adrenal cortex and medulla, lect 18/19 Flashcards

(41 cards)

1
Q

where is the adrenal glands located

A

sits on the kidneys

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2
Q

function of mineralocorticoids

A

regulate salt and water retention at the kidney

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3
Q

function of glucocorticoids

A

increase plasma glucose levels

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4
Q

the adrenal gland is actually composed of what two glands

A
  • adrenal cortex
  • adrenal medulla
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5
Q

the adrenal cortex is composed of what three layers? What hormone does each layer secrete

A
  • zoma glomerulosa (outmost layer): aldosterone
  • zona fasciculata: cortisol
  • zona reticularis: sex steroids (androgens)
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6
Q

what hormones does the adrenal medulla secrete

A

epinephrine and norepinephrine

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7
Q

hormones secreted from the cortex are derived from what compound

A

cholesterol

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8
Q

List the regulation steps that cause the release of adrenal cortex hormones

A
  • hypothalamus secretes corticotropin-releasing hormone (CRH) which acts on corticotrophs of AP
  • anterior pituitary releases adrenocorticotropic hormone (ACTH)
  • adrenal cortex secretes cortisol, aldosterone, and adrenal androgens
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9
Q

corticotropin releasing hormone acts on what cells types in the anterior pituitary

A

corticotrophs -> cause secretion of ACTH

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10
Q

ACTH has what two functions

A
  1. activates cholesterol desmolase which acts on cholesterol to form pregnenolone, a product that then can differentiate into hormones
  2. stimulates adrenal gland growth
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11
Q

function of cholesterol desmolase

A
  • precursor for all adrenocortical steriods is cholesterol
  • first step in synthesis is conversion of cholesterol to pregnenolone by desmolase
  • all 3 layers contain cholesterol desmolase which is stimulated by ACTH
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12
Q

cortisol has what negative feedback mechanisms

A
  1. directly inhibits CRH at hypothalamus
  2. inhibits action of CRH on corticotrophs decreasing ACTH release
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13
Q

CRH released from hypothalamus reaches the corticotrophs in the anterior pituitary and activates what messenger cascade

A
  • G protein
  • adenylyl cyclase/cAMP/PKA
  • activation of L-type Ca2+ channels leads to an increase in Ca2+ that rapidly leads to the release of preformed ACTH
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14
Q

cortisol secretion follows what pattern

A
  • a diurnal rhythm
  • levels begin to increase during sleep, reach highest levels in the am
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15
Q

cortisol is released in response to what? What is the primary function?

A
  • Stress
  • effect of cortisol is to increase the availability of glucose which would protect the CNS from malnutrition or extreme fasting
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16
Q

cortisol increases synthesis of what

A
  • gluconeogenesis -> increased blood glucose
  • increased protein catabolism
  • increases lipolysis, providing glycerol
  • decreases glucose uptake by tissues
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17
Q

aldosterone is a mineralocorticoids that is synthesized in what layer

A

z. glomerulosa

18
Q

what two enzymes are necessary in production of aldosterone from cholesterol

A
  1. cholesterol desmolase
  2. aldosterone synthase
19
Q

why can’t z. glomerulosa produce glucocorticoids and androgens

A
  • zone lacks 17a hydroxylase
20
Q

what causes release of aldosterone

A
  • a drop in ECF and blood pressure
  • a rise in plasma K+
21
Q

ACE is present in which organ

22
Q

function of aldosterone

A
  • stimulates
    • sodium reabsorption
    • potassium secretion
    • net effect: expansion of extracellular fluid
23
Q

what adrenal cortex layer produces androgens

A

Z. reticularis

24
Q

What enzymes are necessary in the production of androgens from cholesterol

A
  • 17 a-hydroxylase
  • 17,20 desmolase (lyase)
25
adrenal androgens are more significant in males or females
* in females, the cortex is the major source of androgens * responsible for the development of pubic and axillary hair and for libido * little signifance in males
26
adrogens produced from adrenal cortex is converted to testosterone in males in what organ
testes
27
primary dysregulation: disorders of adrenal cortex
disorder resides in the actual endocrine gland
28
secondary dysregulation: disorders of adrenal cortex
* dysfunction resides in pituitary
29
tertiary dysregulation: disorders of adrenal cortex
disturbance is explained by a hypothalamic defect
30
Differentiate between cushings syndrome and cushings disease
* **cushings syndrome**: primary adrenal hyperplasia -\> **ACTH levels are low** * **cushings disease**: defect caused by overactive anterior pituitary -\> **excess ACTH**
31
clinical presentation * hyperglycemia * thin skin * muscle wasting * central obesity * round face * buffalo hump * HTN
* cushing's * excess glucocorticoids and androgens
32
What is addison's disease
* primary adrenocortical insufficiency: autoimmune destruction of gland * decreased synthesis in all adrenocorticol hormones * loss of cortisol * loss of aldosterone * loss of androgens
33
clinical presentation * hypoglycemia during stress, anorexia, weight loss, weakness * hyperkalemia, hypotension, mtabolic acidosis * in females: decreased pubic and axillary hair, decreased libido
addisons disease
34
what is secondary adrenocortical insufficiency
* insufficient CRH or failure of corticotrophs to adequately secrete ACTH * plasma ACTH levels are low * clinical features relate to cortisol and androgen deficiency * aldosterone levels are usually normal
35
what is conn's syndrome
* aldosterone secreting tumor -\> aldosterone hypersection * increased Na+ reabsorption -\> HTN * increased K+ secretion -\> hypokalemia * increased H+ secretion -\> metabolic alkalsosis * low renin levels
36
what is adrenogenital syndrome
* hypersecretion of **adrenal androgens** * masculinizing conditions in females * deepened voice * increased muscle mass * amenorrhea * hirsutism * cliotral enlargement * acne
37
what does 21 B-hydroxylase deficiency cause
* cortex does not produce glucocorticoids or mineralocorticoids * steroid intermediates build up and are converted to androgens -\> **androgenital syndrome** * **ACTH levels are high**, because of lack of feedback control or cortisol on the pituitary
38
what does 17a-hydroxylase deficiency cause
* glucocorticoids and androgens are not produced * steroid intermediates build up -\> promote mineralocorticoids production -\> overproduction of mineralocorticoids * **HTN inhibits renin secretion** * **​aldosterone levels are low** because of the symptoms of corticosterone excess
39
synthesis of epi and NE is regulated by
* sympathetic stimulation
40
cortisol activates what molecule that converts NE into epi
phenylethanolamine-N-methyltransferase
41
catecholamine effects on metabolism
* epi mobilizes fuels in times of STRESS to sustain glucose production for use by CNS * skeletal muscle -\> increased glycogenolysis * liver -\> increased glycogenolysis * adipose tissue -\> increased lipolysis