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Endocrine > Posterior pituitary and HPL axis (L4) > Flashcards

Posterior pituitary and HPL axis (L4) Flashcards

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
Q

Mechanism of smooth muscle contraction stimulated by oxytocin

A

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

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26
Q

How long is growth hormone releasing hormone?

A

44 amino acids long

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27
Q

Where is GHRH made and released?

A

In the arcuate nucleus

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28
Q

What is cleaved off of GHRH in the biosynthetic process?

A

GCTP (GHRH C-terminal peptide)

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29
Q

How long is somatostatin?

A

14 amino acids long

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30
Q

Where is somatostatin produced?

A

In the periventricular nucleus

31
Q

What does somatostatin do?

A

Inhibits GHRH pulse frequency in the hypothalamus, and inhibits GH and TSH in the pituitary

32
Q

What two types of somatostatin exist, and where are they each most dominant?

A

SS14 - pituitary

SS28 - intestine

33
Q

Endopeptidases important in the biosynthetic processing of somatostatin

A

Furin, PC1, and PC2

34
Q

What is the main goal of growth hormone?

A

To conserve protein (protein anabolic hormone)

35
Q

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

A

Prolactin

36
Q

What are environmental activators and inhibitors of GH?

A

Activators: starvation, stress, exercise
Inhibitors: obesity, age, and high blood glucose

37
Q

GH is mostly released when and in what fashion?

A

Pulsatile release; greatest during the nighttime

38
Q

Many of the effects of GH are mediated through __

A

IGF-1

39
Q

Primary actions of GH

A

Liver: release of IGF-1
Adipose: increase lipolysis/decrease glucose uptake
Skeletal muscle: increase protein synthesis

40
Q

Indirect effects of GH

A

Mediated through IGF-1

  • Cellular proliferation in visceral organs
  • Bone/cartilage growth
41
Q

IGF-1 is dependent on __

A

The presence of insulin

42
Q

Defects in normal growth are often caused by __

A

defective IGF-1 release or signaling

43
Q

GH excess etiology

A

20% caused by somatotrope tumor

44
Q

Two syndromes caused by excess GH

A

Gigantism and acromegaly

45
Q

When does gigantism occur?

A

Before closing of epiphysial plates in childhood

46
Q

When is acromegaly usually diagnosed?

A

In middle age

47
Q

Physical manifestations of acromegaly

A

Gradual enlargement of hands and feet; protruding of jaw, enlarged lips, tongue, and nose

48
Q

Visceral manifestations of acromegaly

A

Possible increase in organ size

49
Q

Most common cause of acromegaly

A

Pituitary adenoma

50
Q

Etiology of Laron syndrome

A

No GH receptors, so no release of IGF-1

51
Q

Treatment of Laron syndrome

A

IGF-1 supplementation

52
Q

Blood hormone levels in Laron syndrome

A

Lack of IGF-1, normal to high GH due to lack of feedback

53
Q

African pygmies

A

Partial lack of GH receptors, so some IGF-1 is released

54
Q

Adult GH deficiency

A

Increased fat deposition, muscle wasting

55
Q

How is prolactin unique?

A

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
Q

Inhibition of prolactin

A

Tonically inhibited by dopamine

57
Q

Half-life of prolactin

A

20 minutes; not bound to any carrier proteins

58
Q

Stimulus-secretion reflex

A

Prolacin is released in response to suckling

59
Q

Physiologic effects of prolactin

A

Mammary development, breast differentiation, milk formation

60
Q

Components of breast differentiation mediated by prolactin

A

Duct proliferation and branching

Glandular tissue development

61
Q

Components of milk production mediated by prolactin

A

Synthesis of milk proteins (beta-casein and alpha-lactalbumin)
Synthesis of milk sugar: lactose
Synthesis of milk fats

62
Q

What hormones can cause increase in prolactin release?

A

TRH and oxytocin

63
Q

Estrogen and prolactin

A

Increases synthesis of prolactin and hyptrophies lactotrophs

64
Q

Consequences of structural similarity of growth hormone and prolactin

A

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
Q

What percentage of pituitary adenomas are prolactinomas?

A

30-40%

66
Q

Three symptoms of prolactinomas

A

Hyperprolactinemia
Galactorrhea
Reproductive dysfunction from GnRH inhibition

67
Q

Sheehan’s syndrome

A

Caused by excessive blood loss/shock during birth

Partial pituitary destruction results, leading to lack of prolactin and other pituitary hormones

68
Q

How must hormones be measured when evaluating anterior pituitary function?

A

In pairs; must evaluate simulating hormone and actual levels

69
Q

Timing of hormone measurement

A

Must be correlated to the right time of day/age of the patient

70
Q

Dexamethasone suppression test

A

Used typically to diagnose Cushing’s syndrome; dexamethasone inhibits ACTH release. If there is a corticotrophic adenoma, levels will not decrease

71
Q

TRH challenge

A

(Review graph from lecture three)

72
Q

Insulin-induced hypoglycemia should result in . . .

A

increased GH levels

73
Q

Injection of IGF-1 should result in . . .

A

decreased GH levels

Endocrine (11 decks)

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