Pathology of The Endocrine System Flashcards

1
Q

How is balance in the endocrine system maintained?

A

Feedback inhibition

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2
Q

What is included in the endocrine system?

A

Pineal gland, hypothalamus, hypothalamus, pituitary gland, thyroid gland, parathyroid gland, adrenal glands, pancreas
Also ovary, testes and kidneys

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3
Q

What are some disease processes in endocrine organs?

A

Hyperplasia
Atrophy
Tissue damage
Neoplasia
Congenital abnormality

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4
Q

What is the differences between benign and malignant neoplasia?

A

Benign - often circumscribed, localised, cant invade and don’t usually transform
Malignant - cancer, invades, metastasises, and can be fatal

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5
Q

What are some important aspects of endocrine diseases?

A

Endocrine organs have high reserve capacity
Feedback effects may cause endocrine changes
Can have multiorgan effects

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6
Q

Describe the anterior pituitary

A

Adenohypophysis
Secretes ACTH, TSH, GH, prolactin, FSH/LH
Blood supply from hypothalamus
Controlled by release factors from hypothalamus

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7
Q

Describe the posterior pituitary

A

Neurohypophysis
Downgrowth of hypothalamus
Secretes ADH and Oxytocin

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8
Q

What is the most common cause for pituitary hyperfunction?

A

Pituitary adenoma

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9
Q

Describe a pituitary adenoma

A

Usually adults - 35-60years
Most sporadic - 5% inherited
Macroscopic - soft, well circumscribed and mainly an incidental finding

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10
Q

What are the effects pituitary adenoma?

A

If functioning then hormone excess
Prolactinoma, GH secreting and ACTH secreting (Cushing’s)
Non functioning

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11
Q

What large pressure effects can an pituitary adenoma give?

A

Radiograhic abnormalities
Visual field abnormalities
Elevated intracranial pressure
Compression damage - hypopituitarism

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12
Q

What is pituitary hypofunction?

A

75% needs to be lost
Can be compression by tumours
Trauma, infection, TB or sarcoidosis
Sheehan’s syndrome - post partum ischaemic necrosis

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13
Q

Describe the histology of thyroid gland

A

Follicles
Colloids containing thyroglobulin
Epithelial cells - TG synthesis, iodination resorption and release of T3/4
C cells - secrete calcitonin

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14
Q

What are manifestation of thyroid disease?

A

Hyperthyroidism - thyrotoxicosis
Hypothyroidism - myxoedema, cretinism, subclinical
Enlargement - goitre and isolated mass/ nodule

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15
Q

What are the causes of hyperthyroidism?

A

Graves disease - diffuse toxic hyperplasia
Toxic multinodular goitre
Toxic adenoma

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16
Q

Describe Graves disease

A

Autoimmune production of anti-TSH receptor antibodies
Stimulate growth, activity and inhibit TSH binding
More females - peak 20-40yrs
Genetic predisposition
Hyperplasia and hyperfunction

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17
Q

What is the histology for Graves disease?

A

Increased cell activity and cell numbers
Scalloping of colloids

18
Q

What are some causes of hypothyroidism?

A

Hashimoto’s thyroiditis
Iatrogenic - surgery and drugs
Iodine deficiency
Congenital hypothyroidism

19
Q

Describe Hashimoto’s thyroiditis

A

Autoimmune destruction of thyroid epithelial cells
More females - 45-65 yrs
Cytotoxic T cells, cytokine and antibody mediated destruction
Circulating autoantibodies to thyroglobulin and thyroid peroxidase

20
Q

What happens to the thyroid gland in Hashimoto’s thyroiditis?

A

Diffuse enlargement gradual failure

21
Q

Describe the histology of Hashimoto’s thyroiditis

A

Hurthle cell change - ore pink and rounded (more cytoplasm)
Intense infiltration of lymphocytes and plasma cells

22
Q

Describe the process of formation of multinodular goitre

A

Iodine deficiency and goitrogens - impaired synthesis of T3 and T4 - increased TSH - hypertrophy and hyperplasia of epithelium
Then simple to multinodular

23
Q

Describe the histology of multinodular goitre

A

Crowded follicles
Distended colloid filled follicles
Haemorrhage, fibrosis and cystic change
Nodular appearance

24
Q

What can a thyroid nodule be?

A

Dominant nodule in multinodular goitre
Cyst
Follicular adenoma
Carcinoma - differentiated - papillary, medullary, follicular and anaplastic

25
What are the investigations for thyroid nodules?
TFTs US FNA - cytology
26
What are the risk factors for thyroid carcinoma?
FH, chronic inflammatory disease, radiation exposure and obesity
27
Describe follicular adenoma
Mostly non-functioning Circumscribes and encapsulated Histology - small micro-follicles
28
Describe follicular carcinoma
Rare and usually solitary Malignant cells breach capsule Metastases - blood and bones RAS mutation or PAX8/PPARG translocation
29
Describe papillary carcinoma
Usually over 50 yrs BRAF mutation or RET/PTC gene rearrangement Spreads via lymphatics but good prognosis Associated with ionising radiation
30
What is the histology of papillary carcinoma?
Papillary projections, empty nuclei, psammoma bodies and may be cystic
31
Describe medullary carcinoma
Malignant tumour of c cells Produces calcitonin 70% sporadic Some MEN2a, b and familial FMTC - mutations in RET proto-oncogene
32
What is the histology of medullary carcinoma?
Tumour cells Amyloids
33
What is the treatment for thyroid carcinoma?
Surgery, radio-active iodine, external radiotherapy and chemo
34
What is primary hyperparathyroidism?
Often asymptomatic hypercalcaemia Sporadic or familial (MEN1) Adenoma mainly, hyperplasia or carcinoma (rare)
35
What is secondary hyperparathyroidism?
Physiological response to decreased Ca renal failure As feedback loop so increases PTH
36
What are multiple endocrine neoplasia (MEN)?
Inherited disorders with underlying genetic mutation Hyperplasia/ neoplasms of endocrine organs - younger age and multifocal Autosomal dominant
37
Describe MEN1
MEN1 tumour suppressor gene mutation - defect in menin protein involved in regulating cell growth
38
What is affected in MEN1?
Parathyroid hyperplasia and adenomas Pancreatic (hypoglycaemia) and duodenal (ulcers) endocrine tumours Pituitary adenoma
39
Describe MEN2
RET proto-oncogene mutation Medullary carcinoma of thyroid Pheochromocytoma
40
What is involved in MEN2A?
Sipple syndrome Parathyroid hyperplasia Extracellular domain auto-dimerization of RET receptor
41
What is involved in MEN2B?
Neuromas of skin and mucous membrane Skeletal abnormalities Younger patients and aggressive Autoactivation of tyrosine kinase pathway