Physio Ii Test 4 (5): Endocrine - Adrenal Hormones

Front 1

The Regulation of Glucocorticoid Secretion is regulated through at least three levels of signaling.

Back 1

1) CNS - Hypothalamus: Corticotropin releasing hormone (CRH) --> corticotrophs of Anterior pituitary.

2) Anterior pituitary:
Adrenocorticotropic hormone (ACTH) -->zona fasciculata of andrenal gland-->cortisol sectetion

3) Coritsol feed back inhibition to both the hypothalamus and ant. pituitary

Front 2

What class of hormones are made in the andrenal cortex?

Back 2

steroid hormones

Front 3

the primary glucocorticoid is?

Back 3

Cortisol

Front 4

Corticotropin releasing hormone (CRH) function

Back 4

secreted by the CNS-Hypothalamus

Regulates ACTH sectertion by the corticotrophs of the anterior pituitary

Front 5

Adrenocorticotropic hormone (ACTH)

Back 5

secreted by the corticotrophs of the anterior pituitary

secretion regulated by CRH

stimulates secretion/production of cortisol/Glucocorticoid by Adrenal gland

Front 6

What type of hormone is Corticotropin releasing hormone (CRH)?

what endocrine organ is it released from?

Back 6

peptide hormone released by the hypothalamus

Front 7

What factors stimulate release of Corticotropin releasing hormone (CRH)?

Back 7

Release stimulated by genetically programmed signals, stress, hypoglycemia, and cytokines produced during acute inflammation

Front 8

What hormones are involved in Feedback inhibition of the hypothalamus and CRH secretion?

Back 8

Feedback inhibition - ACTH & cortisol

Front 9

What is clinicaly relevant about Adrenocorticotropic hormone (ACTH)?

Back 9

ACTH Contain MSH activity [clinically relevant]

Front 10

What hormones and organs stimulate the release of Adrenocorticotropic hormone (ACTH)?

Back 10

Release stimulated by

CRH (Hypothalamus)

ADH (Anterior Pituitary gland)

Front 11

What hormone and organ is involved in the Feedback inhibition of ACTH?

Back 11

ACTH Feedback inhibition - Cortisol

Front 12

What may occur do to adrenal cortex failure? Why would the skin darken?

Back 12

high levels of ACTH are produced (with MSH that may cause darkening of the skin)

Front 13

what is the function and origin of MSH?

Back 13

α-Melanocyte-stimulating hormone (α-MSH) which is used by the hypothalamus as a neurotransmitter to regulate appetite. α-MSH can increase skin pigment production by melanocytes

Front 14

Steroid hormones act by altering ____ via _____ receptors.

Back 14

Steroid hormones act by altering gene expression via DNA bindingr eceptors.Cortisol acts on Glucorticoid receptors to increase the synthesis ofglycogen synthase, glucose-6-phosphatase,aldolase, and many other enzymes

Front 15

Cortisol acts on Glucorticoid receptors to increase the synthesis of

Back 15

glycogen synthase,

glucose-6-phosphatase,

aldolase,

and many other enzymes

Front 16

___ is the primary glucocorticoid

Back 16

Cortisol

Front 17

what are the important metabolic functions of cortisol?

Back 17

1) Provides resistance to stress by making nutrients available for ATP production
2) Helps maintain a liver glycogen reserve
3) Conversion of amino acids to glucose (gluconeogenesis)
4) Increases rate of protein catabolism
5) Stimulates lipolysis (with exceptions)
6) Inhibits insulin actions (Diabetogenic)
↓ glucose & amino acid uptake by muscle and fat cells
↑ hepatic gluconeogenesis

Front 18

Cortisol is diabetogenic. What does this means and what are the associated effects?

Back 18

Inhibits insulin actions (Diabetogenic)

↓ glucose & amino acid uptake by muscle and fat cells

↑ hepatic gluconeogenesis

Front 19

What is cortisol effect on protein catabolism?

Back 19

stimulates, increases

Front 20

What is cortisol effect on gluconeogenesis and glycogenesis?

Back 20

stimulates, increases

Front 21

What is cortisol effect on lipolysis and lipogenesis?

Back 21

stimulates, increases

Front 22

What is cortisol effect on insulin actions on glucose & amino acid uptake?

Back 22

inhibits, decreases

Front 23

what is protein catabolism?

Back 23

amino acids converted to glucose

Front 24

Glycogenolysis

Back 24

Glycogenolysis is the conversion of glycogen to glucose

(which could occur several hours after a meal or overnight) in the liver or, in the absence of glucose-6-phosphate in the muscle, to lactate.

Front 25

Gluconeogenesis

Back 25

Gluconeogenesis is the formation of glucose from noncarbohydrate sources, such as certain amino acids and the glycerol fraction of fats when carbohydrate intake is limited. Liver is the main site for gluconeogenesis, except during starvation, when the kidney becomes important in the process.

Front 26

Glycogenesis

Back 26

Glycogenesis is the conversion of excess glucose to glycogen

Front 27

Cortisol: Adipose effects

Back 27

Variable lipogenic effects
Enhances the lipolytic actions of Glucagon, GH & Epinephrine

Front 28

Why is cortisol important during fasting?

Back 28

Cortisol is essential for maintaining plasma glucose levels during prolonged fasting. Without cortisol, death would occur soon after depletion of glycogen stores.

Front 29

Cortisol: Liver effects

Back 29

↑glycogenesis (maintains a liver glycogen reserve)
Gluconeogenesis
↑Conversion of amino acids to glucose
Enhances the lipolytic & ketogenic actions of Glucagon, Growth Hormone, & Epinephrine

Front 30

Cortisol: Cardiovascular effects

Back 30

1) Maintains cardiac performance
2)Enhances catecholamine response
3) Increases number of catecholamine receptors
4) Circulatory shock if cortisol is lacking
5) Enhances vasoconstriction
↑ Angiotensin II response
↓PG vasodilator production
6) Decreases vascular permeability

Front 31

Diabetogenic – cortisol acts as an antagonist to insulin effects.

Back 31

Cortisol inhibits the insulin-stimulated muscle and adipose tissue glucose uptake.

Cortisol blocks the inhibitory effect of insulin on hepatic gluconeogenesis.

Net effect of cortisol is increased plasma glucose levels - hyperglycemic hormone.

Front 32

What are cortisol's effect on fat metabolism?

Back 32

Cortisol has permissive effects on the actions of other lipolytic hormones (glucagon, epinephrine, GH).

Cortisol is directly Lipolytic in some adipose tissues.

Cortisol is directly Lipogenic in certain adipose tissues - face and trunk [remember the moon face & abdominal fat, with skinny arms & legs seen with cortisol overdose (Cushing’s syndrome).

Cortisol increases plasma FFA levels

Front 33

Cortisol supports the ____ energy requirements during periods of stress.

Back 33

Cortisol supports the increased energy requirements during periods of stress.

Front 34

cortisol has what affect on vasoconstriction?

Back 34

cortisol enhances vasoconstriction

cortisol constricts blood vessels

Front 35

cortisol has what affect on vasodilation?

Back 35

cortisol decreases vasodilation

cortisol constricts blood vessels

Front 36

How does cortisol constricts blood vessels?

Back 36

↑ angiotensin II response

↓Prostaglandin vasodilator production in epithelial cells

Front 37

what is cortisol effect on vascular permeability?

Back 37

Cortisol decreases vascular permeability

Front 38

Cortisol is lipogenic and increases fat deposit in the ____

Back 38

breaks down fat in the perifery

Front 39

Cortisol is lipolytic and increases fat deposit in the ____

Back 39

increases central fat storage

Front 40

Glucocorticoids have Anti-inflammatory/Immunosupression effects and is used therapeutically for what what disorders?

Back 40

Rheumatoid arthritis (1950 Nobel prize)
Allergic disorders
Prevent transplant rejection

Front 41

what the main type of mineralcorticoid?

Back 41

aldosterone

Front 42

Cushing’s Syndrome

Back 42

Excess cortisol

Front 43

Conn’s Syndrome

Back 43

Aldosterone hypersecreting tumor

primary Hyperaldosteronism

Front 44

Secondary Hyperaldosteronism

Back 44

Excess Aldosterone from high renin-angiotensin

Front 45

Congenital Adrenal Hyperplasia (Adrenogenital Syndrome)

Back 45

Enzyme defect in cortisol synthesis

**Excess Androgens**

Front 46

Addison’s Disease

Back 46

Deficient corticosteroids

Front 47

Secondary adrenocortical Insufficiency

Back 47

Deficient ACTH & cortisol

Front 48

Aldosterone receptors

Back 48

Aldosterone acts by binding to Aldosterone receptors, which are DNA binding transcription factors. Since the physiological effects require changes in protein synthesis, it may take 30 min or more to measure an effect.

Front 49

are the effects of aldosterone immediate?

Back 49

No, the physiological effects require changes in protein synthesis, it may take 30 min or more to measure an effect.

Front 50

what is aldosterone's Major site of action?

Back 50

aldosterone's Major site of action is the kidney (cells of the distal tubule and the collecting duct).

Front 51

Aldosterone: 3 major effects on the kidney

Back 51

1) Increases the activity and number of Na+ / K+ ATPase pumps in the basolateral membrane.

2) Increases the activity and number of epithelial Na+ channels, K+ channels, sodium-chloride-potassium cotransporters, and sodium-hydrogen exchange proteins in the apical membrane.

3)Increases ATP production by the mitochondria

Front 52

Aldosterone Increases the activity and number of Na+ / K+ ATPase pumps in the _____ membrane.

Back 52

Aldosterone Increases the activity and number of Na+ / K+ ATPase pumps in the basolateral membrane.

Front 53

Aldosterone o Increases the activity and number of epithelial Na+ channels, K+ channels, sodium-chloride-potassium cotransporters, and sodium-hydrogen exchange proteins in the ___ membrane.

Back 53

Aldosterone Increases the activity and number of epithelial Na+ channels, K+ channels, sodium-chloride-potassium cotransporters, and sodium-hydrogen exchange proteins in the apical membrane.

Front 54

Aldosterone Increases __ production by the mitochondria

Back 54

Aldosterone Increases ATP production by the mitochondria

Front 55

Aldosterone stimulates the active reabsorption of ___ in the distal tubule and the collecting duct.

Back 55

• Aldosterone stimulates the active reabsorption of Na+ in the distal tubule and the collecting duct.

Front 56

Aldosterone stimulates the active reabsorption of Na+ in the distal tubule and the collecting duct.

what is it's effect on ECF volume and plasma osmolarity?

Back 56

This results in an increase in ECF volume but no change in plasma osmolality.

ADH from the hypothalamus – posterior pituitary regulates the plasma osmolarity.

Front 57

How does aldosterone effect urinary excrertion?

Back 57

Aldosterone stimulates the active reabsorption of Na+ in the distal tubule and the collecting duct.

Thus decreases urinary excretion of NaCl with water following (requires ADH). This results in an increase in ECF volume but no change in plasma osmolality. ADH from the hypothalamus – posterior pituitary regulates the plasma osmolarity.

Front 58

what hormone regulates plasma osmolarity

Back 58

ADH from the hypothalamus – posterior pituitary regulates the plasma osmolarity.

Front 59

What are the main functions of aldosterone?

Back 59

-Increases reabsorption of Na+ in the distal tubule and collecting ducts of the kidney

-Cl- , bicarbonate and water follow sodium, increased blood volume

-Promotes renal excretion of K+ and H+

Front 60

What hormones are involved in the RAASystem?

Back 60

Renin, Angiotensin, and aldosterone

Front 61

Renin

Back 61

proteolytic enzyme released by the juxtaglomerular cells of the kidney
renin cleaves the plasma protein, angiotensinogen, to Angiotensin-I

Front 62

Angiotensin

Back 62

Angiotensin converting enzyme (ACE) removes two amino acids from Angiotensin-I to produce Angiotensin-II

Angiotensin-II causes vasoconstriction and stimulates the release of ADH &

Front 63

what does ACE stand for and what is it's function?

Back 63

Angiotensin converting enzyme (ACE)

removes two amino acids from Angiotensin-I to produce Angiotensin-II

Front 64

function of Angiotensin-II

Back 64

Angiotensin-II binds to Angiotensin-II receptors causing vasoconstriction and stimulating aldosterone & ADH release

Front 65

What increases aldosterone release?

Back 65

1) Angiotensin II
Low BP or fluid volume cause renin release from renal juxtaglomerular cells (also SNS response)
2) increased potassium blood levels
3) increased plasma sodium
4) ACTH (minor)

Front 66

Aldosterone release is Decreased by:

Back 66

Aldosterone release is Decreased by:
Atrial Natriuretic Peptide (ANP)
Dopamine

Front 67

There is an increase in K in the blood how does this affect aldosterone?

Back 67

increases aldosterone secetrion

Front 68

There is an increase in plasma Na how does this affect aldosterone?

Back 68

aldosterone release increased

Front 69

There is an increase in dopamine in the blood, how does this affect aldosterone?

Back 69

aldosterone release decreased

Front 70

There is an increase in Atrial Natriuretic Peptide (ANP)
in the blood, how does this affect aldosterone?

Back 70

aldosterone release decreased

Front 71

When and were is Atrial Natriuretic Peptide (ANP) released?

Back 71

Hormone released from cardiac muscle cells when atrial blood pressure increases (also BNP from ventricles and CNP)

Front 72

What is the function of Atrial Natriuretic Peptide (ANP)?

Back 72

ANP inhibits release of Aldosterone & ADH

released from cardiac muscle cells when atrial blood pressure increases

Simulates increased urine output and produces a decrease in blood volume and blood pressure

Front 73

Natriuretic peptide receptors are

Back 73

membrane-bound guanylate cyclase that serves as the receptor for both atrial and brain natriuretic peptides

NPR3 is associated with G-protein αi (minor)

Front 74

What stimulates the secretion of Renin from Renal Juxtaglomerular
cells?

Back 74

Hemorrhage
Dehydration
Low Na+

which results in decreased fluid volume
upright posture Sypathetic

Front 75

Renin stimulates the conversion of angiotensinogen to

Back 75

Angiotensin I

Front 76

ACE converts Angiotensin I to

Back 76

Angiotensin II

Front 77

Angiotensin II stimulates the adrenal cortex to release what hormone

Back 77

Aldosterone which will act on the kidney

Front 78

A deficiency in what 2 enzymes of corticosteroid synthesis would lead to cortisol deficiency?

Back 78

cytochrome P450 enzymes:

P450-C21 = 21 alpha hydoxylase
P450-C11 = 11 beta hydoxylase

Front 79

cytochrome P450 enzymes do what type of chemical reaction

Back 79

cytochrome P450 enzymes do Hydroxylation!!

Front 80

When is ACTH and cortisol at their lowest levels?

Back 80

right before sleep

Front 81

When is ACTH and cortisol at their highest levels?

Back 81

1-2 hrs before waking up

Front 82

what is the primary glucocorticoid?

Back 82

corisol

Front 83

cortisol effects on insulin

Back 83

cortisol is diabetogenic and inhibits insulin actions
↑ liver gluconeogenesis
↓ glucose and AA uptake by muscle and fat

Front 84

What is a side effect of glucocorticoid therapy (cortisol)? What should they be supplemented with?

Back 84

osteoporosis is a side effect of glucocorticoid therapy and patients should be supplimented with vitamin D

Front 85

Aldosterone acts on the ___ to ___ Na+ reabsorption. What is the effect on H2O?

Back 85

Aldosterone acts on the kidney to increase Na+ (and H2O) reabsorption. Where salt goes, water goes.

Front 86

Aldosterone increase Na+ (and H2O) reabsorption leads to excretion of what ions?

Back 86

Na+ in
K+ and H+ out

Front 87

Aldosterone on distal nephron
Na+/K+ ATPase on ____ membrane

Na+ channels on _____ membrane

Back 87

Aldosterone on distal nephron
Na+/K+ ATPase on basolateral membrane (blood)

Na+ channels on apical membrane (urine/tubule)

Front 88

DHEA is converted to what hormones?

Back 88

DHEA is androgen that is converted to testosterone and estrogen

Front 89

during the regulation of cortisol what androgen production can be increased?

Back 89

DHEA

Front 90

DHEA does not inhibit CRH or ACTH.

What does DHEA inhibit?

Back 90

DHEA inhibits the release of gonadotropin releasing hormone (GnRH), LH, and FSH

Front 91

Cushing’s Syndrome

Back 91

Excess cortisol

Hypersecretion of glucocorticoids

Front 92

Conn’s Syndrome

Back 92

Aldosterone hypersecreting tumor

Front 93

Secondary Hyperaldosteronism

Back 93

Excess Aldosterone from high renin-angiotensin

Front 94

Congenital Adrenal Hyperplasia (Adrenogenital Syndrome)

Back 94

Enzyme defect in cortisol synthesis
Excess Androgens

Front 95

Addison’s Disease

Back 95

Deficient corticosteroids

Front 96

Secondary adrenocortical Insufficiency

Back 96

Deficient ACTH & cortisol

Front 97

Addison disease is due to an infection (TB) or autoimmune disorder that causes the distruction of the adrenal cortex.

How and what hormones will be affected?

Back 97

Addison's disease results in the distruction of the adrenal cortex (salt, sugar, sex).

↓Aldosterone
↓Cortisol
↓Androgens

Front 98

Addison's syndrome results in the destruction of the the adrenal cortex.

since the zona fasciculata is destroyed what hormone deficiency will occur?

Back 98

↓Cortisol will result in an ↑ACTH and Hypoglycemia (↓blood glucose)

↑ACTH with αMSH activity that will cause a darkening of the skin.

Front 99

Addison's syndrome results in the destruction of the the adrenal cortex.

since the zona glomerulosa is destroyed what hormone deficiency will occur?

Back 99

↓Aldosterone:
Blood: ↓ Na+, ↓H2O,
Blood: ↑K+, ↑H+

This results in a ↓ Na+ (and H2O) reabsorption and ↓K+ and ↓H+ excretion. Since ↓H2O, patient will have low BP and is at risk for cardiac arrest

Aldosterone: Na+(H20) in / K+ & H+ out

Front 100

How do you treat Addison's disease?

Back 100

aldosterone and cortisol replacement therapy

Front 101

Is Addison's disease 1° or 2° adrenocortical insufficiency?

Back 101

Addison's disease is 1°adrenocortical insufficiency since it is an internal problem (distruction of adrenal cortex)

Front 102

differences between 1° or 2° adrenocortical insufficiency

Back 102

1° adrenocortical insufficiency = inside problem of adrenal cortex

2° adrenocortical insufficiency= outside problem effecting adrenal cortex

Front 103

hypoglycemia, lethargy, and weakness are linked to 1° or 2° adrenocortical insufficiency?

Back 103

hypoglycemia, lethargy, and weakness are linked to both 1°and 2° adrenocortical insufficiency

Front 104

2° adrenocortical insufficiency is caused by

Back 104

Pituitary failure or tumor (non-ACTH secreting)
Hypothalamic failure (no CRH release)
Autoimmune disease inactivating ACTH

Front 105

Where and why is ANP released?

What does ANP inhibit?

What is the function of ANP?

Back 105

ANP is released from cardiac muscle in response to high blood pressure

ANP inhibits Aldosterone and ADH release

stimulates increased urine output by constricting afferent arterioles in the nephron (↑GFR and ↑Na+ filtered load)
Also inhibits aldosterone from reabsorbing Na+ (↑Na+ excretion)
goal is to decrease blood volume and osmolarity

Front 106

Which of the following produces it’s MAJOR physiological effects by directly binding to a G-protein associated receptor?

1) Renin
2) Cortisol
3) Insulin
4) Growth hormone
5) Aldosterone
6) ANP
7) ADH

Back 106

1) Renin -enzyme
2) Cortisol -steroid
3) Insulin -peptide
4) Growth hormone -peptide
5) Aldosterone -steroid
6) ANP-peptide
7) ADH-peptide

Front 107

What cell type in the adreal gland produces catecolamines?

Back 107

Chromaffin cells in the adrenal medula produce catecolamines
epinephrine
norepinephrine

Front 108

What stimulates the release of catecolamines from the adrenal medulla?

Back 108

Sympathetic preganlionic nerves stimulate the adrenal medulla to release catecolamines (epinephrine and norepinephrine).

Front 109

Catecholamines effects

Back 109

-Stimulate glucagon release
-Modulate insulin release
-Stimulate renin release
-Modulate vasopressin (ADH) release
-Modulate thyroid hormones
may enhance release under some conditions
-stimulate T4 to T3 conversion is some tissues
-Thyroid hormones and cortisol can increase adrenergic receptors and enhance adrenergic responses