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FHB Block 4 > L4- Posterior Pituitary and HPL Axis > Flashcards

L4- Posterior Pituitary and HPL Axis Flashcards

1
Q

How large are AVP and OXY?

A

nonapeptides (9 amino acids) —> relatively short half-life

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2
Q

What is the co-peptide for AVP and OXY?

A

AVP: neurophysin II
OXY: neurophysin I

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3
Q

What is another name for AVP?

A

ADH

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4
Q

Cell bodies that produce AVP are located in which two hypothalamic nuclei?

A

Paraventricular (PVN) and supraoptic (SON)

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5
Q

PVN has two types of cells: magnocellular and parvocellular. Which cell types project to the posterior pituitary?

A

Only magnocellular neurons project to the posterior pituitary

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6
Q

Where do parvocellular neurons project to?

A

Parvocellular PVN neurons that contain AVP project to the median eminence and other brain regions. They are important for regulating mood (anxiety/stress)

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7
Q

AVP in magnocellular SON and PVN are important for maintaining what?

A

Fluid balance

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8
Q

What two factors stimulate the release of AVP from the PVN and SON of the hypothalamus into the posterior pituitary?

A

Increase in plasma osmolality and decrease in blood volume (blood loss greater than 10%)

Small changes in plasma osmolality triggers AVP release prior to thirst

Decrease in blood volume sensitizes the system

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9
Q

How does the sympathetic innervation affect AVP release?

A

AVP is mediated by an increase in sympathetic inputs, which releases magnocellular neuronal inhibition

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10
Q

How does AVP cause vasoconstriction?

A

AVP binds the V1 receptor in vascular smooth muscle cells producing contraction and increasing vascular resistance

V1 receptor is a G-protein coupled receptor and acts through IP3/DAG and phosphorylates myosin light chain kinase

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11
Q

How does AVP lead to reabsorption of water?

A

The principle function of AVP is to increase water reabsorption and conserve water.

AVP binds to V2 receptors in the principle cells of the distal tubule. PKA activation phosphorylates the water channel Aquaporin 2 which is then inserted in the membrane and allows increased water permeability.

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12
Q

What is the definition of diabetes?

A

Excessive urine production

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13
Q

What are the two etiologies of diabetes insipidus?

A

1) Decreased AVP release - most common defect
Hypothalamic or pituitary defect 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, hypokalemia

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14
Q

Are AVP levels increased, decreased or normal in people with Diabetes Insipidus?

A

Normal

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15
Q

Oxytocin is released by magnocellular neurons whose cell bodies are located in what hypothalamic nucleus?

A

PVN

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16
Q

What is the main function of OXY?

A

Induce smooth muscle cell contraction in the breast and uterus.

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17
Q

Describe the feedback regulation of OXY

A

OXY release is regulated by positive feedback loops

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18
Q

Describe the chain of events from binding of OXY to its receptor to smooth muscle contraction

A

OXY binds to G protein-coupled receptors and activates PLC signaling pathways which increases intracellular calcium —> —-> phosphorylation of myosin light chain by MLCK

Remember; myosin is the “switch” in the initiation of smooth muscle contraction

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19
Q

How large is GHRH?

A

44 amino acids- large

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20
Q

GHRH (growth hormone releasing hormone) is produced in what hypothalamic nucleus?

A

Arcuate nucleus

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21
Q

What is the role of GHRH?

A

Stimulate growth hormone from the anterior pituitary

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22
Q

What is the role of growth hormone?

A

Growth hormone increases muscle mass and decreases fat –> promotes lean mass growth

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23
Q

Somatostatin (growth hormone releasing inhibitor) is produced where?

A

Somatostatin is produced in the periventricular nucleus (PeVN)

24
Q

What is the role of somatostatin?

A

Somatostatin inhibits GHRH pulse frequency at the level of the hypothalamus. This inhibits GH and TSH in the pitutiary

25
Q

Where does somatostatin 14 predominate vs 28?

A

SS14: brain
SS28: intestines

26
Q

When is growth hormone released?

A

Predominantly during the night

27
Q

Growth hormone is in the same family as what other pituitary hormone?

A

Prolactin (they are structurally similar)

28
Q

What is the goal of growth hormone?

A

GH is a protein anabolic hormone- the goal is to conserve protein

29
Q

What factors increase vs decrease GH?

A

Increase: stress, exercise, starvation
Decrease: age, high blood glucose, obesity

30
Q

Growth hormone stimulates the release of hormone from the liver?

A

IGF-1

31
Q

Name 5 molecules that stimulate GH release from the anterior pitutiary

A

GHRH, Dopamine, NE/E, amino acids, thyroid hormone

32
Q

Name 4 molecules that inhibit GH release from the anterior pituitary

A

Somatostatin, IGF-1 (negative feedback), Glucose (hyperglycemia), Free fatty acids (obesity)

33
Q

How does GH affect the liver?

A

Stimulates production of IGF-1

34
Q

How does GH affect adipose tissue?

A

Increase lipolysis and decrease glucose uptake

35
Q

How does GH affect muscle?

A

Increase protein synthesis

36
Q

GH stimulation of IGF-1 production in the liver is dependent on what?

A

Insulin! You don’t want to promote growth during times of starvation

37
Q

How does GH affect blood glucose levels?

A

GH mobilizes glucose stores and increases plasma glucose levels

GH is stimulated by hypoglycemia and exercise

38
Q

What hormone is directly responsible for bone/cartilage growth?

A

IGF-1

39
Q

How does IGF-1 affect GH?

A

IGF-1 inhibits GH. Negative feedback

40
Q

When during a person’s life does IGF-1 peak?

A

Puberty

41
Q

GH is a _____trope

A

Somatotrope

42
Q

Differentiate gigantism from acromegaly

A

Gigantism: GH Excess that occurs before closing of the epiphyseal plate during childhood. Leads to long bone growth/extreme height

Acromegaly: GH excess - diagnosed middle aged. Gradual enlargement leads to arthritis, change in facial features, enlarged lips/tongue.

43
Q

What is the most common cause of acromegaly?

A

Pituitary adenoma

44
Q

What is Laron syndrome?

A

Genetic defect in GH receptor –> no production of IGF-1

Plasma GH levels are normal to high (because there is no feedback from IGF-1)

45
Q

What is african pigmy?

A

Partial defect in GH receptor –> some IGF-1 response.

No puberty increase in IGF-1

Childhood is normal height, but no growth spurts occur

46
Q

Describe adult GH deficiency

A

increased fat deposition and muscle wasting

47
Q

Name a lactotrope

A

prolactin

48
Q

Are lactotropes part of the endocrine axis?

A

No- there is only a short feedback loop on hypothalamic dopamine- no unique stimulating factor from the hypothalamus

49
Q

How does dopamine affect prolactin?

A

Prolactin is tonically inhibited by dopamine

50
Q

What is galactorrhea

A

Increased prolactin leads to milky discharge from the breast, known as galactorrhea

51
Q

What is the half-life of prolactin?

A

Prolactin is not bound by serum proteins, and has a relatively short half-life (20 minutes)

52
Q

What stimulates prolactin release?

A

Suckling- a “stimulus-secretion reflex”

53
Q

What 3 things is prolactin responsible for?

A

1) Mammary gland development
2) Breast differentiation
3) Milk production

54
Q

How does estrogen affect prolactin?

A

Estrogen increases prolactin synthesis and lactotrope hypertrophy

55
Q

What is the importance of the fact that GH and prolactin are structurally similar?

A

They are similar enough that at high levels they may bind each other’s receptor –> similar effects

Ex: high levels of GH can result in GH binding to the PRL receptor causing galactorrhea

56
Q

How does prolactin affect GnRH?

A

Prolactin inhibits GnRH release

57
Q

What is Sheehans’ syndrome?

A

Hemorrhage during childbirth –> partial pituitary destruction –> prolactin deficiency

Loss of axillary and pubic hair

FHB Block 4 (15 decks)

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