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Z MD1 Endocrine block > HPA and thyroid > Flashcards

HPA and thyroid Flashcards

0
Q

difference between autocrine and paracrine signalling

A

autocrine - self-regulating hormone paracrine - acts on neighbouring cells

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1
Q

8 hormones produced by the pituitary

A

post - oxytocin and ADP ant - prolactin, GH, ACTH, TSH, FSH, LH

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2
Q

what are the 3 major groups of neurohormones

A

hypothalamus –> anterior pituitary hypothalamus –> posterior pituiatry catecholamines (made by modified adrenal medulla neurons)

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3
Q

what is the definition of a tropic hormone

A

a hormone that controls the secretion of another hormone

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4
Q

which types of hormones are hydrophilic and hydrophobic

A

hydrophilic - peptide hormones, catecholeamines hydrophobic - steroid hormones, thyroid hormones

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5
Q

explain the synthesis and storage of peptide hormones, steroid hormones, catecholamines and thyroid hormones

A

peptide hormones and thyroid hormones and catecholeamines - made in advance and stored in vesicles steroid hormones - synthesised on demand from precursors

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6
Q

which hormone types are bound to carrier proteins

A

steroid hormones and thyroid hormones

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7
Q

what are the two hormone groups of amines

A

catecholeamines and thyroid hormones

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8
Q

what 4 factors can influence the plasma hormone concentration?

A
  • the hormones rate of secretion by the endocrine gland - rate of metabolic activation - extent of binding to plasma proteins - rate of metabolic inactivation and excretion
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9
Q

what are the hormone removal systems

A

steroids - conjugation –> urine and bile amines - specific circulating degrading enzymes large peptides - receptor-mediated endocytosis small peptides - kidneys

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10
Q

what is a permissive hormonal affect

A

hormone cannot exert effects without the presence of a second hormone

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11
Q

what is the difference between a primary and secondary endocrine disorder

A

primary - gland is abnormal secondary - normal gland but abnormal tropic hormone action of activity

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12
Q

what are the 4 things that affect GH secretion

A

ghrelin and GHRH - stimulatory somatostatin and IGF-1 - inhibitory

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13
Q

explain GH insensitivity and what are the levels of hormones involved

A

where GH doesnt properly elicit the release of IGF-1 (high GH and low IGF-1)

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14
Q

why can you only give someone GH intravenously and not orally?

A

because it is a peptide hormone and therefore is metabolised and degraded when orally administered

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15
Q

action of ghrelin in the HPA

A

enhances the effect of GH release by GHRH

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16
Q

how does ghrelin and GHRH stimulate GH release

A

GHRH = elevates cAMP ghrelin = elevates Ca2+ –> both pathways linked to the same output

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17
Q

what are the physical signs of excess GH

A

large nose, lips, jaw, ears, hands and feet out of proportion to the body (acromegaly)

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18
Q

what are the treatment options for a patient with excessive GH

A
  • remove tumour (if relevant) - reduce GH release through somatostatin analogues or dopamine agonist - inhibit GH action through GH antagonist or pegvisomant
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19
Q

why do we use somatostatin analogues (and not just somatostain) when treating excessive GH

A

somatostatin has a very short half life due to enzymatic cleavage and renal elimination - add in D-amino acids which make them more resistant to enzymatic cleavage

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20
Q

what are 2 drugs names that are somatostatin analogues

A

octreotide lanreotide

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21
Q

explain the structure of the GH anatagonists

A

have a different amino acid at position 119 (usually a glycine) - interferes with tyrosine kinase dimerisation –> therefore no receptor activation - competes with normal GH

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22
Q

why do we pegylate GH antagonists

A
  • increases the size –> reduces renal filtration - improves solubility - decreases accessibility for proteolytic enzymes
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23
Q

what is pegvisomant

A

PEGylated GH antagonist with a long half life and adequate affinity

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24
Q

how does radioactive iodine treatment cure Grave’s disease

A

internalised by cells in the thyroid gland –> isotope decays and injures/destroys cells –> thyroid cell death –> reduced thyroxine

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25
Q

what are the two amine drugs that can be used for hyperthyroidism and what are their actions

A

Carbimazole - inhibits thyroid peroxidase propylthiouracil - inhibits thyroid peroxidase and the conversion of T4 to T3

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26
Q

what are the side effects of taking thioamine drugs for hyperthyroidism treatment

A

may cause agranulocytosis may cause hepatotoxicity

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27
Q

what does thyroxine bind to

A

thyroxine binding globulin albumin transthyretin

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28
Q

does T3 or T4 have a longer half life

A

T4

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29
Q

what are the proper names for T3 and T4

A

Liothyronine - T3 Thyroxine - T4

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30
Q

explain the volume of distribution and the half life of T4

A

low volume of distribution and 7 day half life

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31
Q

how do you know whether you have given a high enough dose of thyroxine to a patient

A

you adjust the dose to normalise their TSH levels

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32
Q

what is the recommended daily intake for iodine

A

150micrograms

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33
Q

what causes goitre

A

high production of TSH inducing thyroid cells to proliferate

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34
Q

what is the condition called that is due to maternal iodine deficiency

A

cretinism

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35
Q

which isotope of iodine is used for hyperthyroidism treatment

A

I-131

36
Q

how does iodine act as an antiseptic

A

it is a potent oxidiser - reacts in electrophilic reactions with enzymes of the respiratory chain of microbes as well as with amino acids located in cell membranes and cell wall proteins –> cell integrity destroyed

37
Q

why is organic iodine not toxic

A

because organic iodine does not dissociate to free I2

38
Q

how can excessive iodine intake harm the foetus

A

may develop a goitre themselves so severe as to block the airways and cause suffocation

39
Q

which molecule is associated with increasing iodine deficiency

A

goitrogens - inhibit iodide uptake in the thyroid

40
Q

which hormones influence whole body regulation of fuel use

A

insulin glucagon thyroid hormone leptin

41
Q

how do thyroid hormones alter energy levels

A
  • elevates ATP - elevates acetyl-CoA - elevates NADP and NADPH
42
Q

how do thyroid hormones increase mental alertness and basal metabolic rate

A

proteins of oxidative phosphorylation are upreglated so more ATP is made –> increases the rate of protein synthesis - elevate number of catecholamine (adrenaline) receptors - enhancing catecholamine effects - stimulate the differentiation of brown adipose tissue to generate heat

43
Q

what is the proportion of the production of T3 and T4

A

T3 = 20% T4 = 80%

44
Q

what is peroxidase involved in

A

creates the iodine radicals –> go and find tyrosine –> diiodotyrosine –> T4

45
Q

Does T3 or T4 have a longer half life

A

T4

46
Q

what happens to the anabolism of thyroid hormones when you have too much iodine

A

body starts to make reverse iodine (inactive)

47
Q

where is thyroperoxidase found

A

in the thyroid cell membrane

48
Q

what are the 5 steps of making T3 and T4

A

1) iodide is oxidised to a chemically reactive form by thyroperoxidase 2) iodine reacts with tyrosines in the protein thyroglobulin 3) iodinated tyrosines on the surface of thyroglobulin are enzymically condensed by thyroperoxidase 4) modified thyroglobulin taken up into the thyroid cell 5) peptide links are hydrolysed –> liberating free amino acids, diiodotyrosine and T3 and T4

49
Q

how is iodine taken up into the thyroid cell in the first place

A

TSH acts on its receptor which is an adenylate cyclase –> this activates cAMP –> activates NIS (sodium iodide symporter) –> takes up Iodine and Na ions (gradient for Na/I pump maintained by Na/K ATPase)

50
Q

4 options for treatment of hyperthyroidism

A
  • radioactive iodine treatment - antithyroid drug therapy - surgery/thyroidectomy - thyroid arterial embolization
51
Q

where is most of the circulatory T3 made?

A

in the liver and kidneys (by type 1 deiodinase activity)

52
Q

what is the action of Type 2 deiodinase

A

makes T3 within the cells of the brain, brown adipose tissue and pituitary

53
Q

clinical signs of hypothyroidism

A
  • dry coarse hair - loss of eyebrow hair - puffy face - goitre - weight gain - constipation - brittle nails
54
Q

what are the clinical signs of hyperthyroidism

A
  • hair loss - bulging eyes - sweating - goitre - rapid heart rate - weight loss - frequent bowel movements - warm, moist palms - tremor of fingers - soft nails
55
Q

which part of the pituitary has a neural link and which has a vascular link to the hypothalamus

A

post - neural link (outgrowth of brain) ant - vascular link

56
Q

what are the 2 advantages of the hypothalmic-hypophyseal portal system

A
  • less hormone secretion is needed to elicit a given level of response - tropic hormones are transported directly to pituitary to elicit a response
57
Q

what is the infundibulum

A

the stalk that connects the pituitary to the brain

58
Q

which bone is the pituitary located in

A

the sphenoid bone

59
Q

2 hormones produced by the posterior pituitary and their functions

A

ADH/vasopressin = increase CD permeability –> decrease urine volume oxytocin = milk ejection and uterine contraction

60
Q

what are the 6 hormones produced by the anterior pituitary and which hypothalamic hormones influence them

A

prolactin - PRF (stim) and dopamine (inh) GH - GHRH (stim) and somatostatin (inh) TSH - TRH (stim) ACTH - CRH (stim) LH - GnRH (stim) FSH - GnRH (stim)

61
Q

what are the 6 types of cells in the anterior pituitary

A

corticotrophs –> ACTH thyrotrophs –> TSH and prolactin gonadotrophs –> FSH and LH somatotrophs –> somatotropin and GH mammotrophs –> prolactin

62
Q

what is the pathway for cortisol release

A

hypothalamus releases CRH –> anterior pituitary –> ACTH –> adrenal cortex –> cortisol

63
Q

the release of TSH via TRH receive afferent information from

A

temperature receptors in infants

64
Q

the release of TSH via TRH receive integration through which areas of the brain

A

paraventricular nuclei and neighbouring areas

65
Q

the release of ACTH via CRH receive afferent information through …

A

the limbic system reticular formatino hypothalamic and anterior pituitary cells sensitive to circulating blood cortisol suprachiasmatic nucleus

66
Q

the release of ACTH receive integration through which areas of the brain

A

paraventricular nucleus

67
Q

the release of FSH and LH receive integration through which areas of the brain

A

preoptic area and others

68
Q

the release of prolactin receive integration through which areas of the brain

A

arcuate nucleus and others

69
Q

the release of GH receive integration through which areas of the brain

A

paraventricular nucleus arcuate nucleus

70
Q

what requirements are needed for growth

A

normal mix of growth influencing hormones - GH, T3 and T4, insulin, sex hormones genetic determinants adequate diet no chronic disease or stressful environment

71
Q

size at birth is determined by

A

genetics environment nutrition

72
Q

what are the effects of growth hormone

A
  • metabolic - increase blood FAs and glucose (anti-insulin effects) - soft tissue and skeleton - hyperplasia and hypertrophy on soft tissues and skeleton - increased protein synthesis - increase IGFs from liver
73
Q

explain the transport of GH in the blood

A

half dissolved in plasma and other half bound to a binding protein

74
Q

what makes IGF (somatomedins)

A

liver and paracrine

75
Q

which hormone is needed to close the epiphyseal plates of long bones

A

oestrogen

76
Q

what is psychosocial dwarfism

A

stunted growth due to chronic abuse or neglect

77
Q

What part of the thyroid gland actually produces T3 and T4

A

the colloid (within the thyroid follicle)

78
Q

where is thyroglobulin contained

A

within the colloid

79
Q

What produces calcitonin

A

C cells in the thyroid gland

80
Q

what are the 6 stages of thyroid hormone production

A
  1. follicular cell synthesizes enzymes and thyroglobulin for colloid 2. a Na-I symporter brings in I into the cell. Pendrin transporter moves I- into the colloid 3. enzymes add iodine to tyrosine to make T3 and T4 4. thyroglobulin is taken back into the cell in vescles 5. I/C enzymes separate T3 and T4 from the protein 6. free T 3 and T4 enter the circulation
81
Q

what does stress do to thyroid hormones

A

decreases TRH release –> reduces T3 and T4

82
Q

in infants.. what does cold stimulate

A

increase in TRH production

83
Q

what are the half lives of T3 and T4

A

T3 - 1 day T4 - 6-7 days

84
Q

actions of thyroid hormones

A
  • increase BMR and oxygen consumption –> calorigenic/heat producing - modulate metabolism - sympathomimetic effects
85
Q

what is the difference of the hormone levels and presentation in primary and secondary hypothyroidism

A

primary - T3 and T4 is low while TSH is high with a goitre secondary - T3 and T4 and TRH+/-TSH low with no goitre

86
Q

physiological affects of hypothyroidism

A

decrease BMR and oxygen consumption

decreased energy

increased weight

decreased HR

decreased mentation and reflexes,

fatigue

decreased protein synthesis

myxedema

87
Q

what are the hormone levels in primary, secondary and hypersecreting tumour for hyperthyroidism

A

primary - high T3 and T4 with low TSH - goitre secondary - high T3 and T4 with high TRH+/-TSH - goitre tumour - high T3 and T3 and low TSH - no goitre

88
Q

physiological affects of hyperthyroidism

A
  • increased BMR and O2 consumption - weight loss - heat intolerance - increased HR - increased altertness - exopthalmos

Z MD1 Endocrine block (4 decks)

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