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L42, 43 The Adrenal Gland Flashcards

1
Q

What are the two main parts of the adrenal glands?

A

Cortex and Medulla.

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2
Q

What is the key enzyme family involved in corticosteroid synthesis?

A

P450 cytochrome enzymes.

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2
Q

What hormones are produced by the adrenal cortex?

A

Corticosteroids (Glucocorticoids and Mineralocorticoids) and Androgens.

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2
Q

What are corticosteroids?

A

Steroid hormones produced in the adrenal cortex.

Includes:

Glucocorticoids: Affect glucose metabolism (e.g., cortisol).

Mineralocorticoids: Regulate salt and water balance (e.g., aldosterone).

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2
Q

What is the adrenal cortex hormone precursor?

A

Cholesterol.

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3
Q

What are the three zones of the adrenal cortex from outermost to innermost and hat does each adrenal cortex zone primarily produce?

A

Zona glomerulosa → Mineralocorticoids (Aldosterone)

Zona fasciculata → Glucocorticoids (Cortisol)

Zona reticularis → Androgens

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4
Q

What are adrenal glands?

A

Paired endocrine glands located above the kidneys (one on each kidney).

Each gland consists of two parts:

Adrenal Cortex (outer layer) — produces corticosteroids and androgens.

Adrenal Medulla (inner part) — produces catecholamines (adrenaline, noradrenaline).

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5
Q

What is the medulla of the adrenal gland?

A

Specialized sympathetic ganglion.

Produces catecholamines: adrenaline (epinephrine) and noradrenaline (norepinephrine).

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6
Q

What is the starting material for steroid hormone synthesis?

A

Cholesterol.

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7
Q

How does cholesterol reach the mitochondria?

A

Via Steroidogenic Acute Regulatory protein (StAR) — controls transport from outer to inner mitochondrial membrane (RATE-LIMITING STEP).

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8
Q

How is cholesterol converted to pregnenolone?

A

Enzyme: Cytochrome P450 side chain cleavage enzyme (P450scc, CYP11A1).

Location: Inner mitochondrial membrane.

Reaction: Cleavage between carbon atoms 20 and 22 of cholesterol.

Keywords:

Pregnenolone: Precursor molecule for all adrenal steroids.

P450scc (CYP11A1): Catalyzes cholesterol cleavage.

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9
Q

What regulates P450scc?

A

Requires electrons from adrenodoxin reductase and adrenodoxin.

Stimulated by ACTH (Adrenocorticotropic hormone).

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10
Q

What are glucocorticoids?

A

Class of corticosteroids that regulate metabolism of carbohydrates, proteins, and fats.

Main glucocorticoids: Cortisol and Corticosterone.

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11
Q

How is cortisol transported in the blood?

A

Bound to:

Transcortin (CBG): ~80%

Albumin: ~10%

~5–10% remains free and active.

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12
Q

How does cortisol act on cells?

A

Binds to Glucocorticoid Receptors (GRs) inside the cell.

GR-cortisol complex binds to Glucocorticoid Response Elements (GREs) on DNA to regulate gene expression.

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13
Q

How is ACTH made?

A

Derived from a large precursor protein called pro-opiomelanocortin (POMC).

Processing by prohormone convertase creates ACTH and other peptides (α-MSH, CLIP).

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14
Q

*

How does ACTH regulate adrenal steroidogenesis?

A

Binds to receptors on adrenal cortex cells.

Stimulates cAMP production → activates protein kinase A → increases expression of steroidogenic enzymes (e.g., StAR, CYP11A1).

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15
Q

Metabolic effects of cortisol?

A

Carbohydrates: Increases plasma glucose via gluconeogenesis; inhibits glucose uptake into tissues.

Proteins: Promotes muscle protein breakdown into amino acids for gluconeogenesis.

Fats: Stimulates lipolysis and redistributes fat to trunk and face.

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16
Q

Effects of cortisol on bones?

A

Decreases calcium absorption from gut.

Increases calcium excretion in kidneys.

Inhibits osteoblast activity → Osteoporosis risk.

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17
Q

Effects of cortisol on immune system?

A

Decreases lymphocytes and eosinophils.

Increases neutrophils, red blood cells, platelets.

Reduces inflammation by inhibiting cytokine production and leukocyte migration. ALL THIS WEAKENS IMMUNITY

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18
Q

What is Cushing’s syndrome?

A

Condition caused by prolonged exposure to high cortisol levels.

Causes:

  • Pituitary tumor producing excess ACTH (Cushing’s disease).
  • Ectopic ACTH-producing tumors.
  • Adrenal adenomas.
  • Iatrogenic (prolonged steroid therapy).

Symptoms:
- Central obesity, moon face, buffalo hump.
- Muscle wasting.
-Purple striae.
-Hypertension.
- Osteoporosis.

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19
Q

What is Addison’s disease?

A

Primary adrenal insufficiency (autoimmune destruction of adrenal cortex).

Symptoms:

  • Fatigue, weight loss, hypotension, hyperpigmentation, electrolyte imbalances.

Treatment:

  • Cortisol replacement therapy (hydrocortisone).
  • Sometimes mineralocorticoid (fludrocortisone) replacement.
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20
Q

What is aldosterone?

A

Mineralocorticoid hormone that regulates sodium and potassium balance, blood volume, and blood pressure.

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21
Q

How is aldosterone synthesised?

A

Cholesterol → Pregnenolone (CYP11A1)

Pregnenolone → Progesterone (HSD3B2)

Progesterone → 11-Deoxycorticosterone (CYP21A2)

11-Deoxycorticosterone → Corticosterone (CYP11B1)

Corticosterone → 18-Hydroxycorticosterone → Aldosterone (CYP11B2, Aldosterone synthase).

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22
What regulates aldosterone secretion?
Major regulators: Renin-angiotensin system, plasma K⁺ concentration. Minor regulator: ACTH.
23
How does aldosterone act?
Binds Mineralocorticoid Receptors (MRs) in kidneys. Stimulates: - Na⁺ reabsorption - K⁺ and H⁺ excretion - Water reabsorption → Increase in blood pressure.
24
What prevents cortisol from activating MR? | mineralcorticoid receptors
11β-Hydroxysteroid dehydrogenase type 2 (11β-HSD2): Converts cortisol to cortisone, which does not activate MR.
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# mineralcorticoid-related disease What is Conn’s syndrome?
Primary hyperaldosteronism (adrenal adenoma causing excess aldosterone). Symptoms: - Hypertension -Hypokalemia (low K⁺) -Metabolic alkalosis. Treatment: -Surgical removal of tumor. -Spironolactone (aldosterone antagonist).
26
What is the adrenal medulla?
Inner part of adrenal gland. Acts as modified sympathetic ganglion. Releases adrenaline (80%) and noradrenaline (20%) into circulation.
27
How is adrenaline synthesised?
1. Tyrosine → L-DOPA (tyrosine hydroxylase; rate-limiting step). 2. L-DOPA → Dopamine (DOPA decarboxylase). 3. Dopamine → Noradrenaline (dopamine β-hydroxylase). 4. Noradrenaline → Adrenaline (PNMT; stimulated by cortisol).
28
How is catecholamine release regulated?
Sympathetic nervous system activation. Stressors via hypothalamus. ACTH and cortisol stimulate production but NOT feedback inhibition.
29
How is catecholamine action terminated?
1. Reuptake into nerve terminals. 2. Metabolism by: - COMT (catechol-O-methyltransferase) - MAO (monoamine oxidase) 2. Final metabolite: VMA (Vanillylmandelic Acid), excreted by kidneys.
30
What is Phaeochromocytoma?
Tumor of chromaffin cells in adrenal medulla → Overproduction of catecholamines. Symptoms: - Episodic severe hypertension. - Headache. - Sweating. - Palpitations. - Anxiety. Diagnosis: - Measure urinary VMA and metanephrines. - MIBG scan of adrenal glands. Treatment: - Surgery (α-blocker first, then β-blocker to avoid hypertensive crisis).
31
How does the body respond to stress involving the adrenal gland?
Hypothalamus secretes CRH → Pituitary releases ACTH → Adrenal cortex secretes cortisol (stress hormone). Sympathetic nervous system activates adrenal medulla → Releases adrenaline and noradrenaline.
32
Besides emotional stress, what else can stimulate ACTH release?
Biochemical stressors such as: - Hypoglycemia (low blood sugar) - Surgery - Infection - Trauma - Physical exercise These activate the hypothalamus → CRH release → stimulates ACTH production.
33
What is the "escape" phenomenon in aldosterone physiology?
Although aldosterone increases Na⁺ and H₂O reabsorption, extracellular fluid (ECF) volume only rises by about 15%. Why? Increased atrial natriuretic peptide (ANP) secretion. Pressure natriuresis (kidneys excrete Na⁺ to prevent excessive volume overload).
34
How does excessive liquorice ingestion cause hypertension?
Liquorice inhibits 11β-HSD2 enzyme in kidneys. This prevents cortisol from being inactivated to cortisone. Cortisol activates mineralocorticoid receptors (MRs) → mimicking aldosterone effects → sodium retention, potassium loss → Severe hypertension despite low aldosterone levels.
35
What are features of AME? | apparent mineralcorticoid excess
Severe hypertension Hypokalemia (low potassium) Low renin and aldosterone levels.
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What are dexamethasone and betamethasone?
- Synthetic glucocorticoids. - High potency at the glucocorticoid receptor. - Long duration of action (longer half-life compared to hydrocortisone). Uses: - Suppress inflammation - Treat autoimmune diseases - Used in fetal lung maturation (preterm birth risk).
39
What happens if the adrenal medulla is destroyed?
No significant clinical symptoms. Sympathetic nervous system compensates adequately by direct innervation of tissues. Examples of destruction: malignant invasion of adrenal glands.
40
How do adrenal glands integrate the body’s response to stress?
Two parallel arms: 1. Hypothalamic-Pituitary-Adrenal (HPA) Axis CRH → ACTH → Cortisol → Increases blood glucose, suppresses inflammation, supports energy metabolism. 2. Sympathetic Nervous System (SNS) + Adrenal Medulla Direct SNS stimulation → Adrenaline release → Rapid heart rate, bronchodilation, mobilization of glucose and fatty acids. ✅ Together: maintain homeostasis during stress.
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Why is pregnenolone considered the 'bottleneck' of adrenal steroid hormone synthesis?
Pregnenolone is the first steroid formed from cholesterol inside mitochondria (via CYP11A1). It is the precursor for ALL adrenal steroids: glucocorticoids, mineralocorticoids, and androgens. More pregnenolone = more steroid hormone production overall. Without pregnenolone, no adrenal steroids can be synthesized.
51
How does ACTH stimulate cortisol production at the cellular level?
ACTH binds to the Melanocortin 2 receptor (MC2R) on adrenal cortex cell membranes. This activates adenylyl cyclase, increasing cAMP levels. cAMP activates protein kinase A (PKA) → promotes expression of steroidogenic enzymes and StAR protein. End result: Enhanced cortisol synthesis.
51
What is the "aldosterone escape" phenomenon?
Even though aldosterone promotes Na⁺ and water retention, extracellular fluid (ECF) volume increases only about 15%. Mechanisms limiting fluid overload: - Atrial natriuretic peptide (ANP) release. - Pressure natriuresis: kidneys excrete excess sodium and water.
51
What is the difference between Cushing’s disease and Cushing’s syndrome?
Cushing's disease: Excess cortisol caused specifically by a pituitary ACTH-secreting tumor. Cushing’s syndrome: General term for excess cortisol, regardless of cause (e.g., adrenal tumor, ectopic ACTH production, or steroid therapy).
51
Where are 11β-HSD1 and 11β-HSD2 enzymes located, and what do they do?
11β-HSD1: - Found in: Liver, adipose tissue, brain. - Function: Converts inactive cortisone → active cortisol. 11β-HSD2: - Found in: Kidneys, colon. - Function: Converts active cortisol → inactive cortisone to protect mineralocorticoid receptors from cortisol.
51
What are the clinical consequences of adrenal medulla destruction?
None significant. The sympathetic nervous system compensates adequately through direct innervation of tissues. Loss of adrenal medulla is not life-threatening, but medical teams should be informed if the medulla is removed surgically.
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Why are catecholamine metabolites measured for diagnosing Phaeochromocytoma?
Plasma adrenaline levels fluctuate rapidly (second-to-second) and are unreliable. Metabolites (VMA, metanephrines) are stable and provide a more accurate reflection of chronic catecholamine secretion. Urinary VMA levels are commonly used.

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