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FHB Block 4 > L6- Adrenal Gland Continued > Flashcards

L6- Adrenal Gland Continued Flashcards

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1
Q

What is the primary function of the mineralocorticoids? The secondary function?

A

The mineralocorticoids are hormones that promote sodium retention by the kidney.

Secondarily, they aid in water retention

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2
Q

What is the main mineralocorticoid?

A

Aldosterone

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3
Q

What is the precursor to aldosterone that also has mineralocorticoid action?

A

11-deoxycorticosterone

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4
Q

Which are the primary cells that have aldosterone synthase?

A

Cells of the zona glomerulosa- responsible for the production of aldosterone

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5
Q

What tissues express high levels of MR/therefore are the sites of mineralocorticoid action?

A

Distal tubule in the kidney, colon, salivary ducts and sweat glands.

The main target is the kidney

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6
Q

How does aldosterone affect potassium and sodium in the kidney?

A

Aldosterone stimulates sodium and water reabsorption in the kidney; increases potassium secretion (exchanges Na for K)

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7
Q

What physiologic effect stimulates the release of renin from JGA of the kidney?

A

Decreased blood pressure.

Renin is secreted into the blood and acts like a hormone, although it is not a hormone

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8
Q

What is the action of renin?

A

Cleavage of angiotensinogen (from the liver) to angiotensin I

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9
Q

What enzyme is responsible for the conversion of angiotensin I to the active form, angiotensin II?

A

ACE

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10
Q

What is the action of angiotensin II?

A

Angiotensin II is a vasoconstrictor and stimulates aldosterone release from the zone glomerulosa

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11
Q

Which hormone is the primary regulator of extracellular volume?

A

Aldosterone- stimulates sodium and water reabsorption in the kidneys, stimulates potassium secretion —> increased extracellular fluid volume and blood pressure

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12
Q

What is the primary role of AVP/ADH?

A

Regulator of free water balance -

Stimulates the distal nephron water permeability to increase water retention

This decreases plasma osmolality which secondarily affects sodium concentration in the blood (Na+ is more dilute as more water is reabsorbed from the distal nephron)

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13
Q

How does aldosterone affect change (what happens following binding of aldosterone to the MR)?

A

Aldosterone binding to the mineralocorticoid receptor causes it to dimerize and translocate to the nucleus where it alters transcription of aldosterone-regulated genes

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14
Q

What happens to cortisol in cells that do not have cortisol receptors (GR)?

A

It is converted to the inactive form- cortisone- by 11 beta-HSD2 such that it does not bind to MR

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15
Q

What two hormones bind to the mineralocorticoid receptor?

A

Both mineralocorticoids (aldosterone) and glucocorticoids (cortisol) can bind to and activate the MR.

Glucocorticoids are 10-100 times higher in concentration than mineralocorticoids, but 95% of them are bound to specific binding proteins and therefore biologically inactive

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16
Q

What enzyme is inhibited by carbenoxolone? What is the result?

A

11 beta-HSD2 is inhibited by carbenoxolone. This results in excess MR activation, as cortisol is not converted to its inactive form (cortisone)

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17
Q

What hormones are produced by the zona reticularis?

A

Weak androgens- such as DHEA/DHEAS

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18
Q

DHEA is a precursor for what other hormones?

A

More potent androgens such as testosterone, and also for estrogen

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19
Q

What makes a weak androgen weak?

A

Low binding affinity for androgen receptors

20
Q

In men, 50% of total androgens in the prostate are derived from what?

A

Weak androgen adrenal precurors

21
Q

The STAR protein is stimulated to transport cholesterol into the inner mitochondrial membrane by what hormone? What is cholesterol converted to?

A

ACTH- cholesterol is now converted to pregnenolone

22
Q

The presence/absence of what restricts different zones of the adrenal cortex to producing only certain hormones?

A

The presence/absence of enzymes in the different zones of the adrenal cortex determines which hormones will be synthesized

23
Q

What is the most common cause of congenital adrenal hyperplasia?

A

21 alpha-hydroxylase deficiency

24
Q

What is the result of a 21 alpha-hydroxylase deficiency?

A

Excess androgen production (DHEA) and deficit of mineralocorticoids/glucocorticoids leads to virilization (masculinization), ambiguous genitalia at birth and sodium loss

25
Q

Congenital adrenal hyperplasia deficiencies lead to an increase in what hormone/why?

A

All three enzyme deficiencies (21 alpha-hydroxylase, 11 beta-hydroxylase and 17-hydroxylase) all lead to an increase in ACTH stimulation of the cortex due to lack of negative feedback (all inhibit cortisol production)

Excess ACTH stimulation leads to adrenal hyperplasia

26
Q

What is the major cell type of the adrenal medulla?

A

Chromaffin cells- analogous to a postganglionic post-sympathetic neurons

27
Q

What two hormones are produced in the adrenal medulla?

A

Catecholamines- Epinephrine (most numerous) and norepinephrine

28
Q

What stimulation causes release of EPI and NE from the medulla?

A

Sympathetic stimulation.

EPI and NE are stored in granules in the cells, and released into the blood upon activation.

29
Q

What nerve innervates the adrenal medulla?

A

Splanchnic nerve

30
Q

Other than the adrenal medulla, where else is EPI produced in the body?

A

Nowhere.

The adrenal medulla is the only site of EPI synthesis in the body

31
Q

EPI is released in response to what?

A

Acute stress- pain, cold, perceived danger…

32
Q

NE can be synthesized from what precursor quickly in response to sympathetic stimulation?

A

dopamine

33
Q

What hormone stimulates the conversion of NE to EPI in the adrenal medulla?

A

Cortisol

34
Q

What receptors does EPI act through?

A

Both alpha and beta adrenergic receptors

35
Q

How does EPI affect metabolism?

A

EPI increases glucose release and increases the metabolic rate

36
Q

How does epi affect the cardiovascular system?

A

Vasoconstriction, increases heart rate

37
Q

Differentiate beta-1 from beta-2 receptor location

A

Beta-1 is more important in the heart, beta-2 is more important in skeletal muscle arterioles and the lungs

38
Q

What are the three main targets of epinephrine?

A

Muscle, liver and fat

39
Q

Differentiate the roles of epi and cortisol in response to stress

A

Epi: short-term response to acute stress
Cortisol: long-term response to stress

Acute stress activates the sympathetic nervous system and stimulates the release of NE. NE stimulates CRH to initiate the HPA response to long-term stress

Generally, they both work by mobilizing and redistributing energy stores, and increasing the cardiovascular responsivity

40
Q

What is the half-life of catecholamines?

A

Very short- 10 seconds to 1.5 minutes

41
Q

Catecholamines are degraded by what two enzymes?

A

COMT (catechol-O-methyltransferase) and MAO (monoamine oxidase)

42
Q

What is the metabolic by-product of catecholamine metabolism?

A

vanillylmandelic acid (VMA), which is excreted in the urine

43
Q

What can VMA levels be used to detect?

A

VMA levels can be used to clinically detect tumors producing excess EPI or NE

44
Q

What are pheochromocytomas?

A

Tumors originating from chromaffin cells- leading to overproduction of catecholamines

45
Q

What are the symptoms of pheochromocytomas?

A

Hypertension (with no response to medication), headaches and tachycardia

46
Q

How are pheochromocytomas diagnosed? How are they treated?

A

Diagnosis: Measurements of urinary metanephrines - metabolic by-products of EPI and NE
Treatment: surgery, with use of alpha/beta blockers to block their effects

47
Q

What is known as the 10% tumor?

A

Pheochromocytomas.
10% are: malignant, bilateral, in children, familial, recurrent after 5-10 years, associated with MEN syndrome, present with a stroke and extra-adrenal

FHB Block 4 (15 decks)

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