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Gastro nutrition > Endocrine non pancreas > Flashcards

Endocrine non pancreas Flashcards

1
Q

Describe the size and relations of the pituitary gland?

A
  • 500mg gland suspended from the infundibulum bounded by the walls of the sella turcica in the pituitary fossa of the sphenoid bone
  • Relations
    ◦ Sella tucica is the anterior, posterior and inferior limit, the diaphragmasellae above which lays the optic chiasm is the superior limit. Infundibilum extends through central aperture of this roof
    ◦ Anterior to sella turcica is the optic chiasm, posterior is the mammilary bodies
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2
Q

What is the blood supply of the pituitary gland?

A

Superior and inferior hypophyseal arteries

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3
Q

Describe the cell make up of the lobes of the pituitary?

A

◦ Anterior - chromophils (acidophils and basophils) and chromophobes
‣ 50% somatotrophgs,
‣ 10-25% mamotrophs,
‣ 15-20% corticotrophs,
‣ gonadotrophs 5-10% and
‣ thyrotrophs the rarest <5%
◦ Posterior lobe the nerve endings of hypothalamic neurons
◦ Intermediate lobe <1% and doesn’t secrete

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4
Q

What are the cell types of the anteiror pituitary? Which are most common?

A

◦ Anterior -
‣ 50% somatotrophgs,
‣ 10-25% mamotrophs,
‣ 15-20% corticotrophs,
‣ gonadotrophs 5-10% and
‣ thyrotrophs the rarest <5%
◦ Posterior lobe the nerve endings of hypothalamic neurons
◦ Intermediate lobe <1% and doesn’t secrete

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5
Q

What is the most common cell type in the pituitary? What does it secrete?

A

◦ Anterior -
‣ 50% somatotrophgs, –> growth hormone
‣ 10-25% mamotrophs,
‣ 15-20% corticotrophs,
‣ gonadotrophs 5-10% and
‣ thyrotrophs the rarest <5%
◦ Posterior lobe the nerve endings of hypothalamic neurons
◦ Intermediate lobe <1% and doesn’t secrete

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6
Q

What are the two types of secretory cells in the pituitary?

A

Grandular and agranular

Granular being acidophils and basophils
- Acidophils include mammotrophs, somatotrophs
- Basophils secrete glucoprotein trophic hormones - LH, FSH, ACTH, TSH

Agranular being chomophobes (degranulated secretory cells). melanotrophs, and epithelial supportive cells

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7
Q

What is a chromophil?

A
  • Granular secretory cells - chromophils - two types
    ◦ Acidophils - 80%- secretes
    ‣ Mammotrophs –> prolactin
    ‣ somatotrophin –> growth hormone –> 50% of anterior cells
    ◦ Basophils (20%) secrete glycoprotein trophic hormones
    ‣ TSH - thyrotrophs
    ‣ ACTH - Corticotroph
    ‣ LH - gonadotroph - Leutenising hormone
    ‣ FSH - gonadotroph - follicle stimulating hormone
    ‣ Beta lipotrophin (LPH)
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8
Q

What are the two types of granular secretory cells?

A
  • Granular secretory cells - chromophils - two types
    ◦ Acidophils - 80%- secretes
    ‣ Mammotrophs –> prolactin
    ‣ somatotrophin –> growth hormone –> 50% of anterior cells
    ◦ Basophils (20%) secrete glycoprotein trophic hormones
    ‣ TSH - thyrotrophs
    ‣ ACTH - Corticotroph
    ‣ LH - gonadotroph - Leutenising hormone
    ‣ FSH - gonadotroph - follicle stimulating hormone
    ‣ Beta lipotrophin (LPH)
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9
Q

What are the acidophil cells of the pituitary?

A
  • Granular secretory cells - chromophils - two types
    ◦ Acidophils - 80%- secretes
    ‣ Mammotrophs –> prolactin
    ‣ somatotrophin –> growth hormone –> 50% of anterior cells
    ◦ Basophils (20%) secrete glycoprotein trophic hormones
    ‣ TSH - thyrotrophs
    ‣ ACTH - Corticotroph
    ‣ LH - gonadotroph - Leutenising hormone
    ‣ FSH - gonadotroph - follicle stimulating hormone
    ‣ Beta lipotrophin (LPH)
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10
Q

What are the basophil cells of the pituitary?

A
  • Granular secretory cells - chromophils - two types
    ◦ Acidophils - 80%- secretes
    ‣ Mammotrophs –> prolactin
    ‣ somatotrophin –> growth hormone –> 50% of anterior cells
    ◦ Basophils (20%) secrete glycoprotein trophic hormones
    ‣ TSH - thyrotrophs
    ‣ ACTH - Corticotroph
    ‣ LH - gonadotroph - Leutenising hormone
    ‣ FSH - gonadotroph - follicle stimulating hormone
    ‣ Beta lipotrophin (LPH)
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11
Q

What are the agranular cells of the pituitary”

A
  • Agranuclar secretory cells - chromophobes - degranulated secretory cells
    ◦ Melanotrophs
    ◦ Amphophils are epithelial supportive cells
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12
Q

What type of neurons are in the anterior lobe of the pituitary?

A

Post ganglionic sympathetic fibres

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13
Q

Classify the anterior pituitary hromones by their chemical nature

A
  • Glycoproteins: heterodimers
    ◦ Thyroid stimulating hormone (TSH)
    ◦ Follicle-stimulating hormone (FSH)
    ◦ Luteinising hormone (LH)
  • Peptides - large
    ◦ Corticotropin (ACTH)
    ◦ Pro-opiomelanocortin
    ◦ Growth hormone (GH)
    ◦ Prolactin
  • Oxytocin and vasopressin small cyclic nonapeptides
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14
Q

What are the glycoprotein hormones fo the pituitary?

A
  • Glycoproteins: heterodimers
    ◦ Thyroid stimulating hormone (TSH)
    ◦ Follicle-stimulating hormone (FSH)
    ◦ Luteinising hormone (LH)
  • Peptides - large
    ◦ Corticotropin (ACTH)
    ◦ Pro-opiomelanocortin
    ◦ Growth hormone (GH)
    ◦ Prolactin
  • Oxytocin and vasopressin small cyclic nonapeptides
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15
Q

What are the peptide hormones of the anteiror pituitary?

A
  • Glycoproteins: heterodimers
    ◦ Thyroid stimulating hormone (TSH)
    ◦ Follicle-stimulating hormone (FSH)
    ◦ Luteinising hormone (LH)
  • Peptides - large
    ◦ Corticotropin (ACTH)
    ◦ Pro-opiomelanocortin
    ◦ Growth hormone (GH)
    ◦ Prolactin
  • Oxytocin and vasopressin small cyclic nonapeptides
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16
Q

WHat are the peptide hormones

A
  • Peptide hormones
    ◦ Anterior and posterior pituitary hormones - ACTH, GH, prolactin, vasopressin, oxytocin, pro-opiomelanocortin
    ◦ parathyroid hormone
    ◦ calcitonin
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17
Q

What are the steriod hormones?

A

◦ Adrenocortical hormones
‣ Glucocorticoids
‣ Mineralocorticoids
‣ Androgens
◦ Sex hormones - testosterone, oesotrogen, progesterone
◦ 1 25 dihydroxycholecalciferol

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18
Q

What stimulates release of prolactin?

A
  • Release stimulated by serotoninergic and opioid pathways, gonadotropin releasing factor
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19
Q

What inhibits release of prolactin?

A
  • Release inhibited by somatostatin, with tonic inhibition by dopamine from hypothalamus
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20
Q

What is the function of prolactin?

A

◦ Stimulation of development and growth of mammary glands and milk production
◦ Suppresses LH secretion

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21
Q

What is the pattern of TSH release?

A
  • TSH pulses for 2-3 hours, nocturnal levels double day time
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22
Q

What structure is TSH

A

Dimeric glycoprotein

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23
Q

What inhibits TSH release?

A

◦ Release Inhibited by somatostain, T4 and T3

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24
Q

What causes release of TSH

A

◦ Release prompted by thyrotopin releasing hyromone

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25
Q

What does TSH do

A

◦ Causes production and release of thyroid hormones at the thyroid gland through GPCR Gs

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26
Q

ACTH release caused by?

A

◦ Release promoted by corticotrophin releasing factor from the hypothalamus
◦ Release increased by
‣ Nutritional stress - starvation, low amino acids, hypoglycaemia or low plasma concentrations of fatty acids, ghrelin
‣ Physiological stress - Exercise, excitement, trauma, heat
‣ Opioids
‣ Alpha adrenergic agonists, dopamine agonists, and serotinergic agonist increase release therefore Catecholamines and vasopressin increase release

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27
Q

ACTH release inhibited by

A

◦ Release Inhibited by somatostain and glucocorticoids (cortisol)

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28
Q

ACTH effect

A

◦ Acts on the adrenal cortex causing synthesis and release of glucocorticoids increasing cholesterol and steriod synthesis

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29
Q

LH release prompted by

A
  • Release prompted by gonadotrophin releasing factor from the hypothalamus
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30
Q

FSH release due to

A
  • Release prompted by gonadotrophin releasing factor from the hypothalamus
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31
Q

LH inhibition by

A

Testosterone or oesotrogen

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32
Q

FSH inhibitino by?

A

Testosterone or oesostrogen

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33
Q

LH action

A

◦ Stimulates ovulation and luteinization of ovarian follicles and testosterone secretion in males

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34
Q

FSH action

A

◦ Stimulates development of ovarian folicles and oestrogen synthesis and regulates spermatogenesis in the testes

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35
Q

Prolactin inhibited by

A

◦ Release Inhibited by somatostatin, and tonic inhibitory control by hypothalamus via dopamine D2, somatostatin and GABA

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36
Q

Actions of ACTH

A

◦ Direct - enhances transport of amino acids across cell membranes,m increaseds protein synthesis, increased transcirption of DNA
‣ Increase new bone and cartilage
‣ Increased hepatic glucose production
‣ Decreased skeletal muscle glucose utilisation increasing insulin resistance, enahnced protein synthesis
‣ Promotes release of fatty acids from adipose tissue
‣ Enhanced immune action
◦ Indirect via insulin growth factor 1 released from the liver in response to GH
‣ stimulates DNA, RNA and protein synthesis - bone formation, glucose uptake, myelin synthesis and neuronal survival

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37
Q

Oxytocin mechanism of action

A
  • is a nonapeptide that binds to a Gq-coupled receptor, ostensibly mainly on myometrial cells but also elsewhere - most notably in the CNS.
  • Its non-uterine effects are numerous and fascinating (for example implicated in the origins of social group interaction, sexual arousal, maternal behaviours, and mood regulation).
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38
Q

Vasopressin half life

A

5-10 mminutes

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39
Q

What is the mechansim of vasopressin receptors

A
  • It binds to three main families of receptors:
    ◦ V1a and V1b receptors (Gq-coupled)
    ◦ V2 receptors (Gs-coupled)
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40
Q

EPO comes from?

A

◦ Secreted from modified cortical fibroblasts
◦ Stimulated by hypoxia and angiotensin II
◦ Inhibited by inflammatory cytokines
◦ Effect is increase in the rate of red cell production and maturation

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41
Q

EPO is produced due to?

A

◦ Secreted from modified cortical fibroblasts
◦ Stimulated by hypoxia and angiotensin II
◦ Inhibited by inflammatory cytokines
◦ Effect is increase in the rate of red cell production and maturation

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42
Q

EPO is inhibited by?

A

◦ Secreted from modified cortical fibroblasts
◦ Stimulated by hypoxia and angiotensin II
◦ Inhibited by inflammatory cytokines
◦ Effect is increase in the rate of red cell production and maturation

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43
Q

EPO action

A

◦ Secreted from modified cortical fibroblasts
◦ Stimulated by hypoxia and angiotensin II
◦ Inhibited by inflammatory cytokines
◦ Effect is increase in the rate of red cell production and maturation

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44
Q

Renin released by

A

JG cells

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45
Q

Thrombopoetin released from where

A

PCT

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46
Q

Thrombopoetin released due to? Inhibited by?

A

◦ Stimulated by thrombocytopenia and inflammatory cytokines
◦ Inhibited by itself (negative feedback loop)

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47
Q

Urodilatin secreted by? Does what? Inhibited by? Effect

A

◦ Secreted from DCT cells, directly into the tubule
◦ Stimulated (probably) by increased sodium deliery
◦ Inhibited (presumably) by decreased sodium delivery
◦ The effect to increase sodium reabsoprtion in the collecting duct

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48
Q

Where is vitamin D modified in the kdiney?

A

PCT

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49
Q

What is vitamin D conversion in the PCT catalysed by?

A

‣ hypocalcemia
‣ PTH
‣ low vitamin D levels

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50
Q

Conversion of vitamin D to active form in the kidney is inhibited by?

A

‣ hypercalcemia
‣ low PTH
‣ high vitamin D levels

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51
Q

What role does the kidney have in clearance and metabolism of hormones?

A

Insulin
* 90% cleared by the kidney (proximal tubule)
Gastrin
* 30% cleared by the kidney (probably also proximal tubule)
Other hormones:
* PTH
* Vasopressin
* Oxytocin
* TSH
* Growth hormone
* Luteinising hormone

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52
Q

How large are adrenal glands?

A

5-6g

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53
Q

Where are adrenal glands located

A

anterior superior border of each kidney

◦ Epigastrium, opposite the 11th intercostal end fo the vertebral space and the 12th rib 
◦ Small irregular shaped
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54
Q

What are the regions of the adrenal gland? What hormone does each secrete? What % of the structure does each region take up?

A
  • They are divided into four functionally and anatomically distinct regions:
    ◦ Cortex: 85% of the adrenals
    ‣ Zona glomerulosa, which secretes mainly aldosterone - lack 17alpha hydroxylastherefore unable to make androgens or cortisol
    ‣ Zona fasciculata, which secretes mainly cortisol - the dominant part of the gland; does not have the capacity to make aldosterone
    ‣ Zona reticularis, which secretes mainly androgens
    ◦ Medulla, a modified sympathetic ganglion that secretes catecholamines
    ‣ (80% adrenaline, 20% noradrenaline), composed of chromaffin cells
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55
Q

What are the 3 areas of the cortex of the adrenal gland? What do they each do

A
  • They are divided into four functionally and anatomically distinct regions:
    ◦ Cortex: 85% of the adrenals
    ‣ Zona glomerulosa, which secretes mainly aldosterone - lack 17alpha hydroxylastherefore unable to make androgens or cortisol
    ‣ Zona fasciculata, which secretes mainly cortisol - the dominant part of the gland; does not have the capacity to make aldosterone
    ‣ Zona reticularis, which secretes mainly androgens
    ◦ Medulla, a modified sympathetic ganglion that secretes catecholamines
    ‣ (80% adrenaline, 20% noradrenaline), composed of chromaffin cells
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56
Q

What is produced in the adrenal medulla

A
  • They are divided into four functionally and anatomically distinct regions:
    ◦ Cortex: 85% of the adrenals
    ‣ Zona glomerulosa, which secretes mainly aldosterone - lack 17alpha hydroxylastherefore unable to make androgens or cortisol
    ‣ Zona fasciculata, which secretes mainly cortisol - the dominant part of the gland; does not have the capacity to make aldosterone
    ‣ Zona reticularis, which secretes mainly androgens
    ◦ Medulla, a modified sympathetic ganglion that secretes catecholamines
    ‣ (80% adrenaline, 20% noradrenaline), composed of chromaffin cells
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57
Q

WHat cell type is found in the adrenal medulla

A

Chromaffin cells

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58
Q

How are steriods released in response to stimulation?

A
  • Steroid synthesis in the cortex is from stored cholesterol vesicles, and occurs on demand, on the time scale of minutes
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59
Q

How fast after stimulation of the adrenal gland are steriods released?

A
  • Steroid synthesis in the cortex is from stored cholesterol vesicles, and occurs on demand, on the time scale of minutes
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60
Q

How much cortisol is made per day?

A

30mg with a max of 300mg per day

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61
Q

How is cortisol made?

A

‣ Production
* 4 CYP enzymes and choelsterol ester hydrolase make CS from cholesterol

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62
Q

What causes production of cortisol to increase?

A

‣ It occurs primarily in response to pituitary ACTH release via GPCR (Gs), modulated by:
* Catecholamines
* Angiotensin II
* Vasopressin
‣ Pituitary ACTH is released in a circadian pulse, and also in response to stress of different forms (eg. pain, distress, hypotension, inflammatory cytokines)
‣ Glucocorticoid feedback to the pituitary and hypothalamus downregulates ACTH secretion

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63
Q

WHat triggers aldosterone release?

A

◦ Aldosterone release occurs in response to hypovolemia, sodium depletion, hyperkalemia, and is stimulated by:
‣ Angiotensin II
‣ ACTH
‣ Directly, by hyperkalemia

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64
Q

What is the timescale trend of catecholamine secretion?

A
  • Catecholamine synthesis in the medulla is a constant process that replenishes catecholamine stores, as there is a constant rate of secretion
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65
Q

Catecholamines are are prepared in what fashion within the adrenal medulla?

A
  • Catecholamine synthesis in the medulla is a constant process that replenishes catecholamine stores, as there is a constant rate of secretion◦ Catecholamines are stored in chromaffin granules from which they are released by exocytosis
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66
Q

How much adrenaline is produced per day and released

A

150microg

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67
Q

What is the maximum endogenous adrenaline production amount

A

60 x 150mcg (basal)

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68
Q

Within the medulla what % of cells are adrenaline secreting chromaffin cells?

A

80%
20% are noradrenergic

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69
Q

What stimulates release of adrenaline from the medulla?

A

◦ Release is stimulated by preganglionic sympathetic innervation of the adrenal medulla, with acetylcholine as the neurotransmitter, binding to nicotinic receptors on the chromaffin cells and depolarising them, resulting in granule exocytosis

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70
Q

WHat amino acid is the precurser to adrenal medullary production of hormones/

A
  • Tyrosine, a non-essential amino acid, is the precursor molecule that gets taken up into the adrenal medullary cells.
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71
Q

Is tyrosine an essential or non essential amino acid?

A
  • Tyrosine, a non-essential amino acid, is the precursor molecule that gets taken up into the adrenal medullary cells.
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72
Q
  • Tyrosine is used to make hormone where?
A

Adrenal medulla

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73
Q

How is Tyrosine converted to noradrenaline

A
  • Tyrosine hydroxylase then catalyses the synthesis of L-dihydroxyphenylalanine (DOPA, which was scubaed into dopa), and this seems to be the rate-limiting step for catecholamine synthesis.
  • Dopa is then decarboxylated into dopamine by dopa decarboxylase, the enzyme targeted by anti-Parkinsons drugs, and also the one that uses vitamin B6 as a cofactor (which is where isoniazid interferes with it, causing seizures and lactic acidosis)
  • Dopamine is metabolised into noradrenaline by dopamine β-hydroxylase, which is expressed throughout the central and peripheral nervous system
  • Noradrenaline is converted into adrenaline by phenylethanolamine N-methyltransferase, which is an enzyme only really found in the adrenal medulla (as other sympathetic nerve endings do not secrete any adrenaline). For this reason, an adrenal phaeochromocytoma will secrete adrenaline, whereas a paraganglioma (arising from other sympathetic tissues) will typically secrete only noradrenaline.
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73
Q

How is Tyrosine converted to DOPA

A
  • Tyrosine hydroxylase then catalyses the synthesis of L-dihydroxyphenylalanine (DOPA, which was scubaed into dopa), and this seems to be the rate-limiting step for catecholamine synthesis.
  • Dopa is then decarboxylated into dopamine by dopa decarboxylase, the enzyme targeted by anti-Parkinsons drugs, and also the one that uses vitamin B6 as a cofactor (which is where isoniazid interferes with it, causing seizures and lactic acidosis)
  • Dopamine is metabolised into noradrenaline by dopamine β-hydroxylase, which is expressed throughout the central and peripheral nervous system
  • Noradrenaline is converted into adrenaline by phenylethanolamine N-methyltransferase, which is an enzyme only really found in the adrenal medulla (as other sympathetic nerve endings do not secrete any adrenaline). For this reason, an adrenal phaeochromocytoma will secrete adrenaline, whereas a paraganglioma (arising from other sympathetic tissues) will typically secrete only noradrenaline.
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Perfectly
73
Q

What is the rate limiting step in Catecholamine synthesis?

A

Tyrosine conversion to L-DOPA by tysoine hydroxylase

73
Q

How is dopamine formed

A
  • Tyrosine hydroxylase then catalyses the synthesis of L-dihydroxyphenylalanine (DOPA, which was scubaed into dopa), and this seems to be the rate-limiting step for catecholamine synthesis.
  • Dopa is then decarboxylated into dopamine by dopa decarboxylase, the enzyme targeted by anti-Parkinsons drugs, and also the one that uses vitamin B6 as a cofactor (which is where isoniazid interferes with it, causing seizures and lactic acidosis)
  • Dopamine is metabolised into noradrenaline by dopamine β-hydroxylase, which is expressed throughout the central and peripheral nervous system
  • Noradrenaline is converted into adrenaline by phenylethanolamine N-methyltransferase, which is an enzyme only really found in the adrenal medulla (as other sympathetic nerve endings do not secrete any adrenaline). For this reason, an adrenal phaeochromocytoma will secrete adrenaline, whereas a paraganglioma (arising from other sympathetic tissues) will typically secrete only noradrenaline.
74
Q

How is dopamine converted to adrenaline?

A

DOpamine beta hydroxylase

74
Q

How are steriods broken down?

A
  • Large proteins with 4 main functional regions - nuclear receptors (ligand dependent transcription factors)
  • Effects
    ◦ Nuclear transcription
    ◦ Sit in the membrane influences secondary messenger signalling
    ‣ Immune cell apoptosis
    ◦ Cytosol influence on protein function
    ‣ Anitinflammatory effect
  • Degredation of steriods by ubiquitin proteasome
74
Q

What converted adrenaline to noradrenaline

A

Phenylethanolamine N methyltransferase

74
Q

Describe the glucocorticoid receptor

A
  • Large proteins with 4 main functional regions - nuclear receptors (ligand dependent transcription factors)
  • Effects
    ◦ Nuclear transcription
    ◦ Sit in the membrane influences secondary messenger signalling
    ‣ Immune cell apoptosis
    ◦ Cytosol influence on protein function
    ‣ Anitinflammatory effect
  • Degredation of steriods by ubiquitin proteasome
75
Q

What does the thyroid gland secrete?

A

thyroxine and triiodothyronine

76
Q

What is the effect of TSH

A
  • TSH binds to TSH receptors on thyroid follicular epithelial cells increaasing secretory processes by increasing cAMP
    ◦ TSH also increases iodine trapping
    ◦ Increased iodination via peroxidase
    ◦ Increased coupling reaction to form T4 and T3
    ◦ Increased proteolysis of thyroglobulin increasing release of T4 and T3 into circulation
77
Q

What intracellular mechanism does TSH induce

A
  • TSH binds to TSH receptors on thyroid follicular epithelial cells increaasing secretory processes by increasing cAMP
    ◦ TSH also increases iodine trapping
    ◦ Increased iodination via peroxidase
    ◦ Increased coupling reaction to form T4 and T3
    ◦ Increased proteolysis of thyroglobulin increasing release of T4 and T3 into circulation
78
Q

Where are TSH receptors?

A
  • TSH binds to TSH receptors on thyroid follicular epithelial cells increaasing secretory processes by increasing cAMP
    ◦ TSH also increases iodine trapping
    ◦ Increased iodination via peroxidase
    ◦ Increased coupling reaction to form T4 and T3
    ◦ Increased proteolysis of thyroglobulin increasing release of T4 and T3 into circulation
79
Q

What 4 responses to TSH are there inside thyroid cells?

A
  • TSH binds to TSH receptors on thyroid follicular epithelial cells increaasing secretory processes by increasing cAMP
    ◦ TSH also increases iodine trapping
    ◦ Increased iodination via peroxidase
    ◦ Increased coupling reaction to form T4 and T3
    ◦ Increased proteolysis of thyroglobulin increasing release of T4 and T3 into circulation
80
Q

What is the mechanism of iodine trapping

A
  • Iodine trapping - basolateral second active transport pumping iodine into the interior of the cell to 30x its blood concentration (TSH stimulated)

Chloride - iodide transport protein into follicular lumn

81
Q

What concentration gradient is iodine trapping pumped against?

A
  • Iodine trapping - basolateral second active transport pumping iodine into the interior of the cell to 30x its blood concentration (TSH stimulated)

Chloride - iodide transport protein into follicular lumn

82
Q

Where is the iodine trapped

A
  • Iodine trapping - basolateral second active transport pumping iodine into the interior of the cell to 30x its blood concentration (TSH stimulated)

Chloride - iodide transport protein into follicular lumn

83
Q

What form is iodine in the thyroid?

A
  • Oxidation of iodide to iodine - thyroid peroxidase performs this with hydrogen peroxide accepting the electron (located on the apical membrane of follicular cell) –> iodine is then transported via chloride-iodide transport protein into follicular lumen
84
Q

How does thyroid peroxidase act?

A
  • Oxidation of iodide to iodine - thyroid peroxidase performs this with hydrogen peroxide accepting the electron (located on the apical membrane of follicular cell) –> iodine is then transported via chloride-iodide transport protein into follicular lumen

Thyroid peroxidase also assists binding of thyroglobulin to iodine –> iodination of thyroglobulin

85
Q

What is the catalyst enzyme in the thyroid

A

Thyroid peroxidase

86
Q

What form is iodine in within the plasma? What form is it in the thyroid

A

Iodide in the plasma - ionised

Iodine in the thyroid after oxidation by thyroid peroxidase with electrons accepted by hydrogen peroxide

87
Q

Where is thyroglobulin formed?

A
  • Thyroglobulin synthesied in endoplasmic reticulum and golgi apparatus of the follicular cell is secrteted into the follicular cavity where it bonds with iodine (3 position of tyrosine) in presence of thyroid peroxidase enzyme
88
Q

What relationship does thyroglobulin have to thyroid hormones?

A
  • Thyroglobulin synthesied in endoplasmic reticulum and golgi apparatus of the follicular cell is secrteted into the follicular cavity where it bonds with iodine (3 position of tyrosine) in presence of thyroid peroxidase enzyme
  • Iodination of thyroglobulin at tyrosine 3 site –> monoiodotyrosine and di-iodotyrosine –> oxidative condensation of two di-iodotyrosine leads to formation of T4 and a serine residue
    ◦ Mono-iodotyrosine and dioiodotyrsine leads to T3
    ◦ Catalysed by peroxidase enzyme
    ◦ These are stored in the follicular colloid
89
Q

What is the precurser product for the thyroid hormones

A

Thyroglobulin

  • Iodination of thyroglobulin at tyrosine 3 site –> monoiodotyrosine and di-iodotyrosine –> oxidative condensation of two di-iodotyrosine leads to formation of T4 and a serine residue
    ◦ Mono-iodotyrosine and dioiodotyrsine leads to T3
    ◦ Catalysed by peroxidase enzyme
    ◦ These are stored in the follicular colloid
90
Q

How are T3 and T4 formed?

A
  • Iodination of thyroglobulin at tyrosine 3 site –> monoiodotyrosine and di-iodotyrosine –> oxidative condensation of two di-iodotyrosine leads to formation of T4 and a serine residue
    ◦ Mono-iodotyrosine and dioiodotyrsine leads to T3
    ◦ Catalysed by peroxidase enzyme
    ◦ These are stored in the follicular colloid
91
Q

How are T3 and T4 released

A
  • TSH mediated release via - endocytosis as vesicles containing thyroglobulin mpve from the apical membrane and are cleaved to form T3 and T4 after which they diffuse across the basolateral membrane into capillaries
92
Q

T3 comprises what % of hormonal release from the thyroid?

A

10%

93
Q

T4 comprises what % of released thyroid hormone?

A

90%

94
Q

Where do thyroid hormones bind to their receptors? WHat effect do they have? What cells?

A
  • Cross cell membranes and bind to nuclear receptors increasing gene transcription –> increased intracellular metabolism of almost all cells
    ◦ Growth of tissues and bone
    ◦ Increased basal metabolic rate with increased oxygen consumption, heat production
    ◦ Metabolism - increased glucose absorption, glycogenolysis, gluconeogenesis, lipolysis and protein synthesis + breakdown
    ◦ CNS - potentiates sympathetic nervous system effects, brain development in intrauretiner and neonatal period, mood and psychiatric effects
    ◦ Cardiac and circulatory - icnreased cardiac outptu and heart rate
95
Q

Outline the effects of thyroid hormone physiologically

A
  • Cross cell membranes and bind to nuclear receptors increasing gene transcription –> increased intracellular metabolism of almost all cells
    ◦ Growth of tissues and bone
    ◦ Increased basal metabolic rate with increased oxygen consumption, heat production
    ◦ Metabolism - increased glucose absorption, glycogenolysis, gluconeogenesis, lipolysis and protein synthesis + breakdown
    ◦ CNS - potentiates sympathetic nervous system effects, brain development in intrauretiner and neonatal period, mood and psychiatric effects
    ◦ Cardiac and circulatory - icnreased cardiac outptu and heart rate
96
Q

What increases the release of thyroid hormone?

A

TSH
TRH via TSH

97
Q

What decreases the release of thyroid hormone?

A
  • Factor decreasing release
    ◦ TRH and TSH release are inihibited by T3(negative feedback)
98
Q

Available thyroid hormone is dependent on

A

TSH, TRH

Negative feedback

  • Available thyroid hormone is dependent on the free fraction which can be altered by changes in thyroid binding globulin which is responsible for the protein binding in plasma
99
Q

Describe the size and location fo the thyroid gland

A
  • Large (10-20g) endocrine gland with Two symmetrical lobes separated by an isthmus
  • Anterior to the 2-4th rings of the trachea / C5 - T1
    ◦ Anteriorly - skin, pretracheal fascia, sternothyroid and sternohyoid muscles
    ◦ Superiorly - cricoid cartilage
    ◦ Medially - larynx, trachea, oesophagus and recurrent laryngeal nerve
100
Q

How does the thyroid relate to the trachea?

A
  • Large (10-20g) endocrine gland with Two symmetrical lobes separated by an isthmus
  • Anterior to the 2-4th rings of the trachea / C5 - T1
    ◦ Anteriorly - skin, pretracheal fascia, sternothyroid and sternohyoid muscles
    ◦ Superiorly - cricoid cartilage
    ◦ Medially - larynx, trachea, oesophagus and recurrent laryngeal nerve
101
Q

What are the relations of the thyroid?

A
  • Large (10-20g) endocrine gland with Two symmetrical lobes separated by an isthmus
  • Anterior to the 2-4th rings of the trachea / C5 - T1
    ◦ Anteriorly - skin, pretracheal fascia, sternothyroid and sternohyoid muscles
    ◦ Superiorly - cricoid cartilage
    ◦ Medially - larynx, trachea, oesophagus and recurrent laryngeal nerve
102
Q

What is the blood supply of the thyroid?

A
  • Blood supply - superior and inferior thyroid rtery Owith veinous drainage by superior/middle and inferior thyroid veins
103
Q

What is the nervous supply of the thyroid?

A

SNS from middle cervical ganglion

PSNS vagal

104
Q

Describe the microstructure archietecture of the thyroid?

A
  • Organised into follicles: colloid-containing cavities lined with cuboidal epithelium
  • Colloid is made up of iodinated thyroglobulin, the precursor for thyroid hormone synthesis
105
Q

How is iodine absorbed dietarily?

A
  • Iodine is absorbed from diet as iodide (reduced in the gut) 150-300mcg per day - small intetsine
106
Q

What % of total body iodine is in the thyroid?

A

80%

107
Q

How is iodine moved into the thyroid cells?

A
  • It is concentrated by 30-40 times in the thyroid follicles by the sodium/iodide symporter (NIS) before being transported into the colloid rapidly through multiple proteins (70-80% of body iodine is in the thyroid)
108
Q

Thyroglobulin has what residues which are iodinated by thyroid peroxidase?

A

Tyrosine

109
Q

How many tyrosine residues does thyroglobulin have?

A

66
30 can be iodinated
Of the 25-30 tyrosine residues ionidated up to 16 can be coupled to form 2-8 molecules of finishes T4/T3

110
Q

Where is thyroglobulin made? How is this regulated?

A

◦ Thyroglobulin itself is synthesised in the follicular cell under TSH control

111
Q

How are thyroid hormones stored?

A
  • Iodinated thyroglobulin is stored, and reabsorbed as needed by follicular cells
  • Proteolysis by endopeptidases of thyroglobulin liberates T3 (20%) and T4 molecules (80%)
112
Q

How are thyroid hormones made from thyroglobulin?

A
  • Iodinated thyroglobulin is stored, and reabsorbed as needed by follicular cells
  • Proteolysis by endopeptidases of thyroglobulin liberates T3 (20%) and T4 molecules (80%)
113
Q

Circulating thyroid hormones are in what form

A
  • Released thyroid hormones consist of 80% T4 and 20% T3
  • Circulating T4 and T3 are highly protein bound to thyroid hormone-binding globulin, a chaperone protein in the plasma
114
Q

T4 half life?

A
  • T4 has a longer half life (6-7 days), gradually converted to T3 by peripheral deiodinase enzymes (ubiquitous, but mainly in the liver and kidneys)
115
Q

T3 half life?

A

Hours

116
Q

T4 is converted to T3 how?

A
  • T4 has a longer half life (6-7 days), gradually converted to T3 by peripheral deiodinase enzymes (ubiquitous, but mainly in the liver and kidneys)
117
Q

How does a thyroid hormone enter a cell?

A
  • Entry into cells via various membrane transporters e.g. organic anion transporters
  • Bind to mainly nuclear receptors, which act as transcription factors, modifying protein synthesis (though there are also cytosolic and membrane receptors which have more immediate effects)
  • Most physiologically important actions are mediated by gene transcription and therefore take more than 24hrs to manifest
118
Q

Thyroid hormone function can be divided into?

A

Blood flow
Upregulated functions
Heat proudction
Nutritional

119
Q

How does thyroid hormone effect blood flow?

A

◦ Increased cardiac output due to
‣ increased contractility over 24 hours
‣ decreased peripheral vascular resistance - direct vasodilation occurs rapidly
* Except causes pulmonary vasoconstriction
◦ Increased sympathetic nervous system activity, increased sensitivity to catecholamines
◦ Increased blood flow to
‣ Kidneys - increased clearance of renally cleared substances
‣ Hepatic - increased clearance of metabolised hepatic substances
‣ Increased skeletal blood flow

120
Q

What functions does thyroid hormone upregulate?

A

◦ Psychological and neurodevelopmental effects
◦ Increased gastrointestinal motility and increased appetite
◦ Increased sympathetic nervous system activity

121
Q

How does thyroid hormone effect heat?

A

◦ Increased shivering and nonshivering thermogenesis
◦ Decreased efficiency of mitochondrial electron transport, resulting in heat production
◦ Increased BMR and O2 consumption –> increased respiratory demand, respiratory drive and decreased respiratory muscle power with tendancy toward bronchoconstriction

122
Q

How does thyroid hormone effect nutritional processing?

A

◦ Increased gluconeogenesis –> increased hepatic glucose output
◦ Fat
‣ Increased lipolysis in white adipose tissue –> Increased free fatty acid release
‣ Increased hepatic lipogenesis,
‣ Increased use of lipids as metabolic fuel substrate
‣ Reverse cholesterol transport
◦ Increased hepatic protein synthesis

123
Q

What regulates TRH release?

A

◦ Stimulated by low T4/T3 levels + cold temperature
◦ Inhibited by high T4/T3, fasting, cortisol and leptin

124
Q

What stimulates TRH release

A

◦ Stimulated by low T4/T3 levels + cold temperature
◦ Inhibited by high T4/T3, fasting, cortisol and leptin

125
Q

What inhibits TRH release

A

◦ Stimulated by low T4/T3 levels + cold temperature
◦ Inhibited by high T4/T3, fasting, cortisol and leptin

126
Q

What stimulates TSH release
What inhibits TSH release

A
  • TRH stimulates TSH release
    ◦ Inhibited by high T4/T3 levels, somatostatin, dopamine and cortisol
127
Q

Peripheral conversion of T4 to T3 is regulated by?

A

Peripheral de-iodinase activity

Inhibtied by critical illness, cortisol and starvation

128
Q

How do propylthiouracils work?

A

Prevent synthesis of T3 and T4:
Thiouracils: propylthiouracil - blocks synthesis of T3 and T4 as well as peripheral T4-T3 conversion
Imidazoles: carbimazole - block synthesis of T3 and T4

129
Q

What does carbimazole do?

A

Prevent synthesis of T3 and T4:
Thiouracils: propylthiouracil - blocks synthesis of T3 and T4 as well as peripheral T4-T3 conversion
Imidazoles: carbimazole - block synthesis of T3 and T4

130
Q

How can you reduce the systemic effects of released thyroid hormones?

A

Block peripheral T3 and T4 activity:
β-blockade: propanolol (which also decreases T4-T3 conversion)
Corticosteroids: also decrease T4-T3 conversion

131
Q

Beta blockers work in hyperthyroidism why?

A

xBlock peripheral T3 and T4 activity:
β-blockade: propanolol (which also decreases T4-T3 conversion)
Corticosteroids: also decrease T4-T3 conversion

132
Q

What are thryoid hormones chemically

A

Iodinated tyrosine derivatives

133
Q

Thyroxine absorption and bioavailability

A

Well absorbed
60-80% bioavailability

134
Q

What factors effect oral bioavailability of thyroid hormones?

A

Empty stomach
Pause NG feeds for 1 hour

135
Q

pKa of thyroxine

A

7.43

136
Q

Solubility of thyroxine?

A

Mildly water soluble

137
Q

Vd of thyroxine?

A

0.15L/kg

138
Q

What is thyroxine bound to?

A

Thyroid binding hormone

139
Q

How is thyroxine metabolised and excreted?

A

Deiodinase enzymes to active T3

Hepatic metabolism of inactvie iodinated compoundsH

140
Q

Half life of thyroxine?

A

6-8 days
10% deiodinated per day

141
Q

Mechanism of thyroxine action

A

Endocytosis via transmembrane receptors and binding to nuclear transcription factors

142
Q

What pharmaceutically is important for thyroid hormones?

A

8-15 degrees

143
Q

Bioavailability of T3

A

97%

144
Q

pKa of T3

A

8.4

145
Q

Solubility of T3? Therefore how is it prepared? What effect does this have on its use?

A

Reluctantly water soluble

Alcohol and ammonium hydroxide excipients so CVC needed

146
Q

How much T3 is given in bolus dose in myoxoedema coma

A

5-20mcg

147
Q

Vd of T3

A

1.8L/kg

148
Q

T3 protein binding

A

Less than T4 as 30x less affinity for thyroid bidning globulin

149
Q

Half life of T3

A

6-10 hours
Shorter as less protein bound

150
Q

T3 effects on the heart

A

SNS sensitiser
Inodilator

151
Q

Renal effects of T3/4

A

increased renal blood flow and renal clearance

152
Q

Hepatic effects of T3/4

A

Increased protein synthesis
increased hepatic metabolism of substances

153
Q

GI effects of T3/4

A

Increased motility and appetite

154
Q

T3/4 overdose treatemnt

A

Cholestyromine to reduce enterohepatic recirculation of glucoronidated substances

Plasma exchange
Beta blockade
Glucocorticoids

155
Q

Define hormone

A

A hormone is a chemical messenger produced by a ductless gland which has its action at a distant target cell via a specific receptor.

156
Q

Types of hormones based on types of signalling

A

Autocrine
Paracrine
Neurocrine
Endocrine

157
Q

Group hormones based on structure

A

Lipid hormones
1. Steriods
2. Eicosanoids

Peptide hormones
- Short
- Long
- Glycopeptides

Monoamine derivatives (single amino acid)

158
Q

Steroid hormone examples? WHy are they grouped together?

A

Lipid hormone subclass

Steroids are synthesised from cholesterol, and are released as they are produced (they are not stored). They are highly lipid soluble and act on cytoplasmic and intra-nucleic receptors.
Aldosterone
Testosterone
Oestrogen
Cortisol

159
Q

Eicosanoid hormones e.g.? Formed from?

A

Eicosanoids are formed from cell membrane phospholipid.
Prostaglandins
Thromboxanes
Leukotrienes

160
Q

Peptide hormones characteristics?

A

Peptide hormones are store in granules and released by exocytosis

161
Q

Short chain peptide hormones

A

Short-chain
Insulin
ADH
Oxytocin
ACTH

162
Q

Long chain peptide hormones

A

GH
Prolactin

163
Q

Glycopeptide hormones

A

Proteins with carbohydrate groups.
LH
FSH
TSH

164
Q

Which hormones are derived froma single amino acid?

A

Derived from a single amino acid.
Catecholamines
Stored in granules and act at membrane receptors.
Adrenaline
Noradrenaline
Serotonin
Thyroxine

165
Q

Give examples of peptide vs steriod hormones?

A
166
Q

How are peptide and steriod hormones different structurally and in sysntheiss?

A
167
Q

Precursers of steriod vs peptide hormones

A
168
Q

Storage of peptide vs steriod hormones

A
169
Q

Transport and kinetics of steriod vs peptide hormones

A
170
Q

Hormones of the anterior pituitary

A

FSH, LH
Prolactin
ACTH
TSH
GH

171
Q

Hormones of the posterior pituitary

A

ADH and oxyticin

172
Q

Steriod hormones characteristics

A

Intracellular, lipid soluble
Choleserol based
Nil storage
Globulin bound for transport
DNA alteration
SLow kinetics

Cortisol

173
Q

Peptide hormones charactersitics

A

ADH, insulin

Membrane receptors
Low lipid solubility
Prohormone/hormone storage vesicles
Dissolved in plasma
Secondary messenger systems
Rapidly released

174
Q

Where are osmoreceptors

A

Sensory receptors primarily found centrally and peripherally detecting changes in osmotic pressure

Central: anterior hypothalamus, circumventricular organs (subfornical organ adn organum vasculosum) - BBB deficient blood supply

Peripheral osmorecpeotrs upper GIT and portal vein

175
Q

Receptors of ADH

A

V1a - vascular endothelium, constrcition especially splanchnic and coronary.
- Platelet aggregation
- Hepatic glycognelysis
- Neurotransmission in the spinal cord and brian

V1b - ACTH release posterior pituitary

V2 - renal basolateral membrane inserting aquaporin 2 into luminal membrane and stimulating urea reabsoerption

176
Q

His is ADH metabolised

A

Peptidases in liver and kidney

177
Q

ADH secretion inhibited by

A

ANP
GABA
Opioids

178
Q

Vasopressin clinical uses

A

Catecholamine agent in spetic shock
DI
Control bleeding in vWD and uraemic platelet dysfunction
Hepatorenal syndrome and variceal haemorrhage

179
Q
A

Gastro nutrition (7 decks)

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