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Posterior pituitary and HPL axis (L4) Flashcards

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1
Q

Makeup of oxytocin and vasopressin

A

Both nonapeptides made first as preprohormones

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2
Q

Prohormones of OXY and AVP

A

Oxytocin + neurophysin I,

AVP + neurophysin II

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3
Q

Preprohormones of OXY and AVP

A

9 AAs, glycopeptide, signal peptide, and neurophysin

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4
Q

When is neurophysin cleaved from the peptide?

A

In the secretory granules during transport

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5
Q

What types of cells are located in the paraventricular nucleus?

A

Magnocellular and parvocellular

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6
Q

Which of the two cell types in the paraventricular nucleus projects to the posterior pituitary?

A

Magnocellular

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7
Q

What happens with the parvocellular cells in the PVN that contain AVP?

A

They project to the median eminence and other brain regions to regulate mood/stress

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8
Q

What is the purpose of magnocellular cells in the PVN and SON?

A

Maintaining body fluid homeostasis

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9
Q

AVP is stimulated by what two factors?

A

Increase in osmolality and decrease in fluid volume

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10
Q

Describe the sensitization of AVP neuron with blood volume loss.

A

Blood loss greater than 10% and a decrease in mean arterial pressure increases sympathetic neural input, releasing the inhibition on magnocellular cells

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11
Q

Cellular mechanism of AVP vasoconstrictor effects

A

AVP binds the V1 receptor in smooth muscle, activating PLC to make IP3 and DAG, increasing intracellular calcium concentration. This binds to the calmodulin in the cell, activating myosin light chain kinase, therefore increasing contractions

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12
Q

Cellular mechanism of AVP osmoregulation effects

A

Binds to V2 receptors in the distal tubules of the kidney, activating PKA and stimulating insertion of aquaporin 2 channels in the apical membrane. Water moves transcellularly and exits into the bloodstream through aquaporin 3 and 4 channels

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13
Q

What is the primary dysfunction in diabetes insipidus?

A

AVP defect

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14
Q

What is the most common etiology of diabetes insipidus?

A

Decreased AVP release due to hypothalamic trauma related to trauma, cancer, or infection.

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15
Q

What is the second, less common etiology of diabetes insipidus?

A

Decreased renal responsiveness to AVP. Can be genetic or acquired

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16
Q

Describe genetic diabetes insipidus.

A

X-linked; 90% in males. Mutation in AVP receptor

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17
Q

Describe acquired diabetes insipidus.

A

Nephrotoxicity from lithium treatment, hypokalemia

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18
Q

In the case of diabetes insipidus due to decreased responsiveness to AVP, what are the blood levels of AVP?

A

Normal

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19
Q

Primary clinical presentation of SIADH

A

Hyponatremia in the absence of edema

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20
Q

What percentage of patients have SIADH from primary pituitary dysfunction?

A

Only 33%

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21
Q

Other causes of SIADH (4)

A

CNS disorders (lesions, trauma, infections)
Lung diseases
Extrapituitary tumors
Low sodium: sodium loss due to lack of aldosterone will cause hypovolemia and increased AVP release

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22
Q

By what/where is oxytocin released?

A

Released by magnocellular neurons in the PVN and released in the posterior pituitary

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23
Q

Main function of oxytocin

A

Induction of smooth muscle contraction in the breast tissue and uterus

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24
Q

How is oxytocin regulated?

A

In a positive feedback loop

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25
Mechanism of smooth muscle contraction stimulated by oxytocin
Oxytocin binds to GPCR, activating PLC to increase DAG and IP3, increasing the intracellular calcium concentration. This binds to calmodulin, and the calmodulin:Ca2+ complex activates myosin light chain kinase to induce smooth muscle contraction
26
How long is growth hormone releasing hormone?
44 amino acids long
27
Where is GHRH made and released?
In the arcuate nucleus
28
What is cleaved off of GHRH in the biosynthetic process?
GCTP (GHRH C-terminal peptide)
29
How long is somatostatin?
14 amino acids long
30
Where is somatostatin produced?
In the periventricular nucleus
31
What does somatostatin do?
Inhibits GHRH pulse frequency in the hypothalamus, and inhibits GH and TSH in the pituitary
32
What two types of somatostatin exist, and where are they each most dominant?
SS14 - pituitary | SS28 - intestine
33
Endopeptidases important in the biosynthetic processing of somatostatin
Furin, PC1, and PC2
34
What is the main goal of growth hormone?
To conserve protein (protein anabolic hormone)
35
Growth hormone is in the same family as what other hormone?
Prolactin
36
What are environmental activators and inhibitors of GH?
Activators: starvation, stress, exercise Inhibitors: obesity, age, and high blood glucose
37
GH is mostly released when and in what fashion?
Pulsatile release; greatest during the nighttime
38
Many of the effects of GH are mediated through __
IGF-1
39
Primary actions of GH
Liver: release of IGF-1 Adipose: increase lipolysis/decrease glucose uptake Skeletal muscle: increase protein synthesis
40
Indirect effects of GH
Mediated through IGF-1 - Cellular proliferation in visceral organs - Bone/cartilage growth
41
IGF-1 is dependent on __
The presence of insulin
42
Defects in normal growth are often caused by __
defective IGF-1 release or signaling
43
GH excess etiology
20% caused by somatotrope tumor
44
Two syndromes caused by excess GH
Gigantism and acromegaly
45
When does gigantism occur?
Before closing of epiphysial plates in childhood
46
When is acromegaly usually diagnosed?
In middle age
47
Physical manifestations of acromegaly
Gradual enlargement of hands and feet; protruding of jaw, enlarged lips, tongue, and nose
48
Visceral manifestations of acromegaly
Possible increase in organ size
49
Most common cause of acromegaly
Pituitary adenoma
50
Etiology of Laron syndrome
No GH receptors, so no release of IGF-1
51
Treatment of Laron syndrome
IGF-1 supplementation
52
Blood hormone levels in Laron syndrome
Lack of IGF-1, normal to high GH due to lack of feedback
53
African pygmies
Partial lack of GH receptors, so some IGF-1 is released
54
Adult GH deficiency
Increased fat deposition, muscle wasting
55
How is prolactin unique?
It is not part of an endocrine axis; it uses a short-loop feedback system on hypothalamic dopamine. No unique stimulating factor from the hypothalamus
56
Inhibition of prolactin
Tonically inhibited by dopamine
57
Half-life of prolactin
20 minutes; not bound to any carrier proteins
58
Stimulus-secretion reflex
Prolacin is released in response to suckling
59
Physiologic effects of prolactin
Mammary development, breast differentiation, milk formation
60
Components of breast differentiation mediated by prolactin
Duct proliferation and branching | Glandular tissue development
61
Components of milk production mediated by prolactin
Synthesis of milk proteins (beta-casein and alpha-lactalbumin) Synthesis of milk sugar: lactose Synthesis of milk fats
62
What hormones can cause increase in prolactin release?
TRH and oxytocin
63
Estrogen and prolactin
Increases synthesis of prolactin and hyptrophies lactotrophs
64
Consequences of structural similarity of growth hormone and prolactin
If one of the hormone levels is really high, it can lead to non-specific binding and extra effects of the other hormone (e.g., high GH can lead to galactorrhea)
65
What percentage of pituitary adenomas are prolactinomas?
30-40%
66
Three symptoms of prolactinomas
Hyperprolactinemia Galactorrhea Reproductive dysfunction from GnRH inhibition
67
Sheehan's syndrome
Caused by excessive blood loss/shock during birth | Partial pituitary destruction results, leading to lack of prolactin and other pituitary hormones
68
How must hormones be measured when evaluating anterior pituitary function?
In pairs; must evaluate simulating hormone and actual levels
69
Timing of hormone measurement
Must be correlated to the right time of day/age of the patient
70
Dexamethasone suppression test
Used typically to diagnose Cushing's syndrome; dexamethasone inhibits ACTH release. If there is a corticotrophic adenoma, levels will not decrease
71
TRH challenge
(Review graph from lecture three)
72
Insulin-induced hypoglycemia should result in . . .
increased GH levels
73
Injection of IGF-1 should result in . . .
decreased GH levels

Endocrine (11 decks)

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