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Paediatrics > Ch8 Endocrinology > Flashcards

Ch8 Endocrinology Flashcards

1
Q

Where are corticosteroids made?

A

Zona fasciulata of the adrenal cortex

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2
Q

How much cortisol does the body secrete per day?

A

15-25mg/day (basal levels) and 250-300mg/day during stress

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3
Q

What is the half-life of cortisol?

A

90 mins

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4
Q

What is the HPA control for cortisol?

A

Hypothalamus (CRH) > Pituitary (ACTH) > Adrenal (Cortisol)

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5
Q

What is Addison’s disease?

A

Primary adrenal insufficiency

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6
Q

What is a normal physiological corticosteroid replacement?

A

Hydrocortisone 20mg OM and 10mg ON

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7
Q

Are hydrocortisone and cortisol the same?

A

Yes

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8
Q

What are the equivalent steroid doses to 20 mg hydrocortisone?

A

Prednisolone 5 mg; Methylprednisolone 4 mg; Dexamethasone 0.75 mg;

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9
Q

What are the symptoms of adrenal insufficiency?

A

Fatigue, weakness, arthralgia, anorexia, nausea, hypotension, hypoglycaemia, low Na, high K and addisonian crisis.

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10
Q

How can the basal adrenal function be monitored?

A

Morning cortisol levels

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11
Q

What are the s/e of steroids?

A

CVS - hypertension / low K / high Na Endo - HPA suppression, cushingoid features, stunted growth, high BMs GI - Ulcers and pancreatitis Glaucoma / cataracts Poor wound healing AVN, osteoporosis and muscle weakness Haem - immunosuppression and hypercoagulability

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12
Q

What is the best test for hypocortisolism?

A

8am cortisol

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13
Q

What are the features of Addisonian crisis?

A

Confusion, lethargy, weakness, postural hypotension, hyperthermia, low glucose, high K and low Na.

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14
Q

What is the treatment of Addisonian crisis?

A

100mg IV hydrocortisone stat; followed by 50gm QDS IV fluid resuscitation and correction of electrolyte disturbances

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15
Q

When should mineralocorticoids be administered in adrenal insufficiency?

A

Primary adrenal insufficiency (i.e. when the adrenal gland is destroyed) and not secondary such as with pituitary disease

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16
Q

How can primary and secondary hypothyroidism be distinguished?

A

In primary there is a high TSH whilst in secondary there is a low TSH

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17
Q

What are the anaesthetic complications related to operating on a patient with hypothyroidism?

A

Poor wound healing and cardiac complications

18
Q

What is Schmidt syndrome?

A

Hypothyroidism associated with immune mediated destruction of the adrenal gland

19
Q

What is the treatment for hypothyroidism and adrenal insufficiency?

A

Hydrocortisone 400mg IV over 24 hours before thyroid replacement as this may precipitate an adrenal crisis

20
Q

What are the features of myxoedema coma?

A

Unresponsiveness, hypotension, bradycardia and hypothermia

21
Q

What is the treatment for myxoedema coma?

A
  1. Hydrocortisone 400mg IV over 24 hours (this will correct the electrolyte abn)
  2. Thyroid replacement with 500mcg levothyroxine
  3. IV glucose
  4. IV fluids / warming
22
Q

How does the posterior pituitary gland develop embryologically?

A

This is an evagination of the ventral diencephalon (infundibulum) - these are neural crest cells = neuroectoderm

23
Q

How does the anterior pituitary gland develop embryologically?

A

From the Rathke’s pouch, which is epithelial (ectodermal) tissue from the roof of the mouth. The Rathke’s pouch detachs to form a vesicle which then migrates to form the anterior pituitary

24
Q

What is the median eminance?

A

The recess in the floor of the third ventricle due to the infundibulum aka infundibular recess

25
Q

What is caused by the failure of the separation of the Rathke’s pouch?

A

Craniopharyngeal duct, which can be the source of recurrent meningitis

26
Q

What forms from the anterior portion of Rathke’s pouch?

A

Pars distalis

27
Q

What forms from the posterior portion of Rathke’s pouch?

A

Pars intermedius

28
Q

What is the pars tuberalis of the pituitary gland?

A

The extension of the anterior pituitary gland that wraps around the base of the pituitary stalk

29
Q

Where are remnants of Rathke’s pouch (rathke’s cleft) found?

A

Pars intermedius

30
Q

What type of circulation does the pituitary gland have?

A

Portal

31
Q

Where are hypothalamic hormones released?

A

From neurones in the tuber cinereum that are conveyed to the median eminence of the pituitary stalk via the tuberohypophysial tract. The hormones are released into capillaries of the hypophyseal portal circulation which are transported to the anterior pituitary

32
Q

Where are posterior pituitary hormes synthesized?

A

Magnocellular neuroendocrine neurones in the supraoptic and paraventricular nuceli of the hypothalamus. These pass through the supra-optic hypophyseal tract to the posterior pituitary via the pituitary stalk

33
Q

What is POMC?

A

Proopiomelanocortin - precursor to ACTH, MSH, lipotropin, beta-endorphin and met-enkephalin

34
Q

How is prolactin release from the ant. pituitary controlled?

A

Under dopaminergic inhibition from the hypothalamus. Release is pulsatile with peak at 6 am. Other inhibitory factors are TRH and VIP (vasoactive intestinal peptide).

35
Q

What protein is released in response to GH?

A

IGF-1 (insulin like growth factor 1) is secreted by the liver

36
Q

What hormone suppresses GH release?

A

Somatostatin suppresses release only and does not affect synthesis of GH

37
Q

Where does GH act?

A

Directly on the epiphyseal endplates to stimulate chondrocyte proliferation

38
Q

What hormones stimulate GH release?

A

GHRH and Ghrelin

39
Q

What hormones control TSH release?

A

TRH stimulates and Somatostatin inhibits

40
Q

What controls ADH release?

A

Increase in Serum Osmolality causes ADH release (which results in water reabsorption from the collecting duct). ADH is also a vasoconstrictor.

Paediatrics (13 decks)

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