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BMS 460 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

target cell for GHRH

A

somatotrope (+GH)

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2
Q

target cell for somatostatin

A
  • somatotrope (- GH)
  • thyrotrope (- TSH)
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3
Q

target cell for dopamine

A

lactotrope (- PRL)

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4
Q

target cell for TRH

A
  • lactotrope (+PRL)
  • thyrotrope (+TSH)
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5
Q

target cell for GnRH

A

gonadotropes (+ FSH and LH)

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6
Q

target cell for CRH

A

corticotrope (+ ACTH)

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7
Q

acidophils

A
  • a cell type in the anterior pituitary
  • somatotropes (make GH)
  • lactotropes (make PRL)
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8
Q

basophils

A
  • another cell type in anterior pituitary
  • thyrotropes: make TSH
  • gonadotropes: make FSH, LH
  • corticotropes: make ACTH and MSH (melanocyte-stimulating hormone)
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9
Q

which cell types are affected by hormones released into the blood?

A
  • acidophils
  • basophils
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10
Q

which hormones are released at nerve terminals and what are their target tissues?

A
  • vasopressin (ADH): kidney, vasculature
  • oxytocin: mammary gland, uterus
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11
Q

important note about the hypothalamic-hypophyseal portal system vs hypothalamo-hypophyseal tract?

A

they are two different structures!

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12
Q

what does the PVN primarily secrete?

A
  • firstly, this is the paraventricular nucleus in the hypothalamus
  • primarily secretes oxytocin
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13
Q

what does the SON primarily secrete?

A
  • firstly, this is the supraoptic nucleus in the hypothalamus
  • primarily secretes ADH (antidiuretic hormone, or arginine vasopressin)
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14
Q

review the diagram of the portal system on slide 3!!

A

PLZ

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15
Q

how are hormones from the posterior pituitary transported?

A
  • along axons that accumulate in axon dilations called herring bodies
  • these axons make up the hypothalamo-hypophyseal tract
  • the hormones are transported with the carrier protein neurophysin
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16
Q

review the charts on slide 4!

A

GOTTA REVIEWWWW

17
Q

oxytocin general points

A
  • hormone of love, bonding, trust, divorce, etc.
  • divorce or less likely marriage associated with defective oxytocin receptor
  • basically, it does more than just get produced in mammals during reproductive events
  • also shown to help old muscle work like new (healthy muscle maintenance and repair)
18
Q

what does ADH normally do?

A
  • binds the vasopressin II receptor on collecting duct cells
  • this causes a cAMP-mediated translocation of aquaporin-2 to the apical surface of these epithelial cells
  • aquaporins increase the permeability of water, so water can be reabsorbed
19
Q

what happens with no ADH?

A
  • the body cannot correct hyperosmolality, hypernatremia, polyuria, and polydipsia
  • this is because water can’t be reabsorbed to dilute plasma, so sodium gets very concentrated
20
Q

central diabetes insipidus

A
  • this is DI caused by actual issue with the posterior pituitary making ADH
  • causes include tumors, trauma, surgery
21
Q

nephrogenic diabetes insipidus

A
  • this is DI caused by inability of collecting duct cells to respond to ADH
  • causes include renal diseases, ADH-unresponsive kidney, and drugs like lithium (decrease cAMP)
22
Q

connect alcohol to DI

A
  • alcohol inhibits release of ADH from SON
  • is also acts as an antagonist for aDH in the kidneys
  • this stops aquaporins from getting inserted in collecting ducts
23
Q

connect pregnancy to DI

A
  • placenta secretes vasopressinase
  • this degrades ADH, which creates symptoms of both central and nephrogenic DI
  • normally, plasma vasopressinase falls after delivery
24
Q

describe SIADH

A
  • stands for syndrome of inappropriate ADH secretion
  • opposite of diabetes insipidus
  • patients with SIADH secrete too much ADH or ADH-like substances
  • urine osmolality is too high becuase kidneys reabsorb. too much water from the urine
  • this increases total body water, blood becomes hypo-osmolar, and plasma sodium drops (hyponatremia)
25
Q

two mechanisms of hyponatremia

A
  • dilution of plasma
  • increased excretion of sodium by the kidneys (kidneys increase sodium excretion/decrease sodium filtration in response to expanded plasma volume)
26
Q

describe the pathway of excessive ADH secretion (slide 7)

A
  • start with too much ADH
  • this causes increased water reabsorption by the renal tubule
  • one thing this causes is dilutional hyponatremia, leading to hyponatremia
  • another thing this causes is increased plasma volume
  • increased plasma volume decreases aldosterone secretion, decreases sodium reabsorption, and increases sodium excretion, leading to hyponatremia
  • increased plasma volume also increases glomerular filtration rate, leading to increased sodium filtration, leading to increased sodium excretion

BMS 460 (34 decks)

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