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PHYS - NEURO > 6. NEUROHORMONES > Flashcards

6. NEUROHORMONES Flashcards

1
Q

What are the 8 principal endocrine glands of the body?

A
  1. HYPOTHALAMUS
  2. PITUITARY GLAND
  3. THYROID GLAND
  4. ADRENAL GLAND
    - Adrenal cortex = Aldosterone, cortisol
    - Adrenal medulla = Adrenaline, noradrenaline
  5. PARATHYROID GLAND
  6. PANCREAS
  7. OVARY
  8. TESTES
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2
Q

What hormones does the anterior & posterior pituitary release?

A
  • Anterior pituitary = ACTH, FSH, LH. TSH, GH, PRL

- Posterior pituitary = oxytocin & vasopressin (ADH)

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3
Q

What hormones does the adrenal medulla & cortex release?

A
  • Adrenal medulla = Adrenaline, Noradrenaline

- Adrenal cortex = Aldosterone, cortisol

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4
Q

Describe the principles of the endocrine system

A
  • Mediators travel in the blood stream, slow communication but long term effect
  • Chemical mediators - hormones
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5
Q

Describe the principles of the nervous system

A
  • The nervous system has fast communication but the effects are short lasting or temporary
  • Transmission of electrical impulses
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6
Q

What are neurohormones?

A
  • Neurohormones are produced by NEUROSECRETORY CELLS which are specialised nerve cells
  • The neurohormones are then released into the blood & act on receptors at a distance
  • However, neurohormones can also act as neurotransmitters, autocrine (self) or paracrine (local) factors
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7
Q

Give three classes of hormones

A
  1. PEPTIDE/PROTEIN - synthesised as large precursors which can be cleaved or post-translationally modified.
    - E.g FSH, LH, TSH
  2. AMINO ACID DERVIATIVES - Hormones derived from tyrosine, can also act as neurotransmitters
    - E.g adrenaline, noradrenaline
  3. STEROID HORMONES - Lipids that are derived from cholesterol
    - E.g sex steroids , cortisol
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8
Q

How are the hypothalamus & pituitary associated?

A
  • The hypothalamus & pituitary are joined by the HYPOPHYSEAL NERVE TRACT
  • The infundibulum of the pituitary stalk also connects the two structures
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9
Q

How do hormones released by the hypothalamus act on the pituitary?

A
  • Neurohormones synthesised by the hypothalamus will be carried by neurones projecting into the pituitary
  • The neurohormones will be released into the hypophyseal portal circulation which is a capillary network & portal vein system
  • The hormones will then be released from the pituitary gland
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10
Q

What are the two major hypothalamic neurones?

A
  1. Magnocellular neurones

2. Parvocellular neurones

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11
Q

Describe the magnocellular neurones

A
  • The magnocellular neurones project from the hypothalamus to the posterior pituitary
  • The posterior pituitary is also known as neurohypophysis & produces vasopressin & oxytocin
  • The cell body of the magnocellular neurones is located in the hypothalamus but it projects to the pituitary
  • Magnocellular neuronal cell bodies are located in the:
    1. Paraventricular nuclei
    2. Supra optic nuclei
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12
Q

Describe the parvocellular neurones

A
  • Parvocellular neurones project from the hypothalamus to anterior pituitary
  • The anterior pituitary is also known as adenohypophysis
  • The neurohormones will be released from the neurones into the capillary network to activate specific cells of the pituitary
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13
Q

What does corticotrophin releasing hormone do?

A
  • CRH released from hypothalamus
  • CRH acts on corticotrophs of anterior pituitary
  • ACTH released from anterior pituitary
  • Cortisol released from adrenal cortex
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14
Q

What does the thyrotrophic releasing hormone do?

A
  • TRH released from hypothalamus
  • TRH cats on thyrotrophs of anterior pituitary
  • TSH released from anterior pituitary
  • Thyroid hormones released from thyroid gland
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15
Q

What does growth hormone releasing hormone do?

A
  • GHRH controls release of GH from anterior pituitary
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16
Q

What does somatostatin do?

A
  • Somatostatin/ Growth hormone inhibiting hormone inhibits the release of GH, VIP, TSH, PRL & insulin
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17
Q

What are the specialised cells of the anterior pituitary?

A
  1. Gonadotrophs - release FSH & LH in response to GnRH
  2. Corticotrophs - Release ACTH in response to CRH
  3. Thyrotrophs - Release TSH in response to TRH
  4. Somatotrophs - Control LH in response to GHRH
  5. Lactotrophs - control PRL, in response to dopamine, somatostatin, TRH
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18
Q

What is ACTH & what does it do?

A
  • ACTH (adrenocorticoptrophin hormone) is released in response to CRH produced by the hypothalamus
  • ACTH stimulates the release of glucocorticoids (cortisol) & sex steroids (androgens) from the zona fasciculata of the adrenal cortex
19
Q

Describe the mechanism of cortisol release via the HPA axis?

A
  • CRH released from hypothalamus
  • CRH acts on corticotrophs of anterior pituitary
  • Anterior pituitary releases ACTH
  • ACTH causes release of cortisol & adrenal androgens from adrenal cortex
20
Q

How do cortisol levels change throughout the day?

A
  • Cortisol levels are highest in the morning & decline throughout the day due to the pattern of ACTH secretion from the anterior pituitary
21
Q

Describe the HP-Thyroid axis

A
  • TRH released by hypothalamus
  • TRH acts on thyrotrophs of anterior pituitary
  • TSH released from anterior pituitary
  • Thyroid hormones released from thyroid glad (T3 & T4)
22
Q

What are the two thyroid hormones?

A
  1. T3 - TRIIODOTHRYOXINE
  2. T4 - THYROXINE
    - T4 can be converted to T3 with DEIODINASE
    - T4 is responsible for basal metabollic rate, high T4 = weight loss
23
Q

Describe the synthesis of vasopressin & oxytocin?

A
  • Vasopressin & oxytocin are released from the posterior pituitary
  • They are synthesised in the supraoptic & paraventricular nuclei of the magnocellular neurones which project into the posterior pituitary, where they’re released
24
Q

What is vasopressin & it’s effects?

A
  • Vasopressin is also known as antidiuretic hormone
  • It’s released from the posterior pituitary in response to changes in osmoreceptors of the hypothalamus
    1. Controls osmolalilty - regulates water excretion & thirst
    2. Stimulates contraction of smooth muscle of the kidney to cause vasoconstriction
  • Both of these changes help to regulate blood volume
25
Q

Describe RAAS & it’s interaction with the hypothalamus to release ADH

A
  1. A drop in blood pressure or plasma volume causes teh kidneys to release RENIN
  2. RENIN converts ANGIOTENSINOGEN into ANGITENSIN I
  3. ANGIOTENSIN I circulates in the blood & is converted to ANGIOTENSIN II
  4. ANGIOTENSIN II causes vasoconstriction
  5. ANGIOTENSIN II is detected by the SUB-FORNICAL REGION
  6. Neuronea of the sub-fornical region project to the magnocellular neurones of the hypothalamus releasing vasopressin/ADH
  7. Vasopressin affects the kidneys & increases water retention to regulate blood volume
26
Q

What is oxytocin?

A
  • Oxytocin is synthesised in the hypothalamus & is released by the posterior pituitary
  • Oxytocin levels can elevated during lactation & mating
  • Oxytocin can be produced in response to cervical stretch receptors, stroking, grooming etc.
27
Q

What are the peripheral effects of oxytocin?

A
  1. Stimulates contraction of uterine wall smooth muscle during labour
  2. Contracts myoepithelial cells of mammary glands - lactation
  3. Contracts reproductive duct during sperm ejaculation in males
28
Q

What are the central nervous system effects of oxytocin?

A
  • Oxytocin can be released into central areas of the brain such as the cortex
  • The functions of oxytocin in these areas are not well understood, but it’s thought to be involved in trust, empathy, social bonding & cognition
  • It can therefore be used as treatment for autism, OCD, depression
29
Q

Give examples of hormones that bind to a tyrosine kinase receptor?

A
  • Growth hormone

- Insulin

30
Q

Describe the mechanism of action for tyrosine kinase receptors

A
  1. (GH or insulin) Peptide hormone binds to tyrosine kinase receptor
  2. Leads to dimerisation of the receptor
  3. Activates tyrosine kinases (JAK2/MAPIC)
  4. Tyrosine kinases phosphorylate target proteins to cause signalling cascade
31
Q

Give examples of hormones that bind to a G-protein adenylate cyclase receptor?

A
  • TSH

- ACTH

32
Q

Describe the pathway for G-protein adenylate cyclase receptors

A
  1. TSH or ACTH bind to receptor & activate Gs or Gi protein
  2. Adenylate cyclase can be stimulated or inhibited depending on G protein
  3. Stimulation of AC= increased cAMP & increased PKA
  4. PKA phosphorylates target proteins to cause signalling
33
Q

Give examples of hormones that bind to a G-protein phospholipase C receptor?

A
  • Oxytocin

- GnRH

34
Q

Describe the pathway for G-protein phospholipase C receptors

A
  1. Oxytocin & GnRH bind to receptor coupled to Gq
  2. Phospholipase C is activated which converts PIP2 -> IP3 + DAG
  3. IP3 causes increase in intracellular Ca2+
  4. DAG activates PKC which phosphorylates target proteins
35
Q

Give examples of hormones that bind to a nuclear receptor?

A
  • Sex steroids (testosterone, oestrogen)

- Cortisol

36
Q

Describe the pathway for nuclear receptors receptors

A
  1. Steroid hormones pass through cell membrane as they’re lipophillic, don’t act on surface receptors
  2. Bind to receptors within cytoplasm to form hormone-receptor complex
  3. Hormone-receptor complex enters nucleus
  4. Hormone-receptor complex acts as a transcription factor by binding to a motif in the DNA sequence
  5. Initiates protein synthesis
37
Q

What are diseases caused by too much GH & PRL?

A
  • Too much GH = Acromegaly or Gigantism

- Too much PRL = Hyperprolactinaemia

38
Q

What is hyperthyroidism & hypothyroidism?

A
  • Hyperthyroidsim = too much thyroid hormone

- Hypothyroidism = too little thyroid hormone

39
Q

Give an example of a hypothyroidism disease

A
  • Hashimoto’s disease = too little thyroid
  • Autoimmune disease, antibodies to thyroid hormone
  • Causes: Radioactive iodine treatment, thyroid surgery, pituitary dysfunction
40
Q

Give an example of a hyperthyroidism disease

A
  • Grave’s disease = too much thyroid
  • Autoimmune disease, antibodies attack thyroid gland which mimic TSH causing thyroid production
  • Symptoms: fatigue, goitre, anxiety, weight loss
41
Q

What is adrenal insufficiency & give an example of a disease

A
  • Adrenal insufficiency is when too little adrenal hormones are produced e.g cortisol. The adrenal glands don’t produce enough cortisol
  • Addison’s disease is an example of primary adrenal insufficiency
  • Symptoms: fatigue, darkened skin, irregular menstruation
42
Q

What is Cushing’s syndrome?

A
  • Cushing’s syndrome occurs when there’s too much cortisol production
  • Causes:
  • External steroids (medications e.g asthma)
  • Surgery
  • Adrenal adenoma
  • Cushing’s disease - produces too much ACTH leading to too much cortisol
43
Q

What’s the difference between Cushing’s disease & Cushing’s syndrome?

A
  • Both Cushing’s disease & Cushing’s syndrome result in elevated cortisol levels but have different cortisol
  • Cushing’s disease can lead to Cushing’s syndrom
  • In Cushing’s disease, a pituitary adenoma scretes too much ACTH which results in adrenal hyperplasia causing too much cortisol
  • Whereas, Cushing’s syndrome is simply an increase in cortisol due to other reasons

PHYS - NEURO (18 decks)

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