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Endo > Adrenal Gland Phys (Parfenova) > Flashcards

Adrenal Gland Phys (Parfenova) Flashcards

1
Q

What are the hormones produced in the adrenal gland and what part of the gland specifically makes them?

A

Cortex:
Z. glomerulosa: mineralcorticoids
Z. Fasciculata and reticularis: glucocorticoids, androgens, estrogens

Medulla: Catecholamines: Epi and NE

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2
Q

provide sustained energy source by ↑ gluconeogenesis in liver, ↑ lipolysis, ↑ blood glc (↓glc utilization by tissues)

A

Cortisol (glucocorticoid)

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3
Q

growth and developmental control mediated by…

A

sex hormones: androgens, estrogens

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4
Q

↑ Na reabs and K and H+ secretion

A

aldosterone (mineralcorticoid)

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5
Q

medites immediate response to stress: ↑glc and FA, ↑CV function and performance

A

catecholamines: epi and norepi

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6
Q

describe the transport of adrenalcortical hormones in the blood

A

steroid hormones (i.e. not catecholamines) are about to serum proteins

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7
Q

albumin has (low or high) affinity for adrenalcortical hormones

A

low

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8
Q

90% of cortisol is bound to

A

transcortin (CBP)

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9
Q

the other 10% of cortisol is bound to..

A

nothing! it is the free/active horomone

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10
Q

in general, if you ↑ the % hormone bound to a plasma proteins, you ↑ ____ and ↓ _____

A

↑ t 1/2

↓biological activity

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11
Q

adrenal cortocosteroids are derived from

A

cholesterol

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12
Q

what is the main provider of cholesterol for corticosteroid prodction

A

LDL

*80% from LDL and 20% of cholesterol is synthesized in the adrenal gland

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13
Q

Describe what happens to cholesterol in LDL when it arrives to the adrenal cells

A

LDL binds LDL receptor on adrenal cell surface → internalization via clatherin coated pits → endosome → lysosome → cholesterol is esterfied and stored in cytoplasmic vesicles and LDL receptors are recycled

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14
Q

What are the key enzymes in the synthesis of mineralcorticoids? What steps do they mediate?

A 
cholesterol desmolase (CYP11A1) 
-cholesterol → pregnenolone *rate limiting step

Aldosterone synthetase:
corticosterone → aldosterone

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15
Q

activates cholesterol desmolase (CYP11A1)

A

ACTH

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16
Q

activates Aldosterone synthetase:

A

Ang II

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17
Q

synthetic, potent aldosterone analong (slightly more potent than aldosterone)

A

9alph-fluorocortisol (fludrocortisone)

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18
Q

Effect of ACTH in adrenals

A
  1. stimulates the activity of cholesterol desmolase (CYP11A1)
  2. upregulates LDL receptors to inc cholesterol uptake
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19
Q

(Cholesterol desmolase (CYP11A1) or Aldosterone synthetase) is located in the mitochondria

A

Aldosterone synthetase

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20
Q

describe the regulation of aldosterone synthesis

A

decreased renal perfusion (low BP, vascular dz) → renin secretion → angiotensinogen to ang I (in liver) → ang I to ang II (by ACE) → ang II in adrenal cortex activates aldosterone synthetase → corticosterone to aldosterone

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21
Q

aldosterone target tissues

A

“Aldosterone: Keeps Liquid Volume High (in our) Body”

Kidneys
Lungs
Vasculature 
Heart
Brain

i.e. where mineralcorticoid receptors are found

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22
Q

What glucocorticoids have mineralcorticoid activity?

A

aldosterone (high receptor affinity)
cortisol (high affinity)
Cortisone (low affinity)

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23
Q

How is the selectivity of MR shifted towards aldosterone (when cortisol is also present for binding and it has high affinity ofr MR as well)?

A

11beta hydroxysteroid dehydrogenase converts cortisol to cortisone, which has a lower affinity for MR ∴ aldo can displace it and bind

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24
Q

where does aldo bind MR? (think on cellular level, not organ/tissue)

A

in cytoplasm

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25
Q

describe the what happens when aldo binds MR:

delayed effects and immediate effects

A

aldo-receptor complex translocates to the nucleus →
DELAYED:
binds specific gene promotor → upregulation of…
1. Na/K ATPase
2. ENaC
3. ROMK
4. Sgk1kinase that activates 1-3

all of these ↓ intracell Na and ↑intracell K

IMMEDIATE:

  1. ↑cAMP –IP3 mediated signaling → ↑Ca dept regulation
  2. ↑ activity of kinases (ERK1/2 and JNK)
26
Q

renal effects of aldosterone

A

↑Na reabs (∴ H2O too) – via Na/K ATPase and ENaC
↑ K secretion – via Na/K ATPase and ROMK
↑ H+ secretion – via Carbonic Anahydrase
↑ bicarb production – via CA

27
Q

most potent glucocorticoid our body synthesizes

28
Q

cortisol precursor with moderate potency

A

corticosterone

29
Q

cortisol metabolite with low potency

30
Q

key enzymes in cortisol biosynthesis and the steps they mediate

A
  1. cholesterol desmolate (cholesterol → progenolone)
  2. 11beta-hydroxylase (11deoxycortisol → cortisol)

look at the slide for the others, its probable not worth memorizing

  1. 17alpha hydroxylase
  2. 3beta-hydroxysteroid dehydrogenase
  3. 21beta-hydroxylase

**numbered in order

31
Q

Glucocoticoids bind receptor on PM or intracell?

32
Q

describe what happens once glucocorticoid binds receptor

A

GC-receptor complex translocates to nucleus → binds promoter of target genes →

  1. transactivation (simultanous stimulation and repression) of gene expression
  2. transrepression via NFkB → ↓proinflam cytokines
33
Q

describe overall purpose/goal of glucocorticoids action on carbohydrate and protein metabolism

A

mobilize protein from peripherial tissues to provide glc supply to the brain and other tissues

34
Q

effects of glucocorticoids in the liver

A

↑ gluconeogenesis (from aa)
↑ glycogenesis
↑ protein synthesis to make key enzymes

35
Q

effect of gluconeogeneis in pancreas

A

↑ insulin production (to inc glc uptake)

36
Q

glucocorticoids (activate or inhibit) insulin sensitive glucose transporters. effect of this?

A

inhibit: ↓ glc uptake by most cells (except brain) ∴ producing “insulin resistance”
* recall, glucocorticoids also ↑insulin, so plasma levels of insulin will be high, yet tissues will not be able to utilize it = “insulin resistance”

37
Q

What is the only organ that has enchanced glc uptake in the presence of glucocorticoids

A

brain

**insulin-indept process

38
Q

in the presence of glucocorticoids, protein is broken down everywhere but the

A

liver

**protein synthesis is also inhibited everywhere but the liver

39
Q

What happens to the thymus in the presence of glucocorticoids

A

involution

40
Q

Describe the effect of fat metabolism by glucocorticoidsteroids

A

↑lipolysis (→FA → oxidation )

paradoxically causes fat deposits, at high doses –think moonface

41
Q

What immune cells are the main target of glucocorticoids?

A

macrophages and T lymphocytes

42
Q

glucocorticoids effects on macrophages and T lymphocytes

A

↓ pro-inflammatory cytokines and ↑apoptosis

*will eventually cuase atrophy of lymphoid tissue

43
Q

glucocorticoids effects on immune function

A
  1. lysosomal disruction to ↓ inital stages of infalmmation
  2. prevents edema (↓permiability of capillaries)
  3. ↓leukocyte migration to inflammed area
  4. ↓ T lymphocytes
  5. attenuates fever
  6. prevents immunological rejection of transplant tissue
44
Q

effect of glucocorticoids on skin

A

↓ collagen synthesis

45
Q

effect of glucocorticoids on blood vessels

A

vasoconstriction → HTN

46
Q

effect of glucocorticoids on stomach

A

↑ gastic acid secretion and enzyme production

47
Q

effect of glucocorticoids on blood clotting

A

↓ clotting → bruising

**bc ↓Ca abs and reabs → hypoCa, and Ca is needed in the blood for clotting factors

48
Q

How do glucocorticoids suppress growth

A

↓ Ca abs in intestine and reabs in kidney → hypoCa → ↑PTH → bone demineralization/resorption

49
Q

Cell composition in the adrenal medulla

A

granular chromaffin cells

ganglion cells

50
Q

hormones of the adrenal medulla are dericed from

A

tyrosine

*hormones = epi and NE

51
Q

describe the synthesis of epi

A

tyrosine → DOPA → DA → NE → Epi

52
Q

enzyme that converts NE to epi

A

PMNT (phenlethanolamine N-methyltransferase)

53
Q

what activates PMNT

A

high levels of cortisol

→ ↑↑epi

54
Q

targets of catecholamines

A

alpha and beta adrenergic receptors on…

heart, lungs, muscles, vessels

55
Q

what controls the release of catecholamines

A

sympathetic nervous system

56
Q

intracellular signaling of catecholamine binding alpha or beta adrenergic receptors

A

activate GPCR → AC active → ↑cAMP → pro kinases active

57
Q

describe the steps/pathway of hypothalamic-pit-adrenal axis

A

stress → hypothalamus released CRH → Ant pit releases ACTH → adrenal cortex releases cortisol → metabolic and immune effects

58
Q

describe the negative feedback of the hypothalamic-pit-adrenal axis

A

cortisol

  1. ↓ inhibitory input of hippocampus
  2. ↓ CRH release from hypothalamus
  3. ↓ ACTH production from ant pit
59
Q

consequences of long term dexamethasone treatment

A

↓cortisol production and functional atrophy of hypothalamus-pit-adrenal axis

60
Q

What are the markers for stress in the blood

A

cortisol and ACTH

61
Q

effects of sustained, severe stress

A

continuous stimulation of adrenal hormones → enlargement and adrenocortical hyperfusion → disease…

  • heart disease
  • immunosuppression
  • digestive problems
  • sleep disorders
  • anxiety and depression

…those poor monkeys…

Endo (28 decks)

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