Immunology Block: Mod # 10 - Jitt - Adrenal Cortex/glucocorticoids.

Front 1

glucocorticoids - as a therapy, what can they do generally? what about mineralcorticoid?

Back 1

glucocorticoid analogues are great anti-inflammatory drugs.

blocking mineralcorticoid receptors might be good for stopping hypertension.

remember that the mineralcorticoids are sent out from the outer cortex, and glucocorticoids from the inner cortex.

Front 2

name a couple glucocorticoid analogues

Back 2

hydrocortisone is cortisol.

prendosone is a glucocorticoid analog.

Front 3

what are the main classes of things created in the adrenal cortex?

Back 3

androgens, glucocorticoids, and mineralcorticoids (going inner to outer).

Front 4

what controls excretion from the zona glomerulosa? what about the fasiculata and reticulata?

Back 4

remember it goes GFR - so the G controls mineralcorticoids.

regulated by angiotensin II and potassium.


the rest of the cortex is controlled by ACTH.

Front 5

what's our main glucocorticoid? what's it made from?

how does it circulate?

Back 5

cortisol. comes from cholesterol to pregnanalone.

it circulates mostly (90%) bound to protein - cortisol binding globulin (CBG) and albumen.

Front 6

what enzyme breaks down cortisol?

Back 6

two isozymes.

11-beta-hydroxysteroid dehydrogenase, type1 and type2.

type 1 is in the kidneys and turns cortisol into cortisone (inactive).

type 2 in the liver turns cortisone back into active cortisol.

remember, it's 11-beta-hydroxy-steroid-dehydrogenase.

Front 7

how does cortisol act?

Back 7

there are glucocorticoid receptors I and II. I perceives mineralcorticoids.

it's a steroid, so it ends up in the nucleus, where it works on glucocortoticoid-response-elements (GRE's) where it can up the transcription of at least 10% of human genes.

note that its effects can be either metabolic or anti-inflammatory.

Front 8

what are its metabolic effects? what turns it on?

Back 8

generally it wants to increase the availability of nutrients...so it raises the blood concentration of glucose, triclycerides, and amino acids. it antagonizes insulin, catabolizes proteins, and works on growth-hormone dependent adipose cells to release fat.


upped during stress, trauma, pain, surgery, severe infection.

also, turned on by PRO-infalmatory cytokines (IL2, IL6, Il1, TNF alpha) - this is a feedback inhibition loop.

Front 9

what's cortisone insufficency and cortisone extra?

Back 9

too little = addison's disease.

too much = cushing's.

Front 10

what happens to cortisol secretion if you give exogenous glucocorticoids all the time?

Back 10

it can go down and cause secondary insufficency, which is kinda like addison's disease.

in the example of the kid who was switched from a high dose oral to a low-dose inhaled glucocorticoid, all that time on the high-dose had given him secondary insufficency (inability to make cortisol) - so, when he got an infection, he couldn't mobilize his resources to fight it. he needed to be given hydrocortisone.

Front 11

what are the 2 general reasons for giving glucocorticoids?

Back 11

for replacement in cases of insufficiency, and to decrease inflammation and the immune response in general (organ transplantation).

Front 12

in immunology, what classes of things do glucocorticoids block?

Back 12

blocks both prostiglandin formation/leukotriene formation (from stopping phospolipase A2) and it lowers IL1, IL2, IL6, TNFalpha.