Lecture 4: Posterior Pituitary and HPL Axis Flashcards

(57 cards)

1
Q

What differentiates a preprohormone from a prohormone?

A

signal peptide

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2
Q

AVP associates with neurophysin ___

A

II (has 2 names - vasopressin, ADH, goes with NPII)

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3
Q

Oxytocin associates with neurophysin ___

A

I

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4
Q

Where are the cell bodies for AVP located?

A

In the PVN (paraventricular) and SON (supraoptic)

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5
Q

What are the 2 types of cells in the PVN?

A

1) magnocellular

2) parvocellular

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6
Q

Which type of neuron projects into the posterior pituitary?

A

magnocellular

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7
Q

Where do parvocellular PVN neurons project?

A

median eminence

regulate mood/anxiety/stress

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8
Q

When is neurophysin cleaved from AVP and oxytocin?

A

cleaved from prohormone in secretory granules during axonal transport

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9
Q

AVP release increase when plasma osmolarity __________

A

increases

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10
Q

which comes first, AVP release or thirst sensation?

A

AVP release

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11
Q

AVP release is tonically inhibited by what?

A

baroreceptor stretch and firing

decreased stretching during hypotension so you get DISINHIBITION

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12
Q

When plasma osmolarity increases, do osmoreceptors swell or shrink?

A

SHRINK (inducing AVP release)

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13
Q

GaqPCR stimulates ____

A

Ca++ (leads to vasoconstriction)

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14
Q

What receptors and where does AVP act?

A

V2 receptors on the kidney

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15
Q

What does AVP action do in the principal cells of the distal tubule?

A

phosphorylate aquaporin 2 to move these channels to the apical membrane

SHORT term: quick relocation, not synthesis
LONG term: makes more aquaporin

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16
Q

What are the 2 causes of diabetes insipidus?

A

1) decreased AVP release
2) decreased renal responsiveness to AVP

(AVP release defect is more common)

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17
Q

What causes diabetes insipidus?

A

AVP release problem: trauma, infectious disease

Renal responsiveness problem: genetic problem w/ receptor, lithium, hypokalemia

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18
Q

How do you tell the difference between the two causes of diabetes insipidu?

A

measure AVP levels (if normal, renal problem)

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19
Q

What does oxytocin do?

A

1) target smooth muscle in breast to stimulate milk ejection
2) stretch the cervix at the end of pregnancy
3) cuddling hormone

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20
Q

What stimulates the production of more oxytocin?

A
  • more suckling

- more contractions

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21
Q

What synthetic hormone is used to stimulate labor?

A

Pitocin (oxy synthetic)

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22
Q

What is the oxytocin receptor?

A

GPCRaq

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23
Q

What effects does oxytocin have on the cell?

A

increase IP3 and increase calcium to increase MLC myosin ATPase activity

24
Q

Which axis regulates growth?

A

HPL axis
H = arcuate nucleus GHRH
P = somatotrope GH
L = liver IGF-1

25
Where is GHRH produced in the hypothalamus?
arcuate nucleus
26
What inhibits GHRH at the level of the hypothalamus?
somatostatin | also inhibits GH and TSH in the pituitary
27
Where is somatostatin produced?
1) D cells in the stomach and duodenum (SS28) | 2) PVN of the hypothalamus (SS14)
28
What effect does somatostatin have on GHRH in the hypothalamus? pituitary?
decreases frequency of pulses pituitary: inhibits GH release when there is enough circulating
29
There is an _________ relationship between GHRH and somatostatin?
inverse
30
When during the day does GH peak?
at night during sleep
31
Many downstream target organ effects of GH are mediated through ________
IGF-1 | production is stimulated by GH
32
Describe the negative feedback loop that influences growth
GH released by pit. ----> acts on hepatocytes to stimulate IGF-1 (insulin dependent) ----> IGF-1 inhibits GH
33
Why is GH stimulation of IGF-1 insulin dependent?
because you don't want growth to occur in times of starvation
34
Which hormone is responsible for maintaining lean body mass?
GH
35
What does IGF-1 do?
mimics insulin in muscle but NOT in liver and adipose due to lack of IGF-1 receptors
36
When in life is IGF-1 the highest?
puberty
37
What is the primary job of GH?
decrease adiposity (mobilize glucose in the blood - antagonist to what insulin is doing) increases lipolysis and decreases glucose uptake in fat cells
38
GH ________ (increases/decreases) adiposity and __________ lean body mass
decreases (promotes lipolysis) | increases (promotes protein synthesis)
39
Is growing mediated by GH or IGF-1?
IGF-1!!! Does all the heavy lifting, just needs to be activated by GH
40
What does IGF-1 do?
increases organ size (kidney, pancreas, intestine, islets, skin, bone, heart, lung), function and linear growth
41
True or false: IGF-1 increases glucose uptake in the muscle
FALSE (decreases glucose uptake)
42
What 3 things promote GH decrease?
1) age 2) hyperglycemia 3) obesity
43
What 3 things promote GH increase?
1) stress (NE and ep) 2) exercise 3) starvation
44
What 2 conditions can GH excess lead to?
1) Gigantism (before closing of epiphyseal plate - long bones) 2) Acromegaly (thick bones, pituitary adenoma, enlarged facial features)
45
What does GH deficiency lead to?
dwarfism (chipdren)
46
What are the 2 types of dwarfism?
1) Laron Syndrome (no production of IGF-1, genetic defect in GH) 2) African pygmy (defect in GH receptor, some IGF-1 )
47
How do you treat dwarfism?
IGF-1
48
True or false: lactotropes are NOT part of endocrine axis
TRUE (no stimulating factor from hypothalamus)
49
Prolactin is tonically inhibited by ________
dopamine
50
Is prolactin bound to hormone binding protein?
NO, short half life (20 mins)
51
When is prolactin produced?
in response to suckling (stimulus-secretion reflex)
52
Prolactin is a very potent inhibitor of _______
GnRH
53
Prolactin is in the same family as ____
GH
54
What do prolactinomas lead to?
galactorrhea (milk production/discharge from breast) | reproductive dysfunction because prolactin inhibits GnRH
55
What does prolactin deficiency lead to?
Sheehan's syndrome (occurs as result of excessive blood loss/shock during childbirth)
56
What happens to GH levels during insulin-induced hypoglycemia?
INCREASE
57
What happens to GH levels as IGF-1 is administered?
DECREASE