of the glands]
62
what affect do functioning adrenocortical tumours have?
hyperadrenal syndromes, atrophy of adjacent cortex
63
how are non functioning adrenocortical tumours found?
often incidental – imaging/autopsy
64
what are the appearance of adrenocortical tumours?
Yellow-brown circumscribed Most 2-3cm <30g
65
what are primary adrenocortical carcinomas?
rare, any age More likely functional – virilising Most large >20cm , haemorrhage and necrosis, cystic Metastasises by lymphatics and blood – invades adrenal vein
66
what are metastatic carcinomas?
More common lung, breast
67
what is a type of adrenal medullary tumour?
PHAEOCHROMOCYTOMA
68
describe PHAEOCHROMOCYTOMA?
Adrenal medulla neuroendocrine cells secrete catecholamines → hypertension Usually benign behaviour, can be bilateral Up to 30% inherited – eg MEN 2, SDH 10% extra adrenal (paraganglioma)
69
what is multiple endocrine neoplasia?
Inherited disorders with underlying genetic mutation Hyperplasia/ neoplasms of endocrine organs – younger age, multifocal Several distinct syndromes
70
what distinct syndromes does multiple endocrine neoplasia have?
MEN 1 (Wermer syndrome) MEN 2
71
describe MEN 1 (wermers syndrome)
MEN 1 tumour suppressor gene mutation -defect in menin protein involved in regulating cell growth Parathyroid hyperplasia and adenomas Pancreatic and duodenal endocrine tumours (hypoglycaemia and ulcers) Pituitary adenoma (prolactinoma)
72
what is MEN 2?
RET proto-ongogene mutations Medullary carcinoma of thyroid Phaeochromocytoma
73
what is MEN 2A?
MEN 2A (Sipple syndrome) + Parathyroid hyperplasia Extracellular domain auto dimerisation of RET receptor
74
what is MEN 2B?
+ Neuromas of skin &mucous membrane, skeletal abnormalities + Younger patients, aggressive Autoactivation of tyrosine kinase pathway

Endocrine (35 decks)

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