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Endo/Repro > 03a: Adrenals > Flashcards

03a: Adrenals Flashcards

1
Q

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

A

X = 80-90

Cortex

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2
Q

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

A

X = androgen;

  1. DHEA
  2. DHEAS
  3. Androstenedione
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3
Q

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

A

Cortex;
X = 1-2 weeks

  1. Circulatory collapse (from Na depletion)
  2. Hypoglycemia (if caloric intake limited)
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4
Q

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

A

Steroids;

Lipid-soluble and simply diffuse across membrane to enter circulation

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5
Q

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

A

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

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6
Q

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

A

Bound;

  1. Transcortin, aka CBG (corticosteroid binding globulin)
  2. Albumin
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7
Q

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

A 
X = CBG
Y = albumin
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8
Q

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

A

Glucocorticoids;
X = cortisol
Mineralocorticoids (aldosterone)

Cortisol

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9
Q

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

A

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

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10
Q

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

A

Both

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11
Q

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

A

Cytoplasmic;
Type I

Kidney, colon, salivary/sweat glands

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12
Q

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

A

Cytoplasmic;
Type II

Various tissues

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13
Q

T/F: Cortisol binds Type I cytoplasmic receptors.

A

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

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14
Q

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

A
  1. ZG (but prime regulator is A-II)
  2. ZF*
  3. ZR*
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15
Q

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

A

Rise;
X = cAMP
Production
Y = StAR

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16
Q

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

A

True

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17
Q

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

A 
X = CRH;
Y = paraventricular nucleus of hypothalamus
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18
Q

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

A 
X = CRH;
Y = cortisol

Early morning, before waking (decline through evening)

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19
Q

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

A

False - both inhibited by cortisol

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20
Q

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

A

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

*Low sensitivity in morning means neg feedback less effective

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21
Q

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

A

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

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22
Q

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

A

X = ACTH

Same first 13 AA as alpha-MSH

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23
Q

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

A 
X = cortisol;
Y = catecholamine
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24
Q

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

A

X = cortisol;

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

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25
Q

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

A

Increase; decrease

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26
Q

Cortisol: effect on liver and muscle?

A

Liver: increase gluconeogenesis;
Muscle: increase catabolism

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27
Q

Cortisol: effect on lungs?

A

Increased surfactant production and lung maturation (during development)

28
Q

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

A

Decrease; increase;

Dilute

29
Q

Cortisol: increase bone (resorption/formation).

A

Resorption

30
Q

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

A

False - not liver

31
Q

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

A

False - not in brain

32
Q

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

A

True (increased circulation glucose)

33
Q

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

A

Low;

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

34
Q

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

A

Depress all

35
Q

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

A

X = fetal development

F (insignificant in M compared to testes production)

36
Q

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

A 
X = adrenal androgens;
Y = testosterone (in periphery)
37
Q

Primary function of aldoesterone.

A

Distal nephron:

Increase Na reabsorption (and K secretion)

38
Q

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

A
  1. Angiotensin-II*
  2. Plasma K
  3. ACTH
39
Q

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

A

Increase;

X = StAR

40
Q

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

A 
Increased;
Increase;
X = estrogen;
Synthesis;
Y = angiotensinogen
41
Q

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

A

Low; essentially Na-free

42
Q

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

A

X = 5:1

ATP; lesser (1:4, ATP:catech)

43
Q

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

A

X = tyrosine
NE; Epi
Y = PNMT

44
Q

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

A 
X = convert NE to Epi (in adrenal medulla);
Y = cortisol
45
Q

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

A 
X = cortisol
Y = PNMT

Medullary sinusoids receives blood rich in corticosteroids (which passed through adrenal cortex)

46
Q

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

A

True

47
Q

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

A

X = 10-15 sec!!

48
Q

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

A

False - neuronal and non-neuronal tissue

49
Q

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

A

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

50
Q

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

A 
X = beta-1
Y = alpha and beta-2
51
Q

Adrenal cortex originates from which embryological tissue?

A

Splanchnic mesoderm

52
Q

Adrenal medulla originates from which embryological tissue?

A

Neural crest cells

53
Q

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

A 
X = blood pressure
Y = serum glucose levels
Z = stress
54
Q

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

A

Direct;

Indirect (by permissive action on NE/Epi)

55
Q

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

A

False - aldosterone synthesis ends in sER

56
Q

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

A

Normal: 5-20 mg

Severe Stress: 400 mg

57
Q

About how much aldosterone is normally produced per day?

A

0.25 mg

58
Q

About how much DHEA is normally produced per day?

A

10-20 mg

59
Q

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

A

X = aldosterone

Structure/functional group distribution

60
Q

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

A

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

61
Q

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

A

Hypotension;

Acidosis (and hyperkalemia)

62
Q

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

A

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)

63
Q

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

A 
X = primary hyperaldosteronism
Y = aldosterone-secreting adenoma (benign tumor)
64
Q

Pheochromocytoma is:

A

A tumor of the adrenal medulla

65
Q

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

A

All decrease

Endo/Repro (15 decks)

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