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c. phys exam 3 (w13) > endocrine 3/12/13 > Flashcards

endocrine 3/12/13 Flashcards

1
Q

what is the definition of:

  1. autocrine
  2. paracrine
  3. endocrine
A
  1. autocrine: the hormone leaves one part of the cell but interacts with another part of the same cell (auto=self) Mast cells with histhamine receptors to down regulate themselves
  2. paracrine: the cell releases a hormone that acts locally and has a short half life (inflammation) cells release hormnes
  3. endocrine: ductless hormones, basically the same as paracrine; but goes into blood and works globally (only affects cells with the specific receptor).
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2
Q

what do these mean:

  1. adeno-?
  2. what does that have to do with endocrine?
  3. neuroendocrine?
A
  1. adeno means glands that come from “the gut” during embreyonic stage
  2. most hormones come from adeno- cells.
  3. neuroendocrine: neuro cells that secrete hormones, some other hormones come from this (ADH)
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3
Q

what is half life?

A

the amount of time it takes to break down half of a substance

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4
Q

hormones come in 2 different types: what are they?

A
  1. polar (charged); hydrophillic; amino acid + protein

2. non-polar (non-charged); hydrophobic; cholesterol + protein

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5
Q
  1. how can you change an amino acid?
  2. what does a hydrophillic hormone need to get into a cell?
  3. what does a hydrophobic need to enter the cell?
A
  1. add or subrtract a charge
  2. (protein based)a membrane bound receptor
  3. (cholesterol based) nothing, it passes right through and binds with cytoplasmic receptors or nuclear dna receptors
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6
Q

down regulation vs. up regulation:

  1. what happens if there is too much hormone?
  2. what happens if there is too little hormone?
  3. what happens when hormone levels return to normal levels?
A
  1. the receptors down regulate (become less responsive or less numerous) ex: adenoma in pituitary-secretes too much hormone so receptors down regulate.
  2. receptors up regulate( become more responsive or more numerous)
  3. you will have exaggerated response with up regulated neurons.
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7
Q
  1. what is one of the most important amino acids when it comes to hormones?
  2. what is this amino acid’s function in formation of T3?
  3. what is this amino acid’s role in formation of neurotransmitters?
A
  1. tyrosine
  2. tyrosine + 2 Iodines
  3. tyrosine + O2= dopa (which eventually becomes epi and NE)
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8
Q

A. what is the path of tyrosine to epi (1-4)?

B. what is the rate limiting factor?

A 
A.1. tyrosine +O2 (via tyrosine hydroxylase)= dopa
2. dopa - CO2= dopamine
3. dopamine + O2=NE
4. NE + CH3= epinephrine
B. tyrosine hydroxylase availability
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9
Q

adrenal medulla secretion:

how much epi compared to NE?

A

80% epi to 20% NE

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10
Q

protein derived hormones:

  1. what prefixes will they sometimes have?
  2. track the path of insulin from ribosome to insulin vessicle?
  3. what are uses for the “pre” and “pro” for insulin?
A
  1. “pre”or “pro” or “Pre-pro”.
  2. pre-pro insulin (made by ribosome) > rough ER > pro insulin > golgi apparatus > insulin vessicle
  3. no use, they are garbage
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11
Q
  1. what is the pre-cursor for ACTH?

2. what does it break into and what does each one do individually?

A
  1. pro-opiocortin
  2. breaks into
    a) 2 melanocyte stimulating hormone
    b) 1 ACTH (adeno cortico tropic hormone)
    c) 2 lipotropin (pain regulator (opioid like))
    d) 2 endorphin (pain regulator (opiod like))
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12
Q
  1. what is addisons disease

2. what happens to your skin with addisons disease?

A
  1. addisons is a defeciency in cortisol from adrenal cortex so your body secretes more adeno-corticotropic hormone (trying to stimulate more cortisol)
  2. hyper pigmentation d/t hyper secretion of ACTH (since melanocyte stimulating hormone comes along with it).
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13
Q
  1. what is squelene?

2. what does it turn into?

A
  1. oil from the liver of dog fish (sharks)

2. cholesterol

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14
Q
  1. cholesterol goes to skin and uses _____ then goes to what organs to make what vitamin?
  2. what causes adult ricketts?
A
  1. goes to skin and uses UV light, then goes to kidneys and liver to form vitamin D
  2. liver and kidney issues cause a lack of vitamin D synthesis (vitamin D helps the intestines absorb calcium for the bones)
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15
Q
  1. steroids come from what?
  2. ___ ____ is an enzyme that converts ____ into___, which is converted into ___
  3. where does this enzyme do the first conversion?
A
  1. cholesterol
  2. cholesterol desmolase converts cholesterol to pregnenolone whic is then converted to progestagens.
  3. mitochondria
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16
Q

progestagens have 2 possible pathways:

  1. what is one pathway?
  2. what is the other pathway?
A
  1. 21-hydrolase turns progestagen into either a mineral corticoid (aldosterone) or glucocorticoid (cortisol)
  2. progestagens are converted to androgens which some is then converted to estrogens.
17
Q

what happens if there is a mutation of 21-hydrolase?

  1. female?
  2. male?
A
  1. all progestagens end up shunting toward the androgens side, the child becomes hyper masculinized and becomes a female hermaphrodite.
  2. males develop precocious puberty d/t high testerone levels cause male pattern facial hair and fusion of epiphysiseal plates causing a small hairy man.
18
Q
  1. how do you calculate metabolic clearance rate?

2. how does the body deal with hormones (5 ways)

A
  1. rate of hormone disappearance from blood (divided by) hormone concentration in blood
  2. a) hormone binds to receptor and is taken out of circulation
    b) hormone binds permanently to receptor; when receptor dies and is broken down, so is hormone
    c) receptor it binds to may take it in and degrade it
    d) liver can detoxify it and dump it into bile
    e) if small enough, kidney can dump it in urine
19
Q
  1. what is the hormone feedback mechanism?

2. what happens if the negative feedback mechanism doesnt work?

A
  1. the gland secretes an hormone which is taken into the tissue. when the tissue is done, the tissue sends a hormone (message) telling the gland telling it to shut down.
  2. the gland never turns off (i.e. goiter (not making enough T3 or T4 to shut the gland down- thus gland hypertrophies) or graves disease when TSH is mimic’d)
20
Q

what are the only 2 NORMAL positive feedback mechanisms in human beings that have no negative controls?

A
  1. first phase of female reproductive cycle

2. clotting

21
Q

second messenger systems:(adenylate cyclase) steps 1-4

  1. whent the (polar) hormone stimulates the membrane bound receptor, what happens?
  2. what is GS
  3. what happens to the GS protein then?
  4. what does the alpha GTP portion do?
A
  1. polar hormone stimulates membrane bound receptor with G protein (second messenger) GS
  2. GS= stimulatory G protein
  3. the GS protein is broken into 3 pieces; the alpha GTP part drifts
  4. binds to adenylate cyclase
23
Q

second messenger systems (adenylate cyclase: continued) steps 5-7

  1. when this GTP gets done, what is released?
  2. what does adenylate cyclase do?
  3. what does cAMP do? what does its product do?
  4. what controls the duration of this system?
A
  1. adenylate cyclase causes the GTP to loses a phosphate and becomes GDP which goes back to the receptor site.
  2. adenylate cyclase turns ATP + 2P into CAMP,
  3. cAMP activates protein kinase A (kinase A activity is with metabolism but also stimulates cAMP phosphodiesterase)
  4. System controlled by cAMP phosphodiesterase (which breaks down cAMP-negative feedback). once cAMP is gone, the hormone has to re-start the cycle.
24
Q

secondary messengers (phospholipase c) steps 1-4

  1. what is the second pathway of the hormone to GTP?
  2. what does alpha GTP bind to ?
  3. what happens to GTP then?
  4. what happens to the PIP2 phospholipid (2 things)?
A
  1. hormone releases GTP alpha unit
  2. GTP attaches to phospholipase C
  3. Phospholipase C caises GTP to lose a phosphate and becomes GDP and goes back to receptor site
  4. phospholipase C breaks down PIP2 (a phospholipid) which becomes DAG & glycerol with 2 fatty acids along with a sugar called IP3
25
Q

secondary messengers (phospholipase c (part 2)) 5-9

  1. what is IP3? what does it do?
  2. what does the IP3 receptor on smooth ER do?
  3. what does the calcium do?
  4. what happens with DAG?
  5. what does calmodulin do?
A
  1. IP3 is a sugar; goes to smooth ER receptor stimulating it
  2. causes the release of Ca++ into cytoplasm
  3. calcium goes to bind with calmodulin then goes back into smooth ER
  4. DAG + calcium work together to control protein kinase C
  5. calcium also binds to calmodulin activates cAMP phosphodiasterase
26
Q

how can 2 hormones work in conjunction

A

one can prime the cell for the other-ex:cortisol primes cell for HGH

26
Q
  1. insulin has an enzyme associated with its membrane bound receptor; what is it?
  2. what does it do?
  3. what is it called?
A
  1. a kinase
  2. adds a phosphate to somthing
  3. janus
27
Q

what 2 things activate protein kinase C

A

dag and calcium

28
Q

what opens the calcium channels on the smooth ER?

A

IP3

29
Q

what does PIP2 break down into?

A

IP3 and Dag with Glycerol bound to 2 fatty acids)

30
Q

what activates calmodulin?

A

calcium

31
Q

what does calmodulin activate?

A

cAMP phosphodiesterase

32
Q

difference between adenylate cyclase and phospholipase c second messenger systems.

A
  1. Adenlyate cyclase uses GTP
    phospholipase C uses GTP
  2. Adenylate cyclase uses phosphate to convert ATP to cAMP
    phospholipase C IS CONVERTED to PIP2 using phosphate
  3. A. cyclase: cAMP stimulates Protein Kinase A
    phospholipase C: PIP2 splits into IP3 and DAG
  4. A. cyclase: protein kinase A releases cAMP phosphodiesterase
    Phospo. C: IP3 stimulates calcium channels on smooth ER causing calcium release
  5. Phospho.C: calcium and DAG stimulate Protein Kinase C; calcium stimulates calmodulin which activates cAMP phosphodiesterase.

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

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