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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
What 3 things are needed for dx of acromegaly?
1. Increased serum IGF-1 2. Failure to suppress serum GH w/ OGTT 3. Pituitary enlargment on MRI
26
What effect does Prolactin have on GnRH?
Decreases GnRH
27
What effect does somatostatin have on GH and TSH?
Decreases GH and TSH
28
Most pituitary tumors are considered what; aggressivness; and how are they classifed based on hormone secretion?
- 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
What are 3 examples of hormone producing pituitary adenomas?
1) Prolactinoma 2) Acromegaly (adults); gigantism (child) 3) Cushing's disease
30
Prolactin is synthesized by; inhibited by; primary action; and what does it suppress?
- 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
What are the major factors stimulating Prolactin?
- Pregnancy **(estrogen)** - Breast-feeding (suckling) - Sleep - Stress - **TRH**
32
FSH and LH are secreted by; promotes secretion of; regulated by?
- 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
Why are the major symptoms of PRL excess galactorrhea and infertility?
Suppression of GnRH, which decreases FSH and LH
34
How does prolactin support the actions of estrogen and progesterone in breast development?
- At puberty: stimulate proliferation and branching of mammary ducts - During pregnancy: stimulates growth and development of the mammary alveoli
35
Describe how prolactin, estrogen, and progesterone are involved in lactogenesis?
- 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
What are the clinical consequences of hypopituitarism on GH, FSH/LH, TSH, ACTH, and ADH?
37
What are the causes of hypopituitarism?
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
What is Sheehan syndrome; common patient presentation?
- **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
Explain the regulation of oxytocin secretion from start to its target tissue.
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
Explain the regulation of ADH secretion from start to its target tissue.
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
What are the 5 triggers for ADH secretion and what receptors sense each of these triggers?
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
Secretion of ADH is most sensitive to?
Plasma osmolarity changes
43
What are the receptors for ADH on blood vessels and in the kidneys; activation of these receptors causes what?
Blood vessels: V1 receptors - **vasoconstriction** Kidney: V2 receptors - **increased reabsorption of water** - Increased blood pressure and increased blood volume
44
Explain the difference between central and nephrogenic diabetes insipidus (DI); plasma ADH levels; causes of both?
**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
What drug is used to treat central DI and can it be used to treat nephrogenic DI?
- 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
If a patient presents with polyuria and is urinating large volumes what disease should you be thinking of?
Central or nephrogenic DI
47
What are the pathophysiological changes in SIADH?
- Excessive secretion of ADH - Excessive water retention - Hyponatremia - Hyperosmolarity fails to inhibit ADH release
48
What are the treatments for SIADH?
- Fluid restriction - IV hypertonic saline (3%) - V2 receptor antagonist (on kidneys) - Demeclocycline
49
What are the major factors inhibiting prolactin?
- Dopamine - Dopamine agonists - Somatostatin - Prolactin via **neg. feedback**

Endo/Repro I Exam 1 (12 decks)

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