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FHB - Endocrine & Reproductive > Lecture 6 (73): Adrenal Gland Part 2 > Flashcards

Lecture 6 (73): Adrenal Gland Part 2 Flashcards

1
Q

What are the 3 layers of the adrenal medulla and which hormone is associated with it?

A
  1. zona glomerulosa = Mineralocorticoids
  2. zona fasciculata = Glucocorticoids (cortisol)
  3. zona reticularis weak androgens (DHEAS)
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2
Q

What are mineralcorticoids?

What is the primary endogenous mineralcorticoid?

What is its precursor?

A
  1. Steroid hormones that regulate sodium/water balance
  2. Aldosterone – primary endogenous mineralocorticoid; other steroid hormones can have mineralocorticoid actions
  3. Example: 11-Deoxycorticosterone (precursor of
    aldosterone) has mineralocorticoid action
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3
Q

Where is aldosterone (MR) expressed highly? 5

A
  1. distal tubule in kidney
  2. Colon
  3. Salivary ducts
  4. Sweat ducts
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4
Q

What is aldosterone’s main target?

A

Kidney

  • promotes sodium and water reabsorption in the kidney
  • increases potassium secretion
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5
Q

Describe the Renin-Angiotensin-Aldosterone System.

  1. What stimulates Renin release from the kidney?
  2. What forms?
  3. What converts AI to AII?
  4. What is the function of A II?
A

Decreased blood pressure stimulates renin release from kidney (juxtaglomerular apparatus).

Renin cleaves angiotensinogen (from liver) to angiotensin I.

Angiotensin converting enzyme (ACE) converts to angiotensin II.

Angiotensin II is a vasoconstrictor and stimulates aldosterone.

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6
Q

State which performs the following functions (Aldosterone or AVP/ADH)

  1. primary regulator of extracellular volume
    - Stimulates sodium and water reabsorption in kidney
    - Stimulates potassium excretion

Net Result = increased extracellular fluid volume and blood pressure (sodium in extracellular space retains water)

A
  1. ALDOSTERONE
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7
Q

State which performs the following functions (Aldosterone or AVP/ADH)

  1. primary regulator of free water balance
  • Stimulates distal nephron water permeability –
  • increased water retention
  • Decreases plasma osmolality which secondarily affects sodium concentration in the blood
A

AVP/ADH

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8
Q

Kidney: Cortisol is normally converted to the inactive *CORTISONE by what?

What happens if this enzyme is defective?

Licorice (glycyrrhetinic acid) does what?

A
  1. 11β-HSD2
  2. Certain drugs (carbenoxolone) will inhibit 11β-HSD2 resulting in excess MR activation.
  3. also inhibits 11β-HSD2 – excessive consumption can lead to increased sodium and water retention.
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9
Q

What enzyme converts Cortisone to the active CORTISOL?

A

Local production of Cortisol by 11β-HSD1 potential pathogenic role in DM T2 – novel drug target

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10
Q

What is the major compound in the Zona Reticularis?

A

DHEA/S; metabolite = androstendione

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11
Q

DHEA:

  1. Is the precursor for what androgen? Where is it converted
  2. Declines with what?
  3. Weak or strong androgen? Why?
  4. Increases what in women? Primary source of _____ and _____ in post-menopausal women.
A

Precursor for the more potent androgen testosterone, and for estrogens – converted in reproductive tissues.

50% of total androgen precursors in adult male prostate comes from adrenal

Declines with age – peaks between 20 – 30.

“weak androgen” due to its low binding affinity for androgen receptors (AR).

Increases libido in women; primary source of androgen and estrogen in postmenopausal women

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12
Q

What is the primary product of the zone fasciculata?

Important enzymes?

Where is 17 alpha - hydroxyls made?

A

Cortisol

enzymes:
cholesterol side chain cleavage
21alpha - hydroxylase
11-alpha-hydroxylase

17alpha - hydroxylase
MADE ONLY IN Z.fasciculata and z. reticularis

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13
Q

Congenital Adrenal Hyperplasia is a deficiency in which enzyme?

What is in excess amount?

What are the clinical implications?

A

21α hydroxylase deficiency - results in excess DHEA, no mineralocorticoids or glucocorticoids

Most common cause of CAH

Clinical indications: virilization (masculinization) ambiguous genitalia at birth, sodium loss

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14
Q

CYP21A2: 21α-hydroxylase deficiency

State 3 major things affected.

Clinical implications?

A
  1. No cortisol
  2. No aldosterone/MR activity
  3. Increased androgens
Clinical presentation:
Hypotension
Hyperkalemia
High plasma renin
Masculinization
High ACTH
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15
Q

What is the primary product of the zone glomerulosa?

What are the clinically relevant enzymes?

A

Primary Product: Aldosterone

  1. Cholesterol side chain cleavage
  2. 21alpha-hydroxylase
  3. 11-alpha-hydroxylase
  4. 17-alpha-hydroxylase (only made in z.fascuculata and z. reticularis)
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16
Q

CYP11B1, is a deficiency in what?

what are the levels of the following:

  1. Cortisol
  2. Aldosterone
  3. androgen

What are the clinical implications?

A

11-hydroxylase deficiency

No cortisol
Low aldosterone, but high MR activity
Increased androgens

Clinical presentation:
Hypertension* due to excess 11-deoxycorticosterone
Hypokalemia
Masculinization
High ACTH
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17
Q

What is the primary product of Zona Reticularis?

A

DHEA/S

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18
Q

What is deficient in CYP17?

A

17α-hydroxylase deficiency

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19
Q

CYP21A2: 21α-hydroxylase deficiency

what are the levels of the following:

  1. Cortisol
  2. Aldosterone
  3. androgen

Clinical implications?

A
  1. No cortisol
  2. No aldosterone/MR activity
  3. Increased androgens
Clinical presentation:
Hypotension
Hyperkalemia
High plasma renin
Masculinization
High ACTH
20
Q

CYP11B1, is a deficiency in what?

what are the levels of the following:

  1. Cortisol
  2. Aldosterone
  3. androgen

What are the clinical implications?

A

11-hydroxylase deficiency

No cortisol
Low aldosterone, but high MR activity
Increased androgens

Clinical presentation:
Hypertension* due to excess 11-deoxycorticosterone
Hypokalemia
Masculinization
High ACTH
21
Q

What is deficient in CYP17?

what are the levels of the following:

  1. Cortisol
  2. Aldosterone
  3. androgen

Clinical presentation?

A

17α-hydroxylase deficiency

Clinical presentation:
Hypertension
Hypokalemia
Feminization/
pseudohermaphroditism
High ACTH
22
Q

What 2 important enzymes are found in
fasciculata and glomerulosa?

What enzyme is found only in fasciculate and RETICULARIS?

What enzyme is ONLY in GLOMERULOSA

A

21α-hydroxylase

11-hydroxylase

  1. 17α-hydroxylase

Aldosterone Synthase

23
Q

Where is 11β-HSD1 and 2
?

What are the functions of both?

A

Kidney (type 2)

1 = convert cortisone to CORTISOL

2= opposite

24
Q

What gene is defective and affects the following enzymes:

  1. Cholesterol Side Chain cleavage
  2. 21α-hydroxylase
  3. 11-hydroxylase
  4. 17α-hydroxylase
  5. Aldosterone synthase
  6. 11β-HSD1 and 2
A
  1. CYP11A1
  2. CYP21A2
  3. CYP11B1/CYP11B2
  4. CYP17
  5. CYP11B2
  6. not P450 family
25
Q

_____ in z. glomerulosa can be called 11-hydroxylase or aldosterone synthase

11-hydroxylase deficiency syndrome refers to defect in _____ (z. fasciculata)

A

CYPB2

CYP11B1

26
Q

Minerlcorticoid2 Receptor (MC2R) is what type of receptor?

A

ACTH

27
Q

ACTH TARGETS IN ADRENAL:

  1. Stimulates the conversion of?

Where do the following occur?

  1. Cellular ____
  2. Biosynthesis of _____ & _____
  3. Enzyme?

WHERE
1. Stimulates conversation of dopamine to _____ where?

A

Steroid Biosynthesis:
1. Stimulates conversion of cholesterol to pregnenolone by activating StAR activity

Adrenal COrtex:

  1. Stimulates cellular hypertrophy
  2. Stimulates biosynthesis of cortisol
    - Stimulates biosynthesis of DHEA (CYP17)
  3. Stimulates 11β-hydroxylase (CYP11B1)

Adrenal Medulla:
1.Stimulates conversion of dopamine to norepinephrine in Adrenal Medulla

28
Q

Adrenal medulla:

Originates from same _________ that forms sympathetic ganglia.

Medullary cells are innervated by ______

Considered to be modified _______

A
  1. neural crest area
  2. sympathetic preganglionic fibers.
  3. post-ganglionic sympathetic neurons (no dendrites or axons).
29
Q

Adrenal Medulla:

  1. Cords of _____ shaped epithelial cells.
  2. Most cells release _______ – stored in granules.
  3. Rapid release under _______ NS control
A
  1. Polyhedral
  2. epinephrine
  3. sympathetic
30
Q

How are chromaffin cells made?

Where are they found?

A
  1. “Chromaffin” cells: Catecholamines bind to chrome salts. Reaction oxidizes to brown color.
  2. Adrenal medulla
31
Q

Catecholamines like dopamine, norepinephrine, and epinephrine.

What is the rate limiting enzyme in their production?

A
  1. Tyrosine Hydroxylase

2.

32
Q

What does tyrosine hydroxylase convert?

A

Converts tyrosine to XDOPA (precursor of dopamine)

33
Q

Catecholamines like dopamine, norepinephrine, and epinephrine.

What is the rate limiting enzyme in their production?

Where does the pathway stop?

What converts dopamine to NE?

______ stimulates conversion of norepinephrine to epinephrine – only where??

A
  1. Tyrosine Hydroxylase
  2. Pathway stops at dopamine in the dopaminergic neurons in brain.
  3. Peripheral nerves convert dopamine to norepinephrine (ACTH sympathetic stimulation)

NE to E = cortisol

  1. Cortisol, adrenal medulla.
34
Q

What hormone does the following describe?

Response to acute stress: (pain, cold, perceived danger)

Rapid activation/rapid return

Mediated by the sympathetic nervous system – innervated by splanchnic nerve

A

Epinephrine

35
Q

What are the 3 main targets of epinephrine?

What functions does it affect in these tissues?

A
  1. Muscle, liver, fat
  2. Glycogenolysis: ATP release for local energy (no glucose-6-phosphotase in skeletal muscle)
    - Release glucose into blood in the liver (via glycogenolysis)
    - Increase glucagon release from Alpha cells of the pancreatic islets
    - increase TAG degradation in adipose tissue
36
Q

What receptors does epinephrine act through?

How does it affect the following:

  1. Pupil
  2. Sweat
  3. GI and bronchial muscle?
A

BOTH alpha and beta adrenergic

Arousal

  1. pupil dilation, 2. sweating,
  2. GI and bronchial muscle relaxation
37
Q

How does epinephrine affect the following:

  1. Metabolism
  2. Cardiovascular
A
  1. Glucose release,
    increase metabolic rate
  2. Vasoconstriction, increased heart rate (tachycardia)
38
Q

Which is higher in the following scenario (NE or Isoproterenol:

  1. alpha adrenergic mediated
  2. Beta - adrenergic
A
  1. alpha adrenergic mediated - NE
  2. Beta - adrenergic
    - Isoproterenol
39
Q

What are the coordinated efforts of cortisol and EPI in stress response?

A
  1. Acute stress activates the sympathetic NS and stimulates the release of NE.

NE stimulates CRH to initiate HPA response to long-term stress

Feedback loops occur at multiple levels

40
Q

Where does the break down of EPI and NE to COMT and MAO occur?

A
  1. Adrenal Medulla
  2. Liver
  3. Kidney
41
Q

Where does conversion of the followng occur:

  1. Metenephrine to MAO
  2. DHPG to COMT and AD
  3. Normetanephrine to MAO

and all of these finally to VMA

A

LIVER and Kidney

42
Q

What is the breakdown product of NE and E

either:
Metenephrine or Normetanephrine

A
  1. Epinephrine Metenephrine

2. NE and Normetanephrine

43
Q

What are pheochhromocytomas?

What are the symptoms?

DIagnosis?

Treatment?

A
  1. tumors originating from chromaffin cells.
  2. Diagnosis: measurements of urinary metanephrines
  3. surgery, pre-surgery: alpha/beta blockers
44
Q

Why are pheochromocytoma the 10% tumor?

A

Because ~10 percent of pheochromocytomas are:

Malignant (90% benign)

Bilateral (found in both adrenal glands: 90% arise in just one of the two adrenal glands)
In Children (90% in adults)

Familial (10% will have a family member with the same type of tumor)

Recur (10% will come back in 5 - 10 years)

Associated with MEN* syndromes (patients with rare syndromes of endocrine tumors)

Present with a stroke (10% of these tumors are found after the patient has a stroke)

Extra-Adrenal (found within nervous tissue outside of adrenal glands)

45
Q

What are the extra-adrenal sites of pheochromocytomas?

A

Extra-adrenal sites of pheochromocytomas:

Sympathetic nerve chain along the spinal cord

Overlying the distal aorta (main artery from the heart)

Within the ureter (collecting system from the kidney)

Within the urinary bladder (And 90% in the adrenal glands)

FHB - Endocrine & Reproductive (17 decks)

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