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endocrine exam 1 > adrenal gland hormones > Flashcards

adrenal gland hormones Flashcards

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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?

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A

located almost entirely in the principal cells of the distal neuron

24
Q

mineralocorticoids are ____ hormones

Study These Flashcards
A

life saving or salt saving

saves you from dying from dehydration

25
hyposecretion of aldosterone leads to
hyperkalemia--cardiac toxicity (too much calcium) | decreased ECF -- shock
26
hypersecretion of aldosterone
decreased H+ --alkalosis (high blood pH) hypokalemia--muscle weakness or paralysis increased ECF --hypertension
27
aldosterone promotes--
transport of sodium, K, and H in kidney tubules, sweat glands, colon, and salivary gland ducts
28
how is aldosterone synthesis and secretion regulated?
-ECF potassium concentration -renin-angiotensin system (controls pressure and volume of body fluid) Minor--ECF sodium concentration and adrenocorticotropic hormone
29
urinary potassium excretion is directly related to
1. plasma aldosterone concentrations | 2. ECF potassium concentrations
30
plasma levels of aldosterone are directly related to
plasma K concentrations
31
increased aldosterone levels increase ______ excretion to help maintain normal ECF K levels
K
32
high potassium intake increases ____ excretion
K
33
what is the renin system?
decreased arterial pressure--> renin--> angiotensinogen--> angiotenin I--> angiotensin II--> renal retention of salt and water and vasoconstriction--> increased arterial pressure
34
what is important in regulation of aldosterone secretion?
renin
35
____ is a powerful stimulator of aldosterone synthesis and secretion
angiotensin II
36
how does angiotensin work to stimulate aldosterone synthesis and secretion?
- 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
aldosterone escape
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
cortisol secretion is under control of
ACTH
39
what is the precursor protein of ACTH
POMC
40
how is POMC synthesized
in hypothalamus and stimulated by corticotropin-releasing factor
41
negative feedback of cortisol
increase in plasma cortisol inhibits synthesis of CRF and secretion of ACTH
42
CRF stimulates secretion of ?
ACTH
43
effects of carbohydrates
- stimulate gluconeogenesis (esp. liver) - decrease blood glucose - elevate blood glucose
44
effects of proteins
- decrease synthesis except in liver - increase catabolism except in liver - increased synthesis in liver and plasma - decrease amino acid transport, except to liver
45
effects of fats
increase mobilization and utilization of fatty acids
46
cortisol increases--
glucose, free fatty acids, amino acids
47
what increases within minutes of acute trauma?
plasma and adrenal concentrations of corticosteroids
48
cortisol effects on calcium balance
-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
long term glucocorticoid excess can lead to---
osteopenia and osteoporosis
50
stages of inflammation
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
how does cortisol help prevent inflammation?
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
most common cause of Cushing's syndrome
excess ACTH (high ACTH and cortisol levels)
53
addison's disease
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
addisonian crisis
inability to deal with stress
55
cushing's syndrome
hyperadrenalism signs--buffalo torso, moon face, hirsutism, acne symptoms--elevated blood glucose, protein catabolism, muscle weakness, suppressed immunity, osteoporosis, purplis striae
56
causes of cushing's syndrome
``` adrenal hyperplasia -increase pituitary ACTH -hypothalamic dysfunction pituitary tumors -nonpituitary tumors (ectopic)--ACTH, CRH adrenal neoplasia -adenoma -carcinoma iatrogenic ```
57
metabolic effects of cushing's disease
- 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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