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NEUROSCIENCE 2 > LECTURE 6 - central endocrine glands > Flashcards

LECTURE 6 - central endocrine glands Flashcards

1
Q

What is the pituitary gland and where is it found?

A
  • master gland
  • controls all other glands
  • 2 parts; posterior and anterior
  • sits below hypothalamus
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2
Q

What is the hypothalamus?

A
  • collection of brain nuclei (or centres)
    Important functions:
  • homeostasis and primitive functions
  • controls autonomic function via brainstem autonomic centres
  • controls endocrine function via pituitary gland
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3
Q

What does the hypothalamus respond to?

A

Environmental factors
e.g. light, stress, fear etc

Neural signals
e.g. visceral afferents from heart, liver, stomach

Hormones
Negative feedback

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4
Q

What are the properties of hypothalamic hormones?

A
  • small peptides with short half lives (t1/2)
  • release is pulsatile => rapid effects on the release of cognate anterior pituitary hormone
  • can be used clinically in acute challenge experiments to check pituitary function
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5
Q

Describe the differentiation between the lobes of the pituitary glands

A

ANTERIOR

  • hormones regulated by secreted hypothalamic factors
  • controls circulation
  • hormones released into blood supply

POSTERIOR

  • synthesised in hypothalamus and transported via neuronal projections
  • structurally continuous with the hypothalamus, remains attached by the hypophyseal (or pituitary stalk)
  • gets info from nervous system
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6
Q

What are some anterior pituitary hormones?

A

Cell type - hormone - function

Thyrotroph - TSH - thyroid hormone regulation
Corticotroph - ACTH - regulation of adrenal cortex
Gonadotroph - LH/FSH - reproductive control
Somatotroph - GH - growth
Lactotroph - PRL - milk production

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7
Q

What are some posterior pituitary hormones?

A

Cell type - function

ADH (vasopressin) - water regulation
Neurophysins - important in ADH synthesis
Oxytocin - birth, breast milk expression

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8
Q

What are tropic hormones?

A

Hormones that target other endocrine glands

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9
Q

What is TSH?

A

Thyroid stimulating hormone

  • aka thyrotropin or thyrotrophin
  • made in thyrotrophs in response to pulsatile TRH release from hypothalamus
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10
Q

How can the pituitary gland regulate thyroid activity?

A
  • hypothalamus receives signal

- produces TRH (thyroid releasing hormone) the reacts with ant. pituitary to produce TSH

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11
Q

What are some thyrotroph problems?

A

Pituitary failure

  • primary hypothyroidism = problem with thyroid itself
  • secondary hypothyroidism = problem due to fault elsewhere e.g. not enough TSH production

Pituitary tumour = secondary hyperthyroidism

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12
Q

What hormones are produced by the gonadotrophins?

A

LH and FSH

  • made in anterior in response to GnRH
  • 60% secrete both, 18% secrete only LH and 22% only FSH
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13
Q

Explain the effects and mechanism of action of LH and FSH

A
  • regulate testosterone biosynthesis and spermatogenesis
  • regulate the menstrual cycle and fertility in the ovary
  • both act through cell membrane receptors coupled to G proteins => elevations in cAMP and activation of protein kinase A
  • pulsatile secretion essential for actions
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14
Q

What is ACTH and how is it synthesised?

A

Adrenocorticotrophic hormone - aka adrenocorticotrophin
- polypeptide of 39 amino acids

Synthesis:

  • large precursor Pro-opiomelanocortin (POMC) is the source of several important biologically active substances
  • ACTH = cut from POMC
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15
Q

How is cortisol released in response to ACTH?

A
  • stress = hypothalamus releases CRH (corticotrophin releasing hormone)
  • interacts with receptor to cause release of ACTH
  • interacts with receptor to cause cortisol release from adrenal cortex
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16
Q

What are the effects of ACTH?

A
  • ACTH stimulates G-protein receptor coupled to cAMP
  • this stimulates the enzyme that converts cholesterol to cortisol or sex steroid precursors
  • ACTH rises with stress - this is used clinically to test corticotroph function following insulin challenge
17
Q

How is prolactin regulated?

A
  • made by increasing number of lactotrophs
  • maintained by -ve feedback
  • production of dopamine inhibits production of prolactin, but can be unregulated by TRH and VIP (vasoactive intestinal peptide)
  • dopamine release from hypothalamus regulated by stress, sleep and suckling stimulus
18
Q

What are the effects of prolactin?

A
  • lymphocyte regulation
  • osmoregulation
  • steroid production
  • stimulates mammary gland development
  • maintains lactation
19
Q

What are prolactinomas?

A
  • tumour of pituitary gland (most common one)
  • interferes with HPG axis resulting in infertility and other ailments
  • treatment = dopamine agonist e.g. bromocriptine

Hypothyroidism can lead to hyperprolactinaemia due to elevations in TRH –> increased prolactin production

20
Q

What are the properties of growth hormone?

A
  • aka somatotropin
  • released throughout life
  • pulsatile release
  • stimulated by low glucose, exercise and sleep
  • effects mediated by GH and IGF1
21
Q

What are the stimulatory factors regulating GH release?

A
  • GHRH
  • dopamine
  • catecholamines
  • excitatory amino acids
  • thyroid hormone
22
Q

What are the inhibitory factors regulating GH release?

A
  • somatostatin
  • IGF1
  • glucose
  • FFA
23
Q

What can result from an excess or deficiency of GH?

A

Excess:

  • excessive amounts of IGF1 => abnormal growth of tissue or skeleton
  • -> acromegaly and gigantism

Deficiency or resistance:

  • GH receptor mutations - Laron syndrome dwarfism - treated with IGF1
  • GH deficiency - treated with recombinant hGH
24
Q

What are the causes of hypopituitarism?

A

hypopituitarism = diminished hormone secretion

Causes:

  • pituitary tumour
  • brain surgery
  • trauma (road accidents)
  • blocked blood supply, bleeding, inflammation
  • autoimmunity
  • infection
25
Q

What is arginine vasopressin?

A

AKA antidiuretic hormone (ADH)

  • nonapeptide secreted from posterior pituitary
  • synthesised and packaged with a carrier protein (neurophysin) in the secretary granules
  • granules move down to the ends of the fibres
  • both released upon stimulation of the nerves
26
Q

How is ADH secreted?

A
  • acts on collecting ducts of kidney
  • CD intrinsically impermeable to water
  • ADH stimulates production of water channels and their incorporation into the walls of the CD
  • this allows reabsorption of free water from tubular fluid
  • can convert a very dilute using to a concentrated one

(increase ADH to retain water)

27
Q

What are the effects of an ADH excess or deficiency?

A

ADH excess
- caused by variety of conditions e.g. head trauma, secreting tumours

SIADH = syndrome of inappropriate ADH secretion

  • hyper water retention leads to highly concentrated urine
  • hypo water retention = excess water excretion
28
Q

How does ADH link to diabetes insipidus?

A
  • ADH controls serum osmolarity
  • if posterior pituitary damaged, ADH may be reduced and urine cannot be concentrated
  • Polyuria (XS urine production) and polydipsia (XS drinking) are a result of diabetes
  • Hypernatraemia and increased serum osmolarity result
  • diagnosed by having a dilute urine in the context of concentrated plasma
29
Q

What does oxytocin do?

A
  • stimulated contraction of smooth muscle of breast and uterus
  • can be given to induce labour
  • plays roles in milk ejection reflex and parturition (birth)
30
Q

What aren neuro-endocrine reflexes?

A
  • occurs when neuro-endocrine cells secrete hormones from the neural axon terminals into the blood in response to some neural signal
  • e.g. oxytocin

NEUROSCIENCE 2 (32 decks)

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