Adrenal Gland

Front 1

Describe the 3 layers of the cortex

Back 1

1) Zona glomerulosa: aldosterone
2) zona fasiculata: cortisol + androgens
3) zona reticularis: cortisol + androgens

Front 2

Describe the medulla of the adrenal gland

Back 2

No zones; release epinephrine + norepinephrine

Front 3

Developmental
adrenal gland. 1) What's the size of the fetus? 2) What produces DHEA? 3) What disappears?

Back 3

1) In the fetus, the adrenal gland is proportionally
much larger, up to 1/3 the size of the kidney.
2) Most of the cortex is then a “fetal” zone producing
predominantly the androgen DHEA.
3) After birth the fetal zone disappears, leaving the “definitive” cortex, although the inner, reticularis
layer is not recognizable until about 3 years of age.

Front 4

Describe blood supply

Back 4

Part of the arterial blood supply to the adrenal forms a plexus
in the connective tissue capsule and perfuses the gland through
a radial system of sinusoids draining to the medulla.

This means that blood reaching the medulla from this route
is enriched in the cortical hormones.

Front 5

Describe the creation of corticosterone and aldosterone

Back 5

Cholesterol -> Pregnenolone -> Progesterone -> Corticosterone -> Aldosterone

Front 6

Describe creation of cortisol

Back 6

Cholesterol -> pregnenolone -> 17-hydroxyprogesterone -> cortisol

Front 7

How do you import cholesterol from the outer to the inner mitochondrial membrane?

Back 7

Use StAR protein- steroidogenic acute regulatory protein; LDL carries cholesterol esters via lipid droplet and can be broken down into cholesterol. Once its carried into the mito via StAR, its converted to Pregnenolone.

Front 8

How is pregenolone made into cortisol and where in the cell does this take place?

Back 8

Pregnenolone must be made into 17-OH preg (carried out of mito this way). Travels to SER where it becomes 11-deoxycortisol. Then it travels back into the mito where its converted to cortisol. Now it can leave the mito into the circulation

Front 9

Describe the following steroids: Pregnanes (C21); Androstanes (C19); Estranes (C18)

Back 9

Pregnanes: aldo and cortisol
Androstanes: androgens (DHEA and androstenedione)
Estranes: estrogens, estrone, estradiol, estriol

Front 10

What class of hormones is cortisol from?

Back 10

Glucocorticoids; highest secretion rate and highest plasma concentration (2nd to DHEA-S)

Front 11

What class is aldosterone from?

Back 11

Mineralocorticoid; low secretion and plasma concenration

Front 12

What class is DHEA, DHEA-S, and androstenedione from?

Back 12

Androgen; DHEA has moderate secretion rate, low plasma concentration. DHEA-S has very high plasma concentration, Androstenedion has low secretion rate and low plasma concentration

Front 13

Of cortisol, aldosterone, and androgens, which is mostly bound to proteins?

Back 13

Cortisol and androgens

Front 14

Of cortisol, aldosterone, and androgens, which has the longest half life?

Back 14

cortisol by far

Front 15

Describe the mode of action of steroid hormone

Back 15

1) Interstitium: steroid hormone can travel directly through membrane into cytosol
2) Cytosol: steroid hormone binds to receptorprotein comple, heat shock protein dissociates; activated receptor goes to nucleus
3) Once in nucleus, gets translated to mRNA and creates affected sequence

Front 16

Describe how cortisol is ultimately secreted beginning from hypothalamus

Back 16

Stress + Nonstress neural inputs > (hypothalamus) increase CRH secretion > Increase plasma CRH > (Anterior pituitary) increase ACTH secretion > increase plasma ACTH > (adrenal cortex) increase cortisol secretion > increase plasma cortisol > (target cells of cortisol) respond to increased cortisol

Front 17

Describe when plasma ACTH increases and plasma cortisol increases?

Back 17

Huge spike overnight of both

Front 18

What does definciency of 21-hydroxylase enzyme lead to?

Back 18

Pregnenolone increases, which leads to increase of adrenal androgens (women may get male characteristics)

Front 19

What does administration of synthetic glucocorticoids lead to?

Back 19

Leads to decreased ACTH. The ACTH layers atrophy, therefore body cannot synthesize its own ACTH

Front 20

What are the effects of increasing cortisol on the liver, muscle, and adipose?

Back 20

If cortisol increases, you get less uptake of gluc + aa by muscle. Muscle will increase protein breakdown and decrease protein synthesis, leading to increase plasma aa's. If you have decrease glucose entry to adipose, adipose will increase TG breakdown and increase plasma FFAs. Increase in plasma aa's and plasma glycerol will both stimulate gluconeogenesis in liver, leading to increased plasma glucose

Front 21

What are the effect of glucocorticoids on the CNS?

Back 21

taste, hearing + smell increase in acuity with adrenal cortical insufficinecy; and decreases in Cushing's disease. Reduce corticotropin releasing hormone, and ADH secretion

Front 22

What effect do glucocorticoids have on cardiovascular system?

Back 22

increase sensitivity to vasoconstrictor agents, maintain microcirculation.

Front 23

What effect do glucocorticoids have on GI tract?

Back 23

increase gastric acid secretion, decrease gastric mucosal cell proliferation

Front 24

What effect do glucocorticoids have on liver?

Back 24

Increase gluconeogensis

Front 25

What effect do glucocorticoids have on lungs?

Back 25

INcrease matruation and surfactat during fetal stage

Front 26

What effect do glucocorticoids have on pituitary gland?

Back 26

decrease ACTH secretion (acute) + synthesis (chronic)

Front 27

What effect do glucocorticoids have on kidney?

Back 27

Increase GFR (needed to excrete dilute urine)

Front 28

What effect do glucocorticoids have on bone?

Back 28

Increase resorption, decrease formation

Front 29

What effect do glucocorticoids have on muscle?

Back 29

Decrease fatigue, increase protein catabolism, decrease glucose oxidation, decrease insulin sensitivity, decrease protein synthesis

Front 30

What effect do glucocorticoids have on the immune system?

Back 30

Decrease mass of thymus and lymp nodes; decrease blood concentrations of eosinophils, basophis, and lymphocytes; cellular immunity decreases

Front 31

What effect do glucocorticoids have on connective tissue?

Back 31

decrease fibroblast activity, decrease collagen synthesis

Front 32

What is Cushing's disease?

Back 32

Tumor in pituitary gland that increases ACTH, increases cortisol; increase in weight (increase central fat, decrease peripheral fat) (moon face); 2ndary hypersecretion of cortisol (pituitary adenoma)

Front 33

What is Cushing's syndrome?

Back 33

High levels of glucocorticoids not specific to any source

Front 34

What's Addison's disease?

Back 34

Too little cortisol; primary hyposecretion of all adrenocorticoids

Front 35

Describe how adrenal androgens contribute to testosterone, estrogen, in adult male and adult females.

Back 35

In adult males adrenal androgens appear to
contribute less than 5% of total testosterone

In adult females up to 50% of T may derive
from adrenal androgens.

In post menopausal women 100% of E derives
from adrenal androgens.

Front 36

How does aldosterone increase in circulation?

Back 36

1) Liver secretes angiotensinogen and enters blood stream
2) Kidneys then secrete renin which helps convert angiotensinogen to angiotensin I
3) converting enzyme makes angiotensin I to angiotensin II
4) Angiotensin II induces adrenal cortex to secrete aldosterone, then this goes into the blood stream

Front 37

How does increased plasma aldosterone effect cortical collecting ducts?

Back 37

1) increases sodium reabsorption and potassium secretion such that less sodium is excreted and more potassium is excreted

Front 38

What is 11BHSD enzyme and what do they do?

Back 38

11β-Hydroxysteroid dehydrogenase (HSD11B) is the name of a family of enzymes that catalyze the conversion of inert 11 keto-products (cortisone) to active cortisol, or vice versa,[1] thus regulating the access of glucocorticoids to the steroid receptors. The mineralcorticoid receptor is stimulated by both aldosterone and cortisol, but there is a mechanism that protects the body from excess aldosterone receptor stimulation by glucocorticoids, which happen to be present at much higher concentrations than mineralcorticoids in the healthy individual. The mechanism consists of an enzyme called 11 β-hydroxysteroid dehydrogenase (11 β-HSD). This enzyme co-localizes with intracellular adrenal steroid receptors and converts cortisol (an active mineralcorticoid) into cortisone, a relatively inactive metabolite with little affinity for the mineralocorticoid receptors.

Front 39

What is primary hypersecretion of aldosterone known as?

Back 39

Conn's disease

Front 40

What can congential adrenal hyperplasia cause?

Back 40

usually due to 21-hydroxylase deficiency; depending on severity leads to lack of mineralocorticoid activity and androgen excess

Front 41

How are catecholamines transported in blood? What is their half life?

Back 41

Catecholamines are transported in the blood mostly
in loose association with plasma albumin that acts
as a low affinity, high capacity transporter.

Catecholamines have very short half-lives in the circulation – of the order of 10-15 seconds

Front 42

what is the most notable adrenal medulla disease state?

Back 42

primary hypersecretion