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1. Human Development > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the activation pathway of protein hormones?

A

Preprohormone moves through ER to become inactive prohormone. Golgi complex transforms this into active compound

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2
Q

How do protein hormones travel through the plasma?

A

Unbound, as they are H2O-soluble

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3
Q

How do protein hormones trigger a cellular response?

A

Bind to surface receptors and activate cAMP second messenger pathway

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4
Q

Where are steroid hormones made?

A

Smooth ER. Steroid glands have a high concentration of smooth ER. Steroid hormones are synthesised on demand

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5
Q

How do steroid hormones travel through the body?

A

Bound to carrier molecules. Extends half life as well

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6
Q

How do steroid hormones trigger a response

A

Enters cell freely or bound, moves to nucleus to bind to hormone response element

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7
Q

What amino acid are amino acid hormones derived from?

A

tryptophan or tyrosine

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8
Q

What hormones does the anterior pituitary release? (6)

A

Prolactin, TSH, FSH, LH, ACTH, GH

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9
Q

What hormones does the posterior pituitary release? (2)

A

Oxytocin, ADH

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10
Q

Where are hormones secreted by the PP synthesised?

A

Hypothalamic supraoptic nuclei and paraventricular nuclei

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11
Q

A primary pathology indicates a problem in what gland?

A

Peripheral endocrine gland

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12
Q

What are examples of peptide hormones? (4)

A

GnRH, GHRH, prolactin, insulin

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13
Q

What are examples of glycoprotein hormones? (4)

A

TSH, LH, FSH, hCG

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14
Q

What are examples of seroid hormones? (5)

A

Aldosterone, cortisol, oestrogen, progesterone, testosterone

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15
Q

What are the five types of hormone release?

A

Pulsitile, cirrcadian, diurnal, infradian, seasonal

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16
Q

What are two different techniques to measure hormone concentration?

A

ELISA and radioimmuniassay

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17
Q

What are the two parts of the anterior pituitary lobe?

A

Pars distalis, pars tuberalis

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18
Q

What are the two parts of the neuro intermediate pituitary lobe?

A

Pars intermedia, pars nervosa

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19
Q

What are the two parts of the posterior pituitary lobe?

A

Pars nervosa, infundibulum

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20
Q

What are the hypothalamic hormones? (7)

A

GnRH, GHRH, CRH, TRH, somatostatin, PRH, prolactin inhibitory hormone

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21
Q

What are the actions of prolactin?

A

In pregnancy promotes additional breast development and milk production

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22
Q

What does hyperprolactinaemia cause (3)?

A

Galactorrhoea, gynaecomastia, infertility in males and females

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23
Q

How is hyperprolactinaemia treated?

A

With D2 agonists bromocriptine or cabergoline

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24
Q

What is the metabolic effect of GH on protein?

A

Anabolic

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25
Q

What is the metabolic effect of GH on fats and carbohydrates?

A

Catabolic

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26
Q

What does hypersecretion of GH cause?

A

Gigantism before fusion of epiphyses. Acromegaly after fusion of epiphyses

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27
Q

What does hyposecretion of GH cause?

A

Adult GH deficiency after fusion of epiphyses. Short stature before fusion of epiphyses

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28
Q

What is the treatment for acromegaly?

A

With D2 agonists bromocriptine or cabergoline. Also long-lasting somatostatin

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29
Q

What is the treatment for small stature?

A

Recombinant hGH (somatropin) or recominant hIGF-1 (mecasermin)

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30
Q

What are the two actions of ADH?

A

Vasoconstriction and increased water re-absorption

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31
Q

What are the actions of oxytocin (3)?

A

Uterine contractions

Milk ejection

Social behaviour

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32
Q

When is the thyroid gland enlarged?

A

During adolescence
During pregnancy
During lactation
During later portion of menstrual cycle

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33
Q

What is the blood supply to the thyroid gland?

A

Superior and inferior thyroid arteries

34
Q

What two cell types make up the thyroid gland?

A 
C cells (secrete calcitonin)
Follicular cells (secrete T3 and T4)
35
Q

How does thyroid hormone cause a feedback mechanism?

A

T3 feeds back on thryotrophs to decrease TSH and to decrease release of TRH from hypothalamus

36
Q

How is thyroid hormone synthesised?

A
  1. Na-I sympoter brings I into the cell and pendrin moved iodine into the follicle
  2. Follicular cell syntheses enzymes and thryoglobulin for colloid
  3. Thyroid peroxidase adds iodine to tyrosine to make T3 and T4
  4. Thyroglobulin is taken back into the cell in vesicles
  5. T3 and T4 are released into bloodstream
37
Q

What is the T1/2 for T4 and T3, respectively?

A

7 and 1 day(s)

38
Q

How does T3 trigger a cellular response?

A

Interacts with nuclear receptors and dimerizes with retinoid X receptor; binds to TRE on DNA

39
Q

What are the effects of thyroid hormone?

A

Increased O2 consumption and heat production
Increased cardiac muscle contractility
Increased sensitivity to catecholamines
Increased gut mobility
Increased erythropoiesis
Increased bone turnover
Increased protein turnover and decreased muscle mass
Increased cholesterol degradation
Increased metabolic turnover of hormones and drugs

40
Q

What are the effects of hyperthyroid secretion?

A 
Nervousness and anxiety
Sweating
Heat intolerance
Palpitations
Fatigue
Weight loss
Tachycardia
Tremor
Thyroid bruit
41
Q

What are the effects of hypothyroid secretion?

A 
Cold intolerance
Weight gain
Constipation
Slow reflexes
Dry skin
Hoarse voice
Slow movements 
Coarse hair and skin
42
Q

What is the cause of Hashimoto’s?

A

Autoimmune disease in which antibodies attach the thyroid gland

43
Q

What is the treatment for hypothyroidism?

A

Thyroxine (T4) - low dose every single day

Liothyronine (sodium salt of T3) - every 2-4 days

44
Q

What is defined as iodine deficiency?

A

Less than 50 micrograms per day

45
Q

What is the dietary iodine requirement?

A

150 micrograms per day

46
Q

What is myxoedema?

A

Swelling of the skin and underlying tissues giving a waxy consistency, typical of patients with underactive thyroid glands

47
Q

What is the common cause of hyperthyroidism?

A

Graves’ disease - autoimmune

48
Q

What is Exophthalmos?

A

Bulging of the eye anteriorly out of the orbit (mucopolysaccharide deposition)

49
Q

What is the treatment for hyperthyroidism?

A

Antithyroid drugs like:

  1. Carbimazole
  2. Propylthiouracil (inhibits thyroid peroxidase)
  3. beta-blockers
  4. Propranolol
  5. Radioiodine (irritates follicular cells)

Treat for 12-18 months

Can also do surgery

50
Q

What are the three zones of the adrenal gland?

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

51
Q

What hormones does zona glomerulosa secrete?

A

Aldosterone

52
Q

What hormones does zona fsciculata secrete?

A

Glucocorticoids

53
Q

What hormones does zona reticularis secrete?

A

Sex hormones

54
Q

What precursor is ACTH derived from?

A

POMC

55
Q

What are the effects of cortisol?

A

decrease cell glucose uptake decrease cell glucose use increase gluconeogenesis decrease protein synthesis increase protein breakdown decrease Ca2+ absorption in gut increase Ca2+ excretion in kidney decrease activity of osteoblasts increase activity of osteoclasts

56
Q

Cortisol has a higher affinity for mineralocorticoid receptors than glucocorticoid receptors. How do aldosterone sensitive tissues remain unaffected by this?

A

11-beta-hydroxysteroid dehydrogenase converts cortisol into inactive cortisone

57
Q

What types of 11-beta-hydroxysteroid dehydrogenases are there?

A

Isoform 1, expressed in liver, adipose and muscle. Converts to cortisol

Isoform 2, expressed in aldosterone sensitive tissue. Converts to cortisone

58
Q

What is Cushing’s syndrome?

A

Prolonged exposure to elevated levels of cortisol or exogenous glucocorticoid drugs

Due to pituitary producing excess ACTH

59
Q

What are the symptoms of Cushing’s syndrome?

A 
Moon face
Thin arms and legs with pendulous abdomen
Thin skin
High BP
Poor wound healing
Red cheeks
Red striation
60
Q

What is the treatment for Cushing’s?

A
  1. Inhibit steroid biosynthesis: metyrapone
    Ketoconazone
  2. Inhibit ACTH release: pasireotide, cabergoline
  3. Inhibition of glucocorticoid receptor: mifeprestone
61
Q

What does aldosterone do?

A

Acts on the distal convoluted tubule to increase sodium reabsorption and increase excretion of potassium

62
Q

What is the key of Addisons?

A

Chronic adrenal insufficiency

Primary -> destruction of adrenal gland
Secondary –> lack of ACTH

63
Q

What are the clinical features of Addisons?

A

Weakness, fatigue, anorexia, weight loss, hyperpigmentation, hypotension

64
Q

What is the main type of thyroid cancer?

A

Papillary thyroid cancer (PTC)

65
Q

What endocrinological disease causes striae?

A

Cushing’s

66
Q

What is Pheochromocytoma?

A

Tumour of adrenal gland resulting in too much EN and NEN

67
Q

How does Pheochromocytoma present?

A

Headaches, palpitations, sense of doom, chest pain, sweating, weightloss

68
Q

How do you diagnose Pheochromocytoma?

A

24 hour urinie catecholamines or metanephrines either 24H or plasma

69
Q

How do you treat Pheochromocytoma?

A

Surgical removal after alpha and beta blockade with phenoxybenzamine and doxazosin

70
Q

What is the most significant clinical feature in Conn’s syndrome?

A

Raised aldosterone

71
Q

Confirmation of primary hyperaldosteronism?

A

Measurement of PRA and aldosterone in salt-replete individuals

Selective venous sampling

72
Q

Treatment of Conn’s?

A

Remove the adenoma and drug treatment (spironolactone, eplerenone)

73
Q

Summarises, what are the diseases with hypo and hyperaldosteronism?

A

Hypo - addisons

Hyper - cushings, Pheochromocytoma, Conn’s

74
Q

Describe the arterial supply to the thyroid gland

A

Arterial supply to the thyroid gland is via the superior and inferior thyroid arteries. These arise from the external carotid and subclavian arteries respectively.

75
Q

what is produced by parafollicular cells?

A

Calcitonin

76
Q

what is produced by follicular cells in the thyroid?

A

Thyroid hormon

77
Q

What happens during suckling, hormone wise?

A

Suckling stimulates production of vasoactive intestinal factor (VIF) in the hypothalamus whilst simultaneously inhibiting dopamine release.

Suckling stimulates paraventricular and supraoptic nuclei in the hypothalamus to produce oxytocin, which travels to the posterior pituitary gland where it is released into the circulation.

78
Q

What does oxytocin do for lactation?

A

Oxytocin stimulates myoepithelial cells to contract, pushing milk into the duct, therefore increasing intramammary pressure. This is also known as the let-down reflex.

79
Q

What is the emergency treatment of Addison’s (Adrenal Crisis)?

A

Supportive therapy
IV fluids
High-dose IV hydrocortisone (100mg QDS)

80
Q

What is the maintenance treatment for Addison’s disease?

A

Mineralocorticoid (fludrocortisone)
Glucocorticoid (hydrocortisone/prednisolone)

[Decreased libido] - dehydroepiandrosterone (DHEA)

1. Human Development (18 decks)

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