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human development - endocrinology Flashcards

1
Q

what are the two types of glands?

A
  • endocrine (inside the body)
  • exocrine (outside the body)
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2
Q

what is the difference between endocrine and exocrine glands?

A
  • endocrine glands are directly released into circulation
  • exocrine glands are released outside of the body, via a duct
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3
Q

what is a hormone?

A
  • a chemical substance
  • secreted without the benefit of a duct
  • acts at long ranges
  • often slowly
  • on distant organs or tissues
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4
Q

what are the types of actions by hormones?

A
  • paracrine (hormone is released and acts upon adjacent cell)
  • autocrine (hormone is released and acts upon the same cell that it was released from)
  • neurocrine (messenger is released from one neurone, to act on the next neurone)
  • endocrine (hormone is secreted directly into the circulation)
  • neuroendocrine (messenger is released from a neurone into the circulation)
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5
Q

what type of hormone action is histamine release from mast cells?

A

paracrine

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6
Q

what type of hormone action is interleukin release?

A

autocrine

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7
Q

what type of hormone action is dopamine inhibition of prolactin release?

A

neuroendocrine

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8
Q

why is the endocrine system important?

A
  • maintains internal environment
  • in response to changes in the external environment
  • important for growth and development, puberty and sexual maturation
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9
Q

what is thyroxine?

A
  • a thyroid hormone
  • derivative of tyrosine
  • with added iodine molecules
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9
Q

what are the catecholamine derivatives of tyrosine?

A
  • adrenaline
  • dopamine
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10
Q

what are the four glycoprotein hormones?

A
  • thyroid stimulating hormone (TSH)
  • follicle stimulating hormone (FSH)
  • luteinising hormone (LH)
  • human chorionic gonadotropin (hCG)
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10
Q

what are glycoprotein hormones made up of?

A
  • alpha (species specific) and beta chain (hormone specific)
  • carbohydrate
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11
Q

what are the three steroid hormones?

A
  • mineralocorticoids (affects water and electrolyte balance)
  • glucocorticoids (affects carbohydrate and protein balance)
  • sex steroids (affects sexual characteristics)
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12
Q

give an example for each type of steroid hormone

A
  • mineralocorticoids (aldosterone)
  • glucocorticoids (cortisol)
  • sex steroids (oestrogen, testosterone, progesterone)
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13
Q

describe the receptor mechanism between adrenaline and protein kinase A

A
  • adrenaline binds to a G protein coupled beta adrenoreceptor
  • this activates adenylyl cyclase
  • this increases intracellular concentrations of cAMP
  • this activates protein kinase A, to provide the catalytic unit which can phosphorylate other enzymes to produce a response
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14
Q

describe the receptor mechanism involving PLC, DAG, IP3 and protein kinase C

A
  • ligand binds to receptor which activates Gq protein
  • this activates PLC, which acts on membrane phospholipids to form DAG and IP3 (second messengers)
  • IP3 binds to endoplasmic reticulum and causes the release of calcium
  • DAG acts on protein kinase C to activate it, which also elevates intracellular calcium concentrations
  • other enzymes become phosphorylated to produce a response
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15
Q

what hormones circulate in free form and bound form?

A
  • catecholamines: free form
  • thyroid hormones: mainly bound form
  • proteins/peptides: mainly free form
  • steroid hormones: mainly in bound form
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16
Q

what is the chain of enzymes to get adrenaline from tyrosine?

A
  • tyrosine
  • DOPA
  • dopamine
  • noradrenaline
  • adrenaline
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17
Q

how are different hormones stored and released?

A
  • catecholamines: stored in secretory granule or vesicle
  • peptide hormones: stored in secretory granule, released via exocytosis due to Ca2+ conc. contents are released while the granule is recycled
  • thyroid hormones: stored in a colloid as part of thyroglobulin
  • steroid hormones: not stored, made from cholesterol which are stored in lipid droplets.
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18
Q

what are the type of releases of hormones?

A
  • pulsatile: episodic release of hormone
  • circadian: based of a 24hr cycle
  • diurnal: synchronised to day/night
  • infradian: based on longer than 24hr cycle
  • seasonal
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19
Q

how are oestrogen and progesterone released in women?

A
  • hypothalamus releases GnRH
  • which acts on anterior pituitary
  • causes releases of FSH and LH to the ovaries
  • FSH causes follicle maturation and the release of oestrogen
  • LH acts on the corpus luteum and causes the release of progesterone
  • both oestrogen and progesterone act in a negative feedback system with the anterior pituitary, to stimulate or inhibit the release of FSH and LH
  • progesterone can also act in a negative feedback system with they hypothalamus to stimulate or inhibit the release of GnRH
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20
Q

how does a pulsatile release of GnRH from the hypothalamus affect FSH and LH?

A
  • releases FSH and LH
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21
Q

how does a sustained release of GnRH from the hypothalamus affect FSH and LH?

A
  • inhibits release of FSH and LH
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22
Q

describe the hormone binding of catecholamines and protein peptides

A
  • largely hydrophilic
  • do not associate with plasma proteins
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23
Q

describe the hormone binding of steroid hormones and thyroid hormones

A
  • lipophilic
  • highly bound to plasma proteins
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24
Q

what is the scientific name for the pituitary gland?

A

hypophysis

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25
Q

what is the pituitary gland divided into?

A
  • anterior lobe (adenohypophysis) contains endocrine hormones
  • posterior lobe (neurohypophysis)
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26
Q

describe the organisation of the hypothalamus and pituitary (supraoptic nucleus)

A
  • nerves in the supraoptic nucleus make contact with capillaries in the portal system (runs from the hypothalamus to the adenohypophysis)
  • neurones release factors into portal system, which stimulate or inhibit release of hormones from endocrine cells
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27
Q

describe the organisation of the hypothalamus and pituitary (paraventricular nucleus)

A
  • nerves in paraventricular nucleus make contact with neurohypophysis)
  • hormones are directly released into blood supply and are carried away by venous drainage
  • to present their effects onto the peripheral system
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28
Q

what is a tropic hormone?

A

a hormone released by an endocrine gland, which acts upon another endocrine gland

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29
Q

what is a trophic hormone?

A

a hormone which stimulates growth in target tissues. they may cause hypertrophy (increase in cell size) or hyperplasia (increase in cell number)

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30
Q

explain the hypothalamic-pituitary axis

A
  • CNS input + other input
  • hypothalamus
  • releasing hormone
  • anterior pituitary
  • tropic hormone
  • peripheral gland (endocrine gland that is not in the nervous system)
  • hormone
  • target
  • effect
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31
Q

how many hormones are produced by the anterior pituitary?

A

6

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32
Q

what hormones are produced by the anterior pituitary?

A
  • FSH (follicle stimulating hormone)
  • LH (leutinizing hormone)
  • TSH (thyroid stimulating hormone)
  • ACTH (adrenocortico tropic hormone)
  • prolactin
  • GH (growth hormone)
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33
Q

what do FSH and LH act upon?

A

testes, ovaries

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34
Q

what does TSH act upon?

A

thyroid gland

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35
Q

what does ACTH act upon?

A

adrenal gland

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36
Q

what does prolactin act upon?

A

mammary glands

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37
Q

what does GH act upon?

A

bones, tissues, liver

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38
Q

what is somatostatin?

A

growth hormone release inhibiting hormone

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39
Q

what is inhibin?

A

a hormone produced by the ovaries, which feed back to the gonadotropes in the anterior pituitary; inhibiting the release of FSH

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40
Q

describe the control of hormone production in males with FSH and LH.

A
  • hypothalamus releases GnRH to the gonadotropes in the anterior pituitary
  • this releases FSH and LH to the testes
  • LH acts on Leydig cells in the testes, which produces testosterone.
  • LH and FSH acts on Sertoli cells, which are involved in spermatogenesis
  • the increase in testosterone inhibits the hypothalamus and anterior pituitary from GnRH, FSH and LH release respectively
  • Sertoli cells produce inhibin which acts upon the anterior pituitary to inhibit the release of FSH and LH
41
Q

when is the secretion of prolactin increased?

A
  • during pregnancy (to promote additional breast development)
  • during lactation (production of milk)
42
Q

what is the prolactin inhibitory factor?

A

dopamine
- acts on D2 receptors to inhibit prolactin release

43
Q

what is the prolactin releasing factor?

A

thyrotropin releasing hormone

44
Q

how is the release of prolactin controlled?

A
  • suckling of the breasts stimulates mechanoreceptors in the nipple
  • this sends signals to the hypothalamus, which inhibits the release of dopamine to the anterior pituitary
  • this means more prolactin is released to the milk gland cells in the breasts, ultimately stimulating milk production.
  • mechanoreceptors sending signals to the hypothalamus also stimulates oxytocin release from the posterior pituitary to the myopepithelial cells in the breasts
  • this ultimately stimulates milk ejection by contraction
45
Q

what is the role of prolactin and oxytocin in milk production?

A

prolactin - stimulates milk gland cells to produce milk

oxytocin - stimulates myoepithelial cells to eject milk through contraction

46
Q

what is hyperprolactinaemia?

A

excess production of prolactin
- causes galactorrhea (excess milk secretion)
- causes gynaecomastia (excess breast growth in both males and females)
- causes infertility

47
Q

how would you treat hyperprolactinaemia?

A
  • D2 agonists
  • bromocriptine
  • cabergoline
48
Q

what effects do growth hormone have on blood glucose levels?

A
  • increases blood glucose levels
  • by having anti-insulin effects
49
Q

what are the actions of growth hormone?

A
  • stimulates growth of long bones until fusion of epiphysis
  • increase in size of viscera
  • anabolic effects of protein
  • catabolic effects on fat and carbohydrates
50
Q

what does hypersecretion of growth hormone cause clinically?

A

hypersecretion:
- gigantism (body grows very tall) before fusion of epiphysis
- acromegaly (abnormally large hands and feet) after fusion of epiphysis

51
Q

what does hyposecretion of growth hormone cause clinically?

A

hyposecretion:
- short stature before fusion of epiphysis
- adult growth hormone deficiency after fusion of epiphysis

52
Q

what are the two posterior pituitary hormones?

A
  • oxytocin
  • arginine vasopressin
  • differ by amino acids 3 and 8
  • both hormones have 2 Cys and disulphide bridge
53
Q

how are oxytocin and arginine vasopressin synthesised?

A
  • neurophysins are precursors in the cell bodies of the supraoptic nucleus and paraventricular nucleus
  • neurophysin 1 is associated with the synthesis of oxytocin
  • neurophysin 2 is associated with the synthesis of arginine vasopressin
54
Q

what is another name for arginine vasopressin?

A

anti-diuretic hormone (ADH)

55
Q

what stimulates the release of arginine vasopressin (ADH)?

A
  • decrease in total body water
  • decrease in blood pressure
  • hyperosmolarity (detected by hypothalamic osmoreceptors)
  • low plasma vol (detected by baroreceptors)
  • angiotensin II
56
Q

what are the actions of arginine vasopressin (ADH)?

A
  • increase in water reabsorption to increase blood volume
  • vasoconstriction to increase systemic vascular resistance
  • these both ultimately cause the increase in blood pressure
57
Q

where is the thyroid located and what does it consist of?

A
  • sits on trachea
  • 2 lobes joined by an isthmus
58
Q

when does the thyroid become an enlarged?

A
  • during pregnancy
  • during lactation
  • in adolescence
  • during later portion of menstrual cycle
59
Q

what is the blood supply to the thyroid gland and where does this originate from?

A
  • superior and inferior thyroid arteries
  • which arise from the external carotid artery and subclavian artery
60
Q

where are parathyroid glands located?

A

embedded between the thyroid glands

61
Q

what is the function of parathyroid glands?

A
  • to produce parathyroid hormone
  • which is involved in Ca2+ metabolism
  • parathyroid hormone is released during low plasma Ca2+ concentration levels
  • to raise Ca2+ concentration levels
62
Q

what are the types of cells in a thyroid gland?

A
  • follicular cell: responsible for making thyroid hormones
  • parafollicular cell/ C cell: involved in Ca2+ metabolism, when Ca2+ concentration in the plasma is high
63
Q

what controls the basal metabolic rate?

A
  • thyroid hormones
64
Q

what is calcitonin?

A

a peptide hormone secreted by parafollicular cells

65
Q

how is the synthesis and release of thyroid hormones regulated?

A
  • hypothalamus releases thyrotropin releasing hormone (TRH)
  • TRH stimulates thyrotrophs in anterior pituitary to release TSH or thyrotropin
  • TSH stimulates thyroid gland to synthesise and release thyroid hormones
66
Q

what protein is the main component of the colloid?

A

thyroglobulin

67
Q

what is actively transported into the follicular cell?

A

iodine via a sodium/iodide transporter

68
Q

what causes oxidation and activation of the iodide inside the follicular cell, at the apical membrane?

A

thyroid peroxidase

69
Q

what is oxidised iodine used for in terms of thyroid hormone synthesis?

A

it is added to tyrosine residues in the thyroglobulin to form thyroid hormones

70
Q

what is T3 and T4?

A
  • T3: tri-iodothyronine
  • T4: thyroxine
71
Q

what type of receptors do thyroid hormones interact with?

A

nuclear receptors

72
Q

how do thyroid hormones enter a cell

A
  • diffusion
  • or specific carrier
73
Q

what happens when T4 (thyroxine) is taken up into cells?

A
  • deionisation into T3, which enters the nucleus and binds to the thyroid receptor
  • thyroid receptor dimerises with retinoid X receptor
  • this binds to thyroid hormone responsive element, which targets gene expression
74
Q

what is hashimoto’s thyroiditis?

A
  • autoimmune disease
  • hypothyroidism
  • one produces antibodies to thyroglobulin or thyroid peroxidase
  • this prevent’s the synthesis of thyroid hormones
  • commonly treated with thyroxine
75
Q

what organ is the adrenal gland associated with?

A

kidney (adrenal gland sits on top of kidney)

76
Q

what are the two portions of the adrenal gland called?

A
  • outer portion: adrenal cortex
  • inner portion: adrenal medulla
77
Q

what are the three layers of the adrenal cortex called?

A
  • zona glomerulosa
  • zona fasciculata
  • zona reticularis
78
Q

what hormones do the adrenal medulla secrete?

A
  • 80% adrenaline
  • 20% noradrenaline
79
Q

what class of hormones does the adrenal cortex secrete?

A

steroid hormones

80
Q

what does the zona glomerulosa lack and what hormone does it secrete?

A
  • lacks 17 alpha hydroxylase
  • secretes aldosterone
81
Q

what does the zona fasciculata lack and what hormone does it secrete?

A
  • doesn’t lack 17 alpha hydroxylase
  • lacks aldosterone synthase
  • secretes cortisol
82
Q

what does the zona reticularis lack and what hormone does it secrete?

A
  • lacks aldosterone synthase
  • secretes androstenedione and DHEA
83
Q

explain the regulation of cortisol synthesis in the adrenal cortex

A
  • hypothalamus secretes corticotropin releasing hormone (CRH)
  • CRH acts on the corticotrophs of the anterior pituitary to secrete adrenocorticotropic hormone (ACTH)
  • ACTH stimulates the adrenal cortex to synthesise and release cortisol
  • cortisol feeds back to the corticotrophs of the anterior pituitary to decrease the release of ACTH and on the hypothalamus, to inhibit release of CRH
84
Q

what receptors does cortisol act upon?

A

glucocorticoid receptors

85
Q

what is a circadian rhythm?

A

24hr cycles that are part of the body’s internal clock. they are physical, mental and behavioural changes
ie. body reaches highest body temp at 7pm

86
Q

what factors stimulate CRH release from the hypothalamus?

A
  • circadian rhythms
  • stress
87
Q

what type of receptor does ACTH act upon?

A
  • melanocortin 2 receptor
  • MC2R (G-protein coupled receptor)
88
Q

what happens when ACTH binds to its MC2R receptor?

A
  • activates adenyl cyclase
  • which increases cAMP levels
  • activates protein kinase A
  • which activates cholesterol ester hydrolase, allowing the release of cholesterol from lipid droplets
  • protein kinase A also stimulates desmolase, the rate limiting step
  • this leads to increased synthesis of cortisol
89
Q

how is cholesterol converted into cortisol?

A
  • cholesterol (after being released from lipid droplets) is taken up by the mitochondrion
  • it is converted into pregnanolone using cholesterol desmolase
  • pregnanolone is transferred to the SER, where it is converted to 11-deoxy-cortisol
  • 11-deoxy-cortisol is taken up by the mitochondrion again and converted into cortisol
  • cortisol is highly lipid soluble, so it then diffuses out of the cell
90
Q

how do steroid hormones lead to an increase in gene transcription?

A
  • due to its lipophilic nature, steroid hormones diffuse into the cell and bind to a cytoplasmic receptor.
  • this causes the dissociation of the heat shock protein on the receptor
  • the hormone-receptor complex dimerises and translocates to the nucleus (steroid hormones can interact with nuclear receptors)
  • the complex binds to a specific hormone responsive element on DNA, which increases mRNA production, and subsequently increases protein synthesis
91
Q

what receptor does cortisol have a higher affinity for?

A

mineralocorticoid receptor > glucocorticoid receptor

92
Q

how is cortisol’s higher affinity for mineralocorticoid receptors managed?

A
  • 11 beta hydroxysteroid dehydrogenase is an enzyme that has two isoforms and can either convert cortisol (active) to cortisone (inactive,) or the other way round
93
Q

where are the two isoforms of 11b-HSD expressed?

A
  • 11b-HSD1 is expressed in the liver, adipose and muscle tissue (converts cortisone into cortisol)
  • 11b-HSD2 is expressed in aldosterone sensitive tissues (converts cortisol into cortisone)
94
Q

what are the adverse effects of glucocorticoids?

A
  • increase in blood glucose
  • hyperglycaemia
  • decrease in bone density
  • osteoporosis
  • suppression of response to infection
  • suppression of endogenous glucocorticoid production
  • iatrogenic Cushing’s syndrome (prolonged exposure to high levels of circulating cortisol)
95
Q

what are the effects of Cushing’s syndrome?

A
  • increased susceptibility to infection
  • increased appetite
  • obesity
  • osteoporosis
  • negative nitrogen balance
  • (may be caused by Cushing’s disease which is a pituitary tumour that leads to increased production of ACTH)
96
Q

what are the effects of aldosterone?

A
  • effects on the distal tubule and collecting duct of the kidney
  • increase number of Na+ channels in the apical membrane
  • increase in Na+/K+ ATPase channels in the basolateral membrane
  • leads to increased Na+/K+ exchange
97
Q

what is spironolactone?

A
  • aldosterone antagonist
  • used as sparing K+ diuretic
98
Q

what is Addison’s disease?

A
  • chronic adrenal insufficiency
  • primary adrenal insufficiency due to destruction of adrenal cortex (unable to produce either cortisol or aldosterone)
  • secondary adrenal insufficiency due to lack of ACTH
99
Q

what are the clinical features present for Addisons’s disease?

A
  • weakness, fatigue, anorexia, weight loss
  • gastrointestinal disturbances
  • hypotension
  • hyperpigmentation
  • salt craving
  • postural symptoms
100
Q

what treatment is available for Addison’s disease?

A
  • replacement therapy with fludrocortisone
101
Q

what is the principle mineralocorticoid secreted from the adrenal gland?

A
  • aldosterone
  • secreted from the zona glomerulosa
  • acts on the renal distal convoluted tubule to promote the retention of sodium and excretion of potassium

from science to clinical practice (5 decks)

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