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Endo/Repro Exam 1 > 3. Hypothalamic-Pituitary Relationships > Flashcards

3. Hypothalamic-Pituitary Relationships Flashcards

1
Q

Another name for the pituitary gland is the _________. What two structures is it made up of?

A

Pituitary gland= hypophysis.

  • anterior pituitary (adenohypophysis) epithelial portion that is a collection of endocrine cells.
  • posterior pituitary (neurohypophysis) neural portion that is a collection of axons.
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2
Q

What connects the hypothalamus to the pituitary gland?

A

Hypophysial stalk.

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3
Q

If big enough, a pituitary tumor can cause what?

A

Dizziness and vision problems, or both because it can compress the optic chiasm.

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4
Q

Describe the connections between the hypothalamus** and the **posterior pitutary.

A
  • The connection between the two is neural.
  • The CB of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) in the hypothalamus extend axons to the posterior putuiary.
    • SON will secrete ADH.
    • PVN will secrete oxytocin.
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5
Q

Describe the relationship between the hypothalamus and the anterior lobe of the pituitary.

A
  • The relationship between the hypothalamus and the anterior pituitary is neural and hormonal.
  • Hypothalamus is connected to the AP by hypothalamus-hypophysial portal vessels.
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6
Q

Hypothalamus is connected to the AP by hypothalamus-hypophysial portal vessels. What is the purpose of this feature?

A

The HHP provides blood to the anterior pituitary. It allows hormones from the hypothalamus to be delivered directly and in high concentration, without them showing up in our systemic circulation in high concentrations.

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7
Q

It is important to keep the activity of the endocrine axes at a set point via negative feedback mechanisms.

How are hypothalamic neurons secreted?

A

In a pulsitile manner based on our circadium rhythm.

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8
Q

What is the difference between a 1°, 2° and 3° endocrine disorder?

A

1° endocrine disorder- low or high levels of a hormone d/t defect in endocrine gland.

2° endocrine disorder- low or high levels of a hormone d/t defect in pituitary gland.

3° endocrine disorder- lor or high levels of a hormone d/t defect in hypothalamus.

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9
Q

Each hormone from the anterior lobe are secreted from different cell types, except FSH and LH.

What are these cell types?

A
    1. Gonadotrophs -> release FSH and LH
    1. Corticotrophs -> release ACTH
    1. Thyrotrophs -> release TSH
    1. Lactotrophs -> release prolactin
    1. Somatotrophs -> release GH
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10
Q

AP hormones are organized into families based on their structure and function. What are these 3 families?

A
  1. ACTH family
  2. FSH, LH and TSH family (FLaT family)
  3. Prolactin and GH family
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11
Q
  1. Hypothalamus releases somatostatin onto somatotrophs of AP -> ____ GH secretion
  2. Hypothalamus releases GHRH onto somatotrophs of the AP -> ___ GH secretion
A

1. inhibiting

2. stimulating

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12
Q
  1. Hypothalamus releases PIF (dopamine) onto lactotrophs of AP -> ____ prolactin secretion.
  2. Hypothalamus releases TRH onto lactotrophs of the AP -> ___ prolactin secretion.
A

1. Inhibiting

2. Stimulating

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13
Q

Hypothalamus releases GnRH onto gonadtrophs of AP -> ____ LH and FSH secretion

A

stimulating

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14
Q

What is acromegaly?

A

Prolonged, excessive secretion of GH in adults, after the epiphyseal plates have closed. Excessive growth of soft tissue, cartilage and bone in hands, feet and face. Symtoms develop gradually.

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15
Q

Draw the regulation of growth hormone secretion and describe the feedback loops.

A
  • Secretion of growth hormone AP is controlled by 2 pathways: stimulatory (GHRH) and inhibitory (somatostatin)

Three feedback loops:

  • Ultrashort: GHRH, through an ultrashort feedback loop, inhibits its own production in the hypothalamus.
  • Long feedback loop: Somatomedins stimulate the release of somatostatin at the hypothalamus, a long feedback loop.
  • Short feedback loop: Somatomedins inhibit the anterior pituitary release of GH through a short feedback loop and GH stimulate release of somatostatin from hypothalamus.
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16
Q

When the anterior pituitary secretes [GH], it has a trophic effect on target tissue. One of those target tissue, the ______, secretes _________, which does what?

A
  • The liver
  • Somatomedin (IGF-1), resulting in inhibition. Somatomedins BOTH
    • inhibit the anterior pituitary release of GHRH through a short feedback loop,
    • stimulate the hypothalamic release of somatostatin via a long feedback loop.
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17
Q

If we think someone has acromegaly, the first thing. we do is measure IGF-1 levels. Why not levels of growth hormone?

A

GH level fluctuate throughout the day. IGF-1 levels, on the other hand, remain constant.

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18
Q

We think someone has acromegaly. We measured IGF-1 levels and they were elevated. What is the next step to properly diagnose the patient?

A
  • Give oral glucose.
    • Typically, glucose should decrease secretion of GH.
    • If serum GH is NOT supressed: ACROMEGALY.
  • Perform a pituitary MRI​
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19
Q

How can we remove a pituitary tumor?

A
  • Use a endoscope via a transphenoidal approach.
  • If the tumor is > 1cm, use radiation.
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20
Q

How is growth hormone secreted an when is it secreted the most?

A
  • Pulsitile manner
  • When sleeping and higher during puberty than young kids or adults.
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21
Q

A defiency in growth hormones can be due to what 4 things?

A
  1. Decreased secretion of GHRH from the hypothalamus.
  2. Decreased secretion of GH from the AP.
  3. Failure to make somatomedins in the liver.
  4. Receptors are resistant to GH or somatomedin.
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22
Q

An excess of GH can be due to what?

A
  1. Growth hormone secreting pituitary tumor
    1. Before puberty -> gigantism
    2. After: acromegaly
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23
Q

People with acromegaly see increases in periosteal bone growth, organ size, extremity size and what else?

A

Insulin resistance and glucose intolerance.

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24
Q

GH has 3 metabolic functions such as what?

A

1. Diabetogenic effect (increases blood glucose).

2. Increase in protein synthesis and organ growth.

3. Increase in linear growth.

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25
Q

GH has three metabolic effects:

  1. Diabetogenic effect (increases blood glucose).
  2. Increase in protein synthesis and organ growth.
  3. Increase in linear growth.

Describe #1.

A

GH causes insulin resistance.

  • As a result, we have decrease uptake of glucose and utilization by target tissues, causing an i_ncrease in blood glucose levels_.
  • Increases lipolysis in fat tissue

AS A RESULT: we will also have high blood insulin levels.

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26
Q

GH has three metabolic effects:

    1. Diabetogenic effect (increases blood glucose).
    1. Increase in protein synthesis and organ growth.
    1. Increase in linear growth.

Describe #2.

A
  • GH causes an increase in uptake of AA–> makes DNA, RNA and protein–> increase body mass and organ size. This is mediated by somatomedins.
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27
Q

GH has three metabolic effects:

    1. Diabetogenic effect (increases blood glucose).
    1. Increase in protein synthesis and organ growth.
    1. Increase in linear growth.

Describe #3.

A

GH –> makes DNA, RNA and protein–> increases metabolism in cells that make cartilage and causes chondrocyte proliferation–> increasing linear growth.

This effect is is mediated by somatomedins.

28
Q

Describe the changes of insulin-like growth factor 1 and growth hormone in the fasting state.

A

When fasting, we see:

  1. Increase in growth hormone.
  2. Decrease in somatomedin (IGF-1).
  3. Decrease in insulin.

This decreases protein synthesis and growth–> thus, we mobilize other calories such as fats to get NRG.

29
Q

Draw the regulation pathway of prolactin.

A
30
Q

Hyperprolactinemia will supress what?

A
  • Too much prolactin will cause it to negatively feedback and prevent the release of GnRH from the hypothalamus, decreasing the amount of FSH and LH released from the AP–> ovaries and prolactin released to the breasts.
31
Q

Hyperprolactinemia (high prolactin secretion) causes __________ because prolactin inhibits GnRH secretion.

A

infertility

32
Q

Instead, the first line of treatment for hyperprolactinemia is usually medical treatment with a __________

A

DA AGO

33
Q

Prolactin will cause _______ secretion of GnRH.

A

decrease.

34
Q

Somatostatin will cause decrease secretion of ________.

A

1. GH

2. TSH

35
Q

CRH will cause increase secretion of __________.

A

1. ACTH

2. MSH

36
Q

Most pituitary turmors are ____________, which are spontaneous. Nearly all are benign/malignant and slow/fast-growing Functional tumors release an active/inactive hormone, while clinically non-functioning adenomas release active/inactive hormones.

A
  • Pituitary adenomas.
  • Benign and slow-growing.
  • Functional tumors- active hormone
  • Non-functioning adenomas- inactive hormones.
37
Q

Hormone producing pituitary adenomas release a shit tone of active hormone into the blood. Patients will usually experience symptoms related to what?

A

the hormone in the body.

38
Q

Pituitary failure can cause a deficit of GH, FSH/LH, TSH, ACTH and ADH.

What are the consequences of the first three.

A
  1. Decreased GH–> children are short but no effect on adults
  2. Decreased FSH and LH–> infertility, hypogonadism and decreased sperm in M. Hypogonadism, mentrual irregulatirty in F.
  3. Decreased TSH-> hypothyroidism.
39
Q

Pituitary failure can cause a deficit of GH, FSH/LH, TSH, ACTH and ADH.

What are the consequences of the last 2.

A
  • Decreased ACTH -> loss of pigmentation, hypoadrenalism
  • Decreased ADH -> diabetes insipidus.
40
Q

What is Sheehan syndrome?

A

When pregnant, the puitary gland is enlarged and more prone to infarction. If this happens, it results in postpartum hypopituitarism. Pts will have agalactorrhea, difficulties lactating, amenorrhea (gonadal insuff) and hypothyroidism.

41
Q

Posterior pitutary secretes ADH and oxytocin.

  • ADH neurons have CB primarily in the SON in the hypothalamus.
  • Oxytocin neurons have CB in the PVN of the hypothalamus.

How is oxytocin synthesized, processed and secreted?

A
42
Q

Posterior pitutary secretes ADH and oxytocin.

ADH neurons have CB primarily in the SON in the hypothalamus.

Oxytocin neurons have CB in the PVN of the hypothalamus.

How is ADH synthesized, processed and secreted?

A
43
Q

What are triggers for ADH secretion?

A
  1. Decrease BP will activate cardiac and aortic baroreceptors–> send signal to hypothalamus via sensory neuron–> trigger ADH production and release.
  2. Decrease arterial stretch d/t low blood volume will activate atrial stretch receptors–> send signal to hypothalamus via sensory neuron–> trigger ADH production and release.
  3. Increase osmolarity will activate hypothalamic osmoreceptors–> send send signal to hypothalamus via interneuron–> trigger ADH production and release.

Other: Angiotensin II, sympathetic stimulation, dehydration

44
Q

The secretion of ADH is most sensitive to changes in ________.

A

Plasma osmolarity.

45
Q

What are the actions of ADH?

A
  1. Vasoconstriction of blood vessels via V1 receptors.
  2. Increases water absorption in the kidneys via V2 receptors.

RESULT:

INCREASE BP and BV.

46
Q

What is the mechanism of ADH action in the renal collecting duct?

A
  1. Stimuli for ADH secretion.
  2. ADH is goes from bloodstream –> V2 receptor on the principal cell, located on the BL side.
    • G-protein
  4. ATP–> cAMP via AC.
    • PKA
  6. Adds AQP2 channels to the apical membrane.
47
Q

Under normal conditions, we have ______ amount of ADH in the body.

A

Medium amount.

48
Q

Dina is dehydrated (hyperomostic). How can expect her body to react?

A
    1. Hypothalamus detects too little water
    1. Posterior pituitary releases ADH.
    1. Kidneys remove less water from the blood, so less is lose in urine.
    1. Urine is more concentrated.
49
Q

Dina is overhydrated (hypoomostic) and Dillon has a brain h_emorrhage (hypERvolemia= volume expansion)_. How can expect her body to react?

A
    1. Hypothalamus detects too much water.
    1. Pituitary gland releases less ADH.
    1. Kidneys remove MORE water from the blood, so more is lost in urine.
    1. Large amount of dilute urine.
50
Q

Even when plasma osmolarity is low, a large enough change in volume ______ can cause ADH secretion.

A

Contraction.

51
Q

Hypervolemia (volume expansion) _____ ADH secretion even when plasma osmolarity is ______.

A

inhibits

higher than normal

52
Q

How does central diabetes insipidus (DI) affect ADH secretion?

What the Tx?

A
  • CDI: the posterior pituitary does not secrete ADH (low plasma ADH) d/t damage to the pituiary or destruction of hypothalamus.
  • Person makes large. volumes of dilute urine and body fluids increase in concetration (increase serum osmolarity and Na+)
  • Tx: desmopressin to prevent water excretion.
53
Q

How does nephrogenic diabetes insipidus affect ADH secretion?

What the Tx?

A
  • Nephrogenic DI: Kidneys cannot respond to ADH (high plasma ADH)
  • Causes: lithium, chronic disorders
  • Tx: desmopressin does not work.
54
Q

How can we differentiate between primary polydipsia and diabetes insipidus.

A

Water deprivation test!

  1. Let pt drink night before test, but give them breakfast with no fluids.
  2. Weight pt
  3. Do not give pt fluid for 8 hours; weight every 1-2 hours.
  4. When patient empties bladder, measure urine volume and osmolarity. Also, measure plasma osmolarity.
  5. If suggest DI: let pt drink (no more than twice urine volume of period of fluid deprivation) and give desmopressin
  6. Measure plasma and urine osmolarity, urine volume.
55
Q

read. central vs. nephronic DI chart

A
56
Q

What is SIADH?

A
  • Too much ADH secretion; too much water rentention. Our body becomes hypoosmolar, however this fails to inhibit ADH release.
57
Q

What are the pathophysiology changes seen in the lung and posterior pituitary in SIADH?

A
  • Small-celll lung carcinoma and lymphomas can cause excess secretion.
  • Adrenal insufficiency, drugs , trauma and CNS disorders on the posterior pituitary can also cause excess water retention.
58
Q

HPA Axis

Major hypthalamic and pituitary hormone:

Regulation:

A
  • CRH from the hypothalamus binds to the anterior pituitary to produce ACTH.
  • ACTH –> blood –> binds to adrenal CTX –> stimulates synthethsis of cortisol.
  • Cortisol can feedback and inhibit ACTH release from AP and CRH release from hypothalamus
59
Q

HPG Axis

  • Peripheral target organs:
  • Peripheral hormones:
  • Regulation of axis:
A
  • Peripheral target organs: testes and ovaries
  • Peripheral hormones: testosterone and estrogen
  • Regulation of axis: testosterone and estrogen can inhibit GnRH from the hypothalamus and FSH/LH from the AP.
60
Q

What does IGF do?

A
  • induces growth effects in other tissues, but also inhibits growth hormone production from the pituitary and stimulates somatostatin release from the hypothalamus.
61
Q

How is growth hormone and IGF-1 affected in a fasting state?

A
  • Growth factor is upregulated
  • IGF-1 is down-regulated.
  • Thus, we do not grow while we are fasting, but growth hormone still increases lipolysis.
62
Q

Glucose temporarily _________ growth hormone secretion.

A

down-regulates

63
Q

Growth hormone has a diabetogenic affect.

What does this mean?

A
  • Growth hormone has a diabetogenic effect, and increases blood glucose concentration.
    • ​This can cause insulin resistance. It does this by decreasing glucose uptake and utilization by target tissues but increasing lipolysis and adipose tissue.
64
Q
  1. Explain how the regulation of prolactin secretion differs from the secretion of most

anterior pituitary hormones.

A

In people who are not pregnant or lactating, prolactin is inhibited by DA.

Prolactin can inhibit itself by stimulating th release of DA and it inhibits GnRH, and thus, FSH and LH.

65
Q

b.Explain the impact of water restriction on urine osmolality in both central and

nephrogenic diabetes insipidus

A

Even following water deprivation, a patient with diabetes insipidus will have hypoosmolar urine.

  • A patient with central diabetes insipidus however will have low plasma ADH,
  • A person with peripheral (nephrogenic) diabetes insipidus will have high plasma ADH, as the body attempts to store water due to the water deprivation.

Endo/Repro Exam 1 (14 decks)

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