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BPK205 - Human Physiology > Endocrine (2) > Flashcards

Endocrine (2) Flashcards

1
Q

Classification of hormones

A

Based on source, neuronal control of release, receptor type, chemical structure, and function

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2
Q

3 main classes of hormones

A

peptide, steroid and amine derived

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3
Q

where are peptide hormones made and then stored

A

= made in advance by endocrine cells all over the body and stored in vesicles for release WHEN THEY ARE NEEDED

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4
Q

Describe the transgression of a peptide hormone

A

Initially made as a large inactive preprohormone which has 1 or more copies of the final peptide hormone

Series of post translational modifications converts preprohormone to prohormone to then a hormone

Released by exocytosis into ECF, and diffuses into blood

Response most likely involves altered activity of target proteins

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5
Q

Describe the half life of a peptide hormone

A

= short. seconds to minutes

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6
Q

where are steroid hormones made and then stored

A

made from cholesterol, in the adrenal cortex, kidney, skin, gonads, and placenta

  • Final form is lipophilic so these cannot be stored, they are made on demand by lipophobic precursors that may be stored in intracellular compartments
  • SER = has enzymes needed for steroid synthesis
  • GOOD THAT THE CELL HAS LOTS OF SER!!!
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7
Q

discuss the release, half life and response of steroid hormones

A

Released: by simple diffusion into blood, transported bound to carrier proteins

Longer half life: hours

Response: slow and genomic when involving intracellular receptors, but fast and non-genomic when involving membrane receptors

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8
Q

where are amine hormones made and then stored

A

made in pineal gland, adrenal medulla and thyroid

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9
Q

where is amine derived from

A

mostly tyrosine

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10
Q

what is tyrosine

A

a building block for thyroid hormones which have similar characteristics to steroid hormones

  • helps release catecholamines which have similar characteristics to peptide hormones
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11
Q

exocrine

A

secretion to the outside and leaves the body

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12
Q

Acinar cells and dust cell are a form of

A

exocrine secretion

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13
Q

acinar cell and dust cell secretion

A

form of exocrine

Acinar cells and dust cells secrete pancreatic enzymes into the lumen of the SI to break down food

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14
Q

F cell secretion

A

form of exocrine

F cells secrete pancreatic polypeptide

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15
Q

endocrine

A

secretion into the bloodstream and stays inside

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16
Q

examples of endocrine secretion

A

Alpha cells secrete glucagon

Beta cells secrete insulin

Delta cells secrete somatostatin which inhibits release of hormones like insulin and glucagon

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17
Q

Diverse hormonal actions

A

Hormones can regulate cellular processes

Cellular mechanism of action depends on presence/location of target receptors, and the specific signaling pathway

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18
Q

Cellular processes regulated by hormones

A
  1. rate of enzymatic reactions
  2. transport of ions/molecules across cell membranes
  3. gene expression and protein synthesis
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19
Q

Pituitary gland

A

example endocrine organ: fusion of anterior and posterior

anterior part = endocrine tissue that secretes 6 true hormones
- Release of hormones is controlled by neurohormones from the hypothalamus
- TSH thyroid stimulating hormone, and prolactin
posterior part = neural tissue that secretes 2 neurohormones made in the hypothalamus
- antidiuretic hormone, vasopressin and oxytocin

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20
Q

parts to a reflex loop

A

stimulus
sensor
input signal
integrating center
output signal
target
response

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21
Q

negative feedback loop ex: parathyroid hormone

A

Low plasma calcium conc

parathyroid cell senses calcium conc

parathyroid hormone systemically acts as an integrating center

target is bone and kidneys as they have storage depots of calcium and filter calcium too

result is increase in bone absorption, kidney reabsorption of calcium, and the production of calcitriol leads to increased intestinal absorption of calcium

which all leads to a response of increased plasma calcium conc

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22
Q

types of hormones interactions

A

SPUFT
3. synergism
4. permissiveness
1. up/down regulation
5. functional antagonism
2. trophic hormones

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23
Q

synergism

A

The interaction of 2 hormones has a greater affect than the individual ones added\

Not well understood or greatly predictable

24
Q

permissiveness

A

When a hormone cannot produce its full effect without the presence of another hormone, that hormone is permissive to the hormone it needs

Molecular mechanisms for this are not well understood

25
Q

up/down regulation

A

change in number of receptors cause long term effects that take days or weeks to occur

26
Q

up regulation

A

an increase in receptor numbers in response to decreased hormone conc

Trying to maintain response despite low hormone conc

27
Q

down regulation

A

a decrease in receptor numbers in response to increased hormone conc

Usually involves endocytosis of membrane receptors

28
Q

functional antagonism

A

interaction of hormones with opposite actions

Do not need to share receptors or signaling pathways
Ex. insulin and glucagon

29
Q

tropic hormones

A

hormones that cause a release of another hormones

Ex. neurohormones of the hypothalamus, and hormones of the anterior pituitary

30
Q

Types of ligand-receptor interactions

A

agonist vs antagonist

competitive vs non competitive antagonist

31
Q

agonist vs antagonist

A

Agonist = a ligand that binds to a receptor and enhances its activity
- Can have opposite effects in different tissues
- Adrenaline dilates blood vessels in skeletal muscle but constricts blood vessels in intestines

Antagonist = a ligand that binds to a receptor and inhibits its activity

32
Q

competitive vs noncompetitive antagonist

A

Competitive antagonist = a ligand that binds to a receptor and inhibits its activity, but its binding site is the same as the agonists
- Can be flushed out by an increased agonist conc

Noncompetitive antagonist = a ligand that binds to a receptor and inhibits its activity, but it binds to a different site on the receptor than the agonist
- OR binds to the same active site but it cannot unbind which makes it an irreversible antagonist
- Cannot be washed out by increased agonist conc

33
Q

what affects ligand-receptor interactions

A

specificity and competition

34
Q

specificity

A

= when receptors show preference for a particular ligand/type of ligand

  • Very specific = binds very few ligands
  • Non specific = able to bind many different ligands
  • Ligands can also show specificity for receptors
35
Q

competition

A

= when many ligands compete for the same receptor active site

  • Typically one ligand has higher affinity and binds better than other
  • The overall affect of each ligand is reduced in comparison to 1 ligand
36
Q

how to measure ligand-receptor interactions

A

dose response curves

37
Q

dose response curves: function and components

A

Measures the % response to an agonist conc
- If agonist conc is high enough, the receptors will be saturated and there will be maximal response

EC50 = effective concentration: agonist conc producing 50% of the max response
- Easy to measure on semilog scale using sigmoidal curve

38
Q

dose response curves: competitive antagonist s

A

Competitive antagonists make it harder for agonist to bind and elicit response
- Increasing the comp antagonist will increase the EC50

39
Q

dose response curves: noncompetitive antagonists

A

Noncompetitive antagonists change the availability of binding site OR irreversibly block the binding site
- Increasing the noncomp antagonist will decrease the max possible response

40
Q

Properties of hormones

A
  1. cell-to-cell communication molecules
  2. binding to target receptors initiates cellular response
  3. communication is eventually terminated
  4. half life
41
Q

how do hormones act as cell to cell communication molecules

A
  1. via chemical signals; usually v. low concentration
  2. may be secreted by a cell or group of cells (gland)
  3. transported by blood to distant target tissues
    - May act on one/many tissue types
42
Q

what does the initiation of the cellular response depend on?

A

the receptor that the hormone binded to, and the signaling pathway of the target cells

43
Q

how is communication eventually terminated

A

by limiting secretion, removing/inactivating the hormone, or by terminating the target cell activity

44
Q

what is half life a measure of

A

the time for the hormone conc in blood, to reduce by 1/2
- basically a measure of hormone stability

45
Q

peptide hormones are lipophobic, what does this tell us

A

peptide hormones therefor bind to membrane receptors, in order to cross the membrane
- this activates 2nd messenger systems

46
Q

2nd messenger systems

A

small molecules and ions that relay signals received by cell-surface receptors to effector proteins

47
Q

what are steroid hormones made of

A

cholesterol: all steroid hormones have a similar structure based on cholesterol

48
Q

why do steroid hormones that bind to intracellular receptors, have a slow genomic response?

A

because these this is a modulation or regulation of gene activity

49
Q

neurohormones

A

hormones that secrete via neural tissue
- not true hormones
- ex: catecholamines

50
Q

why are thyroid hormones similar to steroid hormones

A
  • lipophilic
  • made on demand from lipid precursors stored in the thyroid
  • requires carrier proteins
  • long half life
  • elicit slow genomic responses
51
Q

3 examples of steroid hormones

A

testosterone
aldosterone
estrogen

52
Q

gland

A

= a collection of secretory cells
- if not in a gland, secretory cells can be scattered amongst other epithelial tissue cells
… like goblet cells that secrete mucus

53
Q

portal circulatory system

A

a specialized modification where 2 sets of capillaries are connected in series by a set of small veins

54
Q

why is the portal circulatory system used

A

used for efficiency: hormones need to get to the anterior pituitary, not into the blood stream

55
Q

which is the true endocrine organ

A

anterior pituitary

56
Q

how does the release of a hormone in the anterior pituitary work

A
  1. hypothalamic neurons synthesize neurohormones and release them into the capillaries of the portal system
  2. portal veins carry the neurohormones directly to anterior pituitary, where the neurohormones will act on the endocrine cells
  3. endocrine cells release their peptides into the 2nd set of capillaries for distribution to the rest of the body

… ex: prolactin hormone will go to their target organs, mammary glands

BPK205 - Human Physiology (5 decks)

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