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7.2. The function of the adrenal cortex. Flashcards

1
Q

I. Adrenal gland (suprarenal glands)
1. Describe the structure of adrenal gland?

A

Bilateral structures located above the kidneys
- Outer cortex (75%) (~4g):
+) Composed of cortical cells
+) Synthesize adrenocortical hormones
- Inner medulla (25%):
+) Composed of chromaffin cells
+) Synthesize NE + E

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2
Q

I. Adrenal gland (suprarenal glands)
2. Describe the blood supply of adrenal gland

A

Blood supply: flows from cortex to medulla
- Important, because medulla will get information about the cortex and the cortex can control NE + E synthesis of medulla

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3
Q

I. Adrenal gland (suprarenal glands)
3A. What are the 3 zones of cortex?

A

1) Zona glomerulosa (15%): produce
mineralocorticoids (ex: aldosterone)
MOST IMPORTANT

2) Zona fasciculata (75%): produce glucocorticoids (ex: cortisol)

3) Zona reticularis (10%): produces
androgens (ex: DHEA[S])

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4
Q

I. Adrenal gland (suprarenal glands)
3B. What does Zona glomerulosa produce?

A

1) Zona glomerulosa (15%): produce
mineralocorticoids (ex: aldosterone)
MOST IMPORTANT

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5
Q

I. Adrenal gland (suprarenal glands)
3C. What does Zona fasciculata produce?

A

Zona fasciculata (75%): produce glucocorticoids (ex: cortisol)

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6
Q

I. Adrenal gland (suprarenal glands)
3D. What does Zona reticularis produce?

A

Zona reticularis (10%): produces
androgens (ex: DHEA[S])

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7
Q

II. Hormones
1. What are 3 types of hormones produced by adrenal gland?

A
  1. Mineralocorticoids (ex: aldosterone)
  2. Glucocorticoids (ex: cortisol)
  3. Androgens (ex: DHEA[S])
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8
Q

I. Adrenal gland (suprarenal glands)
2. What are the features of Mineralocorticoids?

A

Will affect/control the plasma minerals
- Aldosterone
- DOC = deoxycorticosterone
- (cortisol) – has some mineralocorticoid activity

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9
Q

I. Adrenal gland (suprarenal glands)
3. What are the features of Glucocorticoids?

A

Will affect blood plasma glucose concentration
- Cortisol
- Cortisone (11β HSD1 – convert ineffective cortisone to effective cortisol)
- Corticosterone
- Synthetic glucocorticoids (clinical importance: medication)

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10
Q

I. Adrenal gland (suprarenal glands)
3. What are the features of Androgens?

A

Not really hormones, but precursors
- DHEA (S) -> (dehydroepiandrosterone) ->precursor of androgens + estrogens

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11
Q

III. Biosynthesis of hormones
1. All of the adrenocortical hormones are ____

A

Steroids (hormones)

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12
Q

III. Biosynthesis of hormones
2. What are the feature of adrenocortical hormones?

A
  • All of the adrenocortical hormones are steroids (hormones)
  • Hydrophobic: can cross the PM by passive diffusion
  • No storage of these hormones
    => They are synthesized from cholesterol-ester, which is stored in lipid droplets
    => Source of cholesterol:
     LDL (low density lipoproteins)
     De novo synthesis (from acetate)
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13
Q

III. Biosynthesis of hormones
3. Are there any storage for adrenocortical hormones?

A
  • No storage of these hormones
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14
Q

III. Biosynthesis of hormones - Enzyme responsible for biosynthesis
4. What does Regulation of hormone secretion mean?

A

Regulation of hormone secretion means regulation of amount + activity of enzymes.

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15
Q

III. Biosynthesis of hormones - Enzyme responsible for biosynthesis
5. What are the 2 enzyme families for Biosynthesis of hormones?

A

1) CYP– cytochrome p450 oxidases
2) HSD– hydroxysteroid dehydrogenase

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16
Q

III. Biosynthesis of hormones - Enzyme responsible for biosynthesis
6. What is the role of CYP11 A1?

A

Enzyme responsible for the cleavage of the side-chain of the cholesterol
- Catalyze the cholesterol pregnenolone (reaction occurs in the mitochondria)

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17
Q

III. Biosynthesis of hormones - Enzyme responsible for biosynthesis
7. How can the cholesterol get into the mitochondria from the cytoplasm?

A
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18
Q

III. Biosynthesis of hormones - Zona glomerulosa cells (mineralocorticoids)
8. What is the role of CYP11B2?

A

CYP11B2 = aldosterone synthase, 3 reactions/activities:
1) 11-hydroxylase activity
2) 18-hydroxylase activity
3) 18 oxidase activity
=> NO CYP17 ENZYME!

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19
Q

III. Biosynthesis of hormones - Zona glomerulosa cells (mineralocorticoids)
9. Make a schematic diagram of aldosterone production

A
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20
Q

III. Biosynthesis of hormones - Zona glomerulosa cells (mineralocorticoids)
10. What is/are the enzyme(s) in Zona glomerulosa cells ?

A

CYP11B2

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21
Q

III. Biosynthesis of hormones - Zona fasciculata cells (glucocorticoids)
11. What is/are the enzyme(s) appear in Zona fasciculata cells (glucocorticoids)?

A

CYP17

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22
Q

III. Biosynthesis of hormones - Zona fasciculata cells (glucocorticoids)
12. Make the schematic diagram of cortisol production

A

CYP17 + CYP11B1  cortisol

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23
Q

III. Biosynthesis of hormones
13A. What happen if CYP11B2 is genetically modified (no activity)?

A

If CYP11B2 is genetically modified (no activity), it will only effect the synthesis of the aldosterone

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24
Q

III. Biosynthesis of hormones
13B. What happen if CYP21A2 is genetically modified (no activity)?

A

if CYP21A2 is modified, it will affect both aldosterone + cortisol biosynthesis

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25
III. Biosynthesis of hormones - Zona reticularis 14. Describe the process of hormones biosynthesis in Zona reticularis
- Here the CYP17 has both hydroxylase + lyase activity - DHEA(S) => androstenedione (precursor for testosterone + estradiol in the gonads)
26
III. Biosynthesis of hormones 15. Make a general schematic diagram for hormones biosynthesis in adrenal gland
27
IV. Hormone secretion and transport 1. What are the common features of cortisol and aldosterone?
Both cortisol and aldosterone are hydrophobic materials which require plasma binding proteins to keep them in the blood plasma
28
IV. Hormone secretion and transport 2. What are the features of cortisol?
- 90% bound to CBG (corticosteroid binding globulin = transcortin) - 7% bound to albumin - 3-4% free (equilibrated with hormone concentration in the cytoplasm) - Thalf (half-life) = 60-90 min [cortisol]Total >>(1000x)[aldosterone]Total [cortisol]free >(100x) [aldosterone]free
29
IV. Hormone secretion and transport 3. What are the features of Aldosterone?
- 60% bound to albumin + CBG - 40% free (hormone-fraction) - Thalf (half-life) = 20 min
30
V. Synthetic glucocorticoids 1. What are examples of Synthetic glucocorticoids?
Examples: methylprednisolone (GC activity = 10) and dexamethasone (GC activity = 20) - Elimination from blood plasma: (1) mainly in the liver (2) oxidation, conjugation
31
VI. What are the features of Receptors for adrenocorticol hormones?
32
VII. Aldosterone 1. What are the receptor and target cells for Aldosterone?
1. Receptor: mineralocorticoid receptor (MCR) 2. Target cells: - Principal cells in the kidney (nephrons) - Exocrine glands (duct cells in sweat/salivary glands) - Colon (epithelial cells)
33
VII. Aldosterone 2. What does mineralocorticoid receptor (MCR) bind to?
MCR binds to aldosterone (MC), but it can also bind to cortisol (GC)PROBLEM, because of the free hormone concentration - [cortisol]free >(100x) [aldosterone]free, therefore the receptors will always be activated by the huge concentration of cortisol
34
VII. Aldosterone 3. How can the target cells detect the increase of aldosterone?
- Target cells will eliminate the cortisol - 11β-HSD2 will catalyze cortisol => cortisone (=cannot bind to MCR) - Aldosterone will then be the only hormone that can activate the receptor
35
VII. Aldosterone 4. What is the consequence of Inhibition of 11β-HSD2?
- Cortisol will not be removed, but maintain a continuous MCR activity - The symptoms/consequences will be similar to hyperaldosteronism => AME = apparent mineralocorticoid excess syndrome
36
VII. Aldosterone 5. What are the effects of mineralocorticoids (MCs)
37
VII. Aldosterone 6. What is the consequence of Continuous aldosterone administration?
Will lead to hypokalemia + alkalosis => Na+-reabsorption↑ (transient)
38
VII. Aldosterone - Continuous aldosterone administration 7. What is the escape mechanism for Na+-reabsorption↑?
- A process that will (1) inhibit the Na+-reabsorption and (2) ↑Na+-excretion - Results in ↑ EC volume + BP => ↑GFR (will decrease the direct consequence of the aldosterone on the Na+-reabsorption) => natriuresis (excretion of Na+ in urine) ANP- effect
39
VII. Aldosterone 8A. Make a schematic diagram for Regulation of aldosterone secretion?
40
VII. Aldosterone 8B. Explain the regulation of aldosterone secretion
- When the BP decreases, there is a low Na+-uptake, ECF volume decreases and the sympathetic tone increases => will cause an increase in renin secretion which causes ANG II production. - ACTH is released in response to cellular need and stress, such as bleeding or diarrhea to increase hormone release. - In the case of ANP (atrial natriuretic peptide), it is produced in response to high blood volume/venous return in the atria and it inhibits renin secretion, thus decreasing ANG II and aldosterone. - This will increase Na+-excretion and cause blood volume to decrease.
41
VII. Cortisol 1. How is cortisol made?
CORTISONE --- (11β-HSD1) --- > CORTISOL
42
VII. Cortisol 2. How is cortisol secreted?
- Cortisol is secreted in bursts in response to the pulsatile secretion of ACTH. - The largest burst is 2 hours before waking up
43
VII. Cortisol 3. What is cortisol generally associated with?
Cortisol is generally associated with higher stress and pain levels.
44
VII. Cortisol 4. Why are many effects of cortisol considered permissive?
- Many of its effects are considered permissive, in that it does not directly initiate the response itself, but is necessary to allow a response to occur. - For example, cortisol does not directly stimulate glycogenolysis, but cortisol enhances the glycogenolysis effects of glucagon.
45
VII. Cortisol 6. What are the target cells for cortisol?
all of the cells have this type of receptor => will result in many effects (13)
46
VIII. Effects of cortisol 1. What are effects of cortisol based on?
All of these effects are based on the regulation of gene expression due to the IC receptors
47
VIII. Effects of cortisol 2. What are the effects of cortisol?
1. Metabolic effects - Protein, lipid and carbohydrate metabolism 2. Immunosuprressive and anti-inflammatory effects 3. Calcium and bone metabolism 4. Connective tissue 5. Fetal development 6. Delivery of the baby 7. Adrenal medulla 8. Adenohypophysis 9. Stomach 10. CNS 11. Negative feedback 12. Kidney 13. Permissive effects
48
VIII. Effects of cortisol - Metabolic effects 3A. What are metabolic effects of cortisol?
1. Carbohydrate metabolism: glucocorticoids (GC) will ↑[glucose]plasma 2. Protein metabolism 3. Lipid metabolism
49
VIII. Effects of cortisol - Metabolic effects 3B1. What is the effect of cortisol on carbohydrate metabolism?
1) Gluconeogenesis in the liver 2) Cortisol will ↓ usage of glucose by peripheral cells (skeletal muscle, adipocytes)
50
VIII. Effects of cortisol - Metabolic effects 3B2. What is the effect of cortisol on Gluconeogenesis in the liver?
1. Direct effect of cortisol ↑ -> can↑ expression of all enzymes involved in gluconeogenesis 2. Insulin – usually has an inhibitory effect on gluconeogenesis - When [cortisol] is high -> [glucose]plasma is also high -> ↑insulin -> inhibit the gluconeogenesis, BUT cortisol will ↑ the effect of insulin => Inhibit the inhibitory effect of insulin -> activate gluconeogenesis - The other effect of insulin, glycogen synthesis (liver), will not be inhibited
51
VIII. Effects of cortisol - Metabolic effects 3B3. How does cortisol decrease usage of glucose by peripheral cells (skeletal muscle, adipocytes)?
- The cortisol will inhibit the GLUT4 expression (required for uptake of glucose) and also the insulin-signaling will be inhibited
52
VIII. Effects of cortisol - Metabolic effects 3C. What is the effect of cortisol on protein metabolism?
- It will reduce the IC protein content (reduction of protein) by ↓ protein synthesis + ↑degradation (proteolysis) in the skeletal muscle, adipocytes and lymphoid tissue - The protein synthesis in the liver is not affected -> [protein]plasma↑ - Due to degradation of proteins[amino acids]plasma↑ -> AAs will serve as substrates for the gluconeogenesis (liver)
53
VIII. Effects of cortisol - Metabolic effects 3D. What is the effect of cortisol on Lipid metabolism?
- ↑lipolysis in adipose tissue -> FFA + glycerol (serve as a substrate for gluconeogenesis) - Cortisol will ↑ the appetite/food uptake -> lipids in the body↑ -> lipids will be stored, BUT there will be translocation of the storage from the peripheral parts of the body (extremities) to the central part of the body -> central obesity => Is a symptom to recognize the overproduction of the cortisol - ‘’moon face’’ => Peripheral tissues: lipolysis => Central part: lipid accumulation of the body
54
VIII. Effects of cortisol 4A. What is effect of cortisol on Immunosuprressive and anti-inflammatory effects?
Effects on immune cells - Cortisol prevents the development of the immune response (stops the inflammatory effect)
55
VIII. Effects of cortisol 4B. Give examples of immune effects by cortisol?
56
VIII. Effects of cortisol 5. What is the effect of cortisol on Calcium and bone metabolism?
- Ca2+-absorption/re-absorption occurs in the kidneys + GI-tract - Cortisol will inhibit Ca2+-abs./re-abs. -> hypocalcemia -> PTH↑ - Bone metabolism: in the osteoblast cells, the expression of the RANK ligand↑ -> osteoporosis (bone will lose Ca2+-content)
57
VIII. Effects of cortisol 6. What is the effect of cortisol on Connective tissue?
- Collagen synthesis + fibroblast proliferation↓ => Effects wound healing and causes development of striae (striations of skin)
58
VIII. Effects of cortisol 7. What is the effect of cortisol on Fetal development?
- GCs required for normal development of organs like: CNS, retina, GI-tract, lungs - In case of the lungs, the surfactant production/secretion is under the control of GCs => add additional GCs to increase surfactant production in early pregnancies
59
VIII. Effects of cortisol 8. What is the effect of cortisol on Delivery of the baby?
- GCs initiate the birth of the newborn (especially the GCs produced in the newborn)
60
VIII. Effects of cortisol 9. What is the effect of cortisol on Adrenal medulla?
- GCs will activate that enzyme (methyltransferase enzyme) that is required for the epinephrine production (NE --- [GC] --- > E) - If no GCs are present, it cannot happen in the adrenal medulla - Huge concentration is required for this reaction, can only happen when GC production in the fasciculata cells is activated
61
VIII. Effects of cortisol 10. What is the effect of cortisol on Adenohypophysis?
- In the adenohypophysis, the GH-production/secretion↑ - The IGF-1 production in the liver is inhibited (IGF-1 responsible for indirect effect of GH)
62
VIII. Effects of cortisol 11. What is the effect of cortisol on Stomach?
- The GC can inhibit the inhibitory effect of PG (prostaglandins) on the acid secretion => ↑HCl (gastric acid) production of stomach
63
VIII. Effects of cortisol 12A. What is the effect of cortisol on CNS?
Acute effects: - ↑memory, ↑learning + motivation, ↑arousal Chronic effects (GC present for a long time): - ↓attention, ↓behavior, ↓flexibility, depression
64
VIII. Effects of cortisol 12B. What are acute effects on CNS caused by cortisol?
- ↑memory, ↑learning + motivation, ↑arousal
65
VIII. Effects of cortisol 12C. What are Chronic effects on CNS caused by cortisol?
Chronic effects (GC present for a long time): - ↓attention, ↓behavior, ↓flexibility, depression
66
VIII. Effects of cortisol 13. What is the effect of cortisol on negative feedback?
Negative feedback on the CRH + ACTH production => regulation of cortisol production
67
VIII. Effects of cortisol 14. What is the effect of cortisol on kidney?
- In the kidney, the cortisol is required for the maintenance of the GFR - Cortisol also causes impermeability of the collecting duct -> H2O-reabsorption cannot occur (‘’cortisol works against ADH’’)
68
VIII. Effects of cortisol 15. What are the permissive effects of cortisol?
These effects will not increase the effect of cortisol by themselves, but ↑ expression of something, for example: - β1-AR in the heart - α1-AR in vessels => if GC production is impaired, the expression of these receptors will be decreased -> normal regulations will not work
69
IX. Regulation of cortisol production 1. Make a schematic diagram of Regulation of cortisol production
70
IX. Regulation of cortisol production 2. What are the effects of ACTH
1. Immediate activity (seconds/minutes: change of the activity of proteins 2. Subsequent response (hours): change of expression of proteins 3. Long lasting consequence (days/weeks): affect the total mass of the gland tissue (mass↑)
71
IX. Regulation of cortisol production 3. What are the 3 types of stress?
1) Physical stress: trauma, fraction, surgery, tissue damage, pain, extreme cold/heat 2) Psychological stress: emotional, smell, danger, bad news, visual experience 3) Biochemical stress: hypoglycemia, infection (production of mediators etc.)
72
IX. Regulation of cortisol production - Glucocorticoids and stress 4. What is the effects of glucocorticoids when it comes to stress?
All the effects in the blue box will depress the stress sensation (IMPORTANT FOR SURVIVAL!) 1. Gluconegenesis 2. Protein mobilization 3. Fat mobilization 4. Stabilizes lysosomes => RELIEVE STRESS
73
X. Cushing syndrome/disease 1. What are the causes of Cushing syndrome/disease?
74
X. Cushing syndrome/disease 2. What are the causes for high cortisol production?
75
X. Cushing syndrome/disease 3A. What are the causes for Cushing syndrome/disease?
76
X. Cushing syndrome/disease 3B. What happen when [cortisol] is ↑↑?
- When [cortisol] is ↑↑, they can also stimulate MC receptors, because the target cells of the MC are not able to remove all of the cortisol => MCR are stimulated.
77
XI. Conn’s syndrome What are the features of Conn’s syndrome?
- EC volume↑, Pmean↑↑, [Na+]pl↑ (bc H2O-intake↑ = normalize [Na+]) - Hypokalemia (weakness – membrane potential etc.), alkalosis
78
XII. Addison’s disease: (adrenal insufficiency) 1. What are the features of Addison’s disease: (adrenal insufficiency)?
79
XII. Addison’s disease: (adrenal insufficiency) 2. What happen if MC production↓?
- MC production↓ -> Pmean↓ -> blood + EC volume↓ => Hyperkalemia, metabolic acidosis
80
XII. Addison’s disease: (adrenal insufficiency) 3. What happen if GC production↓?
GC production↓ -> resistance against stress↓ -> [glucose]plasma↓ => acidosis
81
XII. Addison’s disease: (adrenal insufficiency) 4. What happen if there is a Lack of negative feedback?
ACTH (≈MSH) production↑↑ => MC1R (on surface of melanocyte) => melanin↑ => pigmentation↑
82
XIII. Enzyme deficiency: (andro-genital syndrome) 1. What are the features of Enzyme deficiency: (andro-genital syndrome)?
83
XIII. Enzyme deficiency: (andro-genital syndrome) 2. What happen if there is a mutation in CYP21A2?
Mutation in CYP21A2: aldosterone + cortisol↓ - Lack of negative feedback => ACTH↑↑ => androgen↑ (uncontrolled increase, bc ACTH is ↑)
84
XIII. Enzyme deficiency: (andro-genital syndrome) 3. What happen if there is a mutation in CYP11B1?
Mutation in CYP11B1 (only in fasciculata cells): only cortisol↓ - Lack of negative feedback => ACTH↑↑ => androgen↑
85
XIII. Enzyme deficiency: (andro-genital syndrome) 4. How can we recognize Enzyme deficiency in children?
We can recognize this disease in children by the ↑androgen production (=andro-genital syndrome) => secondary sex characteristics will develop and appear in younger age

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