endocrine- adrenal glands

Question 1

where are the adrenal glands?

Answer 1

sit adjacent to the kidney

• adrenal medulla= less problems
• adrenal cortex= most endocrine problems

Question 2

adrena medulla secretes?

Answer 2

epinephrine and norepinephrine, which target most cells and activate SNS

Question 3

adrenal cortex secretes? (3)

Answer 3

3 groups of hormones:

1. glucocorticoids (eg cortisol)
2. mineralocorticoids (eg aldosterone)
3. gonadocorticoids (eg androgens)

Question 4

explain glucocorticoids briefly

Answer 4

secreted in response to stress, target most cells to decrease inflammation, alters metabolism of proteins and fats, suppress immune response
-corticosteroids (prednisone, cortisone) treat chronic inflammation

Question 5

explain mineralocorticoids briefly

Answer 5

chief: aldosterone, targets kidneys to increase sodium reabsorption and increase fluid retention which increases BV and increases BP

Question 6

explain gonadocorticoids briefly

Answer 6

androgens are male sex hormones (testosterone)
-very small amount is released from adrenal glands (in men and women), but most is produced in testes, so if excess women will see more effects

Question 7

ACTH=

Answer 7

adrenocorticotropic hormone produced and released by anterior pituitary, stimulates cortex to release cortisol

Question 8

what could potentially cause hypersecretion?

Answer 8

hyperplasia of cells that secrete these hormones—> excess hormones being secreted
tumor (more cells, more secretion)

Question 9

cortisol tumor or hyperplasia=

Answer 9

increased cortisol production—> decreased ACTH due to negative feedback loop

Question 10

pituitary tumor or hyperplasia=

Answer 10

excessive ACTH production, resulting in excessive cortisol production

Question 11

ectopic tumors=

Answer 11

in location in body that is not the gland, but does some function of gland

ex. malignancy in lung produces ACTH like substance which stimulates cortisol production, but negative feedback look is not suppressing this ACTH like substance, so cortisol levels keep rising
- paraneoplastic syndrome

Question 12

what is cushings syndrome?

Answer 12

a common disease with excess cortisol production (glucocorticoid, hypersecretion)

• cortisol catabolizes (breaks down proteins—> leading to weakened muscles)
• proteins have NO stores in body as glucose and lipids do, only exist in structured forms with functions

Question 13

gluconeogenesis in cushings syndrome?

Answer 13

• production of CHO from non-CHO source
• results in increased glucose in blood, altered glucose metabolism
• prolonged hyperglycemia
• insulin resistance
• impaired glucose tolerance, can develop DM

Question 14

cushings- cortisol: hypokalemia and hypertension?

Answer 14

no affect on mineralocorticoid release!!!
excess cortisol results in cortisol taking on some of aldosterones functions?!!?!?
-so now there is na+ and water retention, excess K+ excretion

Question 15

visual manifestations with cushings?

Answer 15

• rounded moon face (excess lipid deposit within body causing fat deposition in face, neck, and abdomen
• buffalo hump: deposits on shoulders

Question 16

what manifestations occur if androgen secretion is elevated in cushings?

Answer 16

• buffalo hump: fat deposits on shoulders
• facial hair and male balding pattern
• females looking masculine

Question 17

diagnosis of cushings syndrome?

Answer 17

• 24 h urine cortisol: urine sample analyzed for cortisol
• late night cortisol (secretion of cortisol is usually low at night, so if its high that is off)
• dexamethasone test: similar function to cortisol so when administered, ACTH levels should decrease due to negative feedback- if not then there is hypersecretion of ACTH
• CT and MRI scan for an adrenal tumor (producing cortisol), or pituitary tumor (producing ACTH) or an ectopic tumor!

Question 18

treatment of cushings syndrome?

Answer 18

• eradicate tumor
• ectopic tumor: enzyme inhibitors to suppress hormone it produces + chemo
• irradicate pituitary (radiation therapy) second line
• adrenalectomy–> 2 adrenal glands, one can be removed but LAST resort

Question 19

what is Conn syndrome?

Answer 19

primary hyperaldosteronism

-RARE—> usually only encountered in the hospital on an endocrine unit

Question 20

etiology of Conns? (3)

Answer 20

• mostly caused by a cortical adenoma (tumor in cortex)
• idiopathic hyperplasia of cortex
• renin secreting tumor in the kidney (renin converts angiotensinogen into angiotensin I, which is converted by ACE into angiotensin II. this produces aldosterone. Over stimulation of RAAS= increased aldosterone production!)

Question 21

manifestations of Conns?

Answer 21

• hypertension… aldosterone causes vasoconstriction, and retention of Na+, increased BV and BP
• hypokalemia due to excretion of K+
• alkalosis, aldosterone normally excretes H+, so if too much is being excreted than there is a loss of H, increased pH

Question 22

treatment of Conns?

Answer 22

excise adenoma if possible
unilateral adrenalectomy for adenoma 
-aldosterone receptor antagonist 
-restrict Na+ intake
antihypertension drugs if it occurs

Question 23

what is Addisons disease?

Answer 23

decreased production of aldosterone (main mineralocorticoid) and cortisol (glucocorticoid) in cortex—> primary cortical deficiency!!

• impacts both mineralocorticoids and glucocorticoids
• slight deficiency of androgens (affects females a lil bit more)

Question 24

adrenal cortex has a functional reserve, meaning?

Answer 24

if there is damage to cortex, it is still able to function, but if function is lost over 90%, cortex is damaged

Question 25

etiology of addisons?

Answer 25

usually classic autoimmunity- antibodies are targeting self antigens in cortex
-could be a non-secretory, non-functional tumor (damages tissue)
side effect of long term steroid use: decreased ACTH released because steroids inhibit it–> decreased ACTH= less aldosterone and cortisol secreted

Question 26

manifestations of addisons?

Answer 26

• hypovolemia (na+ and h20 are excreted because function of aldosterone is to retain it)
• decreased CO—> hypotension, hypoxia, fatigue
• hyperkalemia (not enough K+ excreted)
• poor stress response (general adaptive syndrome… adrenal gland is involved in this)
• poor appetite and weight loss
• atrophic adrenal gland

Question 27

why does hyperpigmentation occur in addisons?

Answer 27

-hyperpigmentation d/t lack of feedback—> aldosterone/cortisol is not secreted, ACTH is not triggered to stop secreting. ACTH is broken down into A.As which can join to form MSH (melanocyte stimulating hormone) which produces melanin, increase in pigment—> darker skin

Question 28

what is the acute complication of addisons?

Answer 28

and addisonian crisis!!!
-deficiency of cortisol resulting from untreated addisons + added physical or mental stress, adrenal cortex cannot cope!!! loss of functional reserve

Question 29

treatment of acute addisons?

Answer 29

-bring cortisol to normal levels, IV fluids stat and IV glucocorticoids

Question 30

treatment of chronic addisons?

Answer 30

hormone replacement d/t deficiency of hormones