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MRCPCH > Endocrinology and Growth > Flashcards

Endocrinology and Growth Flashcards

1
Q

Major drivers of growth in infancy?

A

nutrition and insulin

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2
Q

Major drivers of growth in childhood?

A

growth hormone and thyroxine

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3
Q

Major drivers of growth in puberty?

A

Sex steroids and growth hormone

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4
Q

Effects of PTH on bone?

A

Binds to osteoblasts which signal to osteoclasts to cause resorption of bone and release calcium.

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5
Q

Effects of PTH on kidneys?

A

Active reabsorption of Ca and Mg from the distal convoluted tubule. Decreases reabsorption of PO4.

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6
Q

Effects of PTH on intestine (via kidneys)?

A

Increases intestinal calcium absorption by increasing activated vitamin D. Activated vitamin D increases calcium absorption.

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7
Q

Definition of PCOS?

A

at least two of the following:
(Rotterdam criteria):
- Polycystic ovaries (more than 12 cysts)
- Oligo-ovulation or anovulation
- Hyperandrogenism (clinical or biochemical)

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8
Q

Symptoms of PCOS?

A
  • Oligomenorrhoea (defined as <9 periods per year)
  • Infertility, subfertility
  • Acne, oily skin, increased skin pigmentation
  • Hirsutism, male pattern baldness or alopecia
  • Obesity or difficulty losing weight
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9
Q

How can metformin help in PCOS?

A 
Reduce insulin resistance
Fall in serum androgens
Induce ovulation
Fall in LH
Reduction in weight
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10
Q

What does LH and FSH do in males?

A

LH stimulates the testes -> testosterone.

FSH (and testosterone) causes the testes to produce sperm.

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11
Q

First sign of puberty?

A

enlargement of the testes (once they reach 4 ml, puberty has commenced)

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12
Q

Testicular size denoting commencement of puberty?

A

4mL

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13
Q

Stages of puberty?

A

enlargement of the testes -> lengthening of the penis -> pubic hair -> ejaculation/ facial hair

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14
Q

Brown-Sequard Syndrome features?

A
  • ipsilateral spastic paralysis (corticospinal tract)
  • ipsilateral loss of proprioception and vibration (dorsal column)
  • contralateral loss of pain and temperature sensation (spinothalamic tract)
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15
Q

Effect of cortisol on BP?

A

Increases BP: permits normal response to angiotensin II and catecholamines by up-regulating a1 receptors on arterioles

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16
Q

Effect of cortisol on bone?

A

Inhibits bone formation: decreases osteoblasts, decreases type 1 collagen, decreases absorption of calcium from the gut, increases osteoclastic activity

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17
Q

Most common cause of primary adrenal insufficiency?

A

80 % due to autoimmune destruction (Addison’s disease)

Other causes: congenital adrenal hyperplasia, adenoma, or idiopathic

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18
Q

Most common cause of secondary adrenal insufficiency?

A

exogenous steroid use -> impairment of pituitary/ hypothalamus

other causes: pituitary adenoma, hypothalamic tumors, surgical damage, and Sheehan’s syndrome (maternal ischemic necrosis related to childbirth)

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19
Q

autosomal recessive condition: obesity, retinitis pigmentosa, polydactyly, hypogonadism, and kidney failure

A

Bardet-Biedl syndrome

children lose their vision by adolescence or early childhood

20
Q

complications of thyroidectomy?

A
  • postop haemorrhage and haematoma formation, this can rapidly compress the airway
  • recurrent laryngeal n palsy -> hoarse voice
  • hypoparathyroidism + low Ca due to removal/ damage of parathyroids
21
Q

most common cause of thyroid problems?

A

autoimmunity.

Graves/ Hashimotos

22
Q

What drug can cause thyrotoxicosis?

A

amiodarone

23
Q

What is Riedel thyroiditis?

A

fibrous tissue replacing the normal thyroid parenchyma

causes a painless goitre + hypothyroidism

24
Q

What drugs may cause hypothyroidism?

A

Lithium, Amiodarone

25
Q

Most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

26
Q

Effects of thyroid dysfunction on periods?

A

hypothyroid - menorrhagia

hyperthyroid - oligomenorrhoea

27
Q

Neurological symptoms of hypothyroidism?

A

Decreased deep tendon reflexes

Carpal tunnel syndrome

28
Q

Most common antibodies in Hashimoto’s?

A

anti-Thyroid Peroxidase

29
Q

Most common antibodies in Grave’s disease?

A

TSH receptor antibodies

Thyroglobulin antibodies

30
Q

Mx of thyrotoxicosis?

A

dependent on underlying cause.

Propranolol: to control thyrotoxic symptoms such as tremor

Carbimazole: blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production. (SE: Agranulocytosis)

Radioiodine treatment

31
Q

What is an arrhenoblastoma?

A

rare types of ovarian tumours which most often secrete testosterone -> virilisation of girls

as well as some oestrogen -> precocious puberty.

32
Q

Tx of GnRH-dependent precocious puberty?

A

GnRH agonist

33
Q

most common enzyme deficiency in congenital adrenal hyperplasia?

A

21-hydroxylase deficiency (90% of cases)

-> cortisol deficiency and sometimes an associated aldosterone deficiency and androgen excess

34
Q

2nd most common enzyme deficiency in congenital adrenal hyperplasia?

A

11-beta-hydroxylase

35
Q

features of salt-losing congenital adrenal hyperplasia?

A

Due to aldosterone deficiency, seen in the first few weeks of life as an adrenal crisis

Females have ambiguous external genitalia

36
Q

features of non salt-losing congenital adrenal hyperplasia?

A

Presents during childhood with low glucocorticoids and high androgens

Males present with virilisation age 2-4 years
females - ambiguous external genitalia

37
Q

Characteristics of McCune-Albright Syndrome?

A

At least 2 of 3:
1. polyostotic fibrous dysplasia (fibrous tissue in bones)

  1. café-au-lait spots
  2. autonomous endocrine hyperfunction (eg, gonadotropin-independent precocious puberty)
    +/- hyperthyroidism, acromegaly, and Cushing syndrome.
38
Q

Venous drainage of the adrenals?

A

R adrenal drains directly into IVC

L adrenal drains into L renal vein

39
Q

Physical features of Turner’s syndrome?

A
  • Lymphoedema and rocker bottom feet at birth
  • Short stature
  • Webbed neck
  • Broad chest
  • Less common: multiple naevi, poorly developed nails, ptosis, low hairline
40
Q

Cardiac associations of Turner’s Syndrome?

A
  • most frequently coarctation of the aorta
    aortic dissection
    bicuspid aortic valve
    hypertension.
41
Q

Endocrine features of Turner’s Syndrome?

A

relating to gonadal dysgenesis:
Amenorrhoea
Dlayed or absent puberty
Infertility

42
Q

Mx of Turner’s Syndrome?

A

Growth Hormone to initiate puberty.

Once satisfactory growth and development has been achieved, GH stopped and oestrogen started.
Progesterone is added at the time of puberty to induce withdrawal bleeds.

43
Q

Features of 17-hydroxylase deficiency?

A

congenital adrenal hyperplasia:

  • non-virilising in females
  • inter-sex in boys
  • hypertension
44
Q

Features of 11-beta hydroxylase deficiency?

A

congenital adrenal hyperplasia:

  • virilisation of female genitalia
  • precocious puberty in males
  • hypertension
  • hypokalaemia
45
Q

Where is testosterone produced?

A

Leydig cells.

small amounts produced in the adrenal glands.

MRCPCH (27 decks)

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