Endo(Ost529)-Adrenocorticosteroids-Dr.lookingland(Scribe13)

Front 1

A dysfuntion affecting the gland out in the peripheral that is going to secrete hormone is what type of dysfunction?

Back 1

Primary dysfunction

Front 2

A dysfunction at the pituitary or hypothalamic level is what type of dysfunction?

Back 2

Secondary dysfunction

Front 3

The adrenocortical axis refers to control by what?

Back 3

Brain

Front 4

Mineralocorticoids and aldosterone are controlled by what?

Back 4

Peripheral substrate system

Front 5

In a primary endocrine disorder of the adrenal cortex, what will be lost?

Back 5

GCC and MCC

Front 6

In a secondary endocrine disorder, what will be lost?

Back 6

Only one pathway

Front 7

What is the RLS in the synthesis of GCC and MCC?

Back 7

Uptake and conversion of cholesterol to pregnenolone

Front 8

Where does the uptake and conversion of cholesterol to pregnenolone occur?

Back 8

Zona Fasiculata and Zona Reticularis

Front 9

In the zona reticulata and zona reticularis, what enzyme is used to convert pregnenolone to 17 hydroxy pregnenolone?

Back 9

17-alpha hydroxylase

Front 10

Are steroids stored?

Back 10

NO, there is direct synthesis and release from adrenal cortex--> "ON DEMAND PRODUCTION"

Front 11

What is the major GCC synthesized in humans?

Back 11

Cortisol

Front 12

Once cortisol is out in the plasma, what is cortisol bound to?

Back 12

CBG made by the liver

Front 13

What percentage of cortisol is bound to CBG? What percentage of cortisol is in the free, bioactive form?

Back 13

95% bound
5% free

Front 14

What is the half-life of cortisol?

Back 14

90-110 minutes

Front 15

What type of reaction is the following reacton?
cortisol(free) + CBG <-->cortisol + CBG (bound)

Back 15

Equilibrium reaction-->maintains a fixed level of free cortisol

Front 16

What are the 3 important sites in cortisol?

Back 16

1.17 site
2.20 site
3.A ring

Front 17

Cleavage at what 3 sites render's cortisol inactive?

Back 17

17 site, 20 site, A ring

Front 18

Cleavage at any of the 3 imp. sites on cortisol results in what inactive metabolites?

Back 18

17-ketogenic steroids and 17-ketosteroids

Front 19

What happens to the inactive metabolites of cortisol?

Back 19

They are lost in the urine

Front 20

How can the amount of cortisol being released into the plasma be measured?

Back 20

Measure urine

Front 21

Cleavage of cholesterol at 3 important sites is what type of reaction?

Back 21

Phase I reaction

Front 22

After the phase I reaction of cortisol which produces inactive meatbolites, what can happen next?

Back 22

Phase II conjugation reaction to make the metabolites of cortisol even more water-soluble

Front 23

In the HPA axis, what hormone cannot be measured in the periphery?

Back 23

CRH

Front 24

In the HPA axis, what hormone can be measured in the blood?

Back 24

ACTH

Front 25

What things coming in higher in the brain can override the negative feedback system of the HPA axis?

Back 25

1.psychogenic, emotional, traumatic
2.cytokines-->inflammation
3.diurnal rhythm

Front 26

During sleep what is the overall major physiologic function of the GCC system?

Back 26

To provide glucose to the brain. (during sleep one is fasting)

Front 27

Is the uptake of glucose into the brain insulin dependent or independent?

Back 27

Insulin INdependent

Front 28

During what stage of sleep is the HPA axis activated?

Back 28

Late stage of sleep

Front 29

What are the 3 main physiological actions of GCCs?

Back 29

1.Metabolic (glucose availability for brain)
2.Anti-inflammatory
3.Immunosuppression

Front 30

Where are GCC catabolic? Where are GCC anabolic?

Back 30

1.Catabolic: Periphery
2.Anabolic: Liver

Front 31

Why is the hypersecretion of GCC devastating?

Back 31

B/c it does cause breakdown of tissue in the periphery.

Front 32

How does cortisol exert its anti-inflammatory actions?

Back 32

By long-term actions at the genome (through GCC receptor)

Front 33

What does the HPA-GCC axis do to the immune system?

Back 33

Inhibits immune system

Front 34

Do cells in the zona glomerulosa have 17-alpha hydroxylase?

Back 34

NO

Front 35

What do cells in the zona glomerulosa have?

Back 35

Dehydrogenase enzyme

Front 36

In the mineralocorticoid pathway, what is the precursor that gets shunted through the microsomal enzyme pathways? What is the precursor in the GCC pahtway?

Back 36

1.Mineralocorticoid: Pregnenolone
2.GCC: 17-hydroxy pregnenolone

Front 37

In the mineralocorticoid pathway, are synthesis and release coupled?

Back 37

YES

Front 38

How does the transport of aldosterone differ from the transport of cortisol?

Back 38

Aldosterone is only weakly bound to a plasma protein.

Front 39

What percentage of aldosterone is bound? What percentage is active?

Back 39

5% of aldosterone is bound
95% of aldosterone is free

Front 40

What is the half life of aldosterone compared to the half-life of cortisol?

Back 40

Aldosterone: 20-30 min
Cortisol: 90-110 min

Front 41

Where are both cortisol and aldosterone degraded and secreted?

Back 41

Degraded in liver
Secreted in urine

Front 42

What are the 3 functions of angiotensin II?

Back 42

1.Direct vasoconstriction
2.Increases total peripheral resistance
3.Increase BP

Front 43

What protein acts directly to simulate aldosterone secretion also?

Back 43

Angiotensin II

Front 44

What are the 2 main effects of aldosterone on the kidney?

Back 44

1.Genomic effect
2.Membrane effect

Front 45

What disease state involves adrenocortical insufficiency?

Back 45

Addison's Disease

Front 46

What are the 2 types of insufficiencies with Addison's Disease?

Back 46

1.Primary Insufficiency
2.Secondary Insufficiency

Front 47

In Addison's disease, what are 2 things that MCC insufficiency results in?

Back 47

1.Sodium loss-->dehydration
2.K retention

Front 48

In primary Addison's disease, excess ACTH production causes what?

Back 48

Hyperpigmentation of the skin.

Front 49

What is the difference between primary Addison's Disease and secondary Addison's Disease?

Back 49

1.Primary-->Hypersecretion of ACTH
2.Secondary-->Hyposecretion of ACTH

Front 50

In congential adrenal hyperplasia, what enzyme is deficient?

Back 50

21-beta-hydroxylase

Front 51

What are the 2 effects of congenital adrenal hyperplasia?

Back 51

1.Adrenal hyperplasia
2.Virilization

Front 52

The following are all symptoms of what disease?
-weakness, fatigue, wt. loss, inability to maintain blood glucose levels during fasting
-hyponatremia, hyperkalemia, dehydration
-hyperpigmentation of skin

Back 52

primary and secondary adrenocortical insufficiency

Front 53

The following are all symptoms of what disease?
-Adrenocortical hypertrophy
-Virilization

Back 53

Congential Adrenal Hyperplasia

Front 54

The following are all symptoms of what disease?
-Muscle atrophy, thinning of skin, redsitribution of fat to face and trunk, poor wound healing

Back 54

Cushing's Syndrome

Front 55

The following are all symptoms of what disease?
-HTN, polyuria, polydipsia, muscle weakness and tetany

Back 55

Primary Aldosteronism or Conn's Syndrome

Front 56

Anti-inflammatory activity is high for what drugs?

Back 56

GCCs

Front 57

Salt retaining activity is high for what drugs?

Back 57

MCCs