The Hypothalamus and Pituitary Glands Flashcards

1
Q

*Describe the structure and composition of pituitary gland and its structural and functional relationship to magnocellular and parvocellular hypothalamic neruons

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2
Q

*Discuss the mechanisms by which the neurohormones antidiuretic hormone (ADH) and oxytocin are synthesized and released by magnocellular neurons.

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3
Q

*Diagram a basic scheme illustrating the components and feedback loops of a typical endocrine axis, including central input, hypothalamic releasing factors, pituitary hormones, and a peripheral endocrine gland.

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4
Q

*List the endocrine cell types of the adenohypophysis and the tropic hormones they produce. Describe what the tropic hormones stimulate in target glands.

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5
Q

*Contrast the axes of somatotrophs ad lactotrophs with the classic endocrine axes and explain how they differ

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6
Q

*Discuss the actions of growth hormone (GH) and Insulin-like growth factor I (IGF-I) in the regulation of growth, and the role of growth hormone in the fasted state.

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7
Q

What hormones does the hypothalamus secrete?

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Hypothalamus secretes GnRH, Somatostatin, TRH (thyroid releasing hormone), Dopamine, GHRH (Growth Hormone Releasing Hormone)CRH (cortisol releasing hormone).

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8
Q

Describe the anatomy of hypothalamus, in relation to pituitary gland.

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Hypothalamus:

  • located above the pituitary gland
  • Neural tissue in brain
  • Integrates sensory stimuli (Heat, light, blood pressure) and communicates with pituitary gland
  • Supraoptic nuclei (SON) and paraventricular nuceli (PVN)= which are collection of neurons that project to posterior pituitary gland(neural communication)
  • Releasing hormones secreted into a portal capillary bed and stimulates cells in the anterior pituitary gland.
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9
Q

What is the clinical connection between hypothalamus anatomy and pituitary?

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Tumors in the anterior pituitary can cause vision loss due to compression of the optic chiasm.

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10
Q

describe the posterior pituitary gland and which cells are located there.

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Posterior Pituitary gland- Aka NEUROHYPOPHYSIS

  • Neural tissue- extension of hypothalamus
  • MAGNOCELLULAR cell bodies found in hypothalamus that synthesizes hormones
  • Axons then travel through the median eminence and pituitary stalk, where nerves terminate in the posterior pituitary.
  • Axon potentials then stimulate the release of hormones from posterior pituitary gland into the Vascular capillary bed.
  • Hormones will travel through the bloodstream to target organs.
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11
Q

What hormones are released from posterior pituitary? What is their function? Why are they released?

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Posterior pituitary releases Oxytocin and Vasopressin (ADH, antidiuretic hormone).
Oxytocin functions to stimulate contraction of uterine muscles, for labor and childbirth, and stimulates breast tissue for release of breastmilk (lactation)
Oxytocin released since it is needed during and after birth (push baby out, feed baby milk ).
ADH- used to regulate the amount of water in your body and controlling water loss in your urine.
ADH controlled when dehydrated or overhydrated.
When you are dehydrated, hypothalamus detects this and sends signal to pituitary gland to increase ADH, which will tell kidney to decrease amount of water to be excreted out in urine and reabsorb more water in blood.
ADH also released when you have drop in blood pressure or decreasing blood volume

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12
Q

Describe the Anterior Pituitary Gland and its cells involved.

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Anterior Pituitary Gland: aka ADENOHYPOPHYSIS.

  • PARVOCELLULAR neurons in the hypothalamus secrete releasing hormones into the Hypothalamohypophyseal portal vessels.
  • These hormones then stimulate the anterior pituitary cells to release different trophic hormones into the bloodstream.
  • Those hormones travel to distant target tissues to stimulate secretion of other hormones.
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13
Q

List the hormones that anterior pituitary secrets? What kind of hormones are they?

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Anterior Pituitary gland secretes:  FLATPIG
FSH (Follicle stimulating hormone)
LH: (Luteinizing Hormone)
ACTH (adrenocorticotropic Hormone)
TSH (Thyroid stimulating hormone)
Prolactin
Growth hormone
These are all PEPTIDE/PROTEIN hormones
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14
Q

Explain the role of hypothalamus in relation to the pituitary gland.

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The hypothalamus secretes releasing hormones (RH) and inhibiting hormones (IH) that act on endocrine cells of the anterior pituitary to influence secretion of their hormones.

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15
Q

Describe the relationship between hormones in the hypothalamus, anterior pituitary and target glands

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Hypothalamus secrete hormones: Dopamine, TRH, CRH, Somatostatin, GHRH, and GnRH.
these hormones act on endocrine cells of anterior pituitary.
Dopamine will INHIBIT Prolactin of anterior pituitary. TRH from hypothalamus will release TSH (thyroid stimulating hormone) of anterior pituitary.
CRH (corticotropic releasing hormone) of hypothalamus stimulates release of ACTH in anterior pituitary.
somatostatin INHIBITS Growth hormone, while GHRH (growth hormone releasing hormone) stimulates Growth hormone of anterior pituitary.
GNRH (gonadotropic releasing hormone) stimulates release of FSH and LH of anterior pituitary.
from anterior pituitary to endocrine targets:
Prolactin stimulates breast in NON-ENDOCRINE target
TSH stimulates thyroid gland to produce thyroid hormones (T3, T4)
ACTH stimulates adrenal cortex to produce cortisol and stimulate many tissues
GH (growth hormone) stimulates LIVER to make insulin like growth factors and affect many tissues
the FSH and LH of gonadotropins stimulate endocrine cells of gonads to produce androgens, estrogen and progesterone; which all stimulate germ cells of gonads and many tissues.

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16
Q

What is unique about GH (growth hormone) and Prolactin?

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Growth Hormone and Prolactin are inhibited by hormones from hypothalamus.
Dopamine made by hypothalamus inhibits Prolactin of anterior pituitary
Somatostatin by hypothalamus also inhibits Growth Hormone.

17
Q

What happens if you produce too much dopamine? How will it affect another hormone? What happens if you produce too much somatostatin.

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Too much dopamine will decrease prolactin (since dopamine inhibits prolactin)
If there is no dopamine, you will have increase of prolactin
If there is too much somatostatin, you will decrease growth hormone (since somatostatin inhibits GH)

18
Q

What kind of cell types does the anterior pituitary have? provide examples of cells and what hormones they secrete.

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Anterior pituitary gland cell types: The TROPHS
-Trophic cells STIMULATE OTHER cells
-The cell name tells you what’s being stimulated.
Gonadotrophs- produce FSH, LH, and stimulate the GONADS
-Thyrotrophs- produce TSH and stimulate Thyroid gland
-Corticotrophs- produce ACTH and stimulate Adrenal Cortex
-Lactotrophs- produce prolactin and stimulate MAMMARY gland
-Somatotrophs- produce Growth Hormone and stimulate SOMATIC Cells (to grow)

19
Q

Describe what occurs in the growth Hormone Axis.

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Growth Hormone Axis:
GHRH (growth hormone releasing hormone) stimulates Growth hormone, which will allow GH to pass through blood and impact adipocytes, bone and muscle. Growth hormone will also stimulate the liver to secrete IGF-1 (Insulin-growth Factor).
IGF-1 will then travel through blood and stimulate bone, muscle and adipocytes.
Grehlin also stimulates Growth hormone levels in blood which will further impact bone, adipose tissue and muscle.
somatostatin will inhibit growth hormone which will negatively impact muscle , adipose and bone.
somatostatin receptor ligand will further stimulate somatostatin and inhibit growth hormone.
*GHRH antagonists will inhibit GHRH and prevent any stimulation of GH?
*IGF-1 will inhibit release of GHRH, and inhibit release Growth hormone or decrease effect of muscle, adipose tissue or bone?

20
Q

What kind of effects does Growth Hormone have? Differentiate between catabolic and anabolic.

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Growth hormone has both ANABOLIC and CATABOLIC effects
Anabolic- build up of muscle
Catabolic -break down of muscle or product
GH promotes both anabolic and catabolic processes based on physiological status (Fed vs slow state)

21
Q

Explain the effects of Growth hormone and IGF-1 andhow they depend on metabolic rate (Fed vs Fasted state)

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Growth hormone is ANABOLIC in FED state and CATABOLIC in Fasted state
during fasted state in adipose tissue: there is a decrease in glucose uptake and Increase in lipolysis (break down of lipid (fat), which overal decreases adiposity
During fasted state, gluconeogenesis is activated in the liver, which will stimulate IGF-1. Also, There is a decrease in glucose uptake in the muscle, leaing to lean body mass
During Fed state, GH stimulates Liver to activate RNA synthesis and protein synthesis, and also stimulate IGFBP and increase IGFs. This all leads to activation of IGF-1 that promotes protein synthesis, RNA synthesis, DNA synthesis and increase Cell size and number in kid stage.
Also, in fed state, amino acid uptake increases and protein synthesis increases, causing increase in LEAN Body mass. This will stimulate IGF-1 wihch will stimulate protein synthesis, RNA, DNA< cell size increases in bone, heart and lung. This will also stimulate for amino acid uptake, protein synthesis and RNA synthesis and DNA synthesis in chondrocytes, increasing linerar growth.

22
Q

Describe how Growth Hormone secretion changes throughout life. How does old age affect fat, and bone density?

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Growth hormone rises after birth (higher concentration than adults).
Then during puberty is PEAK period for growth hormone (highest levels)
After puberty, Growth hormone declines, leading into adult life.
Adult life or near senescence, there is a serious decline in Growth hormone due to old age. This is known as Somatopause (like menopause), where there is decline in growth hormone, and IGF-1.
During normal aging, the loss of growth hormone leads to an INCREASE in lean mass, Increase in fat mass and decrease in bone density.
Phenotypes of this will be frailty, muscle atrophy, relative obesity and increase in frequency fractures and disordered sleep (old-age)

23
Q

What are the different growth hormone pathologies?

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Growth Hormone pathologies:

  1. Growth Hormone Oversecretion BEFORE puberty= GIGANTISM
  2. GH Oversecretion AFTER puberty= ACROMEGALY
  3. GH Undersecretion= DWARFISIM (not producing enough GH)
  4. GH receptor deficiency= LARON DWARFISM (due to not being able to use growth hormone)
24
Q

Practice feedback loops, by discussing what would you expect concentrations of GHRH, GH, IGF-1 and Somatostatin to be compared to normal with GH pathologies (acromegaly, dwarfism, laron dwarfism)

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1) someone with acromegaly will produce too much growth hormone (GH overscretion after puberty) and hence increase IGF-1. The increase in IGF-1 will lead to negative feedback and help decrease GHRH (from hypothalamus), in order to stop making growth hormone. This negative feedback will also increase somatostatin (since somatostatin inhibits growth hormone). The Growth Hormone would increase blood glucose and decrease amino acids and increase fatty acids.
2) *someone with dwarfism- would have low GH (growth hormone), low IGF-1, the low IGF-1 would cause their to be stimulation of GHRH to make more GH, and increase in Somatostatin, which inhibits GH and activates dwarfism. This original decrese in GH will cause a drop in blood pressure and increase in amino acids and decrease in fatty acids.
3) *someone with Laron Dwarfism, cannot get GH to be used the right way, so GH will be low, somatostatin will be high (since it inhibits GH), IGF–1 will be low. Due to low levels of IGF-1, positive feedback will stimulate GHRH to release more GH, which eventually stimulates IGF-1, and inhibits somatostatin? Blood glucose will be increased?

25
Q

What determines the effects of Growth hormone and IGF-1?

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The effects of Growth Hormone and IGF-1 depend on METABOLIC STATE (fed or fasted)
Growth Hormone is ANABOLIC in FED state
and CATABOLIC (break down) is FASTED state
Adipose tissue- GH will stimulate adipose tissue and decrease glucose uptake, while increase lipolysis in FED state (hence decreasing adiposity)
Liver: GH will stimulate liver by increasing RNA synthesis, protein synthesis an IGFBP and IGFs in Fed state, meanwhile Increasing Gluconeogenesis in FASTED state (this will lead to stimulation of IGF-1)
IGF-1 will stimulate protein synthesis, RNA synthesis, DNA synthesis and Cell size and number in bone, heart and lung during FED state (increase organ size and increase organ function).
Both stimulation of GH and IGF-1 will stimulate increase in amino acid uptake, protein synthesis, RNA synthesis, DNA synthesis and collagen in fed state. Chondroitin sulfate and cell size and number also increase in fed state for chondrocytes.
MUSCLE- stimulation of GH (growth hormone) will DECREASE glucose uptake in muscle for Fasted state and increase amino acid uptake and protein synthesis in fed state, while increasing lean body mass. IGF also contributes to same trends as GH for muscle.