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imed3004 COPY > Physiology: Endocrine Control Systems II > Flashcards

Physiology: Endocrine Control Systems II Flashcards

1
Q

What does the GnRH do?

A

Stimulates anterior pituitary to produce FSH and LH which is important for oestrogen and progesterone production in females and testosterone production in males.

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2
Q

What does CRH do?

A

Stimulates anterior pituitary to produce ACTH which is important for production of mineralocorticoids, glucocorticoids, and androgens.

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3
Q

What does somatostatin do?

A

it is a general antagonist to the release of prolactin and Growth Hormone.

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4
Q

Which part of the adrenal gland releases mineralocorticoids? What other hormones does it produce?

A

The adrenal cortex, it also produces androgens and glucocorticoids.

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5
Q

How are steroid hormones produced?

A

All start from cholesterol which is converted into pregnanolone. This involves import into mitochondria and production of enzymes.

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6
Q

How is steroid production regulated?

A

via cAMP levels

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7
Q

How is steroid production switched on?

A

Cholesterol is converted to pregnenolone.

Need cholesterol = LDL receptors

StAR = steroidogenic acute regulatory protein

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8
Q

What 2 enzymes are important for the formation of pregnenolone from cholesterol?

A

StAR (Steroidogenic acute regulatory protein)

P450scc (CYP11a1) (Cholesterol side chain cleavage)

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9
Q

What is the rate limiting step of all steroid production?

A

P450scc (CYP11a1) = cholesterol side chain cleavage

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10
Q

What types of enzymes are important for producing all steroids from pregnenolone?

A

Cytochrome P450s (CYPs) -> redox changes such as CYP11a/b1/b2, CYP17a1/19a1/21a2

Hydroxysteroid dehydrogenases (HSDs) = interconversions

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11
Q

How is steroidiogenesis controlled at the cellular level?

A

Different tissues have different enzymes with different specificities.

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12
Q

How does the adrenal cortex produce aldosterone?

A

Adrenal cortex has specific enzymes that enable it to produce androsteniodione -> cortisol -> aldosterone

These enzymes are:

Androstenedione requires CYP17 + 3beta-HSD

Cortisol requires CYP21 + CYP11b1

Aldosterone requires CYP11b2 (aldosterone synthase [corticosterone -> aldosterone]

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13
Q

What enzyme do the testes and ova have that make them produce different products?

A

Testes have 17 beta-HSD which converts androstenedione into testosterone.

Ova produce oestrogen from testosterone via an enzyme called aromatase. This same conversion occurs from androstenedione to oestradiol but the enzymes involved are both aromatase and 17beta-HSD

3 beta-HSD produces progesterone from pregnenolone.

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14
Q

How can the hypothalamus regulate steroidogenesis?

A

Regulated by cAMP in response to hormones like ACTH, AtII, FSH, LH, which all upregulate cAMP.

Upregulation of cAMP results in stimulation of steroid production by StAR which initiates transport of cholesterol molecules into the mitochondria where P450scc can start steroidogenesis.

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15
Q

Which secondary messenger is always involved in steroidogenesis?

A

cAMP

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16
Q

What do mineralocorticoids do?

A

Regulate minerals in the blood (Sodium)

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17
Q

What do glucocorticoids do?

A

Regulate glucose in the blood

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18
Q

What are the 3 layers of adrenal cortex and what do they produce? Why is there this arrangement?

A

Zona glomerulosa (mineralocorticoids)

Zona fasciculata (Glucocorticoids)

Zona reticularis (DHEA and androstenedione)

Deepest layers produce the easiest steroids and they get more complex the more superficial the layer is. The difference between them is the presence of an additional enzyme per layer.

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19
Q

What does the adrenal medulla produce?

A

Catecholamines (A/NA)

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20
Q

What is the consequence of the similarity in the structure of both cortisol and aldosterone?

A

Imperfection in selectivity results in some affinity of both receptors to both molecules. (cortisol injection results in sodium imbalances)

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21
Q

What do mineralocorticoids do? What do they respond to?

A

Produced in zona glomerulosa they respond to both AtII and Increases in local [K+] as well as ACTH to bind mineralocorticoid recptor (Aldosterone receptors) called MR or NR3C2 which activates signal transduction (gene transcription (hours) or heat shock proteins (minutes))

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22
Q

Where are mineralocorticoid receptors expressed?

A

Kidneys

Distal colon

Sweat glands

(Other locations that are not well understood include heart, hippocampus and brown adipose tissue)

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23
Q

What does aldosterone do in the kidneys?

A

Activates K+ and H+ secretion

Increases Na+/K+ - ATPase activity

Activates Na+ reabsorption

Increases BP and blood volume

24
Q

Where are glucocorticoids produced? What hormone is this in response to?

A

In the zona fasciculata of the adrenal cortex mediated by ACTH

25
Q

What is the most dominant glucocorticoid produced?

A

Cortisol (also corticosterone)

26
Q

Where is the glucocorticoid receptor present and what does it do?

A

It is present on almost every cell of the body and it is a receptor transcription factor which activates gene expression.

GR also represses activity of NF-kappaB and AP-1

27
Q

What kind of stressful situations can trigger cortisol release?

A

Physical: Trauma, surgery, exercise

Psychological: Anxiety, depression, crowding

Physiological: Fasting, hypoglycemia, fever, infection

28
Q

What do glucocorticoids do?

A

Help body deal with stress

Regulates cardiovascular, metabolic, and immunological function

Keeps blood glucose levels high keeping brain fed and forcing other body cells to switch to fats and AAs as energy sources

Catabolic: Break down protein

In large quantities, depresses immune and inflammatory response.

Elevates blood [fat]

Elevates blood protein and amino acids

Anti-inflammatory

29
Q

How do glucocorticoids elevate blood glucose levels?

A

Stimulates gluconeogenesis (mobilises AAs, increases conversion enzymes)

Decreases cellular glucose uptake mostly by muscle and adipose tissue.

30
Q

How do glucocorticoids elevate blood proteins/AAs and fatty acids?

A

Mobilises FAs from adipose tissue, also stimulates beta-oxidation -> energy

Mobilises AAs from non-hepatic tissues (enhances liver protein synthesis)

31
Q

How do glucocorticoids carry out anti-inflammatory functions?

A

They inhibit cytokine release or function

Blocks early stage inflammatory inception

Increases healing of inflammation

Suppresses cellular immune response, stabilises lysosomes, reduces vessel permeability

32
Q

How is cortisol secretion secretion controlled?

A

Circadian rhythm controls baseline of cortisol

Stress levels add to it

33
Q

What does ACTH do?

A

Acts on adrenal glands to produce adrenal glucocorticoids which binds cell-surface melanocortin type II receptors. These act on GPCRs: GPCR -> Adenylyl cyclase -> cAMP -> Protein Kinase A

34
Q

Where are ACTH receptors (MC2R) located?

A

Most dense in the zona fasciculata

35
Q

How does ACTH regulate steroid hormone secretion?

A

Stimulates lipoprotein uptake into cortical cells (increase in cholesterol) plus mitochondrial ox-phos genes (to provide energy for steroid synthesis)

Activates StAR (cholesterol -> mitochondria) and P450scc (chol -> pregnenolone)

Stimulates transcription of the steroidogenic enzyme genes (CYP11b1)

36
Q

What gene produces ACTH? What other proteins are produced with ACTH?

A

ACTH produced from POMC (Pre-pro-opiomelanocortin) which concurrently produces endorphin, lipotrophin and melanocyte-stimulating hormone

37
Q

Which hormone is responsible for runner’s high?

A

beta-endorphin binds to opiate receptor triggering “runner’s high”

38
Q

What does lipotrophin do?

A

Stimulates lipolysis and steroidogenesis

39
Q

What does alpha-MSH do?

A

alpha-MSH (Melanocyte Stimulating Hormone) stimulates melanocytes and can darken skin

40
Q

How is ACTH release controlled?

A

CRH and ADH in the hypothalamus stimulate release

Stress stimulates release

Hypoglycaemia stimulates release

Release follows circadian pattern. Highest levels early AM and follows sleep-wake cycle.

Inhibitory neurotransmitters include opioids, GABA, enkephalins, and somatostatin

Stimulatory hormones include serotonin, ADH, alpha and beta adrenergic agonists as well as interleukins

41
Q

What kind of negative feedback does cortisol provide for ACTH release?

A

Cortisol inhibits the pituitary gland and hypothalamus from producing more cortisol.

ACTH also prevents the hypothalamus from producing more CRH thus reducing amount of ACTH.

42
Q

Why is cortisol produced in response to interleukins?

A

To reduce immune response if it is excessive

43
Q

What is addison’s disease?

A

Adrenal insufficiency resulting in low cortisol and aldosterone levels.

this disease can result in low BP and blood glucose thus making people comatose.

44
Q

Why do people with Addison’s disease have darker skin?

A

Patient lacks cortisol so there is no negative feedback to ACTH production resulting in overproduction of ACTH and as we know ACTH is produced with melanin meaning skin will darken as a result.

45
Q

What is cushing’s syndrome?

A

For some reason (usually a hypothalamic tumour) there is an increase in CRH production which increases ACTH production causing:

Rapid weight gain

Central obesity (buffalo hump, moon face)

Hypertension, muscle wasting, poor wound healing

Hypercholesterolaemia, diabetes mellitis (insulin antagonism)

46
Q

What happens to cortical sex hormones?

A

DHEA + androstenedione which is converted in peripheral tissues to testosterone and oestrogen

47
Q

How is Testosterone converted into 5-dihydrotestosterone?

A

5-alpha reductase which is present in some target cells.

48
Q

Which cells of the testes have a blood-testes barrier?

A

Sertoli cells

49
Q

Which cells of the testes produce androgen-binding protein?

A

Sertoli cells

50
Q

Which cells of the testes secrete testosterone?

A

Leydig cells

51
Q

What are the estrogen types in order of potency in their effects?

A

beta-estradiol > Oestrone > Oestriol

52
Q

Where are oestrogens produced and how are they regulated?

A

In granulosa cells + corpus luteum

They are regulated by LH and FSH via cAMP

53
Q

Where is progesterone produced and how is it regulated?

A

Corpus luteum

Regulated by LH via cAMP

54
Q

How is follicular production of estrogen controlled (2 cell model)?

A

The following steps occur in both theca and granulosa cells:

Cholesterol -> pregnenolone -> Progesterone

Then in the theca cell androgens are produced from androgens which are then transferred to granulosa cells for production of estrogen

Both cells get LDL cholesterol for this process.

LH activates theca cells at the start of this process via cAMP.

Granulosa cells’ first 3 steps are also activated by LH

FSH then stimulates granulosa cells to produce aromatase which produces estrogens

55
Q

What do oestrogens do?

A

They bind to their nuclear oestrogen receptors; ERalpha and ERbeta which activate transcription factors.

These transcription factors are important for growth of ovarian follicles + uterine tube motility, cyclical changes in endometrium, increases in blood flow + smooth muscle contractility of the uterus, oestrogen-dominated uterus is more sensitive to oxytocin and increases breast duct growth.

Feedback:

Inhibits FSH

With LH has both positive and negative feedback based on when it is working

56
Q

What stimulates progesterone production?

A

LH

57
Q

What does progesterone do?

A

Binds to nuclear progesterone receptors which activate transcription factors.

Effects:

Uterus (progestational changes in endometrium)

Antioestrogenic effects (prevents uterine contraction)

Breast (Stimulates lobule + alveoli devt, supports lactation)

Brain (Stimulates thermogenesis and respiration)

Feedback: Inhibits LH

imed3004 COPY (50 decks)

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