Endocrine Glands- Adrenal Gland

Question 1

What are the hormones secreted by the four layers of the adrenal gland?

Answer 1

Cortex:
- Zona Glomerulosa: Mineralcorticoids (aldosterone)
- Zona fasiculata: Glucocorticoids ( cortisol)
- Zona reticularis: (androgens)
Medulla: Catecholamines (epinephrine and norepinephrine)

Question 2

What is the feature of the cells that secrete steroid hormone?

Answer 2

• Can synthesize steroids from cholesterols. Also can store in lipid droplets.

Question 3

What are the primary functions of aldosterone in the renal tubule?

Answer 3

Fxn is to promote retention of Na+, secrete K + and H+ on the distal convoluted tubules. Na+ will increase blood pressure

Question 4

What molecules stimulate the secretion of aldosterone?

Answer 4

increased Blood K+ and Angiotensin II

* Decrease in blood pressure.

* Decrease in tissue fluid Na+ concentration.

Question 5

How is renin produced?

Answer 5

• Decrease NaCl activates p38 or ERK1/2 (transcription factors) which then stimulates COX-2 -> COX-2 can stimulate PGE2 ( produced by distal tubule cells) which will bind receptor EP4 on the Juxtaglomerular cells (JGC) which alerts JGC that Na+ levels are low. JGC will produce renin.

Question 6

What are the primary functions of glucocorticoids?

Answer 6

Fxn’s to control metabolism (increases all of the following):

• Gluconeogenesis
• Use of glucose
• Protein catabolism
• Amino acids
• GFR
• Water secretion
• Lipolysis
• Blood Pressure
• Osteoclast activity
• Risk of infection/ suppression of immune status

Question 7

How does ACTH stimulate the synthesis and secretion of cortisol?

Answer 7

• Stimulates LDL uptake
• Stimulate the hydrolysis of cholesterol esters to regenerate free cholesterol
• Enhance cholesterol transport into mitochondria.
• cAMP in cell will help cholesterol in mitochondria convert into pregneolone which will eventually be converted into cortisol and immediately released.

Question 8

What are the three mechanisms that regulate glucocorticoid synthesis?

Answer 8

1. ) Feedback mechanisms ( see below)
2. ) Circadian rhythm
3. ) Stress

Positive feedback:
- ACTH stimulates adrenal cortex to secrete cortisol.
- CRH stimulates anterior pituitary to secrete ACTH
Negative feedback:
- increase in cortisol causes hypothalamus to decrease CRH secretion, and decrease in ACTH secretion

Question 9

How does low-dose dexamethasone suppression work in diagnosing hyperadrenocorticism (Cushing’s
syndrome)?

Answer 9

• LDDS Test:
◦ Normal animal: Low dose dex will decrease endogenous ACTH secretion and this will decrease circulating cortisol concentrations.
◦ Abnormal: They cannot decrease ACTH secretion
◦ 92-95% sensitivity at 8 hours, 5-8% of diseased dogs show suppression ( false negative)

Question 10

How does the ACTH stimulation test work in diagnosing hyperadrenocorticism (Cushing’s syndrome)?

Answer 10

Animals with the condition will show an exaggerated response to exogenous ACTH.

Question 11

What are the characteristic clinical signs of hyperaldosteronism (Conn’s Syndrome)?

Answer 11

Muscle weakness, cervical ventroflexion (head drop), hypertension, blindness, renal failure.

Question 12

What are typical lab test results you may expect for hyperaldosteronism (Conn’s Syndrome)?

Answer 12

◦ Hypokalemia, decreased plasma K+ concentrations
◦ Hypernatremia, elevated plasma Na+ concentrations
◦ Metabolic alk (decreased H+ ( aldosterone increased secretion of hydrogen)
◦ Elevated CK

Question 13

What are the precursor and cells for the synthesis of catecholamines?

Answer 13

Precursor: Tyrosine
2 kinds of chromaffin cells: one contains more epinephrine granules, one contains more norepinephrine cells.

Question 14

How is the synthesis of catecholamines negatively regulated?

Answer 14

All of these mechanisms are feed back inhibition for TH. So TH is rate limiting enzyme.

Question 15

How do different catecholamine receptors, when bound to epinephrine, initiate signal transduction inside a
cell?

Answer 15

• Alpha 1: activates PLC with PIP2-> PLC will activate 2 second messengers, IP3 and DG (DAG?) -> IP3-this promotes the calcium influx into the cell. DG - activates PK-C which will use calcium for protein synthesis and will activate transcription factors. This will create new proteins.
• Alpha 2 and Beta activates AC which uses ATP to make cAMP. This cAMP will activate protein kinase which will cause protein phosphorylation and activate transcription factors.

* Alpha 2: Inhibits adenyl cyclase, reducing cAMP (second messenger).

* Beta: Activates adenyl cyclase, increasing cAMP (second messenger).

Question 16

What are the primary functions of catecholamines?

Answer 16

◦ Glycogenolysis (increases): Breaks down glycogen into glucose, which will cause hyperglycemia.
◦ Gluconeogenesis: Needs a lot of glucose, so it will cause AA, LA, FA, glycerol into glucose to make more glucose.
◦ Lipolysis: Triglycerides will be made into glycerol and fatty acids which will be used to make more glucose
◦ Vasodilation in skeletal muscles will use FA to increase ATP production.
◦ HR will increase, contractility will increase and there will be vasodilation of coronary arteries.
◦ Vasoconstriction in gut, kidneys, and skin (non critical organs.
◦ you will have dilation of bronchial and increased re