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Endo/Repro > 1-30 DSA Adrenal Gland DSA > Flashcards

1-30 DSA Adrenal Gland DSA Flashcards

1
Q

What is 17α-hydroxylase? What does deficiency lead to?

A

Enzyme in mitochondria of adrenal cortex

Helps convert:
pregnenalone into progesterone, then into 11-deoxycorticosterone, and then into corticosterone

Deficiency:
absence of androgens
excess mineralocorticoids

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2
Q

What is 21-hydroxylase? What does its deficiency lead to?

A

Enzyme in mitochondria of adrenal cortex

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3
Q

What are the 3 zones of the adrenal cortex?

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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4
Q

What is the main product of the zona glomerulosa? What is the effect?

A

Mineralocorticoids - 21 carbons

promotes salt and water retentetion

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5
Q

What is the main product of the zona fasciculata? What is the effect?

A

Glucocorticoids - 21 carbons

increase blood glucose

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6
Q

What is the main product of the zona reticularis? What is the effect?

A

Androgens - 19 carbons

testosterone synthesis in testes
estrogen synthesis in ovaries

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7
Q

What is significant about the enzymes in each zone?

A

Each zone has a distinct set of enzymes to produce different hormones- for example the zona glomerulosa lack 17 α-hydroxylase and will only produce mineralocorticoids

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8
Q

Why is it important to know about the enzymes and intermediates in steroidogenesis?

A

important to know because enzyme deficiencies will result in characteristic phenotypes

Deficiencies can be partial, resulting in attenuated clinical symptoms.

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9
Q

What tissues is the adrenal gland derived from?

A

Neuronal (medulla)

Epithelial (cortex)

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10
Q

What is the origin/composition of the medulla?

A

Composed of neural crest-derived chromaffin cells

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11
Q

What is a general effect of cortisol?

A

– Cortisol suppresses formation of neurons and promotes production of epinephrine

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12
Q

What is the blood flow of the medulla? Why?

A

Blood flows from cortex to medulla so cells are constantly exposed to high concentrations of cortisol

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13
Q

What is the percentage of each catecholamine secreted into the blood? Where is it secreted from?

A

Catecholamine-secreted into the blood from the adrenal medulla

80% epi
20% norepi

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14
Q

How is epi and norepi stored?

A

Stored in chromagraffin granules

complexed with ATP, Ca++, chromogranins

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15
Q

What controls synthesis of epi and norepi?

A

Under control of the CRH-ACTH-cortisol axis

  • ACTH stimulates synthesis of DOPA
  • Cortisol increases PNMT- glucocorticoids are necessary for PNMT expression
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16
Q

What triggers release of catecholamine granules?

A

Catecholamines are stored in granules and release is triggered by CNS control (acetylcholine release)
- AKA sympathetic inn.

Released in response to:
stress, exercise, hypoglycemia, and hemorrhagic hypovolemia

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17
Q

What do epi and norepi act on?

A

Act via GPCRs on adrenergic receptors

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18
Q

What are adrenergic receptors classified by?

A

Potency of endogenous and pharmacologic agonists and antagonists

Downstream signaling pathways

Location and density of receptors

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19
Q

What is the primary action and location of alpha 1 receptors?

A

Increases IP3 and Ca++, DAG

Increases vascular smooth mm contraction

At sym postsynaptic nerve terminals

20
Q

What is the primary action and location of alpha 2 receptors?

A

Decreases cAMP

Inhibits norepi release
Inhibits insulin release

sym presynaptic nerve terminals
beta cells on pancreas

21
Q

What is the primary action and location of beta 1 receptors?

A

Increases cAMP

increases cardiac output

In heart tissue, all over

22
Q

What is the primary action and location of beta 2 receptors?

A

Increases cAMP

Increases hepatic glucose output
decrease contraction of blood vessels, bronchioles, uterus

In liver, sm mm of vasculature, bronchioles, uterus

23
Q

What is the primary action and location of beta 3 receptors?

A

Increases cAMP

Increases hepatic glucose output, increases lipolysis

In liver, adipocytes

24
Q

What degrades catecholamines?

A

COMT

MAO

25
Q

What are the actions of aldosterone?

A

Controls Na+ resorption in the extracellular space

– Increases Na+ resorption, increases K+ and H+ secretion (increases expression of Na-K pump and Na/K/Cl pump)

26
Q

How is aldosterone different from ADH?

A

ADH regulates water balance and plasma osmolarity

27
Q

What kind of receptor does aldosterone work on? Where are these receptors located?

A

binds the mineralocorticoid receptor (MR)

In:
kidney
colon
salivary glands
sweat glands
28
Q

What special enzyme do kidney cells have that are responsive to aldosterone?

A

target cells have 11β-HSD2

  • converts cortisol to cortisone
  • cortisone has low affinity for MR

Actions of mineralocorticoids can be limited to aldosterone since cortisol is inactivated in tissues with MR

29
Q

How does lack of aldosterone manifest, symptom-wise?

A

Hyperkalemia
Hypotension
Metabolic acidosis

30
Q

How does excessive aldosterone manifest?

A

Hypokalemia
Hypertension
Metabolic alkalosis

31
Q

What ‘rule’ from renal should you remember when considering aldosterone?

A

H+ tends to follow K+

Aldosterone promotes voiding of K+ and H+
- promotes retention of Na+, H2O follows

32
Q

What is the major regulatory pathway for aldosterone? Is it the same for cortisol?

A

Major: renin angiotensin system

Cortisol is under ACTH regulation

33
Q

What are the steps of the RAAS system?

A

Liver - angiotensinogen
Kidney - renin production

ANG II - Causes an increase in intracellular Ca2+ levels and triggers aldosterone synthesis

34
Q

What induces renin expression?

A

Decreased blood pressure/lower blood volume

Both ANGII and aldosterone increase BP
- both inhibit renin expression

35
Q

Besides RAAS, what also regulates aldosterone production? (minor players)

A

K+

ACTH

36
Q

How does K+ regulation of aldosterone work?

A

Increased extracellular potassium triggers aldosterone synthesis

↑ potassium depolarizes cell membrane and results in an influx of Ca2+, triggers aldosterone synthesis

Regulation: Hyperkalemia → aldosterone secretion → K+ excretion

37
Q

How does ACTH control aldosterone synthesis?

A

Controls the first step in aldosterone synthesis- conversion of cholesterol to pregnenolone

ACTH induces secretion of cortisol, corticosterone, and DOC all of which have weak mineralocorticoid activity

38
Q

What happens to people who oversecrete ACTH?

A

hypertension

39
Q

What is a summary for the actions of cortisol?

A

Increases blood glucose levels

Amino acid mobilization from tissues

Gluconeogenesis in the liver

40
Q

List all 7 actions for cortisol.

A
  1. Increases gluconeogenesis, protein catabolism, lipolysis, and decreases glucose utilization and insulin sensitivity
  2. Anti-inflammatory effects
    •Inhibits phospholipase A2
    •Inhibits histamine and serotonin release
  3. Suppresses immune responses
    •T cell suppression (IL-2)
    •Lyses eosinophils
  4. Maintain vascular responsiveness to catecholamines
    •Maintains normal blood pressure
    •↓ cortisol → hypotension
  5. Inhibition of bone formation
    •Decreases type I collagen
    •Decreases osteoblast activity
    •Decreases gut Ca2+ absorption
  6. Increases glomerular filtration rate (GFR)
    •Causes vasodilation of afferent arterioles
  7. Decreases REM sleep (psychosis)
    •Also increases wake time
41
Q

When do cortisol levels peak? Decrease? What is the name for the pattern of release?

A

Cortisol is released in a diurnal pattern of secretion

  • peaks ~8 am (sounds about right)
  • drops off after 8 pm, stays low through ‘night’ hours

Released in a diurnal pattern

42
Q

What is the immediate action of ACTH?

A

stimulate mobilization of cholesterol and activate cholesterol desmolase

43
Q

What is the long term action of ACTH?

A

stimulate cytochrome P-450 transcription

44
Q

What happens to increased or decreased ACTH levels?

A

↓ ACTH- adrenal atrophy in the fasciculata and reticularis

↑ ACTH- increase adrenal size

45
Q

What happens with excess ACTH?

A

causes hyperpigmentation due to cross-reaction of ACTH with MCR1 on melanocytes or excess production of MSH

46
Q

What are the actions of androgens in females?

A

Presence of pubic and axillary hair, libido

47
Q

What are the actions of androgens in males?

A

Same as testosterone

Men do not need adrenal androgens as they are synthesized in the testes

Endo/Repro (19 decks)

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