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Endocrine > Lecture 4 > Flashcards

Lecture 4 Flashcards

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1
Q

How many aa are AVP and OXY and what makes up the prehormones?

A

9aa

AVP + Neurophysin 2
OXY + Neurophysin 1

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2
Q

Where are the cell bodies of the AVP neurons located? (what 2 nucleuses)

A
  1. Paraventricular nucleus (PVN)

2. supraoptic nucleus (SON)

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3
Q

PVN has two types of cells magnocellular and parvocellular, only magnocellular project to posterior pituitary. What do the Parvocellular PVN neurons that contain AVP do?

A

project to the median eminence and are important for regulating mood (anxiety)/stress
-works synergistically with CRH to produce ACTH

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4
Q

What is AVP in magnocellular SON and PVN important for?

A

maintaining fluid and balance

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5
Q

What happens to the neurophysin on AVP?

A

is cleaved from the prohormone in the secretory granules during axonal transport

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6
Q

What happens to AVP magnocellular neurons when there is an increase in osmolarity?

A

They shrink and release inhibition–>increase in AVP release
-H20 reabsorption and increase BP

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7
Q

Are barorecpors more or less sensitive than osmoreceptors and what happens when there is a decrease in baroreceptor stretch and firing?

A
  • less sensitive 5-10% decrease in blood volume

- 9 and 10th cranial nerve afferents–>increased sympathetic tone

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8
Q

WHat happens if there is a 10% blood loss?

A

more sensitive to changes in plasma osmolarity-shifts curve to the left-smaller changes to get the same avp release

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9
Q

What type of AVP receptor is there in the smooth muscle and brain? kidney?

A

brain and smooth muscle=v1

kindy=v2

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10
Q

What happens when AVP binds its receptor in the muscle?

A
  • stimulate phospholipase C
  • intracellular calcium
  • Ca/calmodulin
  • MLC kinase
  • ->vasoconstriction
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11
Q

What happens when AVP binds its receptor in the kidney?

A
  • PKA
  • phosphorylate aquaporin 2(only found in collecting duct)
  • translocate into the membrane-water reabsorption

-long term-increased synthesis of aquaporin

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12
Q

What is diabetes insipidus?

A

excessive urine production

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13
Q

What are the 2 main causes (etiology) of Diabetes insipidus?

A
  1. decreased AVP release
    - most common defect
    - hypothalamic or pituitary defect “central” due to trauma, cancer, or infectious disease
  2. decreased renal responsiveness to AVP
    Genetic: x-linked mutation in AVP type 2 receptor- 90% males
    Acquired: lithium treatment(interferes with aquaporin channels being put in membrane), hypokalemia
    AVP levels are normal
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14
Q

What does oxytocin do?

A

Targets smooth muscle in the uterus and breast

  • milk ejection and uterine contractions
  • both are positive feedback loops
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15
Q

What is pitocin?

A

Stimulates OXY used to stimulate labor

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16
Q

How does oxytocin work?

A
  1. PLC and IP3–> increased Ca
  2. ca2+ CaM activates MLCK
  3. increase in MCL myosin ATPase activity
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17
Q

What is the HPL axis of growth hormone?

A

H=arcuate nucleus=GHRH
P=somatotrope= GH
L=liver= IGF-I

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18
Q

How big is GHRH and what is it produced in? What does it do?

A

44 aa
produced in arcuate nucleus
stimulates growth hormone from anterior pituitary

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19
Q

What are the two types of somatostatin? Where are they made and what do they have in common?

A

SS28- made by D cells in stomach and duodenum
SS14-made in hypothalamus (PVN ) and pancreatic ductal cells
-have identical amino terminal

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20
Q

What two things does Somatostatin inhibit?

A
  1. hypothalamus-modulates GHRH pulsatility (decreased frequency)
  2. pituitary- inhibits GH release in pituitary
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21
Q

Both somatostatin and GHRH and GH are being made all the time but what is there relationship?

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A

inverse with Somatostatin

22
Q

When is GH mostly made?

23
Q

How does GH relate to IGF-1 production? What is this dependent on?

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A

GH stimulates IGF-1 production in the liver

-insulin dependent -will not do this in absence of insulin-dont want growing during starvation

24
Q

What does IGF-1 do?

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A

mimics insulin in muscles but not liver or adipose due to lack of receptors

25
Is there classical negative feedback with IGF
yes | -IGF-1 inhibits GH in pituitary
26
When doe IGF-I peak?
during critical periods-highest during puberty
27
What does GH do?
Maintain lean body mass liver: stimulate IGF-1 adipose tissue: increase lipolysis and decrease glucose uptake skeletal: increase protein synthesis - increase gluconeogenesis - mobilize glucose stores and increase plasma glucose
28
What does IGF do in the muscle, what does it not do?
doesn't decrease glucose uptake increases aa uptake increases protein synthesis
29
What are GH direct effects?
adipose tissue, liver, muscle
30
WHat is Gh stimulated by?
hypoglycemia and exercise
31
What are the indirect effects of GH mediated by?
IGF which stimulates cell proliferation in visceral organs and bone/cartilage growth
32
How is GHRH made?
1. transcribed as preprohormone 2. signal peptide cleaved pro hormone-->GHRH (1-45) and the c-terminal peptide GCTP 3. GHRH is further processed to its active form
33
How is somatostatin made?
1. endopeptidases Furin, PC1 and PC2 aid in the processing of the mature SS28 and SS14 SS28=intestine SS14=brain
34
What are 5 GH stimulators?
1. GHRH 2. Dopamine 3. Norepinephrine/Epinephrine (exercise) 4. AA (protein building) 5. thyroid hormone - increased by stress, exercise, starvation
35
What are 4 GH inhibitors?
1. somatostatin 2. IGF-1 (neg feed) 3. glucose (hyperglycemia) 4. free fatty acids (obesity) - decreased with aging, high blood glucose and obesity
36
What can GH excess be caused by?
somatotrope tumor (20%)
37
What is gigantism?
extremely rare, occurs before closing of epiphyseal plate during childhood long bones
38
What is acromegaly?
usually diagnosed in middle age gradual enlargement of hands and feet-leads to arthritis changing in facial features-protruding lower jaw, enlarged lips, tongue, nose possible increased organ size *most often caused by pituitary adenoma
39
What are the two types of dwarfism in children related to GH?
1. Laron Syndrome - genetic defect in GH receptor - no IGF-1 Production - treatment with IGF1 can prevent dwarfism - plasma GH levels are normal to high (lack of feedback) 2. African Pygmy - partial defect in GH receptor-some IGF-1 response - plasm levels of GH normal-no pubertal increase in IGF-1(not caught early cause may not know until puberty)
40
Adult GH deficiency caused by and what does it result in?
caused by pituitary tumor/surgery or treatment (76%) | -increased fat deposition, muscle wasting, reduced bone density, risk of fractures, higher LDL, Triglycerides
41
Are lactotropes part of an endocrine axis?
no- normally not released-usually it is inhibited by dopamine -no unique stimulating factor from hypothalamus
42
What happened in some of the early antihypertension drugs that inhibited dopamine?
``` lactation increased prolactin (galactorrhea) ```
43
Is prolactin bound to serum proteins?
no | half life 20 min
44
What is prolactin released in response to?
suckling "stimulus secretion reflex" - can also be stimulated by TRH and OXY - estrogen increases prolactin synthesis and lactotrope hypertrophy
45
What happens when there is excess GH, what will it bind to?
galactorrhea - binds to prolactin - prolactin also inhibits GnRH so excess production of GH will inhibit reproduction
46
What percentage of pituitary adenomas are prolactinomas?
30-40% of all pituitary adenomas
47
What does prolactinomas lead to?
- hyperporlactinemia - galactorrhea-milk production or discharge from breast - reproduction dysfunction-prolactin inhibits GnRH hormone
48
What happens when there is a prolactin deficiency, what syndrome is this?
Sheehan's syndrome Occurs as a result of excess blood loss/shock during child birth (most of the ones that will die will be lactotrophs because those are the ones dividing at that time) partial pituitary destruction usually affects other pituitary cell types-loss of axillary and pubic hair
49
Must hormones be measured in pairs?
yes like acth and cortisol
50
Stimulation/inhibition tests are used to do what?
normal feedback and pituitary function i. e. dexamethasone suppression test i. e TRH challenge Negative feedback effects Example: 1. insulin induced hypoglycemia should result in? increased GH levels 2. Administration of IGF-1 should result in? decreased GH levels
51
What are the physiological effects of prolactin?
1. mammary gland development 2. breast differentiation - duct proliferation and branching - grandular tissue development 3. milk production - synthesis of milk proteins: beta casein and alpha lactalbumin - synthesis of milk sugar: lactose - synthesis of milk fats in epithelial cells

Endocrine (11 decks)

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