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FHB Hormone/Repro > 74 - Post pit and HPL axis > Flashcards

74 - Post pit and HPL axis Flashcards

1
Q

OXY and AVP are transcribed as preprohormones. In the prohormone form, what is the associated co-peptide with each?

A
  • Neurophysin I + OXY

- Neurophysin II + AVP

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2
Q

How many amino acids is AVP?

A

Nonapeptide, 9 AAs

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3
Q

How many amino acids is OXY?

A

Nonapeptide, 9 AAs

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4
Q

What’s another name for AVP?

A

ADH

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5
Q

When is neurophysin cleaved from the prohormone (AVP or OXY)?

A

In the secretory granules during axonal transport

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6
Q

In what hypothalamic nuclei that release AVP (released from the posterior pituitary)?

A

PVN, SON

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7
Q

PVN has 2 types of cells, magnocellular and parvocellular. Which project to the posterior pit?

A

Magnocellular (fluid balance)

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8
Q

While the magnocellular neurons of the PVN are important for fluid balance, what are the parvocellular neurons of the PVN important for?

A

Regulating mood (anxiety) and stress

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9
Q

Increasing plasma osmolality has what effect on osmoreceptors?

A

Shrinkage (release of inhibition, AVP released)

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10
Q

How does low blood volume affect AVP release?

A

Makes AVP sensitivity increase

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11
Q

Decreased mean arterial BP causes a decrease in baroreceptor stretch and firing. How does this affect AVP sensitivity?

A

Increases AVP sensitivity

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12
Q

What is AVP’s general effect on the vasculature?

A

Vasoconstriction

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13
Q

What type of receptor does AVP bind?

What is the 2nd msger cascade?

A

GPCR

GPCR -> PLC -> IP3/DAG -> Ca2+/PKC -> MLC kinase -> vasoconstriction

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14
Q

What is the name of the GPCR that AVP binds to initiate vasoconstriction?

A

V1 (V1R)

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15
Q

What cells does AVP affect in the kidney, and which part of the kidney?

A

Principle cells of DT

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16
Q

*What is the affect that AVP has on principle cells in the kidney? (what is the 2nd msger?)

A 
Aquaporin 2 (AQP2) channels are P'lated by PKA
- AQP2 traffics to luminal membrane, and what is reabsorbed
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17
Q

What is the major symptom of diabetes insipidus?

A

Excessive urine production (polyuria)

- High osmolality also leads to polydypsia

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18
Q

What common psychiatric medication can lead to diabetes insipidus? How?

A

Lithium treatment

- Interferes w/AQP2 trafficking in some way

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19
Q

What are the 2 main etiological causes of diabetes insipidus?
Which is more common?

A
  1. Decreased AVP release (most common)

2. Decreased renal responsiveness to AVP

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20
Q

What are common causes of diabetes insipidus due to decreased AVP release?

A

“Central” hypothalamic or pituitary defect due to trauma, CA, infectious dz

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21
Q

What are common causes of diabetes insipidus due to decreased renal responsiveness to AVP?
Are AVP levels increased, decreased or nl in these cases?

A
  • Genetic X-linked AVP type-2 receptor (V2 or V2R) mutation (90% males)
  • Acquired thru Li tx or hypokalemia

Normal AVP levels in these cases

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22
Q

OXY is released from magnocellular neurons whose cell bodies are in the _______ (nucleus).

A

PVN

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23
Q

What are the main functions of OXY?

A

Induce smooth m. cell contraction in breast and uterus (positive feedback loops)

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24
Q

What is pitocin?

A

Synthetic oxytocin used to induce labor

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25
Q

What is the positive feedback stimulus that causes more more OXY release in terms of the breast?
In terms of the cervix/uterus?

A
  • Suckling of lactating breast

- Stretch of cervix

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26
Q

What type of receptor does OXY bind?

A

GPCR

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27
Q

What is the second msger system for OXY?

A

GPCR -> PLC -> Ca+ -> Ca/Calmodulin -> MLCK -> P’late myosin -> smooth m. contraction.

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28
Q

What is the primary clinical presentation of syndrome of inappropriate vasopressin secretion? (SIADH)

A

Hyponatremia (low Na levels) in the absence of edema.

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29
Q

What are some of the major causes of SIADH? (just read)

A
  • Primary pituitary disorder (33% pts)
  • CNS disorders (lesions, infections, trauma)
  • Lung dz (infections
  • Extrapituitary tumors
  • Low Na+ (*low Na dues to low aldosterone will cause hypovolemia; AVP is triggered by low blood volume and will be secreted despite the decrease in plasma osmolality)
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30
Q

How many AAs long is GHRH?

A

44 AAs

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31
Q

From which hypothalamic nucleus is GHRH released?

A

Arcuate nucleus

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32
Q

What does GHRH stimulate the release of?

A

GH from anterior pituitary

33
Q

What are the 3 target organs of GH?

A

Liver, adipose tissue, muscle

34
Q

What protein whose synthesis is stimulated by GH is responsible for many peripheral growth effects?

A

IGF-1

35
Q

What are GH’s effects on fat tissue?

A
  • Increased lipolysis

- Decreased glucose uptake

36
Q

What are GH’s effects on muscle?

A
  • Increased protein synthesis
  • Decreased glucose uptake
  • Increased AA uptake
37
Q

What are GH’s effects on the liver?

A
  • Increased IGF-1 and IGF-BP
  • Increased GNG
  • Increased protein and RNA synthesis
38
Q

What is the inhibitory hormone for somatotrophs?

A

Somatostatin (inhibits FSH and LH release)

39
Q

Besides GH providing negative feedback on its HPA axis, what other hormone can do this?

A

IGF-1

40
Q

How many AAs long is SS?

A

14 or 28 AA’s, depending on where it’s made

41
Q

SS28 predominates in the ________ and SS14 predominates in the ________.

A
  • Intestines

- Brain

42
Q

How does somatostatin decrease GHRH release in the hypothalamus?

A

Decreases pulse frequency

43
Q

What endopeptidases are important for the formation of SS28?

SS14?

A
  • SS28: Furin

- SS14: PC1/PC2

44
Q

In what pattern/fashion is GH released?

A

Pulsatile release (mostly at night)

45
Q

What is the overall goal of GH release?

A

Anabolism–conserve protein

46
Q

GH is structurally similar to what protein?

A

PRL

47
Q

What activities stimulate GH release?

A

Stress, exercise, starvation

48
Q

What activities inhibit GH release?

A

Aging, high blood glucose, obesity

49
Q

Does NE/E stimulate or inhibit GH release?

A

Stimulate (exercise, stress)

50
Q

Does glucose stimulate or inhibit GH release?

A

Inhibit (hypoglycemia)

51
Q

Do AA’s stimulate or inhibit GH release?

What about FFAs?

A
  • AAs: stimulate

- FFAs: Inhibit (obesity)

52
Q

Does TH stimulate or inhibit GH release?

A

Stimulate

53
Q

How are GH and insulin connected?

A

GH considered a counter-regulatory hormone for insulin (can’t be starving and have growth at the same time)

54
Q

Is IGF independent or dependent on insulin?

A

Dependent

55
Q

When during the lifetime does IGF-1 peak?

A

During critical growth periods (youth)

56
Q

What organs/cells does IGF-1 stimulate to grow?

A

Kidney, pancreas, intestines, islets, parathyroids, skin, CT, bone, heart, lung, chondrocytes

57
Q

What are 2 dz’s due to GH excess or a somatotrope tumor?

What’s the differentiating factor b/w the 2?

A
  1. Gigantism (tumor in childhood- before epiphyseal growth plates finish)
  2. Acromegaly (tumor in middle ages)
58
Q

What are the sx of gigantism?

A

Extreme height due to increased long bone growth

59
Q

What are the sx of acromegaly?

What’s the most common cause?

A
  • Gradual enlargement of the hands and feet (arthritis)
  • Facial changes: protruding lower jaw, enlarged lips, tongue, nose
  • Possible increase in organ size
  • Most common cause is pituitary adenoma
60
Q

What hormone is childhood dwarfism related to?

A

GH deficiency

61
Q

What are 2 forms of childhood dwarfism?

A
  1. Laron syndrome

2. African Pygmy

62
Q

What causes Laron syndrome?
How is it treated?
Are GH levels increased, decreased, or nl?

A
  • Genetic defect in GH receptor, therefore no production of IGF-I.
  • Tx w/ IGF-I can prevent dwarfism
  • Plasma GH levels are normal to high (lack of feedback)
63
Q

What causes African Pygmy?

Are GH levels increased, decreased, or nl?

A
  • Partial defect in GH receptor; some IGF-I response.

- Plasma levels of GH nl; no pubertal increase in IGF-I.

64
Q

What can cuause adult GH deficiency?

What are the signs/sx?

A

Caused by pituitary tumor/surgery or treatment (76%)

  • Increased fat deposition, muscle wasting
  • Reduced bone density, risk of fractures
  • Higher LDL, triglycerides
65
Q

What is unique about lactotrophs compared to others?

What stimulates them from hypothalamus?

A

Not part of an HPA axis

- Dopamine (tonically inhibited)

66
Q

Increased PRL causes what major symptom?

A

Galactorrhea (milk from breast)

67
Q

What is the half-life of PRL?

A

20 min (not bound to proteins)

68
Q

What are the physiological effects of PRL?

A
  • Mammary gland development
  • Breast differentiation
  • Milk production
69
Q

What specific parts of breast differentiation does PRL stimulate?

A
  • Duct proliferation and branching

- Glandular tissue development

70
Q

What specific parts of milk production does PRL stimulate?

A
  • Synthesis of milk proteins (beta-casein and alpha-lactalbumin)
  • Synthesis of milk sugar (lactose)
  • Synthesis of milk fats in epithelial cells
71
Q

Prolactin is in the same family as what hormone?

A

GH (very structurally similar)

72
Q

What’s the usual cause of PRL excess?

A

Prolactinoma (30-40% of all pituitary adenomas)

73
Q

What are the sx of prolactinoma?

A
  • Hyperprolactinemia
  • Galactorrhea
  • Reproductive dysfunction
74
Q

Why does excess PRL cause reproductive dysfunction?

A

*PRL Inhibits GnRH release

75
Q

What’s the dz of PRL deficiency?

A

Sheehan’s syndrome

76
Q

What causes Sheehan’s syndrome (low PRL)?

What are the sx?

A
  • Occurs as a result of excessive blood loss/shock during childbirth
  • Partial pituitary destruction
  • Usually affects other pituitary cell types: loss of axillary and pubic hair
77
Q

How much all hormones be measured? (might need to read)

A
  • Must measure in pairs

- Appropriate time and longitudinally

78
Q

Insulin-induced hypoglycemia should result in __________ GH levels.

A

Increased

79
Q

Administration of IGF-1 should result in __________ GH levels.

A

Decreased

FHB Hormone/Repro (16 decks)

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