The Adrenal Glands Flashcards by Zach Visinoni

ZG —>
ZF —>
ZR —>
AM—>

ZG - mineralcorticoids
ZF - glucocorticoids
ZR - androgens
AM - NE/Epi

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What H regulates the HPA axis?

Cortisol

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What is the effect of cortisol on immunity, liver, muscle, and adipose?

Immunity is decreased.
GNG is active in the liver.
Protein catabolism is activated in muscle.
Lipolysis is activated in adipose.

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What activates the release of CRH?

Stress and the circadian rhythm.

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What is the effect of endogenous cortisol?

Has the same negative effect on ant pit and hypothalamus.

It may lead to a shut down of ACTH production and lead to atrophy of cortisol-producing cells.

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What are the symptoms of Cushing’s Dz?

Obesity
Moon face
Buffalo hump
HTN
Edema
Weakness
Osteoporosis
DM
Acne

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What is the dexamethasone suppression test useful for?

To r/o or r/i Cushing’s Dz.

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What is the function of low dose dexamethasone suppression test?

To indicate pts with CS from others.
If it does not suppress ACTH levels, then it indicates CS.
Cannot be used to specify the source of excess ACTH.

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What is the function of the high dose dexamethasone suppression test?

To determine whether the excess ACTH is from a pituitary-secreting tumor or non-pituitary-secreting tumor.
Performed after the low dose test.

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What happens to levels of CRH, ACTH, and cortisol when there is an adrenal tumor?

CRH: dec.
ACTH: dec.
Cortisol: inc.

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What happens to levels of CRH, ACTH, and cortisol with a pituitary tumor?

CRH: dec
ACTH: inc
Cortisol: inc

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What happens to CRH, ACTH, and cortisol levels when there is an ectopic ACTH-secreting tumor?

CRH: dec
ACTH: dec
Cortisol: inc

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What happens to CRH, ACTH, or cortisol levels during the latrogenic effect?

CRH: dec
ACTH: dec
Cortisol: dec

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What are 4 major causes of glucocorticoid excess (CS)?

Exogenous glucocorticoids (latrogenic)
Pseudo Cushing’s DZ (from anxiety, depression, alcoholism)
ACTH-dependent tumors (ACTH or CRH-secreting tumors)
ACTH-independent tumors (adrenal adenoma/carcinoma)

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In a high dose dexamethasone suppression test, what is suggested by low ACTH levels post administration of dexamethasone?

A pituitary tumor

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In a high dose dexamethasone suppression test, what is indicated by no change in ACTH post administration of dexamethasone?

An ectopic tumor

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What is the plasma [ACTH] in CS patients?

About 90-200 pg/mL ACTH

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What is the primary action of aldosterone?

Increase renal sodium absorption

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4 steps of aldosterone mechanism at the distal nephron

Aldo binds an IC R.
Initiates transcription in nucleus.
Translation of proteins for new channels and pumps.
Increase Na+ reabsorption and increase K+ secretion.

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What membrane proteins allow for Na+ and K+ movement across cell membranes? (3)

Luminal K+ efflux channel
Luminal Na+ influx channel
Basolateral Na+/K+ ATPase

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How is ACTH produced at the ant pit?

What kind of hormone is ACTH?

Post-translational modifications of POMC.

Peptide H.

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How is a-MSH made? Where is it made?

Further processing from POMC —> ACTH —> a-MSH.

In non-pituitary tissues.

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What’s used to detect adrenal gland insufficiency?

Cosyntropin (synthetic ACTH) stimulation test.

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What is the big picture mechanism of the cosyntropic stimulation test?

See notes

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Normal HPA axis

CRH —> AP to produce ACTH —> AG to produce aldosterone and cortisol. RAAS can also act on the AG.

Primary adrenal insufficiency is a problem where? Secondary AI is a problem where? Tertiary AI is a problem where?

1: problem at AG 2: problem at pituitary gland 3: problem at hypothalamus

Causes of primary AI (Addison’s DZ) (4)

1. Autoimmune DZ. 2. Adrenal hemorrhage. 3. Infection (Tb, N. Meningitis). 4. Tumor Mets to AG.

What are 2 causes of adrenal hemorrhage that can lead to primary AI?

Waterhouse-Friedrichsen syndrome: due to N. Meningitis. | Anti-coagulation therapy.

What’s the TTM for AI generally?

Hs that AGs cannot make anymore (replacements for cortisol and/or aldosterone).

What is fludrocortisone?

A replacement drug for aldosterone.

What kind of replacements will pts with secondary AI need?

Cortisol replacement, but not usually aldosterone replacement due to presence of RAAS.

Primary adrenal excess effect on cortisol, CRH, ACTH, hyperpigmentation?

Cortisol: inc CRH: dec ACTH: dec Hyperpigmentation: No

Secondary adrenal excess effect on cortisol, CRH, ACTH, hyperpigmentation?

Cortisol: inc CRH: dec ACTH: inc Hyperpigmentation: Yes

Primary cortisol deficiency effect on cortisol, CRH, ACTH, and hyperpigmentation:

Cortisol: dec CRH: inc ACTH: inc Hyperpigmentation: Yes

Secondary cortisol deficiency effect on cortisol, CRH, ACTH, and hyperpigmentation:

Cortisol: dec CRH: inc ACTH: dec Hyperpigmentation: No

Steroid therapy effect on cortisol, CRH, ACTH and hyperpigmentation:

Cortisol: dec CRH: inc ACTH: dec Hyperpigmentation: No

Primary hyperaldosteronism cause:

Increased aldosterone from AC

What’s Conn’s syndrome?

Adenoma in adrenal cortex that can lead to primary hyperaldosteronism.

Secondary hyperaldosteronism cause:

From increased renin from JGCs.

What is PAC to PRA ratio useful for?

Detecting primary hyperaldosteronism

How does the PAC to PRA ratio test work?

See notes

What enzyme causes cholesterol —> pregnenolone?

Cholesterol desmolase.

What is the 17a-hydroxyl are enzyme active in?

Cortisol and androgen synthesis

What is the 21b-hydroxylase enzyme active in?

Aldosterone and cortisol synthesis

What is the 11b-hydroxylase enzyme active in?

Aldosterone and cortisol synthesis

How are congenital adrenal enzyme deficiencies characterized?

Enlargement of both AGs due to increased ACTH due to low cortisol.

Deficiencies in which enzymes can cause _______?

17a-hydroxylase, 21b-hydroxylase and 11b-hydroxylase can l=cause congenital adrenal hyperplasia.

Low 17a-hydroxylase effects on MCs, cortisol, androgens, BP, [K+]

``` 17a is in cortisol and androgen synthesis. MCs: inc Cortisol: dec Androgens: dec BP: inc [K+]: dec ```

Deficiency in 21b-hydroxylase effects on MCs, cortisol, androgens, BP, [K+], renin:

``` 21b-hydroxylase is active in aldosterone synthesis and cortisol synthesis. MCs: dec Cortisol: dec Androgens: inc BP: dec [K+]: inc Renin: inc ```

Deficiency of 11b-hydroxylase effect on MCs, cortisol, androgens, BP, [K+], renin:

``` 11b-hydroxylase is active in aldosterone and cortisol synthesis. MCs: dec (inc DOC) Cortisol: dec Androgens: inc BP: inc [K+]: dec Renin: dec ```

What’s a pheochromocytoma?

Usually a benign and UL AG tumor that increases catecholamine secretion.

How much catecholamine secretion is E vs. NE?

80% epi, 20% NE

What controls the E/NE synthesis?

CRH-ACTH-cortisol axis

In catecholamine synthesis, what does ACTH activate?

Production of DOPA

What is the effect of cortisol on catecholamine synthesis?

Increases PNMT to increase Epi.

Draw the MOA of NE/E synthesis and executors is

See notes

What is NE/E stored in?

Chromaffin granules that contain ATP, Ca2+ and chromogranins.

What is the function of chromogranins?

Thought to lower osmotic burden of storing NE/E in granules.

Circulating chromogranins can be used as a marker for what?

Sympathetic paraganglion-derived tumors, AKA paragangliomas.

Degradation of catecholamines

See notes

What can be used as a measure of catecholamine product? (4)

NE Epi Metanephrine VMA

How is a DX of Pheochromocytoma confirmed?

Increased levels of catecholamines and their byproducts.

Alpha-1 receptor MOA Tissues Actions

MOA: Gq (inc IP3/DAG) Tissues: SNS nerve terminals Actions: contraction of vascular SM.

Alpha-2 receptor MOA Tissues Actions

MOA: Gi (inhibit cAMP) Tissues: SNS nerve terminals and beta cells of pancreas. Actions: inhibit NE release, inhibit insulin release.

Beta-1 receptor MOA Tissues Actions

MOA: Gs (inc cAMP) Tissues: heart Actions: inc C.O.

Beta-2 receptor MOA Tissues Actions

MOA: Gs (inc cAMP) Tissues: liver, SM of BVs, bronchioles and uterus. Actions: inc liver glucose output, dilation of BVs, bronchioles, uterus.

Beta-3 receptor MOA Tissues Actions

MOA: Gs (inc cAMP) Tissues: liver and adipose. Actions: inc liver glucose output and inc lipolysis.

Alpha and beta-3 receptors prefer which catecholamine?

Prefer NE>epi

Which catecholamine does the beta-1 receptor prefer?

It has no preference

What catecholamine doe the beta-2 receptor prefer?

Prefers Epi>NE