03a: Adrenals Flashcards by Nuna H

Most, (X)%, of the adrenal gland is composed of (cortex/medulla).

X = 80-90

Cortex

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List the specific (X) steroid hormones produced by the zona reticularis.

X = androgen;

DHEA
DHEAS
Androstenedione

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Loss of adrenal (cortex/medulla) results in death within (X) period of time. What are the two main mechanisms behind this?

Cortex;
X = 1-2 weeks

Circulatory collapse (from Na depletion)
Hypoglycemia (if caloric intake limited)

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Secretion of (steroids/catecholamines) from adrenals represents de novo synthesis, since they can’t be adquately stored. Explain.

Steroids;

Lipid-soluble and simply diffuse across membrane to enter circulation

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T/F: Corticosteroids simply diffuse out into the circulation and travel as free hormones.

False - bound to protein (CBG or albumin) in plasma

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Most adrenal steroids in circulation are (free/bound). Those that are bound: to which protein(s)?

Bound;

Transcortin, aka CBG (corticosteroid binding globulin)
Albumin

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Most adrenal corticosteroids are bound to (X) in plasma. And androgens to (Y).

X = CBG
Y = albumin

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Binding of (gluco/mineralo)-corticoids, specifically (X), is favored over (gluco/mineralo)-corticoids. Which has a greater plasma half-life?

Glucocorticoids;
X = cortisol
Mineralocorticoids (aldosterone)

Cortisol

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T/F: Adrenal androgens, such as DHEA, have significantly lower half-lives in plasma compared to cortisol/aldosterone.

False - DHEA more stable half-life (10-20h) and its plasma conc exceeds that of other adrenal steroids

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Clearance of adrenal hormones from body is through (renal/hepatic) mechanisms.

Both

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Mineralocorticoids bind to (membrane/cytoplasmic) type (I/II/III) receptors. These receptors are found in highest concentrations in which locations/organs?

Cytoplasmic;
Type I

Kidney, colon, salivary/sweat glands

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Glucocorticoids bind to (membrane/cytoplasmic) type (I/II/III) receptors. Which locations/organs in body have this receptor?

Cytoplasmic;
Type II

Various tissues

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T/F: Cortisol binds Type I cytoplasmic receptors.

True (it can, though not preferentially); usually intercepted and enzymatically inactivated

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ACTH can bind to receptors on which layers of adrenal cortex? Star the layers in which ACTH is required for normal function.

ZG (but prime regulator is A-II)
ZF*
ZR*

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Binding of ACTH to adrenal cortex receptors causes (rise/drop) in (X), which then leads to (production/degradation) of (Y).

Rise;
X = cAMP
Production
Y = StAR

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T/F: In absence of ACTH, ZR and ZF will atrophy.

True

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Production of ACTH is under control of (X), which is produced in (Y).

X = CRH;
Y = paraventricular nucleus of hypothalamus

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Secretion of (X) follows a circadian rhythm; ACTH and (Y) hormones parallel this. The peak rates of these hormone secretions occur during:

X = CRH;
Y = cortisol

Early morning, before waking (decline through evening)

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T/F: Although ACTH is subject to feedback inhibition by cortisol, CRH secretion is only controlled by higher centers.

False - both inhibited by cortisol

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Circadian rhythm of CRH: the mechanism is a gradual (increase/decrease) in (X) to (Y) of CRH secreting cells as the day proceeds.

Increase;
X = sensitivity
Y = cortisol (neg feedback)

*Low sensitivity in morning means neg feedback less effective

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T/F: Stressful stimuli result in increased CRH levels by making the neurons less sensitive to cortisol neg feedback.

False - mechanism is simply that stress (neural stimulation) overrides diurnal rhythm

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In high concentrations, (X) hormone has melanocyte stimulating effects. Why?

X = ACTH

Same first 13 AA as alpha-MSH

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The function of (X) hormone are diverse and include many that are permissive - particularly for effectiveness of (Y) action.

X = cortisol;
Y = catecholamine

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What’s the mechanism behind (X) hormone’s permissive role in catecholamine action?

X = cortisol;

Up-regulates receptors, thus increasing responsiveness of tissues to catecholamines

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Cortisol: (increase/decrease) vascular integrity of CV and (increase/decrease) immune function/inflammation.

Increase; decrease

Cortisol: effect on liver and muscle?

Liver: increase gluconeogenesis; Muscle: increase catabolism

Cortisol: effect on lungs?

Increased surfactant production and lung maturation (during development)

Cortisol: (increases/decreases) ADH production, (increases/decreases) GFR. Thus, you'd expect (dilute/concentrated) urine.

Decrease; increase; | Dilute

Cortisol: increase bone (resorption/formation).

Resorption

T/F: Cortisol reduces rates of protein synthesis in all tissues.

False - not liver

T/F: Cortisol inhibits glucose transport into cells of all tissues.

False - not in brain

T/F: Effects of cortisol, though in opposition to insulin, promote insulin secretion.

True (increased circulation glucose)

(High/low) levels of cortisol can result in water intoxication. Why?

Low; | High ADH secretion, low GFR, and inability to produce hypotonic urine (eliminate free water)

Elevated cortisol levels (stimulate/depress) production of GnRH, LH, FSH and (stimulate/depress) production of TSH and (stimulate/depress) production of GH.

Depress all

Adrenal androgens are especially important during (X) phase in life. They're also major source of androgens in (M/F).

X = fetal development | F (insignificant in M compared to testes production)

In females, (X) conversion to (Y) contribute to stimulation of axillary and pubic hair growth.

``` X = adrenal androgens; Y = testosterone (in periphery) ```

Primary function of aldoesterone.

Distal nephron: | Increase Na reabsorption (and K secretion)

List the three factors that control aldosterone secretion from ZG. Star the most effective/important.

1. Angiotensin-II* 2. Plasma K 3. ACTH

Mechanism of AII increasing aldosterone production: generally a(n) (increase/decrease) in (X).

Increase; | X = StAR

Aldosterone levels are (increased/decreased) in pregnancy due to (increase/decrease) in (X). This is because (X) increases hepatic (synthesis/degradation) of (Y).

``` Increased; Increase; X = estrogen; Synthesis; Y = angiotensinogen ```

Hyperaldosteronism: you'd expect sweat/saliva to be (high/low) in Na.

Low; essentially Na-free

Chromaffin cells of adrenal medulla store (X) ratio of Epi:NE. What other compound is stored there, in (greater/lesser) quantity?

X = 5:1 ATP; lesser (1:4, ATP:catech)

Catecholamines in medulla are derived from (X). And most of (NE/Epi) is converted to (NE/Epi) via (Y) enzyme.

X = tyrosine NE; Epi Y = PNMT

PNMT is an enzyme that functions to (X). It's inducible by (Y) hormone.

``` X = convert NE to Epi (in adrenal medulla); Y = cortisol ```

(X) increases the proportion of Epi produced in adrenal medulla by inducing (Y) enzyme. How does (X) even come in close proximity to (Y)?

``` X = cortisol Y = PNMT ``` Medullary sinusoids receives blood rich in corticosteroids (which passed through adrenal cortex)

T/F: In circulation, only about half of catecholamines are loosely associated with carrier protein albumin.

True

Half-life of catecholamines in plasma is about (X).

X = 10-15 sec!!

T/F: Adrenal catecholamines are taken up (for reuse/degradation) by neuronal tissue only.

False - neuronal and non-neuronal tissue

Degradation of catecholamines typically carried out by (X) enzyme. The products are then coupled to (Y) and excreted in (stool/urine).

X = MAO (monoamine oxidase) Y = sulfate or glucuronic acid Urine

Epi and NE, although equally effective in stimulating (X) receptors, differ mostly by their effects on (Y) receptors.

``` X = beta-1 Y = alpha and beta-2 ```

Adrenal cortex originates from which embryological tissue?

Splanchnic mesoderm

Adrenal medulla originates from which embryological tissue?

Neural crest cells

In a nutshell, adrenal system controls (X) and (Y) in an attempt to preserve organs/systems in (Z) condition.

``` X = blood pressure Y = serum glucose levels Z = stress ```

In general, cortisol's effect on serum glucose is (direct/indirect) and that on blood pressure is (direct/indirect).

Direct; | Indirect (by permissive action on NE/Epi)

T/F: Both cortisol and aldosterone, following their synthesis, leave mitochondria and diffuse into circulation.

False - aldosterone synthesis ends in sER

About how much cortisol is normally produced per day? And in stressful situation?

Normal: 5-20 mg | Severe Stress: 400 mg

About how much aldosterone is normally produced per day?

0.25 mg

About how much DHEA is normally produced per day?

10-20 mg

The overlap between function or cortisol and (X) hormone can be explained by similarities in:

X = aldosterone Structure/functional group distribution

Hyperaldosteronism: (high/low) serum pH and (high/low) K. Thus, (hypo/hyper)-kalemic (acidosis/alkalosis).

High; Low; Hypokalemic alkalosis (high renal loss of H ions)

Hypoaldosteronism: you'd expect (hyper/hypo)-tension and (acidosis/alkalosis).

Hypotension; | Acidosis (and hyperkalemia)

Key difference(s) between 21-a-hydroxylase deficiency and 11-b-hydroxylase deficiency.

21: no cortisol/aldosterone (high ACTH due to low neg feedback promotes androgen synthesis) 11: No cortisol, but intermediate (11-deoxycorticosteone) buildup leads to mineralocorticoid effect (HT)

Conn's syndrome is essentially (hyper/hypo)-(X) that typically results from (Y).

``` X = primary hyperaldosteronism Y = aldosterone-secreting adenoma (benign tumor) ```

Pheochromocytoma is:

A tumor of the adrenal medulla

In a purely 11-deoxycorticosterone-induced hypervolemia, renin levels would (increase/decrease), A-II would (increase/decrease), and Aldosterone would (increase/decrease).

All decrease