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c. phys exam 3 (w13) > endocrine 3/19/13 > Flashcards

endocrine 3/19/13 Flashcards

1
Q
  1. what is the master gland?

2. which one is second after that?

A
  1. hypothalamus

2. pituitary

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2
Q

what is Rathke’s pouch?

A

a diverticulum of tissue forming upward from the embreyonic mouth; forms the anterior pituitary (or adenohypophysis)

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3
Q
  1. what happens to the Rathke’s pouch (where does it end up sitting)?
  2. what ends up covering it?
A
  1. it pinches and gets encapsulated in the sphenoid bone (in the sella tursica)
  2. the tentaculum (a tough fibrous tent) forms over the top of it
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4
Q

what connects the pituitary to the hypothalamus?

A

pituitary stalk

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5
Q
  1. what is another name for the posterior pituitary?

2. why?

A
  1. neurohypophysis

2. because it is derived from neuro tissue (unlike the anterior pituitary which is derived from GI tissue).

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6
Q

what is the anterior “hump/ bump” of the hypothalamus called?

A

the Median Eminence

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7
Q
  1. where is the supra optic nucleus contained?

2. what does it do?

A
  1. sits above the optic chiasm (where the optic nerves are)
  2. cell bodies for osmoreceptors are there with axons coming down to the neurohypophysis.
  3. these osmoreceptors sense saltiness and either cause secretion (if salty) or holding (if watery) of ADH by posterior pituitary
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8
Q

what else is hooked up to the osmoreceptors for releasing of ADH?

A

right atrium

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9
Q
  1. where is the para-ventricular nucleus?
  2. what does it release?
  3. what does ___ do?
A
  1. close to third ventricle
  2. releases oxytocin
  3. mamary glands have myoepitheilium which have actin and myosin filaments. oxytocin causes them to contract and release breast milk. responds to baby cry etc and cervix stretch/ contraction.
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10
Q
  1. how many amino acids in make up pituitary hormones?

2. of that number, how many are different from each other

A
  1. 12

2. the base 10 are exactly the same from hormone to hormone; only 2 are different

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11
Q
  1. since all of the hormones are basically the same (same 10 base amino acids), does vasopressiun work on myometrium and uterus?
  2. does oxytocin work on the kidneys?
A
  1. yes, but oxytocin is 6x stronger on myometrium and uterus than vasopressin; and conversely,
  2. oxytocin works on some on kidney, but vasopressin is 6x stronger for them.
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12
Q

what does a chaperone protein do?

A

chaparone proteins hook onto neuropeptides and escort them down the axon terminins causing a release of hormones from terminis.

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13
Q

the posterior pituitary is just an extension of the____?

A

hypothalamus

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14
Q

adenohypophysis:

  1. how does the hypothalamus control what is released?
  2. where is capillary bed #1?
  3. what is the name of the vein that drains capillary bed #1 into capillary bed #2?
  4. what is the name of the portal vein that connects capillary bed #2 to cap bed #3?
A
  1. the hypothalamic adenohypophyseal portal system.
  2. capillary bed #1 is in median eminence (portal vein empties capillary bed #1 into capillary bed #2)
  3. long portal vein
  4. short portal vein
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15
Q

where does capillary bed#3 empty into?

A

blood stream

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16
Q
  1. what is GHRH?
  2. what secretes it?
  3. what is its target cell? how does it get there?
  4. what does the somatotrope release?
  5. what is secreted from hepatic (and pancreatic per Pharm) cells to bind with somatotrope as well?
  6. what does this hormone do?
A
  1. growth hormone releaseing hormone
  2. median prominence of the hypothalamus
  3. somatotrope cells in the adenohypophysis; gets there via long portal vein
  4. growth hormone
  5. somatostatin or GHIH (growth hormone inhibiting hormone).
  6. prevent growth hormone secretion
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17
Q
  1. what percent of anterior pituitary is somatotropes?

2. why do we need GH as adults if we are not growing?

A
  1. 30-40%

2. it primes cells for other hormones, control metabolism

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18
Q
  1. what is corticotropic releasing hormone (CRH)? what does it do?
  2. what is the full name of this product?
A
  1. it binds to corticotropes and causes them to release ACTH

2. ACTH is adrenocorticotropic hormone

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19
Q
  1. what is thyrotropic releasing hormone (TRH)?
  2. where does it go to and what does it bind to? what is released?
  3. where does that go, and what does it cause to be released?
A
  1. a hormone made in the median prominence which is released down the long portal vein.
  2. anterior pituitary; binds to thyrotropes which will release TSH
  3. TSH goes to thyroid and causes release of thyroxine
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20
Q
  1. what is GNRH? where is it produced?
  2. what receptors does it stimulate?how much of anterior pituitary is “these” cells?
  3. what is released when it GNRH binds?
  4. what do these hormones do?
A
  1. gonadotropin releasing hormone
  2. stimulates gonadotropes, 3-5% of A.P. are these cells
  3. FSH & LH (follicle stimulating and leutenizing hormones)
  4. maturation of ovum and sperm
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21
Q

what causes the release of GHRH?

A

low glucose, low fatty acids in blood, exercise, sex hormones and starvation.

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22
Q
  1. what is GNRH?
  2. where does it go?
  3. what does it cause to be released?
  4. where does that product go?
A
  1. gonadotropin releasing hormone
  2. goes to gonadotropes of anterior pituitary gland
  3. causes stimulation of LH (leutinizing hormone) and FSH (follicle stimulating hormone)
  4. the gonads for ovum maturation and spermatazoa maturation
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23
Q

what forms your pituitary stalk

A

the long portal vein and the axons

24
Q
  1. what does deep sleep stimulate the hypthalamus to do?
A
  1. secrete growth hormone releasing hormone which goes to the anterior pituitary and causes its somatortophs to secrete GH (or somatotropin)
25
Q
  1. what does somato mean?

2. ,3.what are the differences between somatostatin and somatotropin?

A
  1. somato means body
  2. statin=stasis (=stop)
  3. trope= alter or to change metabolism (=go)
26
Q
  1. what is somatomedin?
  2. where is it secreted?
  3. what does it affect?
A
  1. a negative feed back hormone that tells hypothalamus that its job of causing the secretion of GHRH is done, dont secrete anymore (causes release of somatostatin from hypothalamus).
  2. secreted by the liver
  3. hypothalamus (stoppping signals to cause GH release) and also causes bones to grow
27
Q
  1. what comes from the hypothalamus that causes the anterior pituitary to stop releasing somatotropin (GH)?
  2. so what organs control the release of GH?
A
  1. somatostatin

2. the liver (stomatomedin) causes the hypothalamus to release (somatostatin)

28
Q

when do you want to release GH?

A

in the early morning because it promotes hyperglycemia in the morning to give you the energy to get up.

29
Q
  1. Gh works with what nutrient to help you grow?

2. what does GH work synergistically with to help you grow?

A
  1. protein (causes uptake of amino acids)

2. works synergistically with insulin (you need insulin to grow)

30
Q

what is the process of turning amino acids into protein?

A

translation and transcription

31
Q

metabolism is__bolic and __bolic:

  1. ___causes the building?
  2. ___causes the breakdown?
  3. what are carbs and fats considered?
A
  1. anabolic (the increase of protein)
  2. catabolic (the decrease of potein)
  3. energy suppliers
32
Q
  1. how are fats broken down?
  2. what is made from them?
  3. what happens to them? what is formed?
A
  1. beta oxidation
  2. acetyl groups (acetylacetic acids)
  3. these are linked together into ketone bodies which are used for fuel
33
Q
  1. how much of anterior pituitary is somatotropes?
  2. how much is cortotropes?
  3. how much is gonadotropes?
  4. how much is lactotropes?
  5. how much is thyrotropes?
A
  1. 30-40% somatotropes
  2. 20% corticotropes
  3. 3-5% gonadotropes
  4. 3-5% lactotropes
  5. 3-5% thyrotropes
34
Q
  1. what does GH do to glucose uptake?

2. what does it do regarding liver?

A
  1. inhibits uptake by muscles, prevents uptake by adipocytes

2. causes liver to increase glucose production (via gluconeogenesis, glycogenolysis) inducing hyperglycemia

35
Q
  1. what is acromegaly?

2. what causes it?

A
  1. hyper growth of bones and diabetes
  2. caused by a benign tumor in the anterior pituitary which increases the release of growth hormone; pancreas releases insulin but demand is too high and pancreas burns out.
36
Q
  1. what does stomatomedin cause?

2. why are pygmies short?

A
  1. bone growth

2. they secrete adequate growth hormone but inadequate stomatomedin

37
Q

fibroblasts can do what?

A

can turn into chondrocytes (that make cartilage), adipocytes (that make fat) and osteoblasts (that make bone)

38
Q
  1. epiphyseal plates; what is it made of?

2. what is an osteoblast called once it is encased in bony matrix?

A
  1. start off as chondrocytes and vecome osteoblasts.

2. encased osteoblasts become OSTEOCYTES

39
Q
  1. how much of bone is collagen (protein skeleton)?
  2. what is the wavelength of collagen?
  3. what makes it hard?
A
  1. 90-95%
  2. 640 nm peak to peak
  3. hypoxyapetite deposits (calcium and phsophate) precipitate within these wavelengths
40
Q
  1. what is ground substance made of?

2. what does it look like (individually)?

A
  1. proteoglycans

2. look like centepedes

41
Q
  1. what is a bone unit called?
  2. what is the blood vessel in the middle of an ____?
  3. what do the osteocytes “wade” in? what does it translate to?
  4. what are the “canals” that connect each osteocyte?
  5. what is each layer of bone called?
A
  1. osteon
  2. haversian canal
  3. lacuna ; “little lake” of fluids
  4. canaliculi; “little canal”
  5. lamella
42
Q
  1. what do osteoclasts do?
  2. how do they do this?
  3. what do osteo blasts do?
A
  1. osteoclasts: erode bone and put calcium back into the blood stream
  2. sit like a dome over the bone and secrete citric and lactic acid which breaks down the bone into calcium and phosphorus
  3. osteoblasts: build bone back up
43
Q
  1. how much of the bodies calcium is not in the bones?
  2. where is most of it?
  3. where is the rest of it?
A
  1. all but 1.1%
  2. 1.0% is inside the smooth ER;
  3. 0.1% is extracellular
44
Q

what is the break down of of the last 0.1%?

a) ,b) ,c)

A

a) 41% of 0.1% is accounted for by donnan effect (bound to amino acids)
b) 9% of 0.1% is associated with an ion (cacl2)
c) 50% of the 0.1% is free

45
Q
  1. what causes the donnan effect?
  2. what does this do to calcium levels?
  3. what does excess calcium do?
A
  1. Donnan effect is the binding of calcium to proteins; acidosis (protons) cause calcium to be displaced from the negatively charged proteins (albumin) to become free calcium ions
  2. this almost doubles the calcium levels (from 50% free to (50%+42%)=92% of the 0.1 that is free)
  3. increased calcium increases threshold potential
46
Q

what does vitamin D do with calcium?

A

causes intestines to absorb calcium into apical membrane

47
Q

PARATHYROID

  1. parathyroid hormone; why is it released?
  2. how does it work indirectly? where?
  3. how does it work directly? where?
A
  1. released in response to low calcium;
  2. -indirectly affects intestine absorption of calcium (via vitamin D);
    • causes thick ascending limb of loop of henle to push out calcium into blood for reabsorption
  3. works directly on osteoclasts causing them to break down bone and put more calcium into blood stream
48
Q 
what is it? what is the target cell? what does the target cell release?
1. GHRH
2. GRH (GNRH)
3. CTRH
4. TTRH
5. PRH
6. PIH
7. GHIH (somatostatin)
8. somatomedin
9 oxytocin
10. ADH
A
  1. growth hormone releasing hormone>somatotropes of anterior pituitary>growth hormone>liver
  2. gonadotropin releasing hormone>gonadotropes of anterior pituitary>LH, FSH> gonads
  3. corticotropic releasing hormone>corticotropes of anterior pituitary>ACTH>adrenal glands
  4. thyrodotropic releasing hormone>thyrodotropes of anterior pituitary>TSH>thyroid
  5. prolactin releasing hormone>lactotropes of anterior pituitary>prolactin>myoendometrium of breasts
  6. prolactin inhibiting hormone>lactotropes-stops prolactin
  7. growth hormone inhibiting hormone (somatostatin)>hypothalamus>somatotropes of anterior pituitary-stops growth hormone
  8. somatomedin>liver>somatotropes of anterior pituitary-stops growth hormone
  9. oxytocin (from posterior pituitary via. paraventricuar nucleus)>myoepithelium of breasts, myometrium of uterus
  10. ADH (from hypothalamus-released by posterior pituitary)> blood vessels and kidneys
49
Q

THYROID

  1. what connects the 2 lobes of the thyroid gland?
  2. what is in the fluid filled follicles?
  3. what is at the center of each follicle?
  4. iodine comes in thru a vessel and is taken out in how many passes?
  5. what 2 things surround the follicle
A
  1. isthmus
  2. thyroglobulin
  3. 70 tyrosine molecules
  4. 1 pass
  5. a capillary and an apical membrane
50
Q

THYROID

  1. what pumps the iodine into the follicle
  2. what enzyme puts the iodine into a usable form? what is this form?
  3. what enzyme puts the tyrosine with the iodine?
  4. what is 1 iodine + 1 tyrosine called?
  5. what is 2 iodine + 1 tyrosine called?
  6. how do you get T3 (tri-iodo-thyronine)and T4 (tetra-iodo-thyronine) based on this formula?
A
  1. ATPase pump
  2. apical peroxidase; oxidized form
  3. iodinase
  4. MIT (mono-iodo-tyrosine)
  5. DIT (di-iodo-tyrosine)
  6. T3=MIT + DIT;
    T4=DIT + DIT
51
Q

THYROID

  1. what stimulates the release of T3 and T4?
  2. when TSH causes the release of T3 & T4, what is the ratio (%)?
  3. which one is the active form (the other being inactive)?
  4. since TSH stimulates release/ use of T3 & T4, what does it do to replenish it?
A
  1. cold and excitement
  2. 3% T3 and 97% T4
  3. T3 is active (T4 is inactive)
  4. increases iodine pump activity
52
Q

THYROID

  1. what transports T3 & T4?
  2. what happens to inactive T4 while in the blood?
  3. what does T3 do?
  4. what does this increase in metabolic activity cause?
A
  1. Transport proteins
  2. binds to intracellular proteins and will eventually (after weeks) convert to T3
  3. T3 will bind to nuclear receptors in cristae of mitochondria; cristae become more folded(=more metabolic activity), increases number of /Na+K+ pumps and number of mitochondria
  4. this increases “the furnace” burns more calories (fat, carbs, proteins are broken down), has SNS effect by increasing HR, RR, o2 consumption.
53
Q
  1. what is thyroid storm?
  2. what is a graves disease
  3. what is a goiter
A
  1. increased metabolism from thyroid
  2. an antibody mimics TSH and causes release of T3/T4 causing hyperactivity of SNS and goiter
  3. overgrowth of the thyroid usually due to hyperactivity (can be involved in hypothyroidism as well).
54
Q
  1. what is PRH and its antagonist?
  2. what do they bind to?
  3. what does either one cause (either one of 2 things)?
  4. what is the end product?
A
  1. prolactin releasing hormone and prolactin inhibiting hormone
  2. lactotropes in the anterior pituitary
  3. bind to lactropes to either cause the release of prolactin or inhibit its release.
  4. glands of breasts to cause production of milk or stop production of milk
55
Q
  1. parathytoid hormone affects bone in 2 phases: what are the phases?
  2. what is the first phase?
  3. what is the second phase?
  4. why dont osteoclasts respond directly to parathyroid hormone?
A
  1. Rapid and slow phases
  2. Rapid phase=starts within minutes to hours, receptors on osteocytes and osteoblasts; cytes and blasts release intrinsic factor which stimulates proliferation of more osteoclasts:
  3. slow phase= newly proliferated osteoclasts break down bone to put calcium into blood
  4. osteoclasts dont have parathyroid hormone receptors
56
Q

how is T3 & T4 released?

A

thyroglobin is phagocytocized and they are released

57
Q

what else is T3 good for (as far as development)?

A

CNS development

c. phys exam 3 (w13) (3 decks)

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