Hypothalamo-neurohypohysial system Flashcards

1
Q

Describe the anatomy of the pituitary gland

A

Anterior (adeno)- made up of secretory cells

Posterior (neuro)- made up of nerve axons

The median eminence is the location of the primary comillary plexus which is a part of a portal system linking the median eminence to the anterior pituitary (hypothalamo-adenohypophysial portal system)

The neurohypophysis is made up of nerve axons and some other cells. The nerves have their cell bodies in the hypothalamus and their nerve axons pass down through the pituitary stalk into the neurohypophysis.

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2
Q

What is the hypothalamic nuclei?

A

A collection of cell bodies which send their axons to a particular place. They are in the hypothalamus.

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3
Q

What are the two types of cell bodies?

A
  1. Paraventricular nucleus- located close to the 3rd ventricle. Some of the neurones which originate in the paraventricular nucleus terminate on the walls of the primary capillary plexus, this suggests that secretion have an effect on the anterior pituitary- these are small neurones (parvocellular hormones). The other neurones terminate in the neurohypophysis- these are longer ones called magnocellular neurones. The magnocellular neurones terminate in the neurohypophysis
  2. Supraoptic- lying above the optic chiasma
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4
Q

Which hormones are associated with neurohypophysis?

A
  • vasopressin
  • oxytocin
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5
Q

What is the superchiasmatic nucleus?

A

Some vasopressingergic neurones originate here

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6
Q

Describe supraoptic neurones

A

They are magnocellular and terminate in the neurohypophysis. They release neurosecretions in the neurohypophysis where they terminate. The neurosecretions are HORMONES because they go into general circulation. So:

  1. Neurosecretions leave the hypothalamic supraoptic nuclei
  2. They pass through the median eminence
  3. They terminate in the neurohypophysis

They have herring bodies which are specific for magnocellular neurones from the supraoptic and paraventricular nuclei. Herring bodies are areas where the neurosecretions can be stored and they can also be released from there too.

Supraoptic neurones are either vasopressinogenic or oxytocinergenic

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7
Q

Describe paraventricular neurones

A

They have a magnocellular and parvocellular component. The magnocellular components terminate in the neurohypophysis- they have herring bodies and can release neurosecretions into the general circulation.

Parvocellular neurones are either vasopressinogenic or oxytocinergic

Some parvocellular neurones pass to other parts of the brain, but others will terminate in the median eminence.

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8
Q

What are the molecular differences between vasopressin and oxytocin

A

Vasopressin= Phenylalanine and Arginine in the tail

Oxytocin= Isoleucine and leucine in the tail

they are both nonapeptides

The vasopressin prohormone is cleaved to produce three molecules (AVP, neurophysin, glycopeptide)

The oxytocin prohormone is cleaved to produce two molecules ( oxytocin and neurophysin)

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9
Q

Synthesis of vasopressin (AVP)

A

Pre hormone –> pro hormone –> hormone

The prohormone breaks down into three molecules: vasopressin (AVP), neurophysin, and glycopeptide (most likely prolactin)

This takes place in the nerve axon.

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10
Q

Synthesis of oxytocin

A

Same as AVP but pre-prooxytocin is cleaved to 2 molecules: oxytocin and neurophysin (slightly different structure to the one produced in the synthesis of AVP)- no glycoprotein is produced.

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11
Q

What are the actions of vasopressin?

A

Physiological action in the collecting ducts- stimulates water reabsorption by principle cells.

It has an antidieuretic effect

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12
Q

Describe the 2 vasopressin receptors (v1 and v2)

A

V1 receptors= linked via G proteins to phospholipase C which acts on membrane phospholipids to produce inositol triphosphate IP3 (and DAG- diacyl glycerol). This increases cytoplasmic Ca 2+ and other intracellular mediators (PKC) which produce a cellular response.

V1a- arterial smooth muscle, hepatocytes and CNS neurones / V1b- corticotrophs (ACTH production)

V2 receptors- linked via G proteins to adenyl cyclase which acts on ATP to form cyclic AMP- this activates PKA which in turn activates other intracellular mediators which produce a cellular response. (aquaporins AQP2). present in the collecting duct cells (water reabsorption)- other effects (endothelial cells, facto VIII and von Willbrandt factor)

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13
Q

Action of aquaporins in the cells of the collecting duct (how do they get there?)

A

Hormone (VP) delivered by the blood. Arrives in capillaries to collecting duct and diffuses across to the V2 receptor which is coupled with adenyl cyclase. PKA activated- which also activates other intracellular mediators.

Aquaporin 2 moleucles are synthesised (water channels). They are housed within vesicles inside the cells. The vesicles they are kept is are called aggraphores.

The vesicles move towards/ fuse with the membrane due to the cascade of reactions caused by the VP. The apical membrane is impermeable to water so the only way they can reabsorb water is through the aquaporins. The apical membrane faces the lumen.

There is always an osmotic force pulling water into the cell because NA+ diffuse through from lumen to plasma. There are aquaporins (3 and 4)at the other side of the cell but they’re not as important because they will only release water if AQP2 gets water into the cell.

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14
Q

Describe the physiological action of oxytocin?

A

Major effect is the therapeutic advantages: in the uterus (helps to produce powerful contraction) and mammary gland (myoepithelial cells- milk ejection)

Unwanted effects on the cardiovascular system (vasodilation and tachycarida- constriction of umbilical arteries and veins) and the kidney (anti-diuresis and secondary hyponatraemia)

CNS- maternal behaviour and social recognition

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15
Q

oxytocin and the uterus

A

Rythmic contraction and increased dilation of the cervix.

Increased local prostanoid production.

Uterine actions of oxytocin are suppressed by progesterone and enhanced by oestrogen- the uterus becomes increasingly sensitive to oestrogen close to the birth of baby.

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16
Q

Tend and befriend theory

A

tend- women seek to protect and care for their children

befriend- women seek out and receive social support

17
Q

What are the major clinical uses of oxytocin?

A
  • Induction of labour at term (controlled and IV infusion)
  • Prevention treatment of post-partum haemorrhage- slow iv- local pressor action in uterus suppresses bleeding
  • facilitation of milk let-down- internasal spray
  • Autism- social responsiveness
18
Q

Describe the control of vasopressin

A

vasopressin causes water reabsorption and vasoconstriction

1) when you are dehydrated there is an increase in plasma osmolality. This is the stimulus for vasopressin release. A rise in plasma osmolality is detected by osmoreceptors. The osmoreceptors are in contact with vasopressinergic neurones but also with the blood- they lie outside the blood brain barrier (circumventricular organs). The dehydration of the osmoreceptors leads to a stimulation of the vasopressinergic neurones.
2) Fall in blood pressure is a stimulus for vasopressin. Baroreceptors are stretch receptors which are stimulated by an increase in pressure. Higher the bp, the higher the baroreceptor firing range. Vice versa. The baroreceptor neurone inhibits vasopressin. If bp down, baroreceptor firing range down. Less inhibition of vasopressin so you get vasopressin secretion. It acts as a vasoconstrictor and increase bp. Blood pressure does have to drop quite a bit for this response to happen.

19
Q

Control of oxytocin

A

There is one neuroendocrine reflex arc- it is this one:

It can go to the adenohypophysis to stimulate prolactin production and to the neurohypophysis to stimulate oxytocin production. The oxytocin causes the myoepithelial cells to contract which leads to milk ejection.

A lack of oxytocin can lead to parnutrition and milk ejection effects induced/ replaced by other means

20
Q

What does a lack of vasopressin lead to?

A

Diabetes insipidus

There is either:

  1. absent/ lack of circulating vasopressin- this is known as central (cranial)
  2. End-organs (kidneys) are resistant to vasopressin- this is known as nephrogenic

Both cause excessing urination but there is no problem with filtration of glucose

21
Q

Diabetes insipidus symptoms

A
  • polydipsia- increased thirst
  • polyuria- large volumes of urine
  • urine is very dilute- hypo-osmolar
22
Q

What is syndrome of inappropriate ADH (SIADH)?

A

Too much ADH is being produced

Patients urinate very little and concentrated urine due to the decrease in plasma osmalality

23
Q
A