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Phys II Unit II > 4 Adrenal Gland > Flashcards

4 Adrenal Gland Flashcards

1
Q

The main hormones produced by the adrenal gland belong to what two families?

A

Steroids
• Glucocorticoids
• Mineralocorticoids
• Androgens

Catecholamines
• Epinephrine
• Norepinephrine

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2
Q

Blood supply to the adrenal glands?

A

Receive rich supply of blood from SUPRARENAL arteries (Superior, Middle, Inferior) and venous return by a SINGLE vein

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3
Q

What size are the adrenals?

A

Small, averaging 3-5 cm in length and 1.5-2.5g in weight

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4
Q

Blood flow in the adrenals is in a __________ system, which is important in modulating the activities of enzymes in the adrenal medulla

A

Sinusoid

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5
Q

What are the three layers of the adrenal cortex?

A

Outward to Inward:

Zona glomerulosa —> Aldosterone

Zona fasciculata —> Cortisol

Zona reticularis —> Andgrogens

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6
Q

Synthesis of cortisol and adrenal androgens is under ___________ control while aldosterone is regulated by __________.

A

Cortisol/androgens —> Pituitary ACTH control

Aldosterone —> RAAS and ACTH (but mostly RAAS…)

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7
Q

The adrenal medullae are the extension of, and under control of __________.

A

The sympathetic nervous system

Activation —> release of Epi/NE

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8
Q

Steroid hormones are derived from _______.

A

Cholesterol

Basis for the specialization of steroid synthesis is the presence or absence of enzymes within the different layers of the cortex.

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9
Q

__________ are used clinically to determine the body’s steroid production levels.

A

Urinary ketones

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10
Q

Steroid hormones share this initial step in their biosynthesis:

A

Conversion of cholesterol to pregnenolone via the enzyme Desmolase (aka P450scc or CYP11A1)

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11
Q

Mobilization of cholesterol for the biosynthesis of steroids is mediated by:

A

ACTH, ANG II receptor, and K+ channels

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12
Q

Cholesterol for steroid biosynthesis is derived from:

A

LDL particles from diet

Hydrolysis of cholesterol esters from vesicles

de novo synthesis from acetyl CoA

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13
Q

Free cholesterol is transferred to the mitochondria, then to the inner mitochondrial membrane by…

A

Steroidogenic acute regulatory protein (STaR)

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14
Q

What is the rate-limiting step in adrenal steroid biosynthesis, and upon what does it depend?

A

Conversion of cholesterol to pregnenolone with desmolase, and it depends on STaR

All layers of the cortex contain cholesterol desmolase, which is stimulated by ACTH

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15
Q

In addition to ACTH melanocortin receptors, the zona glomerulosa also has ______________

A

Ang II receptors and K+ channels - key for the regulation of aldosterone synthesis

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16
Q

The zona glomerulosa lacks __________ and preferentially synthesizes __________

A

Lacks 17a-hydroxylase (so can’t produce androgens or cortisol)

Preferentially synthesizes and secretes aldosterone

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17
Q

What are the secretagogues for aldosterone synthesis

A

ANG II*****

Plasma [K+]

ACTH

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18
Q

What is the MOST important secretagogue for aldosterone synthesis?

A

ANG II - the product of the renin-angiotensin cascade

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19
Q

What is the second most important secretagogue in aldosterone synthesis?

A

Plasma [K+]

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20
Q

What is the LEAST important secretagogue in aldosterone synthesis?

A

ACTH - the effect is weak though

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21
Q

Aldosterone is released in response to what physiologic conditions?

A

Decrease in BP or decrease in ECF volume (ie hemorrhage, diarrhea, vomiting)

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22
Q

As a result of aldosterone secretion

A

Water and sodium are retained —> increased circulating volume and increased renal perfusion

Tubular Na+ and Cl- reabsorption, K+ excretion, water retention occur in the DISTAL TUBULE

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23
Q

How does aldosterone bind in the distal tubule?

A

Binds to an intracellular mineralocorticoid receptor (MR1), which then binds to a mineralocorticoid responsive element (MRE) —> Na+ reabsorption, K+ secretion, H+ excretion

Net effect: expansion of extracellular fluid

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24
Q

What is Conn’s Syndrome?

A

PRIMARY HYPERaldosteronism, caused by an aldosterone-secreting tumor.

Classic findings:
• Increased Na+ reabsorption —> HYPERnatremia, fluid retention, HTN
• Increased K+ secretion —> HYPOkalemia
• Increased H+ secretion —> metabolic ALKAlosis
• LOW renin levels (b/c HTN)

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25
Q

How does 17a-hydroxylase deficiency presentation differ from Conn syndrome?

A

Same SSx (HTN, Hypokalemia, metabolic alkalosis) but reduced aldosterone levels b/c corticosteroid excess

26
Q

How do the SSx and 17a-hydroxylase deficiency develop?

A

Glucocorticoids and androgens are not produced (or if so, very little)

Steroid intermediates build up in the Aldosterone pathway due to the 17a block —> promoting mineralocorticoid production

Results in overproduction of 11-deoxycorticosterone and corticosterone, which both have mineralocorticoid function, so little aldosterone is produced

Aldosterone levels are low, b/c of the corticosterone excess and HTN inhibiting renin secretion

27
Q

The zona fasciculata lacks which enzymes?

A

Aldosterone synthase —> no aldosterone

17,20 lyase —> no androgens

28
Q

What is the major product of the zona fasciculata?

A

Cortisol (glucocorticoid)

29
Q

What are the main steps in the regulation of cortisol secretion?

A

Corticotrophin releasing hormone (CRH) from hypothalamus stimulates corticotrophs to release ACTH from anterior pituitary

ACTH stimulates adrenal gland growth and transfers cholesterol into the mitochondria and activates cholesterol desmolase

Cortisol feeds back to directly inhibit CRH

30
Q

What is the only adrenal steroid to feed back and inhibit CRH release from the hypothalamus?

A

CORTISOL!

31
Q

Cortisol levels in the blood reflect a ____________ release of ACTH

A

Circadian and pulsatile

Greatest cortisol secretory activity occurs in the morning and drops throughout the day and evening. ACTH also reflects CRH secretion

During sleep, levels begin to increase and peak shortly after awakening.

32
Q

During periods of stress, ACT secretion is enhanced and is the result of …

A

Increased AMPLITUDE of CRH bursts, rather than frequency

33
Q

The overall metabolic effect of cortisol is to …

A

Increase blood glucose, by enhancing gluconeogenesis

34
Q

Main ways in which cortisol increases blood glucose

A

PROTEIN CATABOLISM - providing amino acids. Protein synthesis is decreased and tissues targeted are muscle and connective tissue

LIPOLYSIS - providing glycerol

Also decreases glucose uptake by tissues

The effect of cortisol is essential for survival during fasting and stress

35
Q

Cardiovascular actions of cortisol

A

Need cortisol for catecholamines to do their job (permissiveness!)

Maintenance of normal BP

Permissive for alpha-1 receptor responsiveness (up-regulates this receptor)

36
Q

Actions of cortisol on bone

A

Inhibition of bone formation

Decreases intestinal and renal calcium absorption, decreasing plasma calcium —> mobilizing calcium from bone

Excessive use of glucocorticoids or chronically high plasma levels of cortisol (from stress) result in BONE LOSS and more fractures

37
Q

Actions of cortisol on connective tissue and muscle

A

Cortisol inhibits fibroblast proliferation and collagen formation

With high amounts of cortisol, the skin things and connective tissue support of capillaries is impaired

Increased proteolysis in muscle, leading to weakness

38
Q

Anti-inflammatory effect/immune actions of cortisol

A

Induces synthesis of lipoprotein, which inhibits phospholipase 2, preventing the release of prostaglandins and leukotrienes

Inhibits production of IL-2. Inhibits release of histamine and serotonin from mast cells

A cortisone shot —> converted to cortisol by liver —> anti-inflammatory effects (but takes 24+ hours to take effect)

39
Q

Disease characterized by decreased synthesis of all adrenocortical hormones as a result of autoimmune destruction of the adrenal gland.

A

Addison’s Disease (Primary adrenocortical insufficiency)

Loss of cortisol —> hypoglycemia during stress, weight loss, muscle weakness

Loss of aldosterone —> hyperkalemia, hypotension, metabolic acidosis, salt craving

Loss of androgens —> In women, decreased pubic and auxiliary hair, decreased libido (doesn’t really affect men b/c their balls also make androgens)

40
Q

Why do individuals with Addison’s disease have hyperpigmentation of skin on elbows, knees, nipples, and scars?

A

Results from increased ACTH secretion (b/c no cortisol feedback). The POMC gene that produces ACTH also contains the a-MSH fragment —> increase melanin (MSH = melanocyte stimulating hormone)

41
Q

Why are cortisol and androgen low but aldosterone normal in secondary or tertiary adrenocortical insufficiency?

A

Because the problem is either CRH insufficiency (tertiary) or failure of corticotrophs to adequately secrete ACTH (secondary) —> low plasma ACTH

Cortisol and androgen production are regulated primarily by ACTH so they will be low but Aldosterone is primarily regulated by RAAS, so they stay normal

Hyperpigmentation does not occur b/c POMC levels are low

42
Q

Cushing’s Syndrome and Cushing’s Disease have the same SSx but the Syndrome is the result of ________ while the disease is from _________.

A 
Syndrome = Primary adrenal hyperplasia
Disease = excess ACTH
43
Q

SSx of Cushing’s Syndrome/Disease

A

Excess glucocorticoids and androgens

Hyperglycemia
Increased proteolysis
Thin skin, easy bruising
Muscle wasting
Central obesity 
Mood face
Acne (androgen driven)
Buffalo hump 
Hypertension
Virilization (androgen driven)

If Syndrome —> LOW ACTH but HIGH cortisol/androgens
If Disease —> HIGH ACTH

44
Q

What organ can also secrete ACTH —> Cushing’s disease?

A

The lungs

45
Q

The major source of androgens for males is …

A

The testes

For females it’s the adrenal cortex for the development of pubic and axillary hair and libido

46
Q

Androgens are also referred to as…

A

17-ketosteroids (because they have a ketone group on C17 🙄

47
Q

21ß-hydroxylase deficiency in uterine results in…

A

Masculinization of the female —> penis-like clitoris and scrotum-like labia

B/c no conversion of progesterone to 11-deoxycorticosterone or of 17-hydroxyprogestrone to 11-deoxycortisol

Also results in sodium loss and hypoglycemia (b/c not producing glucocorticoids or mineralocorticoids either)

Steroid intermediates build up above block and are converted to androgens leading to adrogenital syndrome and increased 17-ketosteroids in urine

48
Q

What ACTH level would you expect in 21ß-hydroxylase deficiency?

A

High, because the lack of feedback control of cortisol on pituitary. Trophic effect of ACTH is seen

49
Q

Synthesis of catecholamines occurs in..

A

Chromaffin cells of the adrenal medullae

Tyrosine conversion to DOPA and then to dopamine occurs in cytosol.

Dopamine enters granules and is converted to NE

Some NE is stored but most is released back into the cytosol and converted to epinephrine (renters granules for storage)

50
Q

____mg of catecholamines are stored

A

5 mg

85% granules store epi
15% store NE

51
Q

Rate limiting step in catecholamine synthesis

A

Tyrosine hydroxylase converting Tyrosine to DOPA

Acute stimulation —> acute activation of tyrosine hydroxylase activity

Chronic stimulation —> increased expression and concentration of tyrosine hydroxylase

52
Q

What activates the last step of catecholamine synthesis (NE to Epi via phenylethanolamine-N-methyltransferase)?

A

CORTISOL!

53
Q

When are catecholamines secreted?

A

Secretion is integral to flight or fight response: perception or anticipation of fear and danger, excitement, and/or trauma

Secretion is also enhanced with hypotension, shock, HF, hypoglycemia

Essentially, it’s an extension fo the neural system

54
Q

Catecholamine effects are …

A

Rapid and short lived. Half time is ~2 minutes

Epinephrine mobilizes fuels in times of stress —> increased glycogenolysis, gluconeogenesis, glucagon secretion, lypolysis; inhibition of glycogen synthesis and insulin secretion

Why mobilize glucose? To sustain it for CNS use

55
Q

What are the CV effects of catecholamines?

A

Increased cardiac contractility

Increased HR

Increased conduction

Increased BP

Increased arteriolar vasoconstriction (esp in renal, splanchnic, and cutaneous beds) to divert blood to muscle and heart

56
Q

Non-CV effects of catecholamines

A

Bronchiolar dilation
Dilation of pupils
Decreased GI activity
Increased alertness

57
Q

The two main enzymes for the degradation of catecholamines?

A

Monoamine oxidase (MAO) - predominant mechanism for NE, occurs mostly in neuronal cytoplasm

Catechol-0-methyltransferase (COMT) - predominant mechanism for Epi, occurs mostly in heart, liver, kidney

58
Q

End product of catecholamine metabolism

A

3-Methoxy-4-hydroxymandelic acid (aka Vanillylmandelic acid or VMA)

Serves as index of SNS activity or pathology - excreted in urine so can be measured there.

59
Q

Adrenomedullary dysfunction is …

A

VERY RARE

Hypofunction: usually surgical removal

Hyperfunction: Pheochromocytoma (catecholamine-secreting tumor—> 20x normal levels) - will have high VMA levels

60
Q

Clinical manifestations of pheochromocytoma

A

HTN, rapid pulse, chest pain

Excessive sweating, HA

Hyperglycemia, fatigue

Usually found in 40s-50s

Phys II Unit II (9 decks)

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