How can you separate endocrine pathologies?
- Over/under production of hormones
- Mass lesions
Describe the pituitary gland
It has an anterior and posterior aspect
Anterior:
- Epithelial cells
- Blood supply by pituitary portal system
Posterior:
- Nervous cells
How is the anterior pituitary controlled? Name the hormones involved and their actions.
It is mainly controlled by the hypothalamus:
- Thyrotrophin releasing hormone STIMULTES Thyroid stimulating hormone
- Dopamine INHIBITS prolactin
- Corticotrophin releasing hormone STIMULATES ACTH
- Growth hormone releasing hormone STIMULATES growth hormones
- Gonadotrophin releasing hormone STIMULATES gonadotrophin
What are the causes of hyperpituitarism?
Usually, a result of a functional tumour
What are the different types of functional adenomas of the pituitary, and the epidemiology surrounding them.
- Prolactin cell (20-30%)
- ACTH (10-15%)
- Gonadotrophin (10-15%)
- Growth hormone (5%)
- TSH (1%)
Up to 20% of all pituitary adenomas are non functioning (cause hypopituitarism)
What are the clinical affects of the different functional adenomas of the pituitary?
Prolactin cell:
- Amenorrhoea
- Galactorrhoea
- Reduced libido
- Infertility
Growth hormone:
- Gigantism (if children) or Acromegaly (if adults)
- Diabetes mellitus, HTN and congestive cardiac failure
Corticotrophin:
- Cushing’s syndrome
What are the causes of hypopituitarism?
- Non functioning pituitary adenomas
- Ischaemic necrosis (Sheehan’s syndrome, DIC, Sickle cell)
- Ablation or radiation
What are the symptoms of hypopituitarism?
- Growth failure
- Amenorrhoea, infertility, reduced libido, impotence
- Hypothyroid, hypoadrenal
- No lactation (if breastfeeding)
What syndromes are associated with over/under regulation of the posterior pituitary?
Posterior pituitary produces:
- ADH
- Oxytocin
ADH is important:
- DI if under production
- SIADH if over production (brain trauma)
What local affects can a mass lesion have at the pituitary?
Optic chiasm compression:
- Bitemporal hemianopia
Signs of raised ICP:
- Papilloedema, headaches
Obstructive hydrocephalus:
- Brain stem compression
What is the thyroid gland’s main role? How is it controlled? What other roles does the thyroid have?
It produces thyroxine.
TSH from the pituitary stimulates the thyroid to take up iodine and it uses iodine to transform thyroglobulin to T3 and T4.
The thyroid also has parafollicular cells which produce calcitonin, which stimulate calcium reabsorption by bone.
What is goitre? What are the types?
This is an enlarged thyroid; it can be:
- Non-toxic
- Toxic
What are the causes of non-toxic goitre?
- Iodine deficiency
- Ingestion of substances which interfere with hormone syntheses (brassicas)
- Hereditary illnesses
- Female puberty
What is thyrotoxicosis? What are the causes of this?
It is a hyperthyroid state, causing a hypermetabolic state.
Primary causes:
- Grave’s disease
- Multinodular goitre
- Adenomas
- Thyroiditis
Secondary causes:
- TSH secreting pituitary adenoma
Non-thyroid:
- Ovarian teratoma (ectopic TSH)
- Factitious thyrotoxicosis
What is grave’s disease? What are the classical features? What is the epidemiology surrounding it? What are its associations?
It is an autoimmune disease mainly powered by antibodies to the TSH receptor on the thyroid, causing a hyperthyroid state.
It classically has a triad of thyrotoxicosis, exophthalmos (40%) and pretibial myxoedema.
It presents in younger adults, more commonly in females.
It is associated with other autoimmune conditions:
- SLE
- Pernicious anaemia
- T1DM
- Addison’s
Give causes of hypothyroidism
Primary:
- Post-ablative therapy
- Autoimmune (Hashimoto’s)
- Iodine deficiency
- Congenital
Secondary:
- Pituitary/hypothalamic insufficiency
What is hashimoto’s thyroiditis? What are the classical features? What is the epidemiology surrounding it?
This is an autoimmune condition which causes a hypothyroid state.
It classically presents with a painless enlargement of the thyroid, and symptoms of hypothyroid disease. On histology, there are lymphoid cells, with germinal centres.
It is common in those aged 45-65, with a much higher risk in females.
What features of nodules may make it more suspicious of neoplasm?
- Solitary
- Solid
- Younger patient
- Male patient
- Cold (does not function)
How can you differentiate the neoplasms of the thyroid? What features may assist in this?
Neoplasms of the thyroid can be divided into:
- Adenomas
- Carcinomas
Adenomas are well circumscribed lesions, within a fibrous capsule. There will be no invasion into the thyroid.
What types of thyroid carcinoma are there? How common are they? What is the pathogenesis involved?
There are 4 types:
- Papillary (75-85%)
- Follicular (10-20%)
- Medullary (5%)
- Anaplastic (<5%)
They are usually as a result of radiation, or MEN (2A and 2B)
Describe the epidemiology, cytology and features of the four thyroid cancers.
Papillary:
- Any age
- Optically clear nuclei, psammoma bodies
- Non-functional
- 10 year survival is 90%
Follicular:
- Middle ages
- Follicular morphology
- Well demarcated
- Metastasises to bone, lung and liver
Medullary:
- Parafollicular cells
- 80% are sporadic, 20% are MEN2 associated (younger patients)
- Calcitonin is deposited as amyloid (Congo red stain)
Anaplastic:
- Elderly patients
- Very aggressive, death within a year
- Commonly metastasises
What are the parathyroid glands. How are they controlled?
They are found in the poles of the thyroid gland. They are controlled by calcium levels, responding to low levels by secreting parathyroid hormone.
What are the effects of parathyroid hormone?
Increase calcium concentration by:
- Increase osteoclast activity
- Increased renal calcium reabsorption
- Increased vitamin D activation
- Increased renal phosphate excretion
- Increased GI calcium absorption
What are the main causes of hyperparathyroidism?
- Solitary adenoma (80-90%)
- Hyperplasia (10-20%) [sporadic or MEN 1 and 2A
- Carcinoma (<1%)
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