Adrenal Cortex: Glucocorticoid

Question 1

plasma profile of glucocorticoids

Answer 1

increased blood glucose, increased FFA, increased AA

Question 2

what releases glucocorticoids

Answer 2

zona fasiculata

Question 3

what hormones are released by the zona fasiculata

Answer 3

progesterone and cortisol

Question 4

what makes progesterone into 17 hydroxyprogesterone

Answer 4

17a hydroxylase

Question 5

what makes 17 hydroxyprogesterone into 11 deoxycortisol

Answer 5

21 beta hydroxylase

Question 6

what makes deoxycortisol into cortisol

Answer 6

11 beta hydroxylase

Question 7

what are the glucocorticoids

Answer 7

cortisol, cortisone, corticosterone

Question 8

how does cortisol circulate

Answer 8

bound to transcortin and albumin

Question 9

half life of glucocortisol

Answer 9

70min aka long

Question 10

when are glucocorticoids released

Answer 10

in response to stress

Question 11

major function of glucocorticoids

Answer 11

increase plasma glucose via gluconeogenesis

Question 12

where are glucocorticoids metabolized

Answer 12

liver and kidney

Question 13

what does cortisol do

Answer 13

1. decrease bone formation, increase bone resorption
2. decrease CT
3. inhibit inflammatory and immune response
4. maintain CO, increase arteriolar tone, decrease endothelial permeability
5. facilitate maturation of the fetus
6. increase glomerular filtration and free water clearance
7. modulate emotional tone and wakefulness
8. maintain muscle function, decrease muscle mass

Question 14

when is cortisol released

Answer 14

increases with waking, possibly increased sensory input and visual processing

Question 15

what chemical is on cortisol

Answer 15

hydroxy group on C11

Question 16

cortisol to cortisone

Answer 16

11b hydroxysteroid dehydrogenase

Question 17

what chemical is one cortisone

Answer 17

ketone on c11

Question 18

regulation of cortisol

Answer 18

CRH–>AP–>ACTH–>adrenal cortex–>cortisol

negative feedback to AP and hypothalamus

Question 19

how is ACTH released in the blood

Answer 19

CRH binds to Gs–>AC–>cAMP–>PKA–>P proteins–>POMC mRNA–>POMC–>ACTH, beta LPH into the blood

Question 20

how are the steroid enzymes released from adrenal gland

Answer 20

ACTH binds to adrenal gland Gs–>cAMP–>PKA–>p proteins–>mRNA–>steroidigenic enzymesto mito–>pregnenolone–>to SER–>back to mito–>glucocorticoids and androgens in blood

Question 21

what steroidogenic enzymes are made when ACTH binds

Answer 21

17 alpha and 21 beta hydroxylase

Question 22

what increases ACTH secretion

Answer 22

1. decreased cortisol levels
2. sleep wake transition
3. stress, hypoglycemia, surgery, trauma
4. psychiatric disturbances
5. ADH
6. alpha adrenergic agonists
7. beta adrenergic antagonist
8. serotonin

Question 23

what decreases ACTH secretion

Answer 23

1. increased blood cortisol
2. opioids
3. somatostatin

Question 24

what is the diabetogenic effect of glucocorticoids

Answer 24

cortisol increases glucose production from non carb sources and increases glucose utilization

Question 25

action of insulin

Answer 25

decrease glycogenolysis, gluconeogenesis, ketogenesis and lipolysis

Question 26

action of glucagon and epinephrine

Answer 26

increase glycogenolysis, gluconeogenesis, ketogenesis, lipolysis

Question 27

what is the effect of glucocorticoids on AA production in the plasma

Answer 27

unbranched AA (alanine) are taken up into tissues faster than branched (leucine) and used more readily so there are increased numbers in the plasma

Question 28

what is the primary metabolic action of cortisol

Answer 28

gluconeogenesis

Question 29

what other actions does cortisol do

Answer 29

increased lipolysis, increased FFA and AA mobilization, decrease fat synthesis, inhibit glucose storage

Question 30

blood effect of glucocorticoids

Answer 30

increased FFA, increased ketone bodies, increased glucose, increase AA

Question 31

what does cortisol inhibit

Answer 31

cyclooxygenase (decreases prostaglandins, thromboxanes)

Question 32

what is cushings disease

Answer 32

excessive long term cortisol exposure

Question 33

sx of cushings

Answer 33

protein depletion, muscle weakness, fat redistribution into central obesity, increased glucose (may be confused with DM), increased Na retention, osteoporosis, suppressed immune system, insomnia

Question 34

normal response of dexamethasone suppression test

Answer 34

ACTH and cortisol will be depressed by low dose of dexamethasone

Question 35

what does the dexamethasone suppression test test

Answer 35

pathophysiology of anterior pituitary and adrenal

Question 36

ACTH secreting neoplasm of pituitary dexamethasone suppression test

Answer 36

low dose of dexamethasone will have little or no effect on ACTH and cortisol, high dose depress ACTH and cortisol

Question 37

ACTH secreting neoplasm of ectopic foci or cortisol secreting tumor of adrenal cortex dexamethasone suppression test

Answer 37

neither low or high dose will have any affect on ACTH or cortisol

Question 38

sx of adrenocortical insufficiency

Answer 38

weight loss, poor appetite, malaise, n/v, abdominal pain, fever, poor stress response, hypoglycemia, skin hyperpigmentation (addisons disease), low bp, vascular collapse, increased K

Question 39

what is cushings disease

Answer 39

hypercortisol, decreased ACTH if cortisol increased

Question 40

what is addisons disease

Answer 40

hypocortisol

Question 41

what is seen in 21b hydroxylase or 17a hydroxylase deficiency

Answer 41

increased ACTH because of decreased/absent cortisol

Question 42

plasma profile in primary addisons disease?

Answer 42

decreased cortisol, increased ACTH, and decreased plasma glucose

Question 43

plasma profile in cushings disease

Answer 43

ACTH, cortisol and plasma glucose all increased secondary disorder

Question 44

plasma profile in 21 b hydroxylase deficiency

Answer 44

increased ACTH, decreased deoxycorticosterone, decreased aldosterone, decreased cortisol, increased dihydroepiandosterone (shunted toward adrenal androgens), increased urinary 17 ketosteroids

Question 45

plasma profile in 17 a hydroxylase deficiency

Answer 45

excess production of deoxycorticosterone and cortisone, causing high blood pressure. cortisol and adrenal androgens (DHEA) are suppressed. aldosterone indirectly suppressed bc high BP (inactivated RAAS)