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IB physiology > Human Endocrinology > Flashcards

Human Endocrinology Flashcards

1
Q

what is endocrinology?

A

study of hormones

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2
Q

where is most (99%) of the total calcium in the body stored?

A

as calcium phosphate salts in bones.

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3
Q

why is it important that cytoplasmic Ca2+ is very low? (around 0.1μM)

A

provides steep gradient for calcium entry from organelles or extracellular fluids

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4
Q

features of Ca2+ in extracellular fluid

A

only about 0.1% of Ca2+, controlled very precisely (within 10% of 2.4mM)

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5
Q

how is Ca2+ present in plasma found ?

A

40% combined with plasma proteins, 10% is combined with smaller anions (e.g. citrate and phosphate) 50% ionised.

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6
Q

where does extracellular calcium bind?

A

fixed, negative charges on extracellular surface of plasma membranes, altering profile of potential gradient. across membrane without altering size of membrane potential. (surface charge screening)

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7
Q

what is the use of surface charge screening with calcium?

A

stabilises the membranes of excitable cells, more difficult to open ion channels.

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8
Q

what is Hypocalcaemia?

A

extracellular calcium levels drop to around 1.5mM, nervous system becomes progressively more excitable.
- tetanic contraction of muscles.

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9
Q

what can servere hypocalcaemia lead to?

A

tetany of laryngeal muscles leading to asphyxiation

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10
Q

what happens in hypercalcaemia

A

depression of nervous and muscular activity. Calcium salts can begin to precipitate out if levels rise higher than 3mM. e.g. calcium oxalate kidney stones

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11
Q

what chemical messengers does calcium homeostasis involve?

A

parathyroid hormone [1,25(OH)2D] and calcitonin

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12
Q

where does calcitonin and parathyroid hormone target?

A
  • Gut (absorb more or less ca2+)
  • Kidney ( modulate our rate of absorption)
  • Bone (change balance between erosion and deposition)
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13
Q

what can present challenges to calcium homeostasis?

A

pregnancy and lactation, egg-laying, poor absorption (vitamin D3 deficiency) and oxalate poisoning

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14
Q

where is parathyroid hormone (PTH) secreted from and where is this located?

A

parathyroid glands, 4 glands located behind the thyroid.

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15
Q

pattern of PTH release

A

circadian rhythm, released in pulses.

innervated by autonomic nerves, helps modulate rhythms

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16
Q

how many amino acids are in the polypeptides

A

84

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17
Q

what is the only significant external stimulus to promote increased PTH release?

A

decrease in plasma free calcium levels. (low internal calcium levels promotes vesicular release)

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18
Q

what kind of receptors respond to PTH and where are they located?

A

G(q)-protein linked and located on plasma membrane

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19
Q

what is the response to increased free calcium levels in the plasma?

A

increase internal calcium levels.

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20
Q

how does PTH work on the bone, kidney and gut to increase Ca2+ levels? (general)

A

negative feedback system to increase plasma calcium levels.

gut via Vitamin D3

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21
Q

what do osteoblasts do?

A

lay down organic matrix of bone, if they become trapped inside the bone = osteocytes.
both blasts and cytes connect to separate bone fluid (high in calcium and adjacent to bone surface) from ECF.
BOTH HAVE MEMBRANE BOUND PTH RECEPTORS.

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22
Q

What is the matrix of the bone composed of? (and where is calcium involved)

A

collagen and proteoglycans. Calcium phosphate salts precipitate on collagen fibres, forming hydroxyapatite crystals.

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23
Q

what are osteoclasts?

A

multinucleate cells that release proteolytic enzymes and acids to help digest and dissolve the bone for bone remodelling.

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24
Q

what takes place in bone remodelling?

A

bone reabsorption by osteoCLASTS and deposition by osteoBLASTS.

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25
Q

what effects does PTH have on the bone?

A 
osteocytic osteolysis (erosion of bone crystals by osteocytes) where Ca2+ released transfered to ECF. 
- osteoblasts inhibited from laying down more bone and produce a paracrine signal stimulating osteoclasts to erode bone (and progenitor cells to differentiate into more osteoclasts)
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26
Q

how does PTH work on the kidney?

A

increases active reabsorption of calcium by Distal convoluted tubule (DCT)

  • inhibits reabsorption of inorganic phosphate ions in PCT, lowering extracellular phosphate levels.
  • stimulates synthesis of active vitamin D3 derivative.
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27
Q

why does PTH cause net phosphate loss despite phosphate absorption from gut and bone being increased?

A

overwhelmed by increased loss of phosphate in urine.

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28
Q

where is Vitamin D3 (cholecalciferol) sythnesised?

A

keratinocytes (specialised skin cells) from cholesterol. [requires exposure to UVB light]

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29
Q

how can Vitamin D3 be obtained in the diet?

A

from dairy products and fish liver oils. (or D2 from fungal sterol ergosterol)

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30
Q

what are liver stores of D3 used for?

A

maintain consistant level of 25-OHD in the plasma which circulates blood bound to a binding protein.

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31
Q

where is 25-OHD taken up?

A

proximal tubules of kidney, if. under influence of PTH converted to active form [1,25(OH)2D], otherwise converted into an inert form .

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32
Q

what are the roles of active 1,25(OH)2D mediated by and what is its main role? (active Vitamin D)

A

mediated by nuclear receptor, most important effect is to increase Ca2+ absorption from gastrointestinal tract.
[ also has minor roles in promoting bone dissolution]

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33
Q

what can a lack of dietary vitamin D3 cause?

A

children - rickets

adults (after growth plates fuse) - osteomalacia.

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34
Q

where is calcitonin secreted from

A

C-cells (clear cells) in thyroid gland

32 amino acid polypeptide

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35
Q

what are the stimuli for calcitonin secretion?

A

increased plasma Ca2+ (main) and gastrin (helps with anticipatory response)

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36
Q

how does calcitonin reduce plasma ca2+ ?

A

rapidly inhibits absorption of bone by osteoclasts. (favours deposition)

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37
Q

what effect does calcitonin have?

A

stabilises Ca2+ homeostasis when turnover between plasma and bone is unusually high. e.g. growth or lactation.

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38
Q

what is somatotropin ?

A

Growth hormone (GH)

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39
Q

where is GH secreted from?

A

somatotrophs (make up 40% of anterior pituitary gland)

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40
Q

what is GH release stimulated by?

A

growth hormone releasing hormone (GHRH) form hypothalamus and ghrelin from the stomach.

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41
Q

what is GHRH inhibited by?

A

somatostatin. (GH promotes synthesis and release of ; short loop negative feedback)

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42
Q

what dies GHRH inhibit?

A

ITS OWN RELEASE ! (ultra short loop feedback)

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43
Q

how is GH found in plasma ad what is its half life?

A

bound to binding proteins, HL = 20 mins

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44
Q

characteristic of GH release

A

erratic pulses ( blood test won’t tell u much about levels)

45
Q

how do GH levels differ between men and women?

A

Men - large peak in early hours of sleep
women - more irregular but mean level higher then men.
(exercise and metabolic cues can also promote release)

46
Q

GH levels pattern over a life time

A

high in childhood, peak at puberty and declining (but not zero) over period of adult life.

47
Q

what receptors does GH activate?

A

membrane based receptors (pre-existing dimers).

48
Q

what happens once GH activates a receptor?

A

receptor activates JAK-2 (janus kinase 2) ; enzyme in cytoplasm which phosphorylates tyrosine resides on proteins.

49
Q

how is GH release affected by hypoglycaemia?

A

related in response to this and low free fatty acids levels (FFA levels) - can be seen in an overnight fast.

50
Q

why is GH released due to hypoglycaemia and low FFA levels?

A

helps to preserve glucose for brain, switching metabolism of peripheral tissues to use of FFAs.
[EFFECTS ANTAGONISTIC TO INSULIN AND ANALOGUS TO CORTISOL]

51
Q

GH Metabolic actions

A
  • causes adipose to release FFAs
  • stimulates hepatic gluconeogenesis and glucose output
  • acts directly on insulin-sensitive target cells e.g muscles and adipocytes to inhibit glucose uptake (diabetogenic effect)
52
Q

which amino acid in particular stimulates GH release?

A

arginine (but is released in response to high amino acid levels)

53
Q

why is GH released in response to high aa?

A

promotes uptake of aa in muscles cells and chondrocytes (a cell which has secreted the matrix of cartilage and become embedded in it.) INCREASES RATE OF PROTEIN SYNTHESIS
- also promotes cellular growth and differentiation

54
Q

what is the control of growth affected by?

A

many factors - genetic, environmental, gender.

many permissive hormones needed (insulin and thyroid) [permissive as don’t CAUSE growth but are NEEDED)

55
Q

4 different types of dwarfism (deficiencies in growth)

A
  • pituitary dwarfism
  • dwarfism of Sindh
  • Laron syndrome
  • achondroplasia (most common , nothing to do with GH)
56
Q

what can cause excess GH secretion as a child and what does this lead to?

A

over secretion from a pituitary tumour, causing gigantism.

57
Q

what causes the extreme hight in gigantism?

A

overstimulation at growth plates of long bones (due to GH). if GH overstimulation occurs after growth plates fuse, height can not increase further (but periosteal bone growth continues)

58
Q

what is acromegaly?

A

due to periosteal bone growth in gigantism. Anti-insulin effects may lead to form of diabetes.

59
Q

which bones do growth hormones help control the growth of?

A

long bones (e.g. limbs)

60
Q

how do growth hormones help growth of limbs

A

chondrocytes (stimulated by GH) lay down cartilage, which becomes calcified and ultimately ossified - allows bone to elongate in growth plate region.

61
Q

life cycle of chondrocytes in growth plates of bones

A

proliferate, hypertrophy and die as cartilage around them calcifies.

62
Q

zones of growth plate in long bones

A

resting zone, proliferative zone, hypertrophic zone and calcifying cartilage.

63
Q

what hypothesis was founded after observing cartilage from rats when incubated with GH alone?

A

“somatomedin hypothesis”

64
Q

what is the somatomedin hypothesis?

A

most actions of GH on growth are MEDIATED by INSULIN-LIKE GROWTH FACTOR 1 (IGF-1 = Somatomedin)
which is released by the liver in response to GH.

65
Q

why are IGFs names like this?

A

structural similarity to proinsulin

66
Q

how does IGF-1 work?

A

forms part of a negative feedback mechanism - increases somatostatin release by the hypothalamus therefore inhibits GH production by pituitary

67
Q

levels of IGF-1 over a life time in plasma

A

increase with age, peaking at puberty and reducing during adulthood (same as GH)

68
Q

how does IGF-1 circulate and what is its half life

A

bound to plasma binding proteins, (IGFBP1 and IGFBP6), half life of 20 hours (compared to 20 mins of GH)

69
Q

what are the levels of IGF-1 binding proteins controlled by?

A

GH and insulin (hormonal control)

70
Q

what challenges the somatomedin hypothesis?

A
  • if liver derived IGF-1 is knocked out, body growth s normal (Sjogren et al, 1999)
  • GH injection into growth plate stimulates growth in that growth plate alone, if repeated with IGF-1 removed, growth in that plate is not stimulated
71
Q

what is “dual effector hypothesis” ? (came after somatomedin hypothesis)

A

suggests that IGF-1 is produced locally, under the influence of GH.
[GH stimulates chondrocytes from precursors in growth plate and also local formation if IGF-1 which driver further growth]

72
Q

current theory of growth at growth plates in long bones

A

number of endocrine, paracrine and autocrat factors being implicated as promoting intracellular growth regulatory pathways.

73
Q

what is used to dissociated between catabolic and anabolic effects of GH (fed vs fasting)

A

insulin - stimulating IGF-1 production by liver, reducing levels of some IGF binding proteins. (increasing free IGF-1)
- Thyroid hormone and fibroblast growth factor 21 (FGF21) also required.

74
Q

what is the role of fibroblast growth factor 21 (FGF21) ?

A

released from liver when fasting, response to free fatty acid levels, promotes “growth hormone resistance” e.g. by reducing amount of IGF-1 produced in response to GH

75
Q

a combination of which molecules is required to promote growth?

A

high GH, low FGF21, sufficient levels of insulin and thyroid hormone. (GH also promoted by high amino acid etc )

76
Q

why isn’t pituitary growth hormone (GH) required before birth? (in utero)

A

IGF-1 and IGF-2 regulated by other hormones; sommatomammotropins and insulin .

77
Q

what are the 2 regions of the adrenal glands?

A

cortex and medulla. (blood flows through the cortex, draining into veins of medulla)

78
Q

adrenal medulla mechanism for hormone release

A

stimulated by sympathetic preganglonic fibres, chromatin cells release CATECHOLAMINE hormones into circulation.

79
Q

which part of adrenal gland is adrenaline made from and where? (and which enzyme)

A

made from noradrenaline by enzyme PNMT (in medulla of adrenal glands)

80
Q

what kind of hormones does the adrenal cortex secrete?

A

corticosteroid hormones, synthesised by cholesterol.

81
Q

in the human fetes , where in the adrenal gland is androgen DHEA synthesised?

A

fetal zone, once born the outer cortex expands to form 3 zones characteristic of adult gland

82
Q

3 regions of adrenal cortex (from outer to inner)

A

Zona ; glomerulosa, fasciculata, reticularis (GFR)

[remember it by GFR - glomerular filtrate rate, but not linked]

83
Q

what does the zona glomerulosa secrete?

A

aldosterone (=mineralocorticoid due to plasma electrocyte effects)

84
Q

aldosterone effects

A

acts on distal tubule of kidney (+sweat glands, salivary glands and gut) to promote reabsorption of Na+ and secretion of K+
[ also promotes secretion of type A intercalated cells of kidney]

85
Q

factors increasing aldosterone secretion

A

increased plasma potassium ion conc and angiotensin II .

ACTH is also a permissive factor. (deficiency in aldosterone without it)

86
Q

what does the bona fasciculata secrete?

A

glucocorticoids (increase blood sugar levels) e.g. cortisol

87
Q

what is secreted in place of cortisol in some other animals? (e.g. rats)

A

Corticosterone.

88
Q

what does the zona reticularis secrete

A

“weak androgens “ e.g. DHEA (dehydroepiandrosterone)

89
Q

how do weak adrogens affect males and females?

A
  • no significance in males as testes secrete large amounts of strong androgen TESTOSTERONE.
  • account for ~50% of circulating androgens in women.
90
Q

importance of weak androgens in women

A

converted into testosterone and 5-alpha-DHT which are responsible for pubic and axillary hair.
- also promote sexual behaviour and libido in women.

91
Q

what is the role of pro-opiomelanocortin (POMC) located in the corticotrophs of the anterior pituitary ?

A

protein precursor from which polypeptide hormones can be cleaved. e.g. Beta-endorphin and melanocyte stimulating hormone (MSH) [associated with colour change in vertebrates]

92
Q

where is ACTH (adrenocortiocotrophic hormone) derived from? (39 amino acid polypeptide)

A

POMC (in anterior pituitary)

93
Q

HPA (hypothalamic pituitary adrenal) axis mechanism to stimulate release of ACTH

A

hypothalamus releases corticotropin-releasing hormone (CRH) stimulating corticotrophs in anterior pituitary to release ACTH

94
Q

what can augment ACTH release during times of stress?

A

ADH

95
Q

what is the effect of ACTH on adrenal CORTEX?

A

stimulatory effect, increases size of cortical cells, needed for normal cortical function.
- Stimulates synthesis and secretion of CORTISOL

96
Q

What molecules are used in negative feed back loops for HPA axis?

A

cortisol and ACTH

97
Q

cortisol release pattern

A

pulses (follows pulsatile release of ACTH)

- follows circadian rhythm, large surge in hours just before waking up.

98
Q

how is cortisol transported around the body and what is its half life?

A

bound to cortisol binding globulin (GBG), half life = 70 mins

99
Q

how does cortisol work? (steroid hormone )

A

binds to cytoplamsic receptor, moves to nucleus to regulate gene expression. (takes hours/days to have an effect)

100
Q

what is physiological stress?

A

anticipation, justified or not, that a challenge to homeostasis looms

101
Q

example of a stressor met my a specific endocrine response

A

hypocalcaemia and PTH

102
Q

stages of “general adaptation syndrome’ invoked by stressors

A
  • ALARM REACTION; sympathetic response as well as HPA axis, Glucocorticoids released.
  • RESISTANCE STAGE; homeostasis is restored (but can have different set points)
  • STAGE OF EXHAUSTION; detrimental effects of chronic stress due to chronically elevated levels of glucocorticoids
103
Q

what is the use of cortisol release in response to hypoglycaemia ?

A

has a glucocorticoid role, important in long term control

104
Q

actions of cortisol in its glucocorticoid role

A
  • breaks down muscle plasma proteins to be used in gluconeogenesis
  • amino acids to glucose stimulated in liver (enzymes)
  • inhibits glucose uptake by muscle and adipose tissue (conserving for brain)
  • promotes FFA release from adipose tissue (directly and permissive as allows adrenaline and GH to have effect)
105
Q

what can happen in humans with a deficiency in both GH and ACTH during strenuous exercise or starvation?

A

fatal hypoglycemia. - Cortisol therefore essential

106
Q

how does cortisol affect the inflammatory process?

A

inhibits many components.

107
Q

how does acute stress affect HPA axis?

A

early activation of some components of immune system but sustained HPA axis activation results in immunosuppression

108
Q

other effects of cortisol (not glucocorticoid role or stress response)

A
  • secreted by fatal adrenal gland for fatal maturation
  • smooth muscle to respond to noradrenaline, adrenaline and angiotensin II
  • affecting mood (jet lag circadian rhythm is set out of cortisol)
  • suppress reproductive function
  • inhibition of bone formation and college synthesis
109
Q

why is it important that distal tubule cells express an enzyme that degrades cortisol? what can this enzyme be inhibited by?

A
  • aldosterone receptor has some affinity for cortisol and cortisol is found in greater concentrations.
  • Glycyrrhetinic acid inhibits it - found in liquorice root
    (will cause you to reabsorb too much Na+, leading to hypertension.)

IB physiology (4 decks)

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