Endocrine Flashcards

1
Q

What are the major effects of prolactin?

A

Promotes milk secretion and maternal behavior

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2
Q

Define lactotrope

A

Cells that synthesize prolactin

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3
Q

What are the major effects of lutenizing hormone (LH)?

A

females: stimulates ovulation
males: stimulates testosterone secretion
- synthesized in gonadotrope cells

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4
Q

What are the major effects of follicle stimulating hormone FSH?

A

females: stimulates ovarian follicle growth
males: stimulates spermatogenesis
- synthesized in ganadotrope cells

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5
Q

What are the positive and negative feedback loops on Prolactin?

A
Positive:
-Breast suckling, TRH, VIP
-moderate levels of estrogen
Negative:
-Dopamine
-high levels of estrogen
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6
Q

What are the positive and negative feedback loops acting on gonadotrope cells that produce LH and FSH?

A

positive:
-GNRH: gonadotropin releasing hormone
negative:
-estogen and testosterone from gonads

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7
Q

What does hyperprolactinema often result from?

A

Prolactinoma-most common pituitary tumor.

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8
Q

What are treatments for hyperprolactinemia?

A

-bromocriptine and cabergoline

dopamine agonists acting on D2 dopamine receptor of the lactotrope

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9
Q

What are the major effects of ADH, anti diuretic hormone (aka vasopressin)?

A

Promotes renal water retention

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10
Q

What is central diabetes insipidus due to?

A

Failure to secrete ADH

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11
Q

What are the major effects of oxytocin?

A

-acts on breast to eject milk and on uterus to cause contractions

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12
Q

What are the major effects of growth hormone on metabolism and stature?

A

metabolism:
-spares glucose utilization, increases availability of FFAs, promotes amino acid uptake and protein synthesis
-decreases adiposity and increases lean body mass
-diabetogenic b/c long term admin of growth hormone can make tissues resistant to effect of insulin
Growth:
-promotes limb and internal organ growth
-net linear bone growth at epiphyses

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13
Q

What are insulin like growth factors IGFs? aka somatomedins

A

-have similar effects to insulin and mediate effects of growth hormone

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14
Q

How does insulin induced hypoglycemia be used to test hypothalamic pituitary axis?

A

Insulin induced hypoglycemia–>following should happen:
ACTH increases–>cortisol
GH increases
oppose the action of insulin

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15
Q

How do mutations in G proteins lead to tumors causing acromegaly or giantism and why are such tumors usually not malignant?

A

mutations in somatotroph G proteins lead to elevated levels of cAMP and hyper secretion of GH. If hyper secretion occurs in youth, results in giantism and if hyper secretion occurs after closure of epiphyses, leads to acromegaly. Not malignant because mutations retain differentiated functions and don’t metastasize.

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16
Q

Why is IGF-1 and not hGH a candidate pharmaceutical to treat Laron syndrome?

A

Laron syndrome is due to resistance to GH b/c of mutations in GH receptor that prevents GH from acting. treatment of IGF-1 to restore growth.

17
Q

Why are calcium homeostasis and phosphate homeostasis linked?

A

99% of calcium is complexed with 85% of phosphate in the body to form hydroxyapatite in bone.

18
Q

Why do circulating Calcium levels need to be controlled?

A

hypocalcemia leads to life threatening tetanic contractions

hypercalcemia leads to impaired mentation and consciousness and muscle weakness

19
Q

How is the synthesis of 1,25(OH)2-VItD regulated?

A
  • liver converts vitD3 to 25(OH)-VitD–>converted in kidney by 1-alpha-hydroxylase to 1,25(OH)2-VItD (active form)
  • fall of calcium, estrogen, prolactin: increases PTH, acts on kidney, increases 1,25(OH)2-VItD to maintain levels
  • negative feedback: on 1-alpha-hydroxylase, which leads to formation of less active metabolites 24,25(OH)2 and 1,24,25(OH)3
20
Q

What is the potential role of 1-alpha-hydroxylase in regulating immune response?

A

-TLR ligands and immune system cytokines may promote synthesis of 1,25(OH)2-VItD in macrophages, which promotes responses that help clear pathogens

21
Q

Why does a deficiency in Vit D lead to depressed levels of 25(OH) Vit D, normal levels of 1,25(OH)2-VItD, and elevated PTH levels?

A

Vit D deficiency leads lower 25(OH)Vit D and to compensatory elevation of PTH, which promotes conversion of 25(OH) Vit D to 1,25(OH)2-VItD.

22
Q

How is PTH synthesis and release regulated?

A

Plasma Ca2+ concentration is the principle regulator. As plasma Ca++ falls, PTH secretion increases.

23
Q

What are the major effects of PTH?

A

-act on bone to promote bone resorption and release of Ca and PO4 ions. PTH acts to increase phosphate and reduce calcium excretion in urine. Also increases formation of 1,25(OH)2-VItD in kidney, leading to increased Ca++ absorption in gut.