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endocrine exam 1 > adrenal gland hormones > Flashcards

adrenal gland hormones Flashcards

1
Q

hormones of the adrenal cortex are called

A

mineralocorticoids and glucocorticoids (androgens)

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2
Q

mineralocorticoids

A

aldosterone

desoxycorticosterone

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3
Q

glucocorticoids

A

cortisol and corticosterone

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4
Q

hormones from the adrenal medulla

A

epinephrine
norepinephrine
(catecholamines)

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5
Q

the adrenal cortex is the source of ____

A

steroid hormones, esp cortisol, androgens, and aldosterone

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6
Q

zones of the adrenal cortex

A

zona reticularis, zona fasciculata, zona glomerulosa

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7
Q

steroid hormones like vitamin D derive from? and are ____ soluble?

A

from cholesterol

fat soluble

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8
Q

cholesterol is made in the—

A

liver

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9
Q

synthesis of aldosterone

A

acetate–> cholesterol–> pregnenolone–> progesterone–>aldosterone

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10
Q

synthesis of cortisol

A

acetate–> cholesterol–> pregnenolone–> progesterone or 17-OH-pregnenolone–> 17-OH-progesterone–> cortisol

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11
Q

synthesis of dehydroepiandrosterone

A

acetate–> cholesterol–> pregnenolone–> 17-OH-pregnenolone–> dehydroepiandrosterone

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12
Q

what is the branch point for synthesis of steroids?

A

pregnenolone

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13
Q

relative effects on mineral metabolism from mineral corticoids

A

aldosterone 90%
deoxycorticosterone 2%
corticosterone slight
cortisol slight

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14
Q

overall effectiveness of endogenous glucocorticoids

A

cortisol 95%

corticosterone 4%

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15
Q

overall effectiveness of synthetic glucocorticoids

A

prednisone 4X cortisol
methylprednisone 5X cortisol
dexamethasone 30X cortisol

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16
Q

_____ has the highest affinity

A

cortisol-binding globulin

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17
Q

albumin

A

binds corticoids

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18
Q

—— % glucocorticoids are bound is plasma proteins; half life —- mins

A

90-95%
60-90 mins
about 60% aldosterone bound; half life 20 min

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19
Q

how do steroids enter cell?

A

diffusion and then bind to receptors in cytoplasm

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20
Q

response elements

A

specific DNA sequences where the hormone-receptor complex binds in the nucleus

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21
Q

how does the hormone-receptor complex exert its effects?

A

altering transcription of genes–> mRNA which directs ribosomal synthesis of proteins

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22
Q

Nearly all the cells in the body have ______ so the effects of ______ are widespread

A

nearly all cells in the body have glucocorticoid receptors so the effects of cortisol are widespread

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23
Q

where are the receptors for aldosterone?

A

located almost entirely in the principal cells of the distal neuron

24
Q

mineralocorticoids are ____ hormones

A

life saving or salt saving

saves you from dying from dehydration

25
Q

hyposecretion of aldosterone leads to

A

hyperkalemia–cardiac toxicity (too much calcium)

decreased ECF – shock

26
Q

hypersecretion of aldosterone

A

decreased H+ –alkalosis (high blood pH)
hypokalemia–muscle weakness or paralysis
increased ECF –hypertension

27
Q

aldosterone promotes–

A

transport of sodium, K, and H in kidney tubules, sweat glands, colon, and salivary gland ducts

28
Q

how is aldosterone synthesis and secretion regulated?

A

-ECF potassium concentration
-renin-angiotensin system (controls pressure and volume of body fluid)
Minor–ECF sodium concentration and adrenocorticotropic hormone

29
Q

urinary potassium excretion is directly related to

A
  1. plasma aldosterone concentrations

2. ECF potassium concentrations

30
Q

plasma levels of aldosterone are directly related to

A

plasma K concentrations

31
Q

increased aldosterone levels increase ______ excretion to help maintain normal ECF K levels

A

K

32
Q

high potassium intake increases ____ excretion

A

K

33
Q

what is the renin system?

A

decreased arterial pressure–> renin–> angiotensinogen–> angiotenin I–> angiotensin II–> renal retention of salt and water and vasoconstriction–> increased arterial pressure

34
Q

what is important in regulation of aldosterone secretion?

A

renin

35
Q

____ is a powerful stimulator of aldosterone synthesis and secretion

A

angiotensin II

36
Q

how does angiotensin work to stimulate aldosterone synthesis and secretion?

A
  • increase in rate of sodium reabsorption from distal nephron and water follows osmotically
  • increase ECF volume which contributes to an increase in blood pressure
37
Q

aldosterone escape

A

when aldosterone is initially infused, sodium excretion falls sharply, but within a day or two, sodium excretion is normal even though aldosterone is still being infused

  • reason–associated large increased in ECF volume and arterial blood pressure
  • these effects trigger other mechs that override the neg effect of aldosterone on urinary sodium excretion
38
Q

cortisol secretion is under control of

A

ACTH

39
Q

what is the precursor protein of ACTH

A

POMC

40
Q

how is POMC synthesized

A

in hypothalamus and stimulated by corticotropin-releasing factor

41
Q

negative feedback of cortisol

A

increase in plasma cortisol inhibits synthesis of CRF and secretion of ACTH

42
Q

CRF stimulates secretion of ?

A

ACTH

43
Q

effects of carbohydrates

A
  • stimulate gluconeogenesis (esp. liver)
  • decrease blood glucose
  • elevate blood glucose
44
Q

effects of proteins

A
  • decrease synthesis except in liver
  • increase catabolism except in liver
  • increased synthesis in liver and plasma
  • decrease amino acid transport, except to liver
45
Q

effects of fats

A

increase mobilization and utilization of fatty acids

46
Q

cortisol increases–

A

glucose, free fatty acids, amino acids

47
Q

what increases within minutes of acute trauma?

A

plasma and adrenal concentrations of corticosteroids

48
Q

cortisol effects on calcium balance

A

-decreased intestinal absorption of Ca
-increased urinary excretion of Ca (hypercalciuria)
=decreased serum Ca
-PTH secretion increases Ca to balance it
—> increased bone resorption
—> decreased bone formation

49
Q

long term glucocorticoid excess can lead to—

A

osteopenia and osteoporosis

50
Q

stages of inflammation

A
  1. release of inflammatory substances (bradykinin and histamine)
  2. increased blood flow–erythema
  3. leakage of plasma from capillaries
  4. infiltration by leukocytes
  5. tissue healing
51
Q

how does cortisol help prevent inflammation?

A
  1. stabilization of lysosomal membranes
  2. decreasing permeability of capillaries
  3. decreasing migration of WBC’s into inflamed area phagocytosis of damaged cells
  4. decreasing T-lymphocyte reproduction which helps to suppress immune system
  5. reducing release of IL-1 from WBC’s which reduces fever
52
Q

most common cause of Cushing’s syndrome

A

excess ACTH (high ACTH and cortisol levels)

53
Q

addison’s disease

A

hypoadrenalism

  • mineralocotricoid deficiency–decreased ECF–shock, hyperkalemia (cardiac toxicity), acidosis
  • glucocorticoid deficiency–decreased blood glucose, decreased mobilization of amino and fatty acids, muscle weakness, decreased resistance to stress
54
Q

addisonian crisis

A

inability to deal with stress

55
Q

cushing’s syndrome

A

hyperadrenalism
signs–buffalo torso, moon face, hirsutism, acne
symptoms–elevated blood glucose, protein catabolism, muscle weakness, suppressed immunity, osteoporosis, purplis striae

56
Q

causes of cushing’s syndrome

A 
adrenal hyperplasia
-increase pituitary ACTH
-hypothalamic dysfunction pituitary tumors
-nonpituitary tumors (ectopic)--ACTH, CRH
adrenal neoplasia
-adenoma
-carcinoma
iatrogenic
57
Q

metabolic effects of cushing’s disease

A
  • increased blood glucose-postprandial hyperglycemia–> adrenal diabetes
  • decreased muscle protein–> severe weakness, decreased immunity, osteoporosis
  • hypertension in 75-80% of cases

endocrine exam 1 (5 decks)

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