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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
how does radioactive iodine treatment cure Grave's disease
internalised by cells in the thyroid gland --\> isotope decays and injures/destroys cells --\> thyroid cell death --\> reduced thyroxine
25
what are the two amine drugs that can be used for hyperthyroidism and what are their actions
Carbimazole - inhibits thyroid peroxidase propylthiouracil - inhibits thyroid peroxidase and the conversion of T4 to T3
26
what are the side effects of taking thioamine drugs for hyperthyroidism treatment
may cause agranulocytosis may cause hepatotoxicity
27
what does thyroxine bind to
thyroxine binding globulin albumin transthyretin
28
does T3 or T4 have a longer half life
T4
29
what are the proper names for T3 and T4
Liothyronine - T3 Thyroxine - T4
30
explain the volume of distribution and the half life of T4
low volume of distribution and 7 day half life
31
how do you know whether you have given a high enough dose of thyroxine to a patient
you adjust the dose to normalise their TSH levels
32
what is the recommended daily intake for iodine
150micrograms
33
what causes goitre
high production of TSH inducing thyroid cells to proliferate
34
what is the condition called that is due to maternal iodine deficiency
cretinism
35
which isotope of iodine is used for hyperthyroidism treatment
I-131
36
how does iodine act as an antiseptic
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
why is organic iodine not toxic
because organic iodine does not dissociate to free I2
38
how can excessive iodine intake harm the foetus
may develop a goitre themselves so severe as to block the airways and cause suffocation
39
which molecule is associated with increasing iodine deficiency
goitrogens - inhibit iodide uptake in the thyroid
40
which hormones influence whole body regulation of fuel use
insulin glucagon thyroid hormone leptin
41
how do thyroid hormones alter energy levels
- elevates ATP - elevates acetyl-CoA - elevates NADP and NADPH
42
how do thyroid hormones increase mental alertness and basal metabolic rate
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
what is the proportion of the production of T3 and T4
T3 = 20% T4 = 80%
44
what is peroxidase involved in
creates the iodine radicals --\> go and find tyrosine --\> diiodotyrosine --\> T4
45
Does T3 or T4 have a longer half life
T4
46
what happens to the anabolism of thyroid hormones when you have too much iodine
body starts to make reverse iodine (inactive)
47
where is thyroperoxidase found
in the thyroid cell membrane
48
what are the 5 steps of making T3 and T4
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
how is iodine taken up into the thyroid cell in the first place
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
4 options for treatment of hyperthyroidism
- radioactive iodine treatment - antithyroid drug therapy - surgery/thyroidectomy - thyroid arterial embolization
51
where is most of the circulatory T3 made?
in the liver and kidneys (by type 1 deiodinase activity)
52
what is the action of Type 2 deiodinase
makes T3 within the cells of the brain, brown adipose tissue and pituitary
53
clinical signs of hypothyroidism
- dry coarse hair - loss of eyebrow hair - puffy face - goitre - weight gain - constipation - brittle nails
54
what are the clinical signs of hyperthyroidism
- hair loss - bulging eyes - sweating - goitre - rapid heart rate - weight loss - frequent bowel movements - warm, moist palms - tremor of fingers - soft nails
55
which part of the pituitary has a neural link and which has a vascular link to the hypothalamus
post - neural link (outgrowth of brain) ant - vascular link
56
what are the 2 advantages of the hypothalmic-hypophyseal portal system
- less hormone secretion is needed to elicit a given level of response - tropic hormones are transported directly to pituitary to elicit a response
57
what is the infundibulum
the stalk that connects the pituitary to the brain
58
which bone is the pituitary located in
the sphenoid bone
59
2 hormones produced by the posterior pituitary and their functions
ADH/vasopressin = increase CD permeability --\> decrease urine volume oxytocin = milk ejection and uterine contraction
60
what are the 6 hormones produced by the anterior pituitary and which hypothalamic hormones influence them
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
what are the 6 types of cells in the anterior pituitary
corticotrophs --\> ACTH thyrotrophs --\> TSH and prolactin gonadotrophs --\> FSH and LH somatotrophs --\> somatotropin and GH mammotrophs --\> prolactin
62
what is the pathway for cortisol release
hypothalamus releases CRH --\> anterior pituitary --\> ACTH --\> adrenal cortex --\> cortisol
63
the release of TSH via TRH receive afferent information from
temperature receptors in infants
64
the release of TSH via TRH receive integration through which areas of the brain
paraventricular nuclei and neighbouring areas
65
the release of ACTH via CRH receive afferent information through ...
the limbic system reticular formatino hypothalamic and anterior pituitary cells sensitive to circulating blood cortisol suprachiasmatic nucleus
66
the release of ACTH receive integration through which areas of the brain
paraventricular nucleus
67
the release of FSH and LH receive integration through which areas of the brain
preoptic area and others
68
the release of prolactin receive integration through which areas of the brain
arcuate nucleus and others
69
the release of GH receive integration through which areas of the brain
paraventricular nucleus arcuate nucleus
70
what requirements are needed for growth
normal mix of growth influencing hormones - GH, T3 and T4, insulin, sex hormones genetic determinants adequate diet no chronic disease or stressful environment
71
size at birth is determined by
genetics environment nutrition
72
what are the effects of growth hormone
- 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
explain the transport of GH in the blood
half dissolved in plasma and other half bound to a binding protein
74
what makes IGF (somatomedins)
liver and paracrine
75
which hormone is needed to close the epiphyseal plates of long bones
oestrogen
76
what is psychosocial dwarfism
stunted growth due to chronic abuse or neglect
77
What part of the thyroid gland actually produces T3 and T4
the colloid (within the thyroid follicle)
78
where is thyroglobulin contained
within the colloid
79
What produces calcitonin
C cells in the thyroid gland
80
what are the 6 stages of thyroid hormone production
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
what does stress do to thyroid hormones
decreases TRH release --\> reduces T3 and T4
82
in infants.. what does cold stimulate
increase in TRH production
83
what are the half lives of T3 and T4
T3 - 1 day T4 - 6-7 days
84
actions of thyroid hormones
- increase BMR and oxygen consumption --\> calorigenic/heat producing - modulate metabolism - sympathomimetic effects
85
what is the difference of the hormone levels and presentation in primary and secondary hypothyroidism
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
physiological affects of hypothyroidism
decrease BMR and oxygen consumption decreased energy increased weight decreased HR decreased mentation and reflexes, fatigue decreased protein synthesis myxedema
87
what are the hormone levels in primary, secondary and hypersecreting tumour for hyperthyroidism
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
physiological affects of hyperthyroidism
- increased BMR and O2 consumption - weight loss - heat intolerance - increased HR - increased altertness - exopthalmos

Z MD1 Endocrine block (4 decks)

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