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Endo/Repro I Exam 1 > Lecture 3: Hypothalamic-Pituitary Relationships > Flashcards

Lecture 3: Hypothalamic-Pituitary Relationships Flashcards

1
Q

Generally, cancers of the pituitary expand up to where; cause what?

A
  • Up into the brain and against the optic nerves
  • Increase in size often associated w/ diziness and vision problems, or both
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2
Q

How is the connection between the hypothalamus and posterior lobe of the pituitary neural; what is secreted?

A
  • Posterior pituitary is a collection of axons whose cell bodies are located in the hypothalamus: SON and PVN
  • Secrete neuropeptides:
  • ADH (most SON)
  • Oxytocin (mostly PVN)
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3
Q

How is the relationship between the hypothalamus and the anterior lobe of the pituitary both neural and hormonal?

A
  • Anterior pituitary is a collection of endocrine cells
  • Secretes hormones: ACTH, TSH, FSH, LH, GH, and Prolactin
  • Connected to hypothalamus by hypothalamic-hypophysial portal vessels
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4
Q

What are the 2 important implications of the hypothalamic-hypophysial portal vessesl providing blood supply to the anterior pituitary?

A

1) Hypothalamic hormones can be delivered directly to the anterior pituitary and in high concentrations
2) The hypothalamic hormones do NOT appear in the systemic circulation in high concentrations

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5
Q

Differentiate between 1°, 2°, and 3° endocrine disorders.

A

1° disorder: low or high levels of hormone due to defect in peripheral endocrine gland

2° disorder: low or high levels of hormone due to defect in the pituitary gland

3° disorder: low or high levels of hormone due to defect in the hypothalamus

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6
Q

What is released by corticotrophs, thyrotrophs, gonadotrophs, somatotrophs, and lactotrophs; which family does each hormone belong to?

A

Corticotroph: releases ACTH (ACTH family)

Thyrotroph: releases TSH (TSH, FSH, LH family)

Gonadotroph: releases FSH and LH (TSH, FSH, LH family)

Somatotroph: releases GH (GH, Prolactin family)

Lactotroph: releases prolactin (GH, Prolactin family)

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7
Q

Hypothalamic hormones are often secreted in what type of manner and are entrained to what?

A

Secreted in a pulsatile manner and are entrained to circadian rhythms

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8
Q

What produces GH, what are its targets, what kind of receptor, and what does it stimulate?

A
  • Produced by Somatotrophs
  • Targets the liver and bone
  • GH receptor linked to JAK-STAT signaling
  • Stimulates somatomedin C (Insulin-like growth factor 1; IGF-1) gene transcription and secretion by liver.
  • Inhibited by IGF-1 and somatostatin
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9
Q

When diagnosing acromegaly what should be measured initially; why?

A
  • IGF-1
  • GH levels fluctuate throughout the day, whereas IGF-1 levels remain constant
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10
Q

What test can confirm the diagnosis of acromegaly?

A
  • Oral glucose tolerance test
  • Inaqduate suppression of serum GH after a glucose load confirms the diagnosis
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11
Q

What is the initial treatment for most patients w/ a pituitary tumor; what if tumor is >1cm?

A
  • Initial is surgery via transsphenoidal approach
  • If > 1cm, radiation therapy is considered
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12
Q

What stimulates the release of GH?

A
  • Fasting/hunger/starvation
  • Hypoglycemia
  • Sleep
  • Stress
  • Hormones of puberty
  • Exercise
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13
Q

What is the diabetogenic effect of GH?

A
  • Increases blood glucose concentration
  • Causes insulin resistance
  • Decreases glucose uptake and utilization by tissues
  • Increases lipolysis in adipose tissues
  • Results in increased blood insulin levels
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14
Q

What effect does GH have on protein synthsis and organ growth; mediated by?

A
  • Increases protein synthesis and organ growth
  • Increases uptake of AA
  • Stimulates synthesis of DNA, RNA, and protein
  • Mediated by somatomedins (IGF-1)
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15
Q

What effect does GH have on linear growth?

A
  • Increases linear growth
  • Stimulates synthesis of DNA, RNA, and protein
  • Mediated by somatomedins (IGF-1)
  • Increases metabolism in cartilage-forming cells and chondrocyte proliferation
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16
Q

Which hormones relevant to GH are released from the hypothalamus?

A
  • GHRH (stimulates release of GH from anterior pituitary)
  • GHIH = somatostatin (inhibits release of GH from anterior pituitary)
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17
Q

Which hormone relevant to GH is released from the anterior pituitary gland?

A

GH = somatotropin

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18
Q

Which hormones relevant to GH are released by the liver?

A
  • Insulin-like growth factor (IGF)
  • Insulin-like growth factor 1 (IGF-1) = somatomedin C
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19
Q

What are Octreotide or lanreotide; why are they used?

A
  • Somatostain analogs
  • Used to treat acromegaly by lowering GH levels in blood
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20
Q

What is Pegvisomant and what is it used for?

A
  • GH receptor antagonist
  • Blocks the effects of GH, used in tx of acromegaly
21
Q

What are the factors that can lead to GH deficiency?

A
  • Decreased secretion of GHRH (hypothalamic dysdunction)
  • Decreased GH secretion
  • Failure to generate somatomedins
  • GH or somatomedin resistance (deficiency of receptors)
22
Q

What is the major cause of GH excess?

A

Mostly due to a GH-secreting pituitary adenoma

23
Q

What are the different consequences of GH excess depending on development stage?

A
  • Before puberty: before closure of bone epiphyses due to IGF-1 stimulated long bone growth (Gigantism)
  • After puberty: Increased periosteal bone growth, organ size, extremity size, coarsening of facial features, insulin resistance, and glucose intolerance (acromegaly)
24
Q

Describe how GH levels change throughout the day, what are the effects of sleep and exercise?

A
  • Fluctuates throughout the day
  • Highest during sleep; distubances of sleep perturb GH levels
  • Peaks w/ exercise
25
Q

What 3 things are needed for dx of acromegaly?

A
  1. Increased serum IGF-1
  2. Failure to suppress serum GH w/ OGTT
  3. Pituitary enlargment on MRI
26
Q

What effect does Prolactin have on GnRH?

A

Decreases GnRH

27
Q

What effect does somatostatin have on GH and TSH?

A

Decreases GH and TSH

28
Q

Most pituitary tumors are considered what; aggressivness; and how are they classifed based on hormone secretion?

A
  • Pituitary adenomas
  • Nearly all pituitary adenomas are benign and slow-growing
  • Functional tumors: adenomas that release an active hormone, usually an excessive amount
  • Clinically non-functioning adenomas: do not release an active hormone
29
Q

What are 3 examples of hormone producing pituitary adenomas?

A

1) Prolactinoma
2) Acromegaly (adults); gigantism (child)
3) Cushing’s disease

30
Q

Prolactin is synthesized by; inhibited by; primary action; and what does it suppress?

A
  • Synthesized by lactotrophs
  • PRL is under tonic inhibition by hypothalamic dopmaine
  • Stimulates and maintains lactation
  • Suppresses GnRH (inhibits LH and FSH)
  • Decreases reproductive function
  • Suppresses sexual drive
31
Q

What are the major factors stimulating Prolactin?

A
  • Pregnancy (estrogen)
  • Breast-feeding (suckling)
  • Sleep
  • Stress
  • TRH
32
Q

FSH and LH are secreted by; promotes secretion of; regulated by?

A
  • Secreted by gonadotropes
  • Promotes estrogen and progesterone secretion in females
  • Promotes testosterone production in males
  • Regulated by hypothalamic GnRH
  • Extreme energy deficits (anorexia nervosa or starvation), extreme exercise, and depression can inhibit GnRH function
33
Q

Why are the major symptoms of PRL excess galactorrhea and infertility?

A

Suppression of GnRH, which decreases FSH and LH

34
Q

How does prolactin support the actions of estrogen and progesterone in breast development?

A
  • At puberty: stimulate proliferation and branching of mammary ducts
  • During pregnancy: stimulates growth and development of the mammary alveoli
35
Q

Describe how prolactin, estrogen, and progesterone are involved in lactogenesis?

A
  • Prolactin levels are high during pregnancy, but lactation doesn’t occur because high level of estrogen and progesterone down-regulate prolactin receptors
  • At birth, inhibition is released when estrogen and progesterone levels drop precipitously, when this occurs lactogenesis is stimulated
36
Q

What are the clinical consequences of hypopituitarism on GH, FSH/LH, TSH, ACTH, and ADH?

A
37
Q

What are the causes of hypopituitarism?

A
  1. Brain damage: TBI, subarachnoid hemorrhage, irradiation, stroke
  2. Pituitary tumors - adenomas (if tumor is large, it can compress the pituitary and affect the release of hormones)
38
Q

What is Sheehan syndrome; common patient presentation?

A
  • Postpartum hypopituitarism due to necrosis of the pituitary gland
  • Most patients present w/ agalactorrhea and/or difficulties in lactation
  • Amenorrhea commonly present
  • Some patients present w/ hypothyroidism
39
Q

Explain the regulation of oxytocin secretion from start to its target tissue.

A

1) Prepro-oxyphysin in the hypothalamus (paraventricular nuclei); signal peptides cleaved and packaged into vesicles as Pro-oxyphysin
2) Flows down the hypothalamic-hypophyseal tract and cleavage of neurophysins occurs.
3) Stored in posterior lobe of pituitary as Oxytocin + NPI
4) Released to its target tissues: breast and uterus for contractions

40
Q

Explain the regulation of ADH secretion from start to its target tissue.

A

1) Starts as prepropressophysin in hypothalamus (suproptic nuclei) and signal peptide is cleaved to package propressophysin in vesicles
2) Release causes cleavage of neurophysins along the hypothalamic-hypophyseal tract
3) Stored in posterior lobe of pituitary as ADH + NPII
4) ADH is released to target tissues: kidneys and arterioles

41
Q

What are the 5 triggers for ADH secretion and what receptors sense each of these triggers?

A

1) Decreased blood pressure —> Cardiac and aortic baroreceptors
2) Decreased atral stretch due to low blood volume —> Atrial stretch receptors
3) Increased Osmolarity (>280 mOsM) —-> Hypothalamic osmoreceptors
4) Increased angiotensin II
5) Sympathetic stimulation
6) Dehydration

42
Q

Secretion of ADH is most sensitive to?

A

Plasma osmolarity changes

43
Q

What are the receptors for ADH on blood vessels and in the kidneys; activation of these receptors causes what?

A

Blood vessels: V1 receptors - vasoconstriction

Kidney: V2 receptors - increased reabsorption of water

  • Increased blood pressure and increased blood volume
44
Q

Explain the difference between central and nephrogenic diabetes insipidus (DI); plasma ADH levels; causes of both?

A

Central - Deficient secretion of ADH from hypothalamus or pituitary (decreased plasma ADH)

  • Damage to the pituitary
  • Destruction of hypothalamus

Nephrogenic - renal insensitivity to ADH (increased plasma ADH)

  • Drugs like lithium
  • Chronic disorders (i.e., polycystic kidney disease, sickle cell anemia)
45
Q

What drug is used to treat central DI and can it be used to treat nephrogenic DI?

A
  • Desmopressin: prevents water excretion, mimics ADH
  • Can be used to tx central, but NOT nephrogenic
  • Central DI is caused by not making ADH, so if an ADH analog is given these patients will respond to it
46
Q

If a patient presents with polyuria and is urinating large volumes what disease should you be thinking of?

A

Central or nephrogenic DI

47
Q

What are the pathophysiological changes in SIADH?

A
  • Excessive secretion of ADH
  • Excessive water retention
  • Hyponatremia
  • Hyperosmolarity fails to inhibit ADH release
48
Q

What are the treatments for SIADH?

A
  • Fluid restriction
  • IV hypertonic saline (3%)
  • V2 receptor antagonist (on kidneys)
  • Demeclocycline
49
Q

What are the major factors inhibiting prolactin?

A
  • Dopamine
  • Dopamine agonists
  • Somatostatin
  • Prolactin via neg. feedback

Endo/Repro I Exam 1 (12 decks)

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