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FHB Endocrinology > L71: Posterior Pituitary and HPL Axis > Flashcards

L71: Posterior Pituitary and HPL Axis Flashcards

1
Q

How is Oxytocin/Vasopressin(AVP) synthesized and processed?

A

Preprohormone (signal peptide, hormone, neurophysin, glycopeptide) -> processed and cleaved -> Neurophysin and Hormone are stored in vesicles

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2
Q

Which neurophysin molcules are associated with AVP and OXY?

A

OXY: Neurophysin I
AVP: Neurophysin II

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3
Q

What are hte 2 types of cells in the PVN?

A

MAgnocellular and Parvocellular

Only magnocellular project to posterior pituitary

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4
Q

Where are the cell bodies that secrete AVP?

A

PVN and SON

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5
Q

Where do the parvocellular PVN neurons project to ?

A

HAve AVP and project to median eminence to regulated mood

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6
Q

What are the AVP in magnocellular SON and PVN important for?

A

Maintaining fluid balance

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7
Q

What’s another name for AVP?

A

ADH: antidiuretic hormone

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8
Q

What stimulates release of AVP from the posterior pituitary?

A

Increase in plasma osmolality
Decrease in blood volume
Blood loss greater than 10% and decrease in mean arterial BP -> AVP release by decreased sympathetic tone (release neuronal inhibition)

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9
Q

How does AVP carry out its vasocontrictor effects?

A

Binds V1 receptor in vascular smooth muscle -> contraction -> increase vascular resistance

PLC/DAG/IP3 pathway

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10
Q

What is the principal funciton of AVP?

A

Increase water reabsorptionand conserve water

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11
Q

How does AVP conserve water?

A

Binds to V2 receptors in the principal cells of distal tubule -> PKA activation -> phosphorylate AQP2 -> insert into membrane -> increased water permeability

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12
Q

What is Diabetes Insipidus?

A

Defect in AVP causing excessive urine production
Due to:
Decreased AVP release (most common): hypothalamic or pituitary defect from trauma, cancer, disease
Decreased renal responsiveness to aVP: Genetic mutation in V2 receptor, or acquired via Li tx or hypokalmeia (Note: AVP levels are normal in these case)

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13
Q

Where is oxytocin released by?

A

MAgnocellular neurons from PVN

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14
Q

What is the function of oxytocin?

A

Smooth muscle cell contraction in breast and uterus

positive feedback loops

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15
Q

What is pitocin?

A

synthetic oxytocin used to induce labor

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16
Q

How does oxytocin signal on target tissues?

A

OXY binds to GPCR -> activate PLC signaling pathway > increase intracellular calcium -> Ca2+ binds Calmodulin -> activate myosin light chain kinase-> phosphorylate myosin filament-> smooth muslce contraction

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17
Q

Where is GHRH produced and what does it do?

A

Arcuate nucleus: stimulates GH from the anterior pituitary

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18
Q

How is GHRH synthesized and processed?

A

Preprohormone -> cleave signal peptide-> prohormone -> processing to form GHRH and C term peptide-> processing to active form

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19
Q

Where is Somatostatin produced and what does it do?

A

Periventricuar nucleus;
Inhibits GHRH pulse frequency at the hypothalamus
Inhibit GH and TSH release in pituitary

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20
Q

What are the dominant forms of somatostain in the intestines and the brain?

A

SS28: intestines
SS14: Brain

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21
Q

What is growth hormone?

A

Produced from somatotrope cells in anterior pituitary

Protein anabolic hormone-> conserve protein

22
Q

What increases GH levels?

A

Stress, exercise, starvation

23
Q

What causes GH levels to decrease?

A

Age, high blood glucose, obesity

24
Q

How is GH released?

A

Pulsatile release mostly at night

25
Q

How are most of hte downstream target organ effects of GH mediated?

A

Through IGF-1 (somatomedins) made in the liver

26
Q

WHat stimulates GH release?

A

GHRH, Dopamin, NE/Epi, Amino acids, Thyroid Hormone

27
Q

What inhibits GH release?

A

Somatostatin, IGF-1, glucose, FFAs

28
Q

Describe the action of GH on peripheral tissues

A

GHRH stimulates GH release from posterior pituitary -> GH act on liver-> stimulate IGF-1 :

Direct GH Effects:
Liver: IGF-1
Adipose tissue: increased lipolysis and decreased glucose uptake
Skeletal Muscle: Increase protein Syntehsis

Indirect GH Effects: via IGF-1

29
Q

What are the direct physiological effects of GH?

A

Direct actions promote lean body mass (inc protein and dec adiposity), mobilize glucose stores, increase plasma glucose

Targets: Liver,Adipose tissue, Muscle

30
Q

What are the indirect effects of GH?

A

Stimulated by IGFs-> cellular differentiation in visceral organs and bone/cartilage growth => increase organ size and linear growth

IGF actions are DEPENDENT on INSULIN (GH stimultion of IGF is decreased in starvation states)

31
Q

What does GH need to mediate its effects through IGF-1?

A

INSULIN

32
Q

How is IGF-1 important for growth?

A

Peaks during critical growth periods -> defects in normal growth patterns usually due to defective IGF-1 receptors or signaling

33
Q

What results with a somatotrope tumor?

A

GH Excess -> Acromegaly, Gigantism

34
Q

What is Gigantism?

A

Somatotrope tumor that occurs before closing of epiphyseal plate during childhood -> leads to increased long bone growth and extreme height

35
Q

What is acromegaly?

A

Diagnosed in middle age
Enlarged hands and feed (arthritis)
changes in facial features (protruding lower jaw, enlarged lips, tongue, nose)
Increased organsize

usually due to pituitary adenoma

36
Q

What happens with GH deficiency?

A

Dwarfism (children)

Adults: Increased fat deposition, muscle wasting

37
Q

What is Laron Syndrome?

A

Genetic defect in GH receptor -> no IGF-1 production -> plasma GH levels are normal-high due to lack of feedback

Tx: IGF-1 to prevent dwarfism

38
Q

What is African Pygmy?

A

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

Plasma GH levels normal but no pubertal increase in IGF-1

39
Q

What is unique about prolactin?

A

Made by lactotropes which are not part of endocrine axis -> short feedback loop on hypothalamic dopamine
No stimulating factor from hypothalamus

40
Q

How is prolactin regulated?

A

Tonically inhibited by dopamine from the arcuate nucleus

41
Q

How is prolactin transporte din blood?

A

Not bound to serum protein

42
Q

What sitmulates release of prolactin?

A

Suckling-> stimulus secretion reflex

Also by TRH and OXY

43
Q

What are the physiological effects of prolactin?

A

Mammary gland development
Breast differentiation
Milk production

44
Q

How does estrogen affect prolactin?

A

Increase prolactin synthesis and lactotrope hypertrophy

45
Q

What is the consequence of the similarity between GHa nd prolactin?

A

Nonspecific binding of either receptor when one is produced in excess
Example: Excess GH -> GH binding to PRL receptor -> galactorrhea

46
Q

What causes prolactin excess and what does it cause?

A

Prolactinomas: hyperprolacinemia, galactorrhea, reproductive dysfunction (prolactin inhibits GnRH release)

47
Q

What is Sheehan’s Syndrome?

A

Prolactin Deficiency due to excessive blood loss/shock during childbirth -> causes partial pituitary destruction

48
Q

How do you evaluate anterior pituitary function?

A

Measure hormone in pairs (ex: ACTH + Cortisol)
Measure at appropriate time or longitudinally (take into account circadian rhythm and age)
Stimulation/Inhibition test to test feedback and pitutiary function (Ex: TRH challenge)
Predict Neg Feedback Effects (Ex: insulin induced hypoglycemia should lead to inc GH levels; Administered IGF-1 should lead to decreased GH levels)

49
Q

What stimulates GH?

A 
GHRH
Dopamine
NE/EPi (Exercise, stress)
Amino acids
Thyroid hormone
50
Q

What inhibits GH?

A

IGf-1
High glucose
Obesity (high FFas)

FHB Endocrinology (10 decks)

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