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Tamsin - Physiology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Describe the connections between the hypothalamus and anterior/posterior pituitary gland

A

There are neural connections between the hypothalamus and posterior pituitary

There are vascular connections between the hypothalamus and anterior pituitary

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2
Q

Where are the cell bodies of the nerves with endings in the posterior pituitary?

A

Supraoptic and paraventricular nuclei - neurons pass to the posterior pituitary via the hypothalamohypohysial tract

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3
Q

What vessels form the primary plexus?

A

Primary plexus - network of fenestrated capillaries on the ventral surface of the hypothalamus

Formed by arterial twigs from the carotid arteries and circle of Willis

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4
Q

What is the median eminence?

A

The portion of the ventral hypothalamus from which the portal vessels arise

This region is OUTSIDE the BBB

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5
Q

What are the principal functions of the hypothalamus?

A
  1. Temperature regulation
  2. Neuroendocrine control of:
    • Catecholamines
    • Vasopressin
    • Oxytocin
    • TSH via TRH
    • ACTH via CRH
    • FSH and LH via GnRH
    • Prolactin via PRH
    • GH via somatostatin and GRH
  3. “Appetite” behaviour
  4. Defensive reactions
  5. Control of body rhythms
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6
Q

What 6 hormones are secreted by the anterior pituitary?

A

Adrenocorticotrophic hormone (ACTH)

Thyroid stimulating hormone (TSH)

Growth hormone (GH)

Follicle stimulating hormone (FSH)

Luteinizing hormone (LH)

Prolactin (PRL)

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7
Q

What are the hypophysiotropic hormones?

A

Hormones secreted into the portal hypophysial vessels from the hypothalamus to the pituitary (secreted by the median eminence)

Corticotropin-releasing hormone (CRH)

Thyroid releasing hormone (TRH)

Growth hormone releasing hormone (GRH)

Growth hormone inhibiting hormone (GIH/somatostatin)

Prolactin inhibiting hormone (PIH)

Gonadotropin releasing hormone (GNRH)

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8
Q

Where are the cell bodies of the neurons that secrete the hypophysiotropic hormones?

A

GNRH - Medial preoptic area

Somatostatin - Periventricular nuclei

TRH - Periventricular nuclei

CRH - Periventriuclar nuclei

GRH - Arcuate nuclei

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9
Q

Describe the anatomy of the anterior pituitary

A

Arises embryolgically as an invagination of the pharynx (Rathke pouch)

Contains endocrine cells that store its characteristic hormones

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10
Q

What are the 5 types of secretory cells identified in the anterior pituitary?

A

Somatrotropes (50%)

Lactotropes (10-30%)

Corticotropes (10%)

Thyrotropes (5%)

Gonadotropes (20%)

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11
Q

What percentage of the ciruclating pool of growth hormone is in the bound form?

A

50% - providing a resevoir of hormone to compensate for the wide fluctuations that occur in secretion

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12
Q

At what age do you have the highest circulating levels of growth hormone?

A

Adolescents > Children > Adults

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13
Q

What are the regulators of GH secretion?

A

GHRH and somatostatin secreted by the hypothalamus

Ghrelin - mainly synthesised and secreted in the stomach, also produced in the hypothalamus

GH acts on the hypothalamus to antagonise GHRH release and stimulate somatostatin release

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14
Q

What factors increase GH secretion?

A
  1. Hypoglycaemia
  2. 2-Deoxyglucose
  3. Exercise
  4. Fasting
  5. Increase in amino acids
  6. Protein meal
  7. Infusion of arginine
  8. Glucagon
  9. Lysine vasopressin
  10. Going to sleep
  11. L-Dopa and alpha-adrenergic agonists that penetrate the brain
  12. Apomorphine and other dopamine receptor agonists
  13. Oestrogens and androgens
  14. Stressful stimuli
  15. Pyrogen

3 BROAD GROUPS: 1-Hypolgycaemia/fasting- threatened decrease in substrate for energy production. 2- Increase in aminoacids in the plasma 3-Stressful stimuli

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15
Q

What stimuli decrease GH secretion?

A

REM sleep

Glucose

Cortisol

FFA

Medroxyprogesterone

GH and IGF-1

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16
Q

What important signalling cascades are activated by Growth hormone?

A
  1. PLC/PIP2/DAG
  2. JAK2-STAT pathway
  • JAK2 is a cytoplasmic tyrosine kinase
  • STATs are a family of cytoplasmic transcription that upon phosphorylation by JAK kinases migrate to the nucleus where they activate various genes
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17
Q

What are the effects of growth hormone on protein/electrolytes?

A

Rise in plasma phosphorus

Fall in BUN and amino acid levels

Increased GI absorption of Ca2+

Reduced Na+ and K+ excretion

Increased excretion of amino acid 4-hydroxyproline

Increase in lean body mass and decrease in body fat

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18
Q

What are the effects of growth hormone on carbohydrate and fat metabolism?

A

Many forms are diabetogenic

  • Increase hepatic glucose output
  • Exert anti-insulin effect in muscle
  • Ketogenic
  • Increases circulating FFA levels

Increases ability of pancreas to respond to insulinogenic stimuli

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19
Q

Describe the role of somatomedins (IGF) in growth

A
  • Insulin like growth factors (IGF) are polypeptide growth factors secreted by the liver and other tissues
  • Circulating somatomedins include IGF-1 and IGF-2
  • Both are tightly bound to proteins in plasma
  • IGF-1 receptor is very similar to insulin receptor. Secretion stimulated by GH.
  • IGF-2 receptor has distinct structure. Largely independant of GH. Role in growth of fetus before birth.
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20
Q

What are the actions of GH and IGF?

A
  • Na+ retention
  • Decreased insulin sensitivity
  • Lipolysis
  • Protein synthesis
  • Epiphysial growth
  • IGF 1 - insulin like activity, antilipolytic activity
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21
Q

What are the effects of pituitary insufficiency?

A

Adrenal cortex atrophies > secretion of adrenal glucocorticoids and sex hormones falls to low levels

Stress induced increases in aldosterone secretion are absent but basal aldosterone secretion and increases induced by salt depletion are normal > Salt loss and hypovolaemic shock do not develop but inability to increase glucocorticoid secretion makes patients sensitive to stress

Growth is inhibited

Thyroid function is depressed to low levels > cold intolerance

Gonadal atrophy

Secondary sexual characteristics disappear

Tendency to become hypoglycaemic -> increased hypoglycaemic effect of insulin

Transient polyuria - ACTH, TSH and GH all have a “diuretic” effect which balances the ADH secretion by the post. pituitary. Selective destruction of the supraoptic post. pituitary causes diabetes insipidus

22
Q

What are the causes of pituitary insufficiency?

A

Tumour

Suprasellar cysts - remnants of Rathke pouch

Sheehan syndrome - infarction of the pituitary secondary to post-partum haemorrhage

23
Q

Name the different hormones secreted by the adrenal cortex and adrenal medulla

A

Outer adrenal cortex - glucocorticoids eg cortisol, mineralocorticoids eg aldosterone

Inner adrenal medulla - catecholamines

24
Q

Describe the morphology of the adrenal medulla

A
  • 28% of the mass of the adrenal gland
  • Interlacing cords of densely innervated granule-containing cells that abut on venous sinouses
  • 2 distinguishable cell types:
    • Epinephrine secreting cells (90%) - larger, less dense granules
    • Norepinephrine secreting cells (10%) - smaller, very dense granules

Paraganglia - cells resembling adrenal medullary cells are found near the thoracic and abdominal sympathetic ganglia

25
Describe the morphology of the adrenal cortex
Three zones: 1. Outer zona glomerulosa (15% of adrenal mass) --\> **aldosterone secretion, formation of new cortical cells** 2. Zona fasciculata (50% of adrenal mass) --\> **cortisol** and androgens 3. Zona reticularis (7% of adrenal mass) --\> **androgens** and cortisol
26
What is the vascular supply to the adrenals?
Arterial - Small branches of the phrenic and renal arteries and the aorta Blood flows from a plexus in the capsule through the cortex to the sinusoids of the medulla. Veinous- From the medulla into a central adrenal vein
27
Describe the synthesis of catecholamines in the adrenal medulla
Norepinephrine is formed by **hydroxylation and decarboxylation of tyrosine** Epinephrine is formed by **methylation of norepinephrine** **Phenylethanolamine-N-methyltransferase (PNMT) is the enzyme that catalyses the formation of epinephrine from norepinephrine** **PNMT is induced by glucocorticoids \> If the glucocorticoid concentration falls (eg after hypohysectomy) epinephrine synthesis falls** Most of the catecholamine output in the adrenal vein is **epinephrine** Norepinephrine is also secreted by noradrenergic nerve endings
28
What are the effects of epinephrine and norepinephrine?
1. Glycogenolysis in liver and skeletal muscle 2. Mobilisation of FFA 3. Increased plasma lactate 4. Stimulation of the metabolic rate 5. Increase force and rate of contraction of the heart (via B1 receptors) 6. **NE** --\> acts via A1 receptors causing **vasoconstriction** * HTN stimulates aortic baroreceptors producing **reflex bradycardia** that overrides direct cardioaccelatory effect of NE 7. **E** --\> acts via B2 receptors causing vasodilation in liver and skeletal muscle --\> TPR drops * Widening pulse pressure but insufficient baroreceptor stimulation to cause bradycardia \> **Cardiac rate and output increase** 8. ​Increased alertness 9. Initial rise in plasma K+, prolonged fall in plasma K+ due to uptake by skeletal muscle
29
What is the threshold for the cardiovascular and metabolic effects of NE and E?
NE = 1500 pg/mL (5 times the resting value) E = 50 pg/mL (2 times the resting value)
30
What are the observed effects of dopamine?
* Renal vasodilation + mesenteric vasodilation * Vasoconstriction elsewhere (increased NE release) * Positive inotropic effect on heart (B1 receptors) * Increased systolic pressure and no change on diastolic pressure * Natriuresis (?inhibits Na/K ATPase)
31
Other than catecholamines, what other substances are secreted by the adrenal medulla?
ATP Chromogranin A Opioid peptides (preproenkephalin role unknown) Adrenomedullin (vasoDepressor polypeptide)
32
Describe the action of ACTH
Binds to high affinity receptors on plasma membrane of adrenocortical cells Activates adenylyl cyclase via Gs Increased formation of pregnenelone and its derivatives Over longer periods - increases the synthesis of the P450s involved in the synthesis of glucocorticoids
33
Describe the action of angiotensin 2
Binds to AT1 receptors in the zona glomerulosa that act via a G protein to activate phospholipase C \> increased PKC \> Conversion of cholestrol to pregnenolone + increased action of aldosterone synthase resulting in increased secretion of aldosterone
34
How is cortisol found in the circulation?
Bound to an alpha globulin called transcortin or corticosteroid binding globulin (CBG) Minor degree of binding to albumin Corticosterone is bound to a lesser degree and therefore has a shorter half life Bound steroids are physiologically inactive The bound cortisol functions as a resevoir
35
Describe the metabolism and excretion of glucocorticoids
Metabolised in the liver Reduced to dihydrocortisol and then to tetrahydrocortisol which is conjugated to glucoronic acid (same glucoronyl transferase catalyst as bilirubin glucoronides) Enzyme 11B hydroxysteroid dehydrogenase: Type 1 ctalyses conversion of cortisol to cortisone+reverse reaction and forms cortisol from corticosterone Type 2 catalyses one way conversion of cortisol to cortisone
36
How is aldosterone excreted?
Converted in the liver to the tetrahydroglucoronide derivative This glucoronide is converted to free aldosterone by hydrolysis at pH 1 and is often referred to as the acid-labile conjugate Less than 1% of the secreted aldosterone appears in the urine as the free from
37
What is the mechanism of action of glucocorticoids?
Bind to glucocorticoid receptors --\> Steroid-receptor complexes act as transcription factros --\> mRNA --\> synthesis of enzymes that alter cell function
38
What are the physiologic effects of glucocorticoids ?
* Effects on intermedullary metabolism * protein catabolism, increased hepatic glycogenesis and gluconeogenesis, glucose-6-phosphatase activity increases \> plasma glucose rises * Permissive action * Must be present for certain metabolic reactions to occur eg glucagon * Inhibit ACTH secretion * Inhibit ACTH secretion * Necessary for vascular reactivity * Necessary for CNS function * Necessary for excretion of water loads * Effects on blood cells and lymphatic organs * Decrease number of circulating eosinophils, basophils * Increase neutrophils, platelets, RBCs in circulation * Inhibit the inflammatory response * Suppress manifestations of allergic disease that are due to the release of histamine
39
Describe the regulation of glucocorticoid secretion
Release is dependant on ACTH from the ant. pituitary Normal basal ACTH release maintains serum levels Increased ACTH in response to stress occurs
40
What are the stimulators of ACTH secretion
Pain Emotion Circadian rhythm Nucleus of the tractus solitarius (chemoreceptor and baroreceptors) Free glucocroticoids inhibit ACTH secretion at the hypothalamic and pituitary level
41
Describe the MOA of aldosterone
Binds to cytoplasmic receptor \> receptor-hormone complex \> moves to nucleus \> transcription of mRNA \> production of protein that alter cell function Rapid effect: Increased activity of epithelial Na+ channels ENaCs by increasing the insertion of these into the cell membrane from a cytoplasmic pool Slower effect: Increased synthesis of ENaCs
42
What are the actions of aldosterone?
Increased reabsorption of Na+ from urine, sweat, saliva, contents of colon Decreased reabsorption of K+ from the urine
43
Primary regulators of aldosterone secretion
Ciruclating ACTH level The RAA system Increased K+ concentration increases release
44
What stimuli increase aldosterone secretion?
Stimuli that increase glucocorticoid secretion * Surgery * Anxiety * Trauma * Haemorrhage Stimuli that do not affect glucocorticoid secretion * High K+ intake, low Na intake * Concentration of IVC in thorax * Standing * Secondary hyperaldosteronism
45
What are the relative potencies of corticosteroids compared with cortisol?
Dexamethasone has 0 mineralocorticoid activity but has the most glucocorticoid activity
46
What are the functions of the thyroid gland?
Stimulates O2 consumption of most cells in the body Helps regulate lipid and carbohydrate metabolism Necessary for growth and maturation Regulates calcium metabolism - seretes calcitonin
47
Describe how iodine is used by the body
Minimum daily iodine intake 150microgram Usual daily take 500microgram About 120microgram/day enters the thyroid 80 microgram/day (2/3) secreted in the form of T3 and T4 40micogram/day (1/3) diffuses back into ECF 20microgram/day lost in stool 20% dietary I- enters the thyroid, 80% excreted in urine
48
Describe the process of iodide transport across throcytes
Na/I symporter (NIS) in the basolateral membrane of thyrocytes pumps 2 Na and 1 I into the cell with each cycle * This is secondary active transport - energy is provided by active transport of Na+ out of thyroid cells by the Na/K ATPase * TSH induces NIS expression and retention of NIS in the basolateral membrane
49
What are the key steps in thyroid hormone synthesis?
**Iodide oxidised** to iodine at interface between thyrocyte and colloid. Iodine is **bound to thyroglobulin** in the colloid. The process is mediated by membrane bound **thyroid peroxidase** 1. Monoiodotyrosine is produced (MIT) 2. MIT is iodinated to diiodotyrosine (DIT) 3. 2 DIT molecules undergo oxidateive condensation to form T4 (removal of alalnine) 4. T3 is formed by condensation of DIT with MIT Thyroglobulin is synthesised in the thyrocytes and secreted into the colloid by exocytosis of granules Thyroid hormones remain part of the thyroglobulin molecules until they are secreted - colloid is then ingested by the thyroid cells, peptide bonds hydrolysed and free T4 and T3 are discharged into capillaries
50
What are the 4 functions of thyroid cells?
Collect and transport iodine Synthesis of thyroglobulin and secretion into colloid Fix iodine to the thyroglobulin to generate thyroid hormones Removal of thyroid hormones from thyroglobulin and secretion into circulation
51

Tamsin - Physiology (4 decks)

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