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physiology 2 > endocrine control 2 > Flashcards

endocrine control 2 Flashcards

1
Q

corticotropin releasing hormones

A

act on anterior pituitary to release adrenocorticotropic hormone
adrenocorticotropic hormone acts on the adrenal cortex mineralocorticoids (aldosterone) glucocorticoids (cortisol) androgens

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2
Q

cholesterol

A

has a large side chain preventing it from being transported into the mitochrondria

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3
Q

how to get cholesterol into the mitochdondria

A

cholesterol dose chain cleavage enzymes

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4
Q

cholesterol once into the mitcochodnira

A

pregnenolone

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5
Q

pregnenolone converted into

A

any steroids

depends on assembly of different enzymes available in the cell

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6
Q

2 main steps of steroidoegensi

A
  1. cholesterol changing to pregneolone

2. pregnenolone changing too all other steroids

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7
Q

cholesterol side chain cleavage

A

P450scc = cholesterol side chain cleavage (rate limiting step) enzyme
transported by AtAR = sterodssogenic acute regulatory protein - transports cholesterol into the mitochondria once the side chain has been cleaved off

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8
Q

changing pregnenlolone into other steroids

A

2 types of enzymes involved

  1. cytochrome P450s (CYPs) - redox changes
  2. hydroxysteroid dehydrogenase HSDs = interconversons
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9
Q

how to make testosterone

A

17bHSD turns androstendone to testosterone

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10
Q

hot to make progesterone

A

Sb-HSD turns pregnenolone not progesterone

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11
Q

adrenal cortex produces

A

androstenedione, cortisol and aldosterone

androstenedione - requires CYP17a1 and 3b-HSD
cortisol - requires CYP21 and CYP11b1
aldosterone - requires CYP11b2 (aldosterone synthase)

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12
Q

testes produced

A

testosterone - 17b-HSD to convert androstenedione to testosterone

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13
Q

ova produce

A

progesterone - 3b-HSD converts pregnenolone into progesterone
oestrogen - requires CYP19a1 converts testosterone into oestradiol

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14
Q

StAR

A

steroidogenic acute regulatory protein
stimulates steroid production (rate limiting transport step)
found in all tissues that can produce steroids
transports cholesterol molecules into the mitochondria
regulated by cAMP

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15
Q

P450scc

A

cholesterol side chain cleavage
rate limiting catalytic step
regulated by cAMP

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16
Q

receptors for trophic hormones

A

activate cyclic AMP to activate StAR and P450scc

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17
Q

corticosteroids

A

mineralocorticoids - cortex hormones regulating minerals
glucocorticoids - cortex hormones that regulate glucose
sex hormones

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18
Q

what produces corticosteroids

A

adrenal glands - adrenal cortex (outer)

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19
Q

zona fasciculata produces

A

cortisol

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20
Q

zona glomerulosa

A

produces aldosterone because it has aldosterone synthase

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21
Q

zona reticularis produces

A

androstenedione

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22
Q

mineralocorticoids

A

produced by the zone glomerulosa of the adrenal cortex

secretion is mediated by primary angiotensin 2, and increase in local potassium

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23
Q

dominant for of mineralocorticoids

A

aldosterone (although some others also have mineralocorticoid function)

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24
Q

mineralocorticoids binds

A

MC - mineralocorticoids receptor in the cytoplasm
expressed in kidney, distal colon, sweat glands
activates signal transduction via gene transcription and heat shock proteins

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25
Q

aldosterone action in kidney

A

binds MC receptor to stimulate activity and expression of sodium channels and Na/K ATPase
increases blood pressure and blood volume

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26
Q

glucocorticoids

A

produce in the zona vessiculata of the adrenal cortex

regulated by ACTH (corticotrophin releasing hormone)

27
Q

dominent form of glucocorticoids

A

cortisol

28
Q

glucocorticoids bind

A

GR - glucocorticoid receptor
ubiquitous - in almost every cell
a receptor transcription factor to activate gene transcription
also represses the function of NK-kappaB and AP-1

29
Q

what do glucocorticoids do

A

helps the body deal with stressful situations
- trauma, surgery, exercise, anxiety, depression, crowding, fasting, hypoglycaemia, fever, infection
regulated cardiovascular, metabolic and immune system function
keeps blood glucose high
breaks down protein for fuel source

30
Q

in large quantitiess of glucocorticoids

A

depresses immune and inflammatory response

also redirects circulating lymphocytes to lymphoid/peripheral tissues

31
Q

glucocorticoids on CHO metabolism

A

elevates blood glucose
- stimulate gluconeogenesis (mobilises AAs, increase conversion enzymes)
decrease cellular glucose uptake (mostly by muscle and adipose tissue)

32
Q

glucocorticoids on lipid metabolism

A

elevates blood fat
mobilises FAs from adipose tissue
also stimulates beta oxidation for energy

33
Q

glucocorticoids on protein metabolism

A

elevates blood [protein, AA]

mobilises AA from non hepatic tissues - enhances liver protein synthesis

34
Q

anti inflammatory processes of glucocorticoids

A

inhibits cytokine release
block early stage inflammatory inception
increases healing of inflammation
surpasses cellular immune response, stabilises lysosomes, reduces vessel permeability

35
Q

ACTH

A

adrenocorticotrophic hormone
acts on adrenal cortex
ACTH stimulate secretion af adrenal glucocorticoids
binds cell surface melanocortin type 2 receptors MC2R

36
Q

ACTH binds melanocortin type 2 receptors

A

activate cAMP

37
Q

MC2R most abundant in

A

zona fasciculata

38
Q

ACTH regulates

A

steroid hormone secretion
stimulates lipoprotein uptake into cortical cells (increase cholesterol) plus mitochondria ox-phos genes (steroid synthesis requires lottos energy)

activates StAR and P450scc
stimulates transcription of the steroidogenic enzyme genes

39
Q

ACTH

A

produced from POMC
pre-pro-opiomelanocortin

concurrently produces endorphin, lipotrophin and melanocyte stimulating hormone

b-endorphin binds opiate receptor
y-lipotropin stimulates lipolysis
a/b/y-MSH stimulates melanocytes and can darken skin

40
Q

stimulation of ACTH release

A

CRH and ADH (hypothalamus)
stress
hypoglycaemia

41
Q

circadian pattern of release

A

highest levels early AM

sleep-wake cycle

42
Q

short term stress response

A

adrenaline and noradrenaline

increase blood glucose, increase blood pressure, increase breathing rate, increase metabolic rate, change in blood flow patterns

43
Q

long-term stress response

A

mineralocorticoids sodium ions and water by kidneys
increase blood volume and blood pressure

glucocorticoids conversion of proteins and fats to glucose and immune system suppressed

44
Q

Addisons disease

A

adrenal insufficiency
not enough cortisol or aldosterone
low blood pressure
low blood glucose
patients lack cortisol so there is no negative feedback fro ACTH
overproduction of ACTH
skin colour darkens (overproduction of melanocyte stimulating hormone)

45
Q

Cushing’s syndrome

A

too much cortisol
may be because of too much CRH (hypothalamus tumour) or too much ACTH (anterior pituitary tumour)
rapid weight gain
central obesity
hypertension, muscle wasting, poor wound healing
hypercholesterolaemia, diabetes melllitus

46
Q

sex hormones synthesised in

A

synthesised in the zona reticularis
DHEA (dehydroepiandrosterone) and androstenedione
converted in peripheral tissues to testosterone, oestrogen

47
Q

testosterone is secreted by

A

leydig cells in the testis in response to LH

48
Q

DHT

A

testosterone is converted to dihydrotestosterone by 5-alpha reductase which is only present in some target cells
amplifies action of testosterone in some target tissues
DHT-R complexes required for development of male external genitalia

49
Q

testosterone feedback control

A

systemic testosterone powerfully inhibits GnRH and LH secretion

50
Q

sertoli barrier

A

blood testes barrier
sertoli cells create locally high concentration of testosterone keeping it trapped in the testes to drive sperm production

concentrated testosterone without negative feedback

51
Q

IV testosterone

A

does not arise testes androgen level

exerts negative feedback and stops production of testosterone

52
Q

oestrogen potency

A

beta-oestradiol>oestrone>oestriol

53
Q

oestrogen produced by

A

granulosa cells (also corpus luteum)
require aromatase activity
regulated by LH and FSH (via cAMP)

54
Q

progesterone

A 
corpus luteum (tiny amount from follicular theca cells) 
regulated by LH (via cAMP)
55
Q

2 cells producing oestrogen

A

theca cells and granuloma cells

56
Q

oestrogen from granuloma cells

A

release oestrogen but can’t make them from scratch themselves - must be supplied with androgens which may come from the adrenal cortex or from nearly theca cells

57
Q

granuloma cells are responsive to

A

LH and FSH

58
Q

process of making oestrogens

A

cholesterol - pregnenolone - progesterone - androgens - oestrogen’s

59
Q

FSH catalises in the production of oestrogen

A

catalyses production of aromatase which converted androgens to oestrogen

60
Q

theca cells are responsive to

A

LH

61
Q

LH catalyses

A

cholesterol > pregnenolone

62
Q

effects of oestrogen

A
  • facilitate growth of ovarian follicles and uterine tube motility
    cyclical changes in endometrium
    increases blood flow and smooth muscle contractility of uterus
    oestrogen-dominatedd uterus is more sensitive to oxytocin
    increases breast duct growth
63
Q

effects of progesterone

A

uterus - progestational changes in endometrium, cervix and vagina
antioestrogenic effects - prevents uterine contraction
breast - stimulates lobule and alveoli development, supports lactation
brain- stimulates thermogenesis and respiration

physiology 2 (21 decks)

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