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Applied Biochemistry > Cell Signaling Pathways: Steroid Hormones > Flashcards

Cell Signaling Pathways: Steroid Hormones Flashcards

1
Q

what groups can steroids be grouped into based on their receptors? (7)

A 
mineralocorticoids 
glucocorticoids 
androgens 
estrogens 
progesterones 
thyroid
vitamin D3
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2
Q

what are natural steroid hormones synthesized form?

A

cholesterol

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3
Q

steroid hormones are lipids, which are fat soluble meaning they can

A

pass freely by diffusion through biological membranes and enter cells without a specific transporter mechanism

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4
Q

in the blood, because of their lipid or hydrophobic properties, steroid hormones circulate bound to

A

specific binding or carrier proteins rather than corticosteroid hormone binding globulin

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5
Q

steroids exert biological effects via two routes (2)

A

a slower genomic response (hours and longer)

faster nongenomic mechanism (minutes)

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6
Q

membrane associated receptors active

A

intracellular signaling pathways to bring about nongenomic actions of steroid hormones

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7
Q

nuclear receptors mediate genomic actions with time frames of

A

hours to days

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8
Q

concentration of estrogen in blood
male:
females (premenopausal):
females (postmenopausal):

A

male: 10-50 pg/ml
females (premenopausal): 30-400 pg/nl
females (postmenopausal): 0-30 pg/nl

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9
Q

concentration of testosterone in blood
males:
females:

A

males: 30-120 mg/nl
females: 2-8 ng/ml

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10
Q

concentration of progesterone in blood
males:
females premenopausal, follicular phase:
females premenopausal, luteal phase:

A

males: <1.0 ng/ml
females premenopausal, follicular phase: <0.70 ng/ml
females premenopausal, luteal phase: 2-20 ng/ml

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11
Q

plasma proteins bind and facilitate the circulation of

A

lipid like (hydrophobic) hormones

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12
Q

retuning acid binding protein binds to

A

retinoid acids

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13
Q

sex hormone binding globulin binds to

A

testosterone and estradiol

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14
Q

vitamin D binding protein binds

A

vitamin D

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15
Q

domain structures of nuclear steroid receptors (3)

A

variable region: what makes each receptor different
DNA binding domain: when hormone binds to receptor, this region reacts with DNA at hormone binding elements (specific sequence of nucleotides)
hormone-binding domains: bind to hormone

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16
Q

where are glucocorticoids synthesized

A

the adrenal cortex

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17
Q

glucocorticoids are a family of compounds which bind to the

A

GC receptor

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18
Q

the name glucocorticoid derives from its role in the regulation of the

A

metabolism of glucose

its synthesis in the adrenal cortex and its steroidal structure

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19
Q

what does glucocorticoids binding to their specific receptor stimulate?

A

transcription of anti-inflammatory proteins and factors

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20
Q

cortisol

A

natural steroid hormone, glucocorticoid

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21
Q

where is cortisol produced?

A

zona fasciculate of adrenal cortex

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22
Q

what is cortisol released in response to?

A

stress and a Leo level of blood glucose

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23
Q

primary functions of cortisol (3)

A

increase blood sugar through gulconeogenesis
suppress the immune system
aid in the metabolism of fat, protein, and carbohydrate

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24
Q

side effect if cortisol

A

decreases bone formation by causing osteocyte apoptosis (or autophagy at lower doses)
(neg effects on bone)

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25
Q

Nobel prize for synthetic corticosteroid

A

Drs. Kendall and Hence, Mayo Clinic; Professor Reichstein, Basel

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26
Q

glucocorticoids may be used in low doses in

A

adrenal insufficiency

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27
Q

are much higher doses, oral and inhaled glucocorticoids are used to suppress various (3) disorders

A

allergic]
inflammatory
autoimmune

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28
Q

inhaled glucocorticoids are the second line treatment for

A

asthma

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29
Q

glucocorticoids are administered as post-transplant immunosuppressants to prevent (2)

A

cute transplant rejection and the graft-versus-host-disease

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30
Q

glucocorticoids do not prevent an infection and also inhibit later

A

reparative processes

31
Q

what is glucocorticoid synthesis is regulated by?

A

corticotrophin releasing hormone by nerves in the hypothalamus

32
Q

corticotrophin releasing hormone stimulates the production of, —- which acts on the adrenal cortex to produce and release —

A

ACTH

cortisol

33
Q

prostaglandin synthesis

A

NSAIDS Inuit COX1 and CO2, variably altering the synthesis of TXA2, PGI2, PGD2, and PGFalpha

TXA2: thromboxane A2
PGI2: prostacyclin
PGD2: prostaglandin

34
Q

sex hormone target tissues (11)

A 
breast
female reproductive track
male reproductive track
bone 
vascular system
CNS
immune system
skin
kidney
lung 
GI
35
Q

osteoporosis

A

a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk of fracture

36
Q

what does bone strength primarily reflect? (2)

A

the integration of bone quality and bone density

37
Q

– million bone fractures annually

A

1.5

38
Q

bone fractures can include (3)

A

hip fractures
vertebral fractures
wrist and other fractures

39
Q

what are the annual consequences of hip fractures?

  • -% will die from complications
  • -% will require long-term care
A

24%

25%

40
Q

worldwide:

    • million hip fractures in 1990
    • million hip fractures in 2050
A

1.7
6.3
lots of diseases are becoming an increasing burden on our aging probation

41
Q

what percentage of women, on average, will suffer at least on osteoporotic fracture?

A

50%

42
Q

how much did osteoporosis cost the US alone in 1997?

A

~14 billion

43
Q

when does bone loss occur in menopausal women?

A

about two years prior to last menses

44
Q

estrogen-deprivation bone loss is completed over - years

A

6

45
Q

estrogen-deprivation bone loss ranges from about -% to -%

A

6-12%

46
Q

men vs women, whole body BMC relative to baseline

A

men don’t have rapid bone loss, just a steady decline

47
Q

SERM

A

selective estrogen receptor modulators

48
Q

raloxifene
uses:
effects/location:

A

SERM
uses: osteoporosis, breast cancer
effects/location: agonist at bone; antagonist a breast and uterus

49
Q

tamoxifen
uses:
effects/location:

A

SERM
uses: breast cancer
effects/location: agonist at bone and uterus; antagonist at breast

50
Q

androgens (5)

A 
DHEA
androstendiol
androstenedione 
testosterone 
DHT
51
Q

clinical uses of androgens (5)

A

male androgen insufficiency
treatment of children with growth failure
bone marrow stimulation in diseases resulting in hypo plastic or aplastic anemia
masculinizing hormone therapy

52
Q

anabolic steroids

A

familiar name for synthetic variants of testosterone

more properly termed anabolic-androgenic steroids

53
Q

anabolic steroids were first synthesized in the 1930s, and are now used to

A

therapeutically induce male puberty and treat chronic wasting conditions such as cancer and AIDS

54
Q

health risks of anabolic steroids include (5)

A 
harmful changes in cholesterol levels 
acne 
high blood pressure
liver damage 
changes in left ventricle of the heart
55
Q

what are the adverse effects of anabolic steroids? (4)

A

significant psychiatric symptoms including aggression and violence, mania, and less frequently psychosis and suicide have been associated with steroid abuse (WWE wrestlers, weight lifters)

56
Q

androgen insensitivity syndrome

A

mutations in the hormone binding region cause absence of hormone binding or qualitative/quantitative changes leading to testicular feminization or Reifenstein syndrome

57
Q

Era point mutations have been found in (3)

A

breast cancer
endometrial cancer
psychiatric diseases

58
Q

“famous” case reported in 1994 of a 28 year old male with incomplete epiphyseal closure, was 80.3 inches tall (still growing). he was found to have a mutation in the —- gene, which demonstrated the importance of

A

ESR1

estrogen in males

59
Q

generalized glucocorticoid resistance

A

mutation in ligand binding domain of GR-alpha. presented with history of fatigue, anxiety, hyperandrogegism, and hypertension

60
Q

hereditary diseases involving steroid hormone receptors and vitamin D receptor

A

hereditary vitamin Resistant rickets, alopecia, intervertebral disc disease, leprosy

61
Q

definition of a non genomic action

A

a response to receptor binding that does not initially influence gene expression, but involves signaling cascades (which may or may not result in gene expression changes)

62
Q

agonists

A

bind to a steroid hormone receptor and trigger signaling pathways characteristic of the original hormone

63
Q

dianabol

A

synthetic agonist of the androgen receptor
membrane of nuclear hormone receptor family, stimulates expression of genes that enhance development of lean muscle mass (anabolic steroid)

64
Q

antagonists

A

bind to the nuclear hormone receptors but do not trigger signaling pathways (like competitive inhibitors)

65
Q

tamoxifen and raloxifene

A 
antagonists of the estrogen receptor 
used in treating and preventing breast cancer because sone breast tumors rely on estrogen mediated pathways for growth. class of compounds, SERM
66
Q

tropical issues (3)

A

environmental and food chemicals which bind to estrogen and testosterone receptors weakly
bisphenol Ai n plastic bottles and plastic water pipes
phytoestrogens in soy products

67
Q

steroid hormones are synthesized from

A

cholesterol

68
Q

steroids hormones act through — or — mechanisms

A

genomic or nongenomic

69
Q

the classical mechanism is through interactions of steroids hormones with

A

nuclear receptors

70
Q

membrane HR also exert modulatory effects on nuclear HR through signaling pathways targeting

A

nuclear HR and co-activators

71
Q

membrane receptor binding of steroid hormones initiates various signaling pathways and activates other TF that can lead to transaction of some genes without

A

HREs

72
Q

sex hormones or their analogs are used in the treatment of a variety of

A

diseases

73
Q

analogs of sex hormones also have a number of — uses that can have serious side effects

A

recreational

Applied Biochemistry (52 decks)

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