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Human phys II, Exam 2 > adrenal cortex and medulla, lect 18/19 > Flashcards

adrenal cortex and medulla, lect 18/19 Flashcards

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

A

lung

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
Q

adrenal androgens are more significant in males or females

A
  • 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
Q

adrogens produced from adrenal cortex is converted to testosterone in males in what organ

A

testes

27
Q

primary dysregulation: disorders of adrenal cortex

A

disorder resides in the actual endocrine gland

28
Q

secondary dysregulation: disorders of adrenal cortex

A
  • dysfunction resides in pituitary
29
Q

tertiary dysregulation: disorders of adrenal cortex

A

disturbance is explained by a hypothalamic defect

30
Q

Differentiate between cushings syndrome and cushings disease

A
  • cushings syndrome: primary adrenal hyperplasia -> ACTH levels are low
  • cushings disease: defect caused by overactive anterior pituitary -> excess ACTH
31
Q

clinical presentation

  • hyperglycemia
  • thin skin
  • muscle wasting
  • central obesity
  • round face
  • buffalo hump
  • HTN
A
  • cushing’s
    • excess glucocorticoids and androgens
32
Q

What is addison’s disease

A
  • primary adrenocortical insufficiency: autoimmune destruction of gland
  • decreased synthesis in all adrenocorticol hormones
    • loss of cortisol
    • loss of aldosterone
    • loss of androgens
33
Q

clinical presentation

  • hypoglycemia during stress, anorexia, weight loss, weakness
  • hyperkalemia, hypotension, mtabolic acidosis
  • in females: decreased pubic and axillary hair, decreased libido
A

addisons disease

34
Q

what is secondary adrenocortical insufficiency

A
  • 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
Q

what is conn’s syndrome

A
  • aldosterone secreting tumor -> aldosterone hypersection
  • increased Na+ reabsorption -> HTN
  • increased K+ secretion -> hypokalemia
  • increased H+ secretion -> metabolic alkalsosis
  • low renin levels
36
Q

what is adrenogenital syndrome

A
  • hypersecretion of adrenal androgens
  • masculinizing conditions in females
    • deepened voice
    • increased muscle mass
    • amenorrhea
    • hirsutism
    • cliotral enlargement
    • acne
37
Q

what does 21 B-hydroxylase deficiency cause

A
  • 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
Q

what does 17a-hydroxylase deficiency cause

A
  • 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
Q

synthesis of epi and NE is regulated by

A
  • sympathetic stimulation
40
Q

cortisol activates what molecule that converts NE into epi

A

phenylethanolamine-N-methyltransferase

41
Q

catecholamine effects on metabolism

A
  • 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

Human phys II, Exam 2 (11 decks)

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