03a: Adrenals Flashcards
Most, (X)%, of the adrenal gland is composed of (cortex/medulla).
X = 80-90
Cortex
List the specific (X) steroid hormones produced by the zona reticularis.
X = androgen;
- DHEA
- DHEAS
- Androstenedione
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)
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
T/F: Corticosteroids simply diffuse out into the circulation and travel as free hormones.
False - bound to protein (CBG or albumin) in plasma
Most adrenal steroids in circulation are (free/bound). Those that are bound: to which protein(s)?
Bound;
- Transcortin, aka CBG (corticosteroid binding globulin)
- Albumin
Most adrenal corticosteroids are bound to (X) in plasma. And androgens to (Y).
X = CBG Y = albumin
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
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
Clearance of adrenal hormones from body is through (renal/hepatic) mechanisms.
Both
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
Glucocorticoids bind to (membrane/cytoplasmic) type (I/II/III) receptors. Which locations/organs in body have this receptor?
Cytoplasmic;
Type II
Various tissues
T/F: Cortisol binds Type I cytoplasmic receptors.
True (it can, though not preferentially); usually intercepted and enzymatically inactivated
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*
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
T/F: In absence of ACTH, ZR and ZF will atrophy.
True
Production of ACTH is under control of (X), which is produced in (Y).
X = CRH; Y = paraventricular nucleus of hypothalamus
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)
T/F: Although ACTH is subject to feedback inhibition by cortisol, CRH secretion is only controlled by higher centers.
False - both inhibited by cortisol
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
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
In high concentrations, (X) hormone has melanocyte stimulating effects. Why?
X = ACTH
Same first 13 AA as alpha-MSH
The function of (X) hormone are diverse and include many that are permissive - particularly for effectiveness of (Y) action.
X = cortisol; Y = catecholamine
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
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.
- Angiotensin-II*
- Plasma K
- 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
