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Y1 LCRS Endocrinology > 4 The Hypothalamo-Neurohypophysial Axis > Flashcards

4 The Hypothalamo-Neurohypophysial Axis Flashcards

1
Q

Q: How do the posterior and anterior pituitary glands differ in terms of where neurosecretion occurs?

A

A: ant= median eminence

post= project all way down to posterior pituitary gland

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2
Q

Q: Describe the principle features of the hypothalamo-neurohypophysial system with the aid of a diagram.

A

A: neural input

paraventricular nuclei // supra-optic nuclei

superior hypophysial artery // median eminence // mammillary body

hypophysial portal vessel
inferior hypophysial artery
pituitary cells |
\/
vasopressin // oxytocin

anterior pituitary // posterior pituitary

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3
Q

Q: What are the 2 types of nuclei in the hypothalamo-neurohypophysial system?

A

A: supraoptic and paraventricular

(where cell bodies lie)

are the 2 different types of populations where each is a group of neurones

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4
Q

Q: What is the main neurone type in the hypothalamo-neurohypophysial system? Where do they terminate?

A

A: magnocellular, neurohypophysis (posterior pituitary gland)

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5
Q

Q: What is the less common neurone type in the hypothalamo-neurohypophysial system? Where do they terminate? Where do they originate? What do they secrete?

A

A: paravocellular- exception since ends in median eminence or another part of brain

originate from paraventricular nuclei

vasopressin

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6
Q

Q: Describe supraoptic neurones including structure. (5)

A

A: equipment to make hormones is in cell body (most neurones secrete vasopressin or oxytocin)

1 leave hypothalamic supraoptic nuclei (where they originate)
2 pass through median eminence
3 terminate in neurohypophysis (end)

herring bodies are present along the axon

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7
Q

Q: What are herring bodies?

A

A: storage sites for posterior pituitary hormones (lie along axon)

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8
Q

Q: Describe paraventricular neurones including structure. (5)

A

A: 1 originate in paraventricular nuclei
2 majority of neurones are magnocellular -> pass down to neurohypophysis
3 some (parvocellular) neurones pass to other parts of brain
4 some (parvocellular) VP neurones terminate in median eminence
5 are either vasopressinergic or oxytocinergic

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9
Q

Q: Compare vasopressin and oxytocin in terms of their chemical structure. (4)

A

A: both are simple peptide with a loop and a tail

differ by 2 aa (vaso has Phe and Arg while oxy has Ile and Leu)

contain disulphide bridges (one) in loop

are nonapeptides since 2-20 aa present

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10
Q

Q: How is vasopressin synthesised? (3)

A

A: pre-prohormone first made in cell body of either supraoptic or paraventricular nucleus; pre-vasopressin which contains signal peptide;SP at start - directs it to where it needs to go

–signal peptide quickly lost as moves towards axon–> prohormone; provaspressin

–cleaved–> vasopressin;AVP (arginine vasopressin + neurophysin;NP + glycopeptide;GP

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11
Q

Q: Where does neurophysin come from and why is it important?

A

A: when provasopressin is cleaved

important in maintaining vasopressin/oxytocin stability- stops it moving out of neurone/herring body and stops degradation by enzymes

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12
Q

Q: How does vasopressin synthesis differ from oxytocin synthesis?

A

A: vasopressin has same sequence as oxytocin synthesis, except that the neurophysin differs slightly (by product when prohormone is cleaved) and the glycopeptide is absent (for oxytocin)

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13
Q

Q: How do the 2 types of vasopressin receptor vary? Action. Linked to _ via _. What does this do- cascade? What’s the type of response produced?

A

A: V1 receptor- vasoconstriction action
linked via G proteins to phospholipase C- acts on membrane phospholipids to produce inositol triphosphate (IP3) and diacyl glycerol (DAG)
increases cytoplasmic [Ca^2+] and other intracellular mediators (PKC)
which produces cellular response

V2 receptor- antidiuretic action
linked via G proteins to adenyl cyclase- acts on ATP to produce cAMP which activates protein kinase A which activates other intracellular mediators
which produces cellular response (aquaporins, AQP2)

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14
Q

Q: What is vasopressin also known as?

A

A: anti-diuretic hormone

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15
Q

Q: What is the effect of vasopressin receptor V1a and V1b in different target cells? (3,1)

A

A: V1a

main= arterial/arteriolar smooth muscle (vasoconstriction)

hepatocytes (glycogenolysis)

CNS neurones (behavioural and other effects)

V1b

corticotrophs (ACTH production)

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16
Q

Q: What is the effect of vasopressin receptor V2? (4)

A

A: main= collecting duct cells (water reabsorption)

other effects (endothelial cells, factor VII and von willeband factor)

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17
Q

Q: What is the principle physiological action of ADH/vasopressin? (3)

A

A: is in renal collecting duct (principle cells)

stimulates water reabsorption

resulting in its antidiuretic effect

18
Q

Q: How does vasopressin work in principle cells/collecting duct? Include basic diagram. (8)

A

A: V2 receptors are

  1. Vasopressin binds to the V2 receptor (basolateral membrane)
  2. activates adenylate cyclase-> converts ATP to cAMP
  3. cAMP activates protein kinase A which stimulates the synthesis of AQUAPORIN 2 molecules

((There are 9 types of aquaporin but AQUAPORIN 2 is the vasopressin dependent aquaporin))

  1. Aquaporins assemble into accumulations called Aggraphores
  2. Under the influence of vasopressin, aggraphores migrate to the luminal apical membrane (facing the inside of the collecting duct)
  3. Once the channels are inserted into the membrane, then water can move into the cells
  4. Water is transported out of the cells and into the blood via AQP3 and AQP4 (aren’t really affected by vasopressin)
  5. An osmotic gradient is needed for the movement of water from the collecting duct, through the principal cells and into the blood

diagram; principle cell (lines kidney tubule)
osmotic gradient across cell —->
tubule lumen; apical membrane | cell | basolateral (serosal) membrane; plasma

19
Q

Q: What are the physiological actions of oxytocin (target cells)? (4) Unwanted effects on? (2)

A

A: major- therapeutic advantage (relating to the healing of disease)

  • uterus (contraction)
  • mammary gland - myoepithelial cells

minor- unwanted effects

  • cardiovascular system
  • kidney

additional physiological
-CNS

20
Q

Q: When does oxytocin levels spike in women?

A

A: end of pregnancy

21
Q

Q: What are the 2 main groups of target cells for oxytocin? What action occurs?

A

A: Uterus during parturition (childbirth)- myometrial cells- contraction -> delivery of baby

Breast during lactation- myoepithelial cells (produce milk)- contraction -> milk ejection

OXYTOCIN IS A CONTRACTOR MOLECULE - it causes constriction

22
Q

Q: Explain oxytocin’s physiological action on the uterus. (3) What enhances and suppresses action?

A

A: promotes

rhythmic contraction; fundus -> cervix
increased local prostanoid production
dilation of cervix (opens birth channel -> delivery)

enhanced by oestrogen
suppressed by progesterone

23
Q

Q: What is a fundus?

A

A: the part of a hollow organ (such as the uterus or the gall bladder) that is furthest from the opening

24
Q

Q: What are prostanoids? When are they made? Action? (2)

A

A: lipid mediators generated by the action of cyclooxygenase
are generated widely in response to diverse stimuli
acting in a paracrine or autocrine manner

25
Q

Q: How does the sensitivity of the pregnant uterus to oxytocin change throughout the pregnancy? Why?

A

A: graph

contractile response to oxytocin (y) and weeks of gestation (x)

0 to 20 is horizontal
stays until around 33 then increases till end (straight like / )

increases near end of term- reason= oestrogen also goes up towards pregnancy end (oest stimulates production of oxytocin receptors and hence uterus is more sensitive to oxytocin)

26
Q

Q: Explain oxytocin’s physiological action on the mammary gland.

A

A: contraction of myoepithelial cells leads to milk ejection

27
Q

Q: What are the 3 physiological actions of oxytocin except uterine contraction and lactation? (1,2,2)

A

A: cardiovascular- pharmacological
constriction of umbilical arteries and veins (important as the foetus is delivered and moves away from the need of the placenta)

renal- pharmacological
anti-diuresis
secondary hyponatraemia (occurs when sodium levels are low)

CNS- physiological
maternal behaviour
social recognition

28
Q

Q: What breaks down collagen (has formed tight membrane that helps child in utero) and allows delivery?

A

A: prostaglandins particularly PGE2

29
Q

Q: Describe the female pattern response driven by oxytocin. What inhibits/has positive effect on oxytocin?

A

A: tend and befriend (typical behavioural stress response = fight/flight which is quite a male pattern response)

tend; women protect and care for their chn
befriend; women seek out and receive social support

testosterone tends to inhibit
oestrogen tends to have a positive effect on oxytocin

30
Q

Q: What are 3 major clinical uses of oxytocin?

A

A: induction of labour at term

prevention treatment of post-partum haemorrhage

facilitation of milk let-down

autism - social responsiveness?

31
Q

Q: What are the 2 homeostatic methods of control of vasopressin? What are they based on (stimulus)?

A

A: 2 methods to control release since 2 major functions
Water Reabsorption based on plasma osmolality
Vasoconstriction based on arterial bp

32
Q

Q: Define plasma osmolality.

A

A: concentration of osmotically active particles in blood

33
Q

Q: Explain the homeostatic method of control of vasopressin where plasma osmolality is the stimulus. (6)

A

A: stimulus of high plasma osmolality (dehydration) received by osmoreceptors in hypothalamus - when higher osmolality in blood than neurone ->

cell body of neurone loses water and shrinks ->

stimulates neurone to fire

  • > more vasopressin (ADH) in blood
  • > more aquaporins -> increases water absorption
  • > decreases plasma osmolality (response)
34
Q

Q: Explain the homeostatic method of control of vasopressin where arterial blood pressure is the stimulus. (5)

A

A: stimulus of decreased arterial bp detected by baroreceptors/volume receptors which have

an inhibitory effect on vasopressin and firing rate is proportional to bp therefore if bp falls you get less inhibitory effect on ADH

  • > more vasopressin produced
  • > increased vasoconstriction
  • > get increased bp (response)
35
Q

Q: What is the neuroendocrine reflex arc? Describe it in relation to oxytocin. (6)

A

A: afferent nerve carries information (stimulus) -> efferent nerves (independent of brain) -> induce response

endocrine effect = doesn’t require brain

direct efferent effect -> produce oxytocin

stimulus; suckling -> neural afferent limb -> hypothalamus (neurone bundle) -> nerve to neurohypophysis -> produce oxytocin -> contraction of the myoepithelial cells in the breast resulting in milk ejection

36
Q

Q: What does lack of oxytocin lead to?

A

A: parturition and milk ejection effects induced/replaced by other means

37
Q

Q: What does lack of vasopressin lead to?

A

A: diabetes insipidus

symptoms of diabetes and little vasopressin are similar hence name

38
Q

Q: What are vasopressin and oxytocin?

A

A: neurohypophysial hormones

39
Q

Q: What causes diabetes insipidus? (2)

A

A: 2 forms

 absence/lack of circulating vasopressin
                               |
                              \ / central (cranial) form (less severe but more difficult to treat)
                               |
                              \ /
                 diabetes insipidus
                              / \
                               | nephrogenic form (often drug induced cause)
                              / \
                               | end-organ (kidneys) resistance to vasopressin (vasopressin is still produced)

causes- headtrauma, certain tumours, autoimmune

40
Q

Q: What are the symptoms of diabetes insipidus? (3) How do you treat it?

A

A: polydipsia (increased thirst)

polyuria (large volumes of urine)

urine is very dilute (hypo-osmolar)

drink more water- not particularly debilitating disease if you have access to clean water

Y1 LCRS Endocrinology (19 decks)

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