Sfos - Lect. 71

Front 1

These organs primarily help to protect against immediate stress, and respond to prolonged changes in food/water deprivation, and death ensues shortly after their absence?

Back 1

Adrenal Glands

Front 2

This part of the adrenal gland synthesizes steroid hormones and is essential to life (cortex/medulla)?

Back 2

Cortex

Front 3

What tissue are the adrenal glands derived from?

Back 3

mesenchyme near the urogenital ridge

Front 4

What are the two fetal layers that are first developed during embryological development of the adrenals?

Back 4

Thick inner (fetal cortex…later degenerates); Thin Outer Cortex >> becomes permanent cortex

Front 5

What are the three concentric layers of the permanent cortex of the adrenal glands?

Back 5

zona glomerulosa; zona fasciculata; zona reticularis

Front 6

What do the steroid-secreting cells of the adrenal cortex take up and store as droplets?

Back 6

cholesterol

Front 7

Cells of the adrenal cortex have a lot of these two organelles?

Back 7

sER and Mitochondria

Front 8

Cells in this zone secrete mineralocorticoids (aldosterone)?

Back 8

zona glomerulosa

Front 9

What primarily controls the rate of aldosterone production?

Back 9

renin-angiotensin system

Front 10

Cells of this zone produce a hormone with widespread effects such as influencing carbohydrate metabolism and depressing the inflammatory response and immune functions?

Back 10

Zona Fasciculata (Glucocorticoids, cortisol), also secreted in Zona reticularis

Front 11

The anterior pituitary produces this hormone, which primarily influnuences the release of glucocorticoids from the Zona Fasciculata, and Zona Reticularis?

Back 11

ACTH (releaseing cortisol); (note: ACTH does also stimulate DHEAS and Aldosterone minimally)

Front 12

The renin-angiotensin system influences the releas of a hormone from which zone in the adrenal cortex?

Back 12

Zona Glomerulosa

Front 13

This zone produces dehydroepiandrosterones (DHEAS), weak androgens that may have effects on inflammatory and immune responses different from those of glucocorticoids?

Back 13

Zona reticularis

Front 14

What is the function of the fetal cortex?

Back 14

produces DHEAS which are converted to androgens and estrogens by the placenta

Front 15

What is the rate limiting step in steroidogenesis?

Back 15

The conversion of cholesterol to pregnenolone

Front 16

ACTH acts on the cells of the fasciculata to accelerate the activity of THIS rate limiting enzyme in cortisol biosynthesis?

Back 16

20,22 - Desmolase

Front 17

What are the three functions of ACTH on the adrenals?

Back 17

increase cortisol; increased activity of biosynthetic pathway leading to DHEAS; stimulatory influence on aldosterone release

Front 18

ACTH increases the release of what 2nd messenger in cortical cells?

Back 18

cAMP

Front 19

Chronic ACTH stimulation is seen in what disease state?

Back 19

Cushing's

Front 20

This hormone promotes the release of ACTH, B-endorphin and B-lipotropin from corticotrophs in the anterior pituitary?

Back 20

CRH (corticotropin releasing factor)

Front 21

What fucntion do epinephrine and ADH play on the corticotroph with relation to CRH?

Back 21

They increase the sensitivity of the corticotroph to CRH

Front 22

CRH given to a patient with either of THESE two hormones/factors is more effective then CRH given alone?

Back 22

epinephrine and ADH

Front 23

B-Endorphins have this property, which is useful for stress adaptation?

Back 23

Analgesic property

Front 24

What are the 4 major secretory control mechanisms for ACTH release?

Back 24

cortisol negative feedback; episodic release (7-15 perday); diurnal rhythm; Stress

Front 25

How does cortisol perform it's negative feedback function?

Back 25

At both the pituitary and hypothalamus (effects CRH release and stimulatory strength)

Front 26

What two properties of hormone effect the physiological response of cells to that hormone?

Back 26

the amount of hormone AND the time that hormone is present

Front 27

All endocrine actions display this mode of transmission?

Back 27

Pulsatility

Front 28

What is the benefit of pulsatile release of hormones as opposed to constant stimulation of hormones?

Back 28

Constant stimulation leads to cells down-regulating their receptors for that hormone; Pulsatility does not

Front 29

What is the diurnal rhythm of ACTH and Cortisol release due to?

Back 29

the diurnal variation in the sensitivity of the hypothalamic set point for cortisol (sleep-wake cycle)

Front 30

At what time of the day is ACTH and Cortisol typically the highest?

Back 30

During the early morning

Front 31

True/False Alterations of the ACTH-Cortisol ryhythm is of diagnostic value in the evaluation of mental disorders such as depression

Front 32

What happens to the negative feedback capability of cortisol on ACTH release under circumstances of severe stress (surgery)?

Back 32

ACTH is released with almost no inhibition by cortisol (though to be mediated by higher centers)

Front 33

What is cortisol bound to in the blood?

Back 33

transcortin or cortisol binding protein (CBP) (80%) and albumin (20%)

Front 34

Where does metabolism of cortisol take place?

Back 34

In the liver

Front 35

True/False Most of the actions of cortisol are directly responsible for the vast processes that are essential to life?

Back 35

False; most of the effects are permissive, required for full expression but not directly needed for initiation of the process

Front 36

While cortisol exhibits both catabolic and anabolic actions, the predominance of it's effects are?

Back 36

Catabolic

Front 37

What are the primary effects of cortisol on carbohydrate metabolism?

Back 37

increases the supply ofr glucose through gluconeogenesis AND decreased utilization

Front 38

How does cortisol decrease the utilization of glucose?

Back 38

reduces the sensitivity of cells to insulin

Front 39

What are the effects of cortisol on protein metabolism?

Back 39

increased protein breakdown and decreased protein synthesis in all tissues except the liver

Front 40

Release of cortisol will do what to amino acid levels in the blood?

Back 40

Increased (protein breakdown)

Front 41

What effects does cortisol have on fatty acid metabolism?

Back 41

increases the mobilization of fatty acids and glycerol from adipose tissue

Front 42

Describe the redistribution of body fat stores which occurs as a result of cortisol?

Back 42

thinning of the extremities and fattening of the trunk and face (centripetal obesity with moon face)

Front 43

In the absence of cortisol what happens to the blood pressure?

Back 43

vasodialtion and drop in blood pressure with no external loss of volume

Front 44

What happens to the GFR in the absence of cortisol?

Back 44

falls (water cannot be excreted as rapidly)

Front 45

What does cortisol do to multiple inflammatory and immune responses?

Back 45

blocks each one

Front 46

How does cortisol decrease immune and inflammatory responses?

Back 46

stabilizes lysosomal membranes; decreases capillary permeability; depresses white cell proliferation and phagocytosis

Front 47

In cushing's disease, the set point for cortisol levels is (higher or lower) than normal?

Back 47

Higher

Front 48

What is the underlying basis of Cushing's disease?

Back 48

pituitary tumor secreting ACTH , yet STILL remains responsive to feedback action of ACTH (set point is now HIGHER)

Front 49

What observation is the definitive diagnostic criteria for Cushing's Disease?

Back 49

Dose required to turn off ACTH is higher than normal but suppresion CAN be achieved

Front 50

What is Primary Hypercortisolism?

Back 50

Cushings Syndrome due to adrenal tumor

Front 51

What occurs to the secretion of CRH and ACTH in primary hypercortisolism?

Back 51

Maximum suppression of ACTH and CRH do to constant cortisol secretion

Front 52

What happens to the normal adrenal tissue next to the adrenal tumor?

Back 52

atrophy (does not get ACTH stimulation)

Front 53

What occurs to the adrenal cortex in patients with ectopic ACTH Cushings syndrome?

Back 53

Hyperplasia (large stimulus by ACTH with no negative feedback)

Front 54

Depression, anorexia and alcoholism can cause Cushings Syndrome HOW?

Back 54

By CRH excess

Front 55

What is normally seen in high-dose glucocorticoid therapy used to treat asthma and athritis?

Back 55

Iatrogenic Cushings syndrome (suppression of the hypothalamus/pituitary)

Front 56

Your patient is suspected with cushings syndrome and has a normal response to a low-dose dexamethasone suppression test, what are you to conclude?

Back 56

Not cushings syndrome

Front 57

A patient suspected of having Cushings has detected plasma ACTH under a low-dose Dexamethasone Suppression Test, what do you Do NEXT?

Back 57

Give High dose test

Front 58

A patient suspected of having Cushings has detected plasma ACTH under a low-dose Dexamethasone Suppression Test, under the high-dose test ACTH is undetectable in the plasma, what is the diagnosis?

Back 58

Adrenal tumor

Front 59

A patient suspected of having Cushings has detected plasma ACTH under a low-dose Dexamethasone Suppression Test, under the high-dose test ACTH is elevated?

Back 59

Ectopic ACTH syndrome

Front 60

A patient suspected of having Cushings has detected plasma ACTH under a low-dose Dexamethasone Suppression Test, under the high-dose test ACTH is normal to elevated, what is the diagnosis?

Back 60

Cushing's DISEASE

Front 61

Hypocortisolism due to adrenal destruction is seen in what disease?

Back 61

Addison's disease

Front 62

What is secondary hypocortisolism due to?

Back 62

failure of the pituitary to produce ACTH

Front 63

What is tertiary hypocortisolism due to?

Back 63

failure of the hypothalamus to produce CRH