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Physiology Exam 3 > Lecture 60-Pituitary Hormones > Flashcards

Lecture 60-Pituitary Hormones Flashcards

1
Q

What is growth hormone (somatotropin) secreted by?

A

Somatotrophs

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2
Q

Stimulators of growth hormones? (6)

A

GHRH
Decreased glucose
Decreased FFA
Increased AA
Hypoglycemia/fasting/starvation
Puberty (estrogen/testosterone)

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3
Q

What are stimulators of growth hormones that play a role in nutrient regulation?

A

Decreased glucose
Decreased FFA
Increased AA
Hypoglycemia/fasting/starvation

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4
Q

What are inhibitors of growth hormones?

A

Somatostatin
Increased glucose, FFA
GH
Obesity
Somatomedins (IGF)

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5
Q

What stimulates somatostatin to be released from hypothalamus?

A

Somatomedins (IGF)

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6
Q

Where are the metabolic actions of growth hormones?

A

Liver, muscle, adipose, bone

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7
Q

What are five things that growth hormones affect?

A

Linear growth, protein synthesis, organ growth, carbohydrate, and lipid metabolism

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8
Q

Direct anabolic actions -> increased ______ absorption from _____, ____ reabsorption from _____, ______ synthesis in the _____.

A

Ca Absorption from gut
P reabsoprtion from kidney
Protein synthesis in liver

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9
Q

Where are IGF-2 (somatomedin A) made?

A

Made in the liver

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10
Q

What affect do indirect anabolic actions via somatomeids have?

A

Increase lean muscle mass, linear bone growth, organ size/function

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11
Q

What are the two direct catabolic effects of growth hormone?

A
  1. Increased gluconeogenesis in liver
  2. Increase lipolysis in adipose tissue
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12
Q

By increasing lipolysis in adipose tissue what is released into the blood? What formation is increased?

A

-Release of FFA into blood
*FFA is used for energy

-increased formation of ketones
*a lot of ketones lead to metabolic acidosis

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13
Q

What does a deficiency of growth hormone result in?

A

Dwarfism

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14
Q

What does excessive growth hormone secretion result in?

A

Acromegaly

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15
Q

What does progesterone do to insulin and growth hormone?

A

Progesterone antagonizes insulin and stimulates growth hormone

Insulin resistance and possible ketoacidosis

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16
Q

Increase growth hormone -> insulin _____ -> _______ketoacidosis

A

Insulin Resistance
Diabetic ketoacidosis

17
Q

What are the (2) hormones released from posterior pituitary?

A
  1. Antidiuretic hormone
  2. Oxytocin
18
Q

What is ADH synthesized by and where?

A

Synthesized by neurons in supraoptic nuclei of hypothalamus

19
Q

What is oxytocin synthesized by and where?

A

Synthesized primarily by neurons in paracentricular nuclei of hypothalamus

20
Q

ADH peptide precursor = __________________

A

Prepropressophysin

21
Q

Oxytocin peptide precursor = ________________

A

Prepro-oxyphysin

22
Q

What are stimulators of ADH secretion?

A

Increased plasma osmolarity
Decreased blood volume (hypovolemia)
Decreased blood pressure
Pain
Nausea
Hypoglycemia
Nicotine, opiates

23
Q

What do all the stimulators of ADH have in common?

A

They all reabsorb water

(Stimulators: increased plasma osmolarity, decreased blood volume (increased plasma osmolarity, decreased blood pressure, pain, nausea, hypoglycemia, nicotine, opiates)

24
Q

What are the inhibitors of ADH secretion?

A

Decreased plasma osmolarity, increased blood volume (hypervolemia), increased blood pressure, ethanol, glucocorticoids

25
Q

What do all the inhibitors of ADH secretion have in common?

A

Don’t reabsorb water—excreted in urine

(Decreased plasma osmolarity, increased blood volume (hypervolemia), increased blood pressure, ethanol, glucocorticoids)

26
Q

What part of the nephron is permeable to water?

A

Distal consulted tubule
Collecting duct

27
Q

When can water be reabsorbed into blood?

A

Under the influence of ADH

28
Q

What are the two major actions of ADH?

A

Kidney and vascular smooth muscle

29
Q

ADH receptor = ______ receptor

A

V2

30
Q

What two things does the ADH receptor use?

A

Adenylyl Cyclades and cAMP

31
Q

What is inserted into the membrane of principal cells in the kidney?

A

Aquaporin 2

32
Q

What type of receptor does vascular smooth muscle contraction use?

A

Uses V1 receptor

33
Q

What is the syndrome of inappropriate ADH secretion?

A

-excess ADH released from posterior pituitary
-hypervolemia and hyponatremia
-urine is very concentration

34
Q

What is peripheral or nephrogenic diabetes insipidus?

A

-posterior pituitary normal but principals cells in collecting duct unresponsive to ADH
-defective V2 receptor
-dilute urine, concentration body fluids
-circulating ADH increases (high)

35
Q

What is central diabetes insipidus?

A

-lack of ADH secretion
-can be at hypothalamus or pituitary
-circulating levels of ADH low
-can’t concentrate urine, large volume dilute urine
-plasma osmolarity increased

Physiology Exam 3 (17 decks)

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