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
What do all the inhibitors of ADH secretion have in common?
Don’t reabsorb water—excreted in urine (Decreased plasma osmolarity, increased blood volume (hypervolemia), increased blood pressure, ethanol, glucocorticoids)
26
What part of the nephron is permeable to water?
Distal consulted tubule Collecting duct
27
When can water be reabsorbed into blood?
Under the influence of ADH
28
What are the two major actions of ADH?
Kidney and vascular smooth muscle
29
ADH receptor = ______ receptor
V2
30
What two things does the ADH receptor use?
Adenylyl Cyclades and cAMP
31
What is inserted into the membrane of principal cells in the kidney?
Aquaporin 2
32
What type of receptor does vascular smooth muscle contraction use?
Uses V1 receptor
33
What is the syndrome of inappropriate ADH secretion?
-excess ADH released from posterior pituitary -hypervolemia and hyponatremia -urine is very concentration
34
What is peripheral or nephrogenic diabetes insipidus?
-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
What is central diabetes insipidus?
-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