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4) Metabolic Endocrinology > 9) Adrenal Gland > Flashcards

9) Adrenal Gland Flashcards

1
Q

What stimulates the release of CRH?

A
  • Decrease in plasma cortisol
  • Hypoglycemia
  • Stress
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2
Q

What inhibits the release of CRH?

A

Increase in plasma glucocorticoids

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3
Q

Where are the adrenal glands located?

A

Above or medial to the upper poles of the kidneys

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4
Q

What is the thickest layer of the adrenal cortex?

A

Zona fasciculata

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5
Q

What are the three zones of the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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6
Q

What is the importance of the structure of the adrenal gland in terms of the proximity between the adrenal cortex and medulla?

A
  • Glucocorticoids produced by the adrenal cortex (cortisone, cortisol) are required for the synthesis of catecholamines
  • Catecholamines are synthesized by the adrenal medulla
  • Glucocorticoids travel from the cortex to the medulla directly
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7
Q

Which hormone does the zona glomerulosa produce?

A

Aldosterone

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8
Q

Which hormone does the zona fasciculata produce?

A

Cortisol

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9
Q

Which hormone does the zona reticularis produce?

A

Sex steroids

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10
Q

Which hormones does the adrenal medulla produce?

A

Catecholamines (epinephrine and norepinephrine)

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11
Q

The zona ________ cannot synthesize cortisol or androgens.

A

glomerulosa

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12
Q

Why can’t the zona glomerulosa synthesize androgens or cortisol?

A

Because it lacks 17a-hydroxylase

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13
Q

Why can’t the zona fasciculata form sex steroids?

A

Because it lacks 17-lyase

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14
Q

What is the first step common to all steroids? Where does it take place?

A
  • Formation of pregnenolone from cholesterol

- Mitochondria

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15
Q

What determines which steroid is produced in a cell or tissue?

A

Tissue-specific expression of enzymes

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16
Q

Where are enzymes for steroid hormone synthesis located within the cell?

A
  • Mitochondria and endoplasmic reticulum

- Steroid intermediates have to shuttle back and forth

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17
Q

How do most steroids differ?

A
  • By minor modifications of side groups

- Often hydroxyl groups

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18
Q

What is the StAR protein?

A
  • Rate-limiting enzyme for the transport of cholesterol

- Carries the cholesterol across the mitochondrial membrane to the inner surface

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19
Q

What is the function of P450scc?

A

Side chain cleavage of cholesterol to pregnenolone

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20
Q

The uptake of cholesterol is regulated by what?

A
  • StAR protein

- Steroid Acute Regulatory protein

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21
Q

StAR is ____-inducible.

A

cAMP

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22
Q

What hormones increase StAR?

A
  • Trophic hormones
  • ACTH in the adrenal gland
  • Gonadotrophins in the gonads
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23
Q

Where is cortisol stored intracellulary?

A

There is NO cellular storage of cortisol

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24
Q

What is cortisol converted to in the liver? For what purpose?

A
  • Inactive cortisone and other metabolites

- For excretion in urine

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25
Q

What are the two main effects of cortisol? (2)

A

1) Carbohydrate and protein metabolism

2) Anti-inflammatory effects

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26
Q

What enzyme converts cortisol to inactive cortisone?

A

Hydroxysteroid dehydrogenase type II

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27
Q

What enzyme converts inactive cortisone to cortisol?

A

Hydroxysteroid dehydrogenase type I

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28
Q

Which hormone can activate the aldosterone receptor?

A

Cortisol

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29
Q

How does the plasma concentration of cortisol compare to aldosterone?

A

Cortisol is 100 to 1000-fold higher than aldosterone

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30
Q

What must aldosterone-specific cells do to assure that they respond specifically to aldosterone?

A

Inactivate cortisol

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31
Q

A deficiency in the enzyme responsible for converting cortisol to cortisone results in what syndrome?

A
  • AME syndrome

- Apparent mineralocorticoid excess

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32
Q

Skin, liver, adipose, CNS, and placenta possess hydroxysteroid dehydrogenase type __.

A

1

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33
Q

Kidney, colon, sweat glands, salivary glands, and placenta possess hydroxysteroid dehydrogenase type __.

A

2

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34
Q

What occurs to hydroxysteroid dehydrogenase type 2 when cortisol levels are too high?

A
  • HSD2 is overwhelmed
  • Cortisol stimulates Na+/K+ exchange in the kidney
  • Causes hypokalemia and hypertension
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35
Q

A component of which food is an inhibitor of hydroxysteroid dehydrogenase type 2?

A

Licorice

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36
Q

What type of receptor is the cortisol receptor?

A

Class I (cytosolic) intracellular receptor

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37
Q

The effects of cortisol are (similar/opposite) to insulin and (similar/opposite) to GH.

A

opposite

similar

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38
Q

What are the effects of cortisol on muscle cells, adipocytes, and lymphocytes?

A

Increase in catabolism

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39
Q

What are the effects of cortisol on the liver?

A
  • Increase in glycogen synthesis

- Increase in gluconeogenesis

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40
Q

What is the overall effect of cortisol on blood glucose and glycogen store?

A
  • Increase in blood glucose

- Despite the increase in glycogen storage

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41
Q

Cortisol is (pro/anti)-inflammatory.

A

anti-inflammatory

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42
Q

How does cortisol affect lymph nodes, the thymus, lymphocytes, and antibodies? How does that affect the patient’s health overall?

A
  • Atrophy of the lymph nodes and thymus (activation of apoptosis)
  • Decrease in lymphocytes and antibodies
  • Patients become susceptible to infections
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43
Q

How is cortisol linked to hypertension through norepinephrine?

A

Cortisol sensitizes arterioles to the action of norepinephrine

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44
Q

How is cortisol linked to carbohydrate metabolism through norepinephrine?

A
  • Permissive effect on the action of norepinephrine on carbohydrate metabolism
  • Glycogenolysis leads to hyperglycemia
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45
Q

How does cortisol affect the CNS?

A

Increased activity of the CNS, leading to euphoria

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46
Q

Cortisol may act as a ___________ because it interacts with its receptor.

A

mineralocorticoid

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47
Q

How does cortisol affect blood glucose, amino acids, and fatty acids? Why?

A
  • Increase in blood glucose, amino acids, and fatty acids by catabolism
  • They are now available to help resist stress
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48
Q

ACTH activates cortisol production via which signalling pathway?

A

G-protein/cAMP

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49
Q

After a long suppression of synthesis of ACTH, what may be needed to allow for ACTH synthesis to resume?

A
  • Time is required

- Hypothalamic axis does not respond well, and requires time to produce the cyclical release of ACTH

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50
Q

Describe the rhythm of cortisol-releasing hormone release.

A

Highest level early in the morning (diurnal rhythm)

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51
Q

What is the transport protein for cortisol?

A

Corticosteroid Binding Globulin (CBG or Transcortin)

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52
Q

Where is CBG synthesized?

A
  • Synthesized in the liver

- Highest affinity for cortisol

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53
Q

What percentage of cortisol is bound to CBG? What percentage is “free” in plasma? What occurs to the rest?

A
  • 75% bound to CBG
  • 10% is free
  • 15% bound to serum albumin
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54
Q

Bound cortisol is protected from what? What is the effect?

A
  • Protected from inactivation by the liver

- Maintains a pool of circulating cortisol by delaying metabolic clearance

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55
Q

How does the liver inactivate free steroids?

A

By increasing water solubility

56
Q

How does Cushing’s disease affect blood glucose?

A
  • Increased levels of blood glucose

- Diabetes mellitus

57
Q

How does Cushing’s disease affect body fat?

A
  • Increased body fat and redistribution

- Central obesity and moonface

58
Q

How does Cushing’s disease affect the immune system?

A

Increased susceptibility to infection

59
Q

Which types of tumours may cause Cushing’s disease?

A
  • CRH-producing tumour
  • ACTH-producing tumour
  • Cortisol-producing adrenal tumour
60
Q

What are the four causes of spontaneous Cushing’s disease?

A

1) CRH-producing tumour
2) ACTH-producing tumour
3) Cortisol-producing adrenal tumour
4) Lack of feedback control by cortisol

61
Q

What is the most common cause of Cushing’s disease?

A
  • Iatrogenic (“brought forth by the healer”)

- Results from chronic glucocorticoid therapy

62
Q

What is the treatment for Cushing’s disease?

A
  • Removing the cause of hypersecretion without permanently damaging the adrenal or pituitary
  • Microsurgery
  • Radiation therapy
  • Pharmacologic inhibition of ACTH secretion
63
Q

What is Addison’s disease?

A

Adrenal hypofunction

64
Q

What is the most common cause of Addison’s disease?

A

The destruction of the adrenal gland by an autoimmune response

65
Q

What are symptoms of Addison’s disease?

A
  • Fatigue
  • Weakness
  • Faintness
  • Nausea
  • Vomiting
  • Low-blood pressure
  • Salt craving
  • Pain in muscles and joint
  • Excessive freckling
66
Q

What causes the excessive freckling in Addison’s disease?

A
  • The pituitary gland is attempting to stimulate the production of cortisol
  • Release of MSH from the production of ACTH from POMC
67
Q

How does Addison’s disease affect kidney function? Why?

A
  • Aldosterone is low or absent
  • Water and sodium loss from the kidney
  • Low fluid volume and low blood pressure
  • Salt appetite
68
Q

How does Addison’s disease affect the liver?

A
  • Liver function decreases due to absent cortisol

- Extremely low sugar

69
Q

How does Addison’s disease affect the stomach?

A
  • Stomach digestive enzymes decrease due to absent cortisol
  • Vomiting, diarrhea, cramps
  • Low fluid volume
70
Q

What is the treatment for Addison’s disease?

A

Life-long glucocorticoid and mineralocorticoid therapy

71
Q

What is the main function of aldosterone in terms of sodium and potassium?

A
  • Recovery of sodium in the renal filtrate

- Enhanced potassium secretion into the urine to balance the charge difference

72
Q

What are the three physical attributes of plasma that maintain homeostasis of the blood system?

A
  • Volume
  • Blood pressure
  • Osmolarity
73
Q

What is the major determinant of blood pressure in arteries?

A

The diameter of arterioles

74
Q

Aldosterone increases sodium reabsorption in which areas?

A
  • Distal tubules of the kidney
  • GI tract
  • Salivary gland
  • Sweat gland
75
Q

The release of aldosterone is mainly under the control of what?

A

Angiotensin II

76
Q

What secretes angiotensinogen?

A

Liver

77
Q

What catalyzes the conversion of angiotensinogen to angiotensin I?

A

Renin

78
Q

What catalyzes the conversion of angiotensin I to angiotensin II? What is it secreted by?

A
  • Angiotensin converting enzyme

- Surface of pulmonary and renal endothelium

79
Q

How does angiotensin II affect blood pressure and arteriole diameter?

A
  • Arteriole vasoconstriction

- Increase in blood pressure

80
Q

How does angiotensin II affect the pituitary gland?

A
  • ADH secretion

- H2O reabsorption at the collecting duct

81
Q

What is the overall effect of angiotensin II?

A
  • Water and salt retention

- Effective circulating volume increases

82
Q

What is the source of renin?

A

Juxtaglomerula apparatus

83
Q

What is the function of macula densa cells in the distal tubule?

A

Detect sodium levels in the kidney tubule

84
Q

What is the function of juxtaglomerula cells?

A

Detect blood pressure and release renin in response to low blood pressure

85
Q

What causes the rapid pressor response of angiotensin II?

A

Change in peripheral resistance through direct vasoconstriction

86
Q

What causes the slow pressor response of angiotensin II?

A

Change in renal function (increased sodium reabsorption both direct and aldosterone-mediated)

87
Q

How does the release of angiotensin II affect the sympathetic nervous system and the adrenal medulla?

A
  • Increase in sympathetic discharge

- Increase in adrenal medullary catecholamine release

88
Q

Aldosterone increases the recovery of ______.

A

sodium

89
Q

How does aldosterone increase the recovery of sodium?

A
  • Promotes the insertion of additional sodium channels into the luminal membrane
  • Adds additional Na+/K+ ATPase channels into the basolateral membrane of the tubule
90
Q

What are the main sites of action of aldosterone?

A
  • Distal tubules and collecting ducts of the kidneys

- Other secretory systems (sweat glands, salivary glands, colon)

91
Q

Aldosterone promotes the retention of ______ and the excretion of ______ and ___ into the lumen of the tubules.

A

sodium
potassium
H+

92
Q

Aldosterone sensitizes arterioles to (vasodilators/vasoconstrictors).

A

vasoconstrictors

93
Q

Does aldosterone act instantaneously?

A

No, it has a lag period of one hour

94
Q

Why does aldosterone have a lag period of one hour?

A

Aldosterone-induced enzymes have to be synthesized de novo

95
Q

What kind of receptors are aldosterone receptors?

A

Intracellular receptors that may activate the expression of a series of genes

96
Q

What are aldosterone-responsive target tissues that are capable of inactivating cortisol to cortisone?

A
  • Kidney
  • Colon
  • Salivary glands
97
Q

AME may be induced by _______.

A

licorice

98
Q

What is the most important regulatory system of aldosterone secretion?

A

Renin-angiotensin system

99
Q

The release of renin by juxtaglomerular cells is activated by what?

A
  • Decrease in plasma fluid volume

- Decrease in plasma osmolarity

100
Q

How does angiotensin II affect glomerular filtration rate?

A

Reduces glomerular filtration rate

101
Q

What are the three major factors that regulate renin release? (3)

A

1) Baroreceptors in the wall of the afferent arteriole (decrease in pressure)
2) Neural input via the sympathetic nervous system
3) NaCl concentration in the lumen of the distal tubules (low NaCl)

102
Q

How does NaCl concentration affect renin release?

A

Low NaCl = low blood pressure = increase in renin

103
Q

What feedback control system regulates renin release?

A

Angiotensin II

104
Q

How do low potassium levels affect aldosterone?

A

Reduces aldosterone

105
Q

How do low potassium levels affect renin?

A

Stimulates renin

106
Q

What is Conn’s syndrome?

A

Hypersecretion of aldosterone

107
Q

What are the two major causes of Conn’s syndrome?

A
  • Adrenal hyperplasia (60%)

- Tumour (40%)

108
Q

Conn’s syndrome results in excess excretion of which ions?

A

Potassium and H+

109
Q

What are the effects of excess excretion of K+ and H+ in Conn’s syndrome?

A
  • Serum alkalosis

- Neuropathy (hypocalcemia)

110
Q

How does Conn’s syndrome affect water homeostasis, sodium reabsorption and blood pressure?

A
  • Increased water retention
  • Increased sodium reabsorption
  • Increased blood pressure
111
Q

What is the function of atrial natriuretic peptide (ANP)?

A
  • Increases the excretion of H2O and sodium

- Reduces blood volume

112
Q

What produces ANP? How is it stored?

A
  • Produced by cardiocytes

- Stored in granules

113
Q

Where are ANP receptors located?

A
  • Glomeruli
  • Medullary collecting ducts of the kidney
  • Zona glomerulosa of the adrenal cortex
  • Peripheral arterioles
114
Q

An (increase/decrease) of sodium and water intake stimulates the release of ANP from cardiocytes.

A

increase

115
Q

How does ANP affect plasma renin and aldosterone?

A

Reduction in plasma renin and aldosterone

116
Q

How does ANP affect renal blood flow, water and sodium excretion?

A
  • Increase in renal blood flow
  • Increase in water excretion
  • Increase in sodium excretion
117
Q

Why does ANP increase sodium excretion?

A
  • Increase in filtration rate

- Inhibition of reabsorption of sodium

118
Q

How does ANP affect vasoconstriction by angiotensin II?

A

Inhibits vasoconstriction by angiotensin II

119
Q

Which sex steroids are synthesized in females? Which are synthesized in males?

A
  • Females: estrogens and progesterones

- Males: androgens

120
Q

The adrenal cortex contributes to the production of which metabolites, implicated in the production of sex steroids? What is it regulated by?

A
  • DHEAS
  • Androstenedione
  • Regulated by ACTH and CRH
121
Q

What is the primary role of sex steroids in the adrenal cortex? When does the release increase in the life cycle?

A
  • Unclear
  • Body hair growth in females (adrenarche)
  • Increase before puberty
  • Responsible for growth spurt in middle childhood
122
Q

What is andrenarche?

A
  • Increased expression of adrenal androgens (without increased cortisol levels)
  • During puberty
123
Q

What is congenital adrenal hyperplasia (CAH)?

A
  • Masculinization of external genitalia at birth

- Excessive androgen production (hyperplasia of the adrenal glands)

124
Q

What does the genitalia of females ressemble in individuals with CAH?

A
  • Labia comes together to look like a scrotum

- Clitoris enlarges to look like a penis

125
Q

How does the primordial gonad become an ovary in a normal female?

A
  • Lack of Y chromosome

- Lack of SRY gene (on Y chromosome)

126
Q

Is the Mullerian duct maintained in males or females? What does it lead to?

A
  • Females

- Uterus oviduct

127
Q

Why don’t males possess the Mullerian duct?

A

Because they possess Anti-Mullerian hormone (AMH)

128
Q

Is the Wolffian duct maintained in males or females?

A

Males

129
Q

What causes the presence of female external genitalia in normal females?

A
  • Lack of testosterone

- Lack of DHT

130
Q

What causes the presence of masculinized external genitalia in CAH females?

A
  • Presence of testosterone (by the adrenal gland)

- Presence of DHT

131
Q

What are the effects of testosterone on the brain in CAH females?

A

Sexual differentiation of the brain

132
Q

Do females with CAH possess a uterus and ovaries?

A

Yes, but they also possess masculinized external genitalia

133
Q

What is the enzyme defect in CAH? What are the effects on the hormones produced by the adrenal gland?

A
  • 21-hydroxylase (autosomal recessive)
  • Low cortisol production
  • Low aldosterone production (salt appetite increases)
134
Q

How does low cortisol production in CAH females affect the hypothalamic pituitary axis?

A

Reduced negative feedback, which increases the secretion of CRH and ACTH

135
Q

What is the treatment for CAH females?

A
  • Surgical correction at birth

- Raise as girls (possess tendency towards male play patterns)

4) Metabolic Endocrinology (15 decks)

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