Adrenal Gland

Question 1

What two anatomical sections can the adrenal gland be divided into? What do the secrete?

Answer 1

Medulla - secretes Adrenaline, Noradrenaline.

Cortex - secretes glucocorticoids and adrenal androgens.

Question 2

Where are the adrenal glands?

Answer 2

Paired glands, located near the kidneys.

Question 3

What 3 areas can the Adrenal Cortex be divided into? How large are they (proportionately)?

Answer 3

Zona Glomerulosa - nearest capsule. Smallest part. Zona Fasiculata - largest part in middle, large no of lipid droplets. Zona Reticularis - nearest medulla. Around 30% of cortex.

Question 4

What is the Zona Glomerulosa? What does it secrete?

Answer 4

ZG is the smallest part of the adrenal cortex. It secretes mineralocorticoids such as Aldosterone.

Question 5

What is the Zona Fascularis? What does it secrete?

Answer 5

Largest part of the adrenal cortex. It secretes Glucocorticoids, e.g. cortisol.

Question 6

What is the Zona reticularis? What does it secrete?

Answer 6

ZR is part of the adrenal cortex, it secretes adrenal androgens (DHEA, Androsteinedione)

Question 7

How can cholesterol be utilised? (3 ways)

Answer 7

Cholesterol esters in vesicles (Finite), Lipoproteins in circulation, or it can be made from Acetate.

Question 8

How does cholesterol get into a cell? How does it then get into the mitochondria?

Answer 8

Cholesterol gets into cell uses StAR. It then gets into mitochondria by conversion into Pregnenolone by CSCC.

Question 9

What is the pathway from Cholesterol to Androgens?

Answer 9

Cholesterol - Pregnenolone - 17ahydroxypregnenolone - DHEA - Androsteinedione - Androgens

Question 10

What is the pathway from Cholesterol to Aldosterone?

Answer 10

Cholesterol - Pregnenolone - Progesterone - Deoxycorticosterone - Corticosterone - Aldosterone

Question 11

What is the pathway from Cholesterol to Cortisol?

Answer 11

Cholesterol - Pregnenolone - 17ahydroxypregnenolone - 17aHprogesterone - Deoxycortisol - Cortisol

Question 12

How can excess ACTH affect pigmentation of skin?

Answer 12

ACTH can bind to MSH receptors when it is in excess, which causes hyperpigmentation.

Question 13

How is Aldosterone synthesis controlled?

Answer 13

RAAS System. Increased AII, Increased K, increase aldosterone. ANP causes a decrease in aldosterone. ACTH does not have a huge effect.

Question 14

What is the RAAS?

Answer 14

Renin from JGA in Kidneys converts Angiotensinogen to Angiotensin I, converted to Angiotensin II, which increases Aldosterone synthesis.

Question 15

How is adrenal androgen synthesis controlled?

Answer 15

ACTH is a potent stimulator.

Question 16

How are Glucocorticoids usually transported in the blood?

Answer 16

Usually transported bound to CBG (Corticosteroid Binding Globulin).

Question 17

What are the main affects of Glucocorticoids?

Answer 17

Anti-inflammatory, Immunosuppressive, Reduce growth in young subjects, Stress response. Increase plasma glucose.

Question 18

What are the actions of Mineralocorticoids?

Answer 18

Aldosterone increases Na retention, and increases K excretion.

Question 19

What is Cushing’s syndrome?

Answer 19

Cushing’s syndrome is an excess of Cortisol. It can be caused by either increased ACTH (pit. dependent - Cushing’s disease) or adrenal tumours (rarer).

Question 20

What are the clinical signs of Cushing’s syndrome?

Answer 20

Pot bellied, Hyperpigmentation, Alopecia.

Question 21

What is Hyperaldosteronism? What is Primary/Secondary?

Answer 21

Excess aldosterone. Primary aldosteronism is a result of a problem with the adrenal gland itself, secondary is other factors e.g. More AII.

Question 22

What are the main consequences of Aldosteronism?

Answer 22

More Na retention, More K excretion. Increase in heart rate, muscle weakness and arrthymias, Hypertension due to increased water and salt in blood.

Question 23

What is Addison’s disease? What are the main causes?

Answer 23

Addison’s disease is Hypoadrencorticism, where there is a lack of mineralocorticoids and glucocorticoids. May be due to adrenal atrophy.

Question 24

What are the main effects of Addison’s disease?

Answer 24

Mainly due to lack of Mineralocorticoids. Hyperkalemic, Bradycardia, Dehydration. Underperfusion.

Question 25

What two tests are important for testing Adrenal functions?

Answer 25

1) ACTH stimulation test

2) Dexamethasone suppression test.

Question 26

What is the ACTH stimulation test? What does it test?

Answer 26

ACTH involves administering Synacthen (ACTH analogue) to test cortisol level effects. It tests adrenal hypo/hyperfunction.

Question 27

What is normal in an ACTH stimulation test?

Answer 27

Double cortisol levels.

Question 28

What does no change in cortisol levels mean in an ACTH stimulation test?

Answer 28

Hypoadrenocorticism, as the adrenal gland does not respond.

Question 29

What does an exaggerated response in cortisol levels mean in an ACTH stimulation test mean?

Answer 29

Hyperadrenocorticism.

Question 30

How can the ACTH stimulation test be used to distinguish between spontaneous hyperadrenocorticism and Iatrogenic hyperadrenocorticism?

Answer 30

Spontanous have a level about 600nmol/l (much exaggerated), Iatrogenic have a similar response to Hypoadrenocorticism.

Question 31

What is the basis of the Dexamethasone Suppression test? What is it used to test?

Answer 31

Dexamethasone is a glucocorticoid analogue. It should suppress cortisol levels.

Question 32

What is normal in a Dexamethasone Supression test?

Answer 32

Reduction of cortisol levels to below 50nmol/l within 8 hours.

Question 33

What would a dog with Adrenal dependent Hyperadrenocorticism show in a Dexamethasone suppression test show?

Answer 33

The dexamethasone would not be able to have a negative effect, so there would be no change in cortisol levels after 8 hours.

Question 34

What would a dog with Pituitary depedent Hyperadrenocorticism show in a Dexamethasone suppression test show?

Answer 34

PDH would should a reduction in cortisol levels, though not as low as a normal animal. It would also increase much quicker.