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Physio Exam 3 - Endocrine > 17 | Adrenal Gland > Flashcards

17 | Adrenal Gland Flashcards

1
Q

fetal adrenal

A

relatively bigger for body size

large steroidogenic fetal zone

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2
Q

embryological origins

A
  • adrenal cortex: mesoderm

- adrenal medulla: neuroectoderm (modified S-ANS)

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3
Q

adrenocorticoids

A
  • adrenal cortical hormones
  • derive from cholesterol
  • specific product based on stimuli and cell enzymes
  • rate limited by cholesterol to pregnenolone
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4
Q

StAR

A

[steroid acute regulatory protein]

  • production promoted by stimulating factors
  • StAR stimulates transport of cholesterol from cytosol to mitochondria
  • in mitochondria, enzymes to yield prenenolone
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5
Q

mineralocorticoid vs. glucocorticoid

A

typically:
- mineralocorticoid: aldosterone
- glucocorticoid: cortisol

  • high levels of each produces alternate effect
  • cortisol can readily bind to and activate MC rec
  • but MC tissues contain enzyme that converts cortisol to cortisone, reducing mC effects
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6
Q

steroid secretion

A
  • de novo synthesis
  • can’t be stored
  • lipid soluble, diffuse across membrane down concentration gradient into circulation
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7
Q

steroids in circulation

A 
bound to plasma binding proteins 
-transcortin OR
-corticosteroid binding globulin (CBG) 
AND 
-albumin
  • binding of GCs favored over MCs, cortisol has longer half life than aldosterone (90 vs. 30 min) in the plasma
  • though stable DHEAs have far longer half life (15 hrs) and far higher plasma concentrations
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8
Q

steroid hormone clearance

A

liver and kidney

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9
Q

mineralocorticoid receptors

A

cytosolic
Type I
-mostly in kidney, colon, sweat, salivary glands

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10
Q

glucocorticoid receptors

A

cytosolic
Type II
-various tissues of the body

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11
Q

ACTH (role in cortisol + androgen production)

A
  • derived from POMC (pro-opiomelanocortin)
  • ACTH is required for function of zona fasiculata and zona glomerulosa
  • circulating level is controlling factor for cortisol and androgen synthesis
  • binding increases cAMP that leads to StAR production
  • can bind to receptors on all 3 cortex layers
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12
Q

circadian rhythm/sensitivity

A

CRH + ACTH subject to feedback inhibition from cortisol
AM: low sensitivity, less negative feedback, higher CRH/ACTH/cortisol
PM: higher sensitivity, more inhibitory feedback, less CRH/ACTH/cortisol
(stress can override diurnal rhythm)

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13
Q

cortisol - “stress hormone”

A

necessary for:

  • vital functions during times of prolonged stress (mostly physiological)
  • permissive function, hormone doesn’t initiate change, but is required for full expression of change
  • can be protective
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14
Q

cortisol + catecholamines

A

-cortisol req. for catecholamines to be effective, increased catecholamine responsiveness to cortisol responsible for many effects of cortisol

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15
Q

++cortisol - blood glucose

A

high cortisol increases BG (glucocorticoid)

-through mechanisms that oppose insulin (wants to store glucose)

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16
Q

++cortisol - catabolism

A

high cortisol promotes catabolism

  • breakdown of protein from muscle and CT to free AAs for gluconeogenesis (increasing BG)
  • also stimulates gluconeogenic enzyme production in liver
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17
Q

++cortisol - glucose use

A

high cortisol decreases glucose use
-inhibits glucose transport into cells (increasing BG)
(not in brain)

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18
Q

++cortisol - protein synthesis

A

high cortisol decreases protein synthesis everywhere except liver

  • reduced AA uptake into muscle
  • increased protein catabolism
  • plasma AA levels rise (can be used for glucose synthesis)
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19
Q

++cortisol - fat metabolism

A

high cortisol increases lipolysis to liberate fatty acids and glycerol for gluconeogenesis
-but increases central fat deposition, while periphery loses fat and muscle mass

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20
Q

++cortisol - CNS

A

high cortisol

  • feedback inhibition of CTH and ACTH
  • perception effects (deficiency can lead to accentuation of senses)
  • initial euphoria then depression
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21
Q

cortisol - cardiovascular effects

A

cortisol is required to maintain the CVS

  • maintains sensitivity to Epi/NE
  • w/out vasodilation and decreased BP
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22
Q

cortisol - developmental effects

A

permissive in maturation of fetal organ systems, intestinal enzymes, pulmonary surfactant

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23
Q

cortisol - renal effects (primary, secondary)

A

free water clearance

  • hypothalamic neurons secreting CRH also release ADH
  • cortisol feedback inhibition both
  • without cortisol, increased CRH and ADH
  • increased ADH, inc H20 reabsorption, dec free water clearance (even with decreased plasma osm)
  • hypotension secondary to low adrenergic receptors without cortisol also increases ADH levels
  • together can cause water intoxication
24
Q

cortisol - bone effects

A

promotes bone breakdown

-in excess enhances osteoclast activity, promoting osteoporosis development

25
Q

cortisol - immune function

A

contains inflammatory response

  • in high doses, suppresses inflammatory response
  • used in synthetic GC’s (prednisone)
  • stabilizes lysosomal membranes, dec capillary permeability, dec phagocyte activity, suppression of IL-1, inhibits eicosanoid production (PGs, leukotrienes)
26
Q

cortisol elimination

A

filtered in glomerulus, appears in urine

also reduced and conjugated in liver, metabolites filtered

27
Q

adrenal androgens - relative production

A
  • large quantities in fetus, important during fetal development
  • postnatally low, but rises during prepuberty (onset of hair growth and secretion)
28
Q

adrenal androgens - females

A
  • major androgen source in adult females
  • converted to testosterone in periphery, contribute to axillary/pubic hair growth
  • some androstenedione converted in periphery to estrogen, major source of E post-menopause
29
Q

DHEA levels

A
  • similar to cortisol as young adult
  • decline with age
  • DHEA-S filtered and excreted
30
Q

aldosterone function

A

-increase Na reabsorption in distal nephron, inc K+ secretion
(increased Na/K pump activity, and number of rec)
-production due to ANII + plasma K+ levels

  • ANII produced due to increased renin from fall in AA perfusion pressure or by S-ANS stimulation
  • renin influenced by Na+/Cl- at MD, electrolyte levels, ANII feedback
31
Q

aldosterone production

A
  • stimulated by ANII by cells of zona glomerulosa
  • increased intracellular 1,4,5-triphosphate, increases StAR
  • levels also inc by inc. E (pregnancy), increased PV
32
Q

hyperaldosteronism

A

hyposmotic sweat and saliva

33
Q

adrenal medulla - structure

A
  • cells are modified postganglionic S-ANS neurons
  • innervated by splanchnic nerves
  • chromaffin cells w/ secretory granules
34
Q

chromaffin granules

A

store catecholamines
5:1 epi:norepi ratio
ATP also present 1ATP:4catecholamines

35
Q

catecholamine synthesis

A

tyrosine to DA to norepineprhine
NE mostly converted to epi
-catalyzed by PNMT, which is inducible by cortisol
-medulla receives blood from cortex, rich in corticosteroids. cortisol can fine tune epi:NE ratio

36
Q

granule release

A
  • secreted in response to S-ANS *ACh/cholinergic stimulation (NOT andrenergic - NE/E)
  • ACh binding, inc Ca2+ levels, promote exocytosis
37
Q

catecholamines in circulation

A

50% free in solution, 50% loosely w/ albumin

  • rapidly cleared (10-15s)
  • taken up by neurons, repackaged or inactivated by MAO
  • non-nueronal tissue, inactivated by MAO or COMT
  • degradation products coupled with sulfate/glucuronic acid, excreted in urine

-almost all epi in circulation adrenal, but circ NE from other sympathetic synapses

38
Q

catecholamine receptors/function

A
  • equally effective on B1
  • NE is potent a agonist, little effect on B2
  • E is more potent a agonist, powerful on B2
39
Q

catecholamine effects

A

stimulate gluconeogenesis, glycogenolysis, lypolysis
-increase BG and FFA levels
-increase CO
in excess: hypertension, headache, anxiety, sweating, palpitations, chest pain, postural hypotension)

40
Q

adrenal gland organization

A 
[cortex - all steroid hormones]
glomerulosa: mineralocoritcoids (aldosterone)
fasciculata: glucocorticoids (cortisol)
reticularis: adrogens, DHEA
[medulla]
catecholamines (E, NE)
41
Q

prednisone

A

synthetic glucocorticoid
acts as a pure GC, no mineralocorticoid effects
(can be used to promote surfactant development in fetus)

42
Q

long term prednisone - immune function

A

depressed immune function (may be goal)

  • inhibition of cytokines, leukotrienes, PGs (inflammatory response mediators)
  • depress lymphocyte and monocyte proliferation
43
Q

long term prednisone - blood sugar levels

A

cortisol normally acts to increase BG

  • BG elevated
  • since GCs have diabetogenic/counter insulin effects, may show similar symptoms
44
Q

long term prednisone - blood pressure

A

cortisol required for CVS response to catecholamines

-increased blood pressure, increased sensitivity

45
Q

long term prednisone - physical appearance

A

(symptoms associated with Cushing’s syndrome)

  • moon face, buffalo hump, central obesity/fat deposition
  • thinned limbs (peripheral fat and muscle breakdown)
  • easy bruising (loss of CT supporting microvasculature)
  • high glucose levels (hyperglycemia), thus also hyperinsulinemia
  • stimulated appetite, overeating (hyperphagia)
46
Q

Cushing’s syndrome vs. disease

A
  • syndrome: excess GC activity (i.e. w/ prednisone)

- disease: pituitary tumor that leads to overproduction of ACTH, and thus oversecretion of cortisol from adrenal galnd

47
Q

long term prednisone - long term consuences

A
  • decreased renal Ca2+ reabsorption, decreased GI uptake of Ca2+ . w/ dec plasma Ca2+, increased PTH to try and raise
  • increased bone reabsorption, increased risk of osteoporosis
  • GC promotes gastric secretions, peptic ulcers. also lack of PGs which provide mucosal protection.
  • impaired sleep and memory (CNS)
48
Q

long term prednisone - consequence of prompt cessation

A
  • circulating prednisone inhibits CRH, ACTH, cortisol
  • zona fasciculata and reticularis will have atrophied
  • with immediate stop, no time for these to grow and patient would have little to no glucocorticoid levels (adrenal insufficiency)
49
Q

high endogenous vs. exogenous cortisol

[hypertension]

A

endo: cortisol has some MC activity, normally controlled by enzyme at rec. not adequate in excess.
- physiological response of aldosterone
- may have higher BP than w/ high exogenous cortisol, increased water retention

50
Q

high endogenous vs. exogenous cortisol

[ACTH levels]

A
  • endo: high endogenous cortisol due to ACTH-producing pituitary tumor
  • exo: negative feedback from cortisol, very low levels of ACTH
51
Q

high endogenous vs. exogenous cortisol

[sex hormones]

A

ACTH stimulates zona fasciculata to produce androgens

  • exo: have low ACTH, low androgens
  • in women excess exogenous cortisol can lead to body hair growth (hirsutism), deep voice, acne
52
Q

Addison’s disease

A

destruction of adrenal gland

  • unable to produce aldosterone, androgens, cortisol
  • can be triggered by illness, trauma, or significant stress
  • high levels of ACTH, no negative feedback
53
Q

Addison’s disease - biological effects

A
  • no cortisol: decrease CVS sensitivity to catecholamines, decreased GC activity
  • no aldosterone: increase Na+ loss, hyponaturemia. low ECF vol and PV.
  • with hyponaturemia, can have hyperkalemia
  • cortisol normally maintains BG, may be hypoglycemic
54
Q

Addison’s disease - hyperpigmentation

A

high levels of ACTH, increased a-MSH levels

-melanin darkens skin

55
Q

Addison’s disease - hypotension

A

without aldosterone, decreased Na+ and water reabsorption

  • low plasma volume, leads to hypotension
  • also have low TPR, venous tone, cardiac contractility, catecholamine sensitivity
56
Q

apparent mineralocorticoid excess

A
  • symptoms: high BP, hypokalemic, alkalosis, low Na+ secretion
  • symptoms of hyperaldosteronism
  • BUT have low aldosterone, and high cortisol levels
  • genetic defect, no enzyme to degrade cortisol at MC receptor
  • would treat with pure GC to induce negative feedback on ACTH, or inhibition of MC receptor
57
Q

phenochromatoma

A

tumor of chromaffin cells, excessive amounts of catecholamines

  • increased peripheral resistance, tachycardia, vasoconstriction
  • hypertension, headaches
  • weight loss
  • increase blood glucose levels (counter insulin effects)

Physio Exam 3 - Endocrine (8 decks)

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