Cell signaling Pathways Steroid Hormoes Flashcards

(59 cards)

1
Q

what are steroid hormones synthesized from

A

cholesterol

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2
Q

describe the composition of steroid hormones

A

they are lipids that are fat soluble and hydrophobic

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3
Q

what are the two routes that steroid hormones use to exert their biological effects

A

a slower genomic response and a faster nongenomic mechanism

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4
Q

what receptors mediate genomic actions

A

nuclear receptors

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5
Q

what receptors exert nongenomic effects of steroid hormones

A

membrane receptors activate intracellular signaling pathways

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6
Q

describe the de novo synthesis of cholesterol

A

2 acetyl coA + acetoacetyl coA -> HMG CoA -> mevalonate ->isopentyl pyrophophsate-> geranyl pyrophosphate + farnesyl pyrophosphate ->squaliene -?lanosterol -> cholesterol

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7
Q

where do steroid hormones undergo structural changes

A

on side chains or inside of rings

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8
Q

what is estrogen derived from

A

testosterone and androgens

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9
Q

what catalyzes the synthesis of estrogen

A

aromatase

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10
Q

describe female progesterone levels

A

they change through puberty and adolescence (increase until menopause)

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11
Q

describe male levels of progesterone

A

relatively constant, low levels

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12
Q

what do plasma proteins do

A

bind and facilitate the circulation of lipid like hormones

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13
Q

what are some lipid soluble hormones that bind to members of the nuclear steroid/thyroxine receptor family

A

cortisol, retinoic acid, thyroxine

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14
Q

what is cortisol derived from

A

cholesterol

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15
Q

what is retinoic acid dervied from

A

metabolite of vitamin A1, doesnt have steroid ring structure

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16
Q

what is thyroxine derived from

A

tyrosine residues in thyroglobulin, does not have steroid ring structure

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17
Q

what are the domain structures of nuclear steroid receptors

A

variable region, DNA binding, hormone-binding

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18
Q

where are glucocorticoids synthesized

A

adrenal cortex

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19
Q

what do glucocorticoids do

A

regulate metabolism of glucose, stimulate transcription of anti-inflammatory proteins and factors

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20
Q

where is cortisol produced

A

zona fasciculata of the adrenal cortex

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21
Q

what type of steroid hormone is cortisol

A

glucocorticoid

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22
Q

when is cortisol released

A

in response to stress and a low level of blood glucose

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23
Q

what are the effects of cortisol

A
  • increase blood sugar through gluconeogenesis
  • suppress the immune system
  • aid in metabolism of fat, proteins and carbs.
  • decreases bone formation by causing osteocyte apoptosis
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24
Q

how are glucocorticoids used in low doses

A

in adrenal insufficiency

25
how are glucocorticoids used in high doses
-oral or inhaled glucocorticoids are used to suppress allergic, inflammatory and autoimmune disorders -asthma -post transplant immunosuppressants to prevent rejection and graft-versus-host disease
26
do glucocorticoids prevent infection
no
27
what is a side effect of glucocorticoid use
inhibit later reparative processes when given post transplant
28
how are glucocorticoids regulated
by corticotrophin releasing hormone by nerves in the hypothalamus stimulating ACTH which acts on the adrenal cortex to produce and release cortisol
29
how do glucocorticoids affect inflammatory responses (mechanism)
-Gc induces lipocortin which inhibits phosphatidyl choline from forming arachidonic acid. - this then inhibits the formation of prostaglandins and thromboxanes by COX and subsequently inhibits vasodilation, capillary permeability and leukocyte attraction - arachidonic acid not forming also inhibits the formation of leukotrienes which are subsequently inhibit phagocytosis, bacterial killing
30
how do glucocorticoids affect immune responses (mechanism)
- GC inhibits the formation of IL-1beta from macrophages which blocks fever and T-cell activation ->B-cell activation and thus antibody production
31
how do NSAIDs inhibit the synthesis of prostaglandins
NSAIDs inhibit cox 1 and cox 2 which alter the synthesis of thromboxanes and prostaglandins
32
what is osteoporosis
a skeletal disorder characterized by compromised bone strength, increasing the risk of bone fracture
33
how do decreasing estrogen levels affect BMD and fractures
-bone loss in women begins 2 years prior to last menses -estrogen mediated bone loss is completed over 6 years -bone loss from estrogen is from 6-12%
34
describe the rate of bone loss as a cause of estrogen decrease
steep decline at first then gradual decline
35
what is the connection between periodontitis and osteoporosis
shared risk factors such as age, genetics, hormone change, calcium, smoking, vitamin D
36
what is the function of selective estrogen receptor modulators (SERMS)
they compete with estrogen for the estrogen receptor so estrogen doesn't bind
37
what are the androgens
DHEA, androstenedione, androstenediol, testosterone, DHT
38
what are the groups of steroid hormones
glucocorticoids, mineralocorticoids, androgens, estrogens, progesterone and vitamin D
39
what is an estrogen responsive element
specific short DNA sequence representing nuclear binding site for estrogen receptor protein and hormone complex
40
when are androgens clinically used
-male androgen insufficiency -treatment of children with growth failure -bone marrow stimulation in diseases resulting in hypoplastic or aplastic anemia - masculinizing hormone therapy
41
what is the receptor for androgen
testosterone receptors
42
what is androgen insensitivity syndrome
mutations in the hormone binding region causing absence of hormone binding or changes leading to testicular feminization
43
what is the estrogen receptor associated with (think diseases)
breast cancer and other tumors, control of bone growth, osteoporosis, and uncontrolled growth of the male skeleton
44
what is generalized glucocorticoid resistance and symptoms
mutation in ligand binding domain of GR-alpha. presented with history of fatigue, anxiety, hyperandrogenism, and hypertension
45
how do steroid hormones circulate the blood
bound to specific binding or carrier proteins
46
how long do genomic actions take
hours to day
47
how long do non genomic effects take
minutes
48
describe the nuclear mechanism of glucocorticoids
-the GC enters the cytoplasm and binds a heat shock protein (hsp) -the release of hsp causes the GC receptor to dimerize -the dimer of the receptor and hormone enters the nucleus to bind to the response element
49
what are anabolic steroids
synthetic variants of testosterone
50
what are anabolic steroids used for therapeutically
to induce male puberty and treat cancer and AIDS
51
what are the health risks of using anabolic steroids
bad cholesterol levels, acne, high BP, liver damage, and changes in the left ventricle of the heart
52
what are the adverse effects of anabolic steroids
psychiatric symptoms like aggression, violence, mania, and less frequently psychosis and suicide
53
what is androgen insensitivity syndrome
mutations in the hormone binding region cause absence of hormone binding or changes leading to testicular feminization
54
what results in estrogen receptor alpha point mutations
breast cancer, endometrial cancer and some psychiatric diseases
55
what is generalized glucocorticoid resistance
mutation in ligand binding domain of GR. symptoms include fatigue, anxiety, hyperandrogenism, and hypertension
56
what are some diseases involved with mutations in the vitamin D receptor
rickets, alopecia, intervertebral disc disease, leprosy
57
what do agonists do and give example
bind to a steroid hormone receptor and trigger signaling pathways characteristic of the original hormone ex: dianabol
58
what do antagonists do and give example
bind to the nuclear hormone receptors but do not trigger signaling pathways ex: tamoxifen and raloxifene (antagonists of estrogen receptor)
59
what are some environmental chemicals that target steroid hormone receptors
-bisphenol A in plastic bottles and plastic water pipes - phytoestrogens in soy prodcuts