Endocrinology Flashcards

1
Q

Hypopituitarism

A

Due to deficiency of hypothalamic releasing hormone or pituitary hormones.

1 or hormones affected.

GH and FSH/LH usually affected late. ACTH and TSH affected first.

Hyperprolactinaemia occurs early due to break in its inhibitory pathway where it inhibits prolactin (PRL) release.

ADH and oxytocin are not affected as these are posterior pituitary hormones…unless hypothalamus involved or post pituitary is squashed by tumour or something.

Particular pituitary syndromes:

1) Congenital GnRH deficiency - Kallman’s syndrome
2) Sheehan’s syndrome - Pituitary infarction occurs for some reason after severe PPH. Rare in developed places
3) Pituitary apoplexy - rapid pit. enlargement due to bleeding into it or infarction. Pituitary becomes hulk - severe headache and visual loss (due to angry hulk in brain)

Treatment - Steroids and thyroid hormones - we need these to live. REPLACE THEM - DUAH

Hydrocortisone to replace steroids
Levothyroxine to replace thyroid hormones

Ensure normal glucocorticoid before replacing the thyroid hormone as the thyroid hormone will increase metabolic demand and without sufficient steroid hormones to assist, an adrenal crisis will occur

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2
Q

Hyperprolactinaemia

A

Normally, PRL under tonic inhibition by dopamine (DA) which the hypothalamus makes.

Pregnancy, severe stress such as exams, and lactation all increase PRL physiologically.

Commonest cause of prolactinaemia is a PRL-secreting pituitary adenoma. This occurs as the pituitary dumps its suppressive dopamine partner so it can live a full life.

Hypothyroidism can also cause increased PRL as TRH also stimulates PRL release.

Drugs include metoclopramide.

If PRL >5000 mU/L - its a bloody prolactin secreting tumour.

Men usually present later as their boobs need to work harder to make milk…so by the time they do their tumour has gotten pretty big.

The person presents with galactorrhoea. Headache and visual field defects if its a pituitary tumour causing it (most likely).

PRL also inhibits GnRH although no-one really knows why. This causes oligo/amenorrhoea and decreased libido, or a floppy one if you’re a guy.

Ix - Check serum PRL. At least 3 measurements.
TFTs to make sure it isnt hypothyroidism
Pituitary MRI to find the ntumour
Pituitary function and visual fields.

Treatment - Get rid of causative drugs
DA agonist - cabergoline (bromocriptine if preggers)
Observe if its just a microadenoma - give DA agnost though!
Transsphenoidal surgical resection is ideal.

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3
Q

What is an endocrine hormone?

A

Hormone produced by ductless glands released directly into the blood

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4
Q

What is an autocrine hormone?

A

A hormone that acts on the cell that itself secreted it

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5
Q

What is a paracrine hormone?

A

A hormone that acts on cells neighboring the cells that secrete it

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6
Q

What is an endocrine hormone?

A

A hormone that acts on distant sites, carried by the blood

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7
Q

What is a phermonal hoormone?

A

A hormone released into the atmosphere

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8
Q

Where are oyxytocin and ADH produced and then stored?

A

Produced in hypothalamus then stored in posterior pituitary gland

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9
Q

What does the pineal gland do?

A

Melatonin: control of body rhythms

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10
Q

Where does the pituitary gland sit

A

Near the optic chiasm in the sella turcica

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11
Q

What does corticotrophin (ACTH) do?

A

Stimulates release of adrenal cortex hormones

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12
Q

What does growth hormone do?

A

Acts on most of our cells - promoted skeletal and muscle growth

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13
Q

What does LH do?

A

ruptures ripe Graafian follicle.

Releases ovarian oestrogens and testicular testosterone

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14
Q

What does FSH do?

A

Promotes follicular growth, and spermatogenesis

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15
Q

What actions does oxytocin have?

A

Stimulates milk release and uterine contractions

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16
Q

What action does vasopressin (ADH) have?

A

Promotes water reabsorption in kidney tubule

17
Q

What do the parafollicular cells embedded in the thyroid produce?

A

They produce calcitonin which acts to inhibit calcium resorption from bone.

These parafollicular cells are so called as they are embedded between the follicles of the thyroid gland

18
Q

What are the 4 pancreatic hormones?

A

1) Insulin - promotes glucose removal from bloodstream
2) Glucagon - increases glucose concentrations in bloodtsream
3) Pancreatic polypeptide - nobody knows what it does
4) Somatostatin: paracrine regulator if insulin and glucagon release?

19
Q

Is the GI tract an endocrine gland?

A

YES! It is actually the largest endocrine gland. Its hormones are mainly peptides:

Cholecystokinin (CCK): releases glucagon, stimulates pancreatic enzymes, contracts gall bladder

Gastric inhibitory peptide: enhances insulin release from pancreas during hyperglycaemia

Gastrin: promotes HCl release, gastric mucosa growth

Gastrin-releasing peptide: release gastrin

Ghrelin: promotes feeding behaviour, stimulates GH release from anterior pituitary

Motilin: contracts upper gut muscles

Neurotensin: function unknown

Secretin: stimulates bicarb release from pancreas and potentiates CCK action

Substance P: function unknown

Vasoactive intestinal peptide (VIP): promotes descending gut relaxation?

20
Q

What hormones does the kidney product?

A

EPO: stimulates RBC production
Renin: enzyme splitting angiotensinogen into angiotensin I

21
Q

What are the 4 ovarian hormones?

A

1) Oestrogens
2) Progesterone
3) Relaxin: a polypeptide that softens the cervix during labour in some animals, promotes water uptake and glycogen synthesis in the uterine myometrium
4) Inhibin: also produced by testis and placenta. It inhibits FSH production

22
Q

Which hormone do fat cells (adipocytes) produce?

A

Leptin. It is important in controlling feeding and energy expenditure. Plays a big role in obesity.

23
Q

What does thyrotoxicosis in children do to their bones?

A

It increases their bone age, resulting in a tall child but they will be small when they reach adulthood: Accelerated growth and early epiphyseal closure (over time)

24
Q

Pathophysiology behind goitre?

A

Stimulation of the TSH receptors of the thyroid by TSH,TSH-receptor antibodies, or TSH receptor agonists, such as chorionic gonadotropin, may result in a diffuse goiter. When a small group of thyroid cells, inflammatory cells, or malignant cells metastatic to the thyroid is involved, a thyroid nodule may develop.

A deficiency in thyroid hormone synthesis or intake leads to increased TSH production. Increased TSH causes increased cellularity and hyperplasia of the thyroid gland in an attempt to normalize thyroid hormone levels. If this process is sustained, a goiter is established. Causes of thyroid hormone deficiency include inborn errors of thyroid hormone synthesis, iodine deficiency,[2] and goitrogens.

A goiter may result from a number of TSH receptor agonists. TSH receptor stimulators include TSH receptor antibodies, pituitary resistance to thyroid hormone, adenomas of the hypothalamus or pituitary gland, and tumors producing human chorionic gonadotropin.