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FHB Exam 4 > Endocrine 4: posterior pituitary, HPL > Flashcards

Endocrine 4: posterior pituitary, HPL Flashcards

1
Q

Describe the structure and processing of AVP/OXY.

A
  • nonapeptide (9 AA)
  • AVP and OXY only differ by 2 AA
  • copeptide = Neurophysin
  • –AVP + NPII
  • –OXY + NPI
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2
Q

Which hypothalamic nucleus does AVP come from?

A

PVN and SON

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3
Q

What is the difference between PVN magnocellular neurons and parvocellular neurons?

A

Magnocellular Neurons - extend to posterior pituitary and are involved in osmoregularity

Parvocellular Neurons - extends to the ME and are involved in stress and anxiety

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4
Q

When is the AVP copeptide cleaved?

A

neurophysin is cleaved during axonal transport (in the secretory vesicles)

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5
Q

Describe the mechanism of how changes in plasma osmolarity stimulate AVP release.

A
  1. Normally, osmoreceptors in the brain are inhibiting magnocellular neurons (no AVP)
  2. increase osmolarity (many solutes, little water) pulls water out of cells
  3. osmoreceptors shrink and relieve inhibition of magnocellular neurons
  4. AVP released and acts on the distal tubule and collecting duct of the kidney to increase water reabsorption
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6
Q

Describe the mechanism by which changes in blood volume stimulate AVP release.

A
  1. Normally, baroreceptors are firing at a high frequency
  2. loss of blood volume leads to decreased MAP
  3. decreased MAP causes lower frequency baroreceptor stimulation
  4. increases sympathetic tone and activates magnocellular neurons to release AVP
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7
Q

What is the biggest stimulus for AVP release?

A
  • changes in osmolarity (very sensitive)

- blood volume (less sensitive; increases sensitivity to osmolarity)

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8
Q

Describe the mechanism of AVP in vasculature.

A
  1. AVP binds to V1R receptor (GPCR)
  2. activation of phospholipase C => IP3 and intracellular calcium
  3. calcium binds to calmodulin
  4. activation of MLC Kinase
  5. contraction of smooth muscle => vasoconstriction
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9
Q

Describe the mechanism of AVP in nephrons.

A
  1. AVP binds to V2R receptor (GPCR)
  2. activation of PKA
  3. increased synthesis of aquaporin 2 channels
  4. aquaporin 2 channels are expressed on the apical membrane of the DT and collecting duct
  5. increased water reabsorption from the lumen => water regulation
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10
Q

What are the primary symptoms of diabetes insipidus?

A
  • polyuria: through the night
  • polydipsia: drinking lots of water
  • NO POLYPHAGIA
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11
Q

What are the primary etiologies of diabetes insipidus?

A

central - decreased AVP release (most common)

nephrogenic - decreased renal responsiveness to AVP

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12
Q

What are causes of central diabetes insipidus?

A

at the level of the pituitary or hypothalamus

  • tumor
  • infection
  • cancer
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13
Q

What are causes of nephrogenic diabetes insipidus?

A
  • genetic: X-linked AVP type 2 receptor (present in males)

- acquired: lithium treatment or hypokalemia (more common)

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14
Q

What is unique about diabetes insipidus caused by decreased renal responsiveness?

A

AVP levels remain normal

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15
Q

How does lithium treatment or hypokalemia affect AVP function?

A

Lithium treatment: lithium gets trapped in renal cells and interferes with AVP trafficking of aquaporins or increases lysosomal degradation of aquaporins

hypokalemia: interferes with countercurrent regulation of kidney

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16
Q

How do you differentiate between the 2 types of diabetes insipidus?

A

water restriction test

  • administer AVP => urination and thirst stops === central
  • administer AVP => symptoms continue === nephrogenic b/c no receptor or other factors so can’t have impact
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17
Q

What are the functions/stimuli of oxytocin?

A
  • uterine contractions due to uterine stretch at the end of pregnancy
  • milk production due to suckling
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18
Q

What is pitocin?

A

oxytocin mimetic used to induce labor

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19
Q

Describe the mechanism of oxytocin action.

A
  1. binds to oxytocin receptor in breast or uterine tissue (same receptor)
  2. phospholipase C => ca-calmodulin => MLC K
  3. activated myosin
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20
Q

What are the components of the HPL axis?

A 
Hypothalamus = arcuate nucleus = GHRH
Pituitary = GH
Liver = IGF-1
21
Q

What are the target sites of GH?

A
  • liver
  • adipose
  • muscle
22
Q

What is the main role of GH?

A

promote lean body mass (muscle production)
inhibit fat production (promote lipolysis)
—-> protein anabolism/conservation

23
Q

Define gigantism.

A
  • excess GH due to somatotrope pituitary tumor
  • onset in childhood
  • increased growth of long bones until puberty closes epiphyseal plates
24
Q

Define acromegaly.

A
  • excess GH due to somatotrope pituitary tumor
  • onset in adulthood (after growth plates have closed)
  • increased growth in flat bones, cartilage, and muscles
  • —- enlarged hands and feet (arthritis)
  • —- enlarged tongue, nose, lips
  • —- wide jaw, midbrow protrusion
25
Q

List 2 types of dwarfism.

A
  • Laron’s syndrome

- African Pygmy

26
Q

Define dwarfism.

A

GH deficiency

onset in childhood

27
Q

Define Laron’s syndrome.

A
  • genetic defect in GH
  • cannot produce IGF1
  • normal to high levels of GH due to loss of IGF1 mediated negative feedback
  • —> will not grow like normal children
    tx: IGF1 can prevent dwarfism
28
Q

Define African Pygmy

A
  • partial defect in GH receptor
  • partial deficiency of IGF1
  • normal GH levels
  • NO increase in IGF1 during puberty
  • —> will grow like a normal child, but will not have a growth spurt during puberty and will remain short.
29
Q

Describe adult onset GH deficiency.

A
  • mostly due to pituitary tumor, surgery, or treatment
  • leads to increased fat deposition, muscle wasting, reduced bone density,
  • higher risk for fractures
  • dysplipidemia (high LDL, triglycerides)
30
Q

What regulates prolactin release?

A
  • dopamine is tonically inhibiting prolactin
  • suckling stimulates prolactin release
  • prolactin acts on a short loop negative feedback to dopamine
31
Q

What pituitary cells release prolactin?

A

lactotrophs

32
Q

How is prolactin transported in the blood?

A

free floating

33
Q

Describe the physiological effects of prolactin.

A
  • stimulating by suckling
  • all things milk: breast differentiation, duct proliferation, glandular tissue development, milk/protein enzyme secretion
  • inhibition of GnRH and reproduction
34
Q

What hormone is prolactin structurally similar to? Why is this important?

A
  • GH
  • if there is excess GH, it will bind to PRL receptors (hence, acromegaly pts have galactorrhea, inhibited reproduction and fertility issues)
35
Q

What are clinical problems with excess prolactin?

A
  • most common pituitary adenomas are prolactinomas
  • lead to galactorrhea
  • inhibits reproduction leading to fertility issues
36
Q

Define Sheehan’s Syndrome.

A
  • during pregnancy, lactotrophs in pituitary are proliferating => pituitary is getting bigger, it is highly vascularized
  • during childbirth, hemorrhage puts the portal system in danger and cause pituitary cell death due to loss of blood supply
  • can lead to loss of lactotrophs and other cell types (ex: loss of axillary and pubic hair)
37
Q

How do you evaluate anterior pituitary function?

A
  • measure hormones in pairs (ex: ACTH/cortisol, GH/IGF1)
  • measure longitudinally and at the right time
  • stimulation/inhibition tests to assess negative feedback and pituitary function
38
Q

Describe the structure and production of GHRH.

A
  • 44 AA
  • made in arcuate nucleus
  • stimulate anterior pituitary to make GH
39
Q

Compare/contrast the 2 structures of somatostatin.

A

SS28

  • produced by D cells in the gut
  • enzyme: Furin and PACE
  • slows gastric contractions
  • more predominant in circulation
  • inhibits GH release at the level of the pituitary

SS14

  • produced by periVN in the hypothalamus and pancreas
  • enzyme: PC1/PC2
  • slows down GHRH pulsatile release in hypothalamus
  • inhibits GH and TSH release from anterior pituitary
  • inhibits glucagon

both have same C-termini

40
Q

Describe the relationship between somatostatin and GHRH release.

A
  • normally, GHRH pulsatility is very frequent
  • SS14 slows down GHRH pulsatility
  • hence, peaks in SS14 coincide with low GHRH and thus, low GH
41
Q

Describe the relationship between somatostatin and GH release.

A
  • not only does SS14 slow down GH release stimulation (by slowing down GHRH release)
  • SS14 directly inhibits GH release from the pituitary
42
Q

When is GH release most active?

A

at night

  • low SS
  • high GHRH/GH
43
Q

List stimulators of GH.

A
  • GHRH
  • catecholamines (dopamine, norepinephrine, epinephrine)
  • AAs (to stimulate protein building)
  • thyroid hormone
  • stress, exercise, starvation (hypoglycemia)
44
Q

List inhibitors of GH.

A
  • IGF1
  • SS
  • hyperglycemia
  • obesity (free FFA)
  • aging
45
Q

Describe direct physiological effects of GH.

A
  • liver: stimulates production and release of IGF1, increase protein synthesis, increase gluconeogenesis,
  • adipose: increased lipolysis, decreased glucose uptake
  • muscle: increased protein synthesis, decreased glucose uptake

OVERALL: lean body mass production, lipolysis/decrease adiposity

lipolysis leads to glucose mobilization and increased plasma glucose levels

46
Q

Describe physiological effects of IGF1.

A
  • negative feedback on pituitary to inhibit GH, on hypothalamus to promote SS
  • protein synthesis in visceral organs, bone, cartilage, etc.
  • increased AA uptake and protein synthesis in muscles
  • mimics insulin in the muscle (glucose uptake)
  • insulin dependent
    PROMOTES GROWTH
47
Q

What is the relationship between IGF1, GH, and insulin.

A
  • IGF1 effects are insulin dependent = no IGF unless insulin is present
  • hyperglycemia = insulin = no GH (glucose uptake), IGF (growth)
  • hypoglycemia = no insulin = GH (glucose mobilization), no IGF (no growth)
48
Q

Describe IGF levels through age.

A

peak during critical growth periods (puberty)

FHB Exam 4 (16 decks)

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