5_Adrenal Flashcards by Drew Spargo

What are the effects of epinephrine?

primarily fight-or-flight

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What are the effects of norepinephrine

strong vasoconstrictor to increase BP

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What is the outermost layer and thinnest of the adrenal cortex?

zona glomerulosa

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What is the middle and thickest layer of the adrenal cortex?

zona fasciculate

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What is the innermost layer of the adrenal cortex?

zona reticularis

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What hormones does the zona fasciculate release?

glucocorticoids

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What hormones does the zona reticularis secrete?

adrenal androgens (DHEA and androstenedione)

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What hormones does the zona glomerulosa release?

aldosterone

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How is the zona glomerulosa regulated?

by AngII and K+

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How is the zona fasciculate regulated?

ACTH

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How is the zona reticularis regulated?

ACTH

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What is a pheochromocytoma?

a medullary tumor that causes a sporadic secretion in response to palpation or anesthetics

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What are the clincal consequences of a pheochromocytoma?

postural hypotension: prolonged increase in catecholamines downregulates GPCRs to cause a reduction in sympathetic tone

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Describe the cellular make-up of the adrenal medulla.

post-ganglionic neurons (“chromaffin cells”) that secrete the catecholamines epinephrine and norepinephrine

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Where are the chromaffin cells derived?

they are sympathoadrenal & derived from the neural crest

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How are norepi and epi synthesized?

from tyrosine - l-dopa - dopamine - norepi - epi

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Where is norepi primarily converted to epi?

in the adrenal gland

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What is the reaction catalyzed by cholesterol desmolase?

cholesterol P450 side-chain-cleavage to yield pregnenolone

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What is the RLS in steroidogenesis?

cholesterol desmolase P450 scc

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What is required for CD450scc activation?

ACTH

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How does ACTH activate CD450scc?

activates G-alpha-S pathway

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What factors increase aldosterone synthesis?

AngII and K+

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What factors decrease aldosterone synthesis?

increased Na (mild decrease in synthesis)

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Where is renin secreted?

JG cells

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Upon response to what factors is renin secreted?

decreased pressure, beta-1 stimulation, decreased NaCl

What are the effects of AngII?

1) thirst, 2) vasoconstriction, 3) aldosterone

What are the major & minor mineralocorticoids?

major: aldosterone; minor: deoxycorticosterone, cortisone

What are the synthetic mineralocorticoids?

agonist: 9-alpha-fludrocortisone; antagonist: spironolactone

For what diseases is 9-alpha-fludrocortisone used?

addisons

For what disease is spironolactone used?

CHF

How does spironolactone work?

prevents aldosterone-MR binding

How does amiloride work?

prevents formation of new Na channels

Where do the mineralocorticoids act (cell types)?

principle cells of CT, also DT and CD

What are the effects of the mineralocorticoids?

Na/H2O reabsorption and K secretion

What are the symptoms of hypokalemia?

muscle weakness and paralysis

What are the symptoms of hyperkalemia?

cardiac toxicity

What are the axes of the RFC?

sodium intake (x normal) vs. BP

What is aldosterone effect?

short-term aldosterone effects due to pressure di-/natriuresis after 24-48h

Where does aldosterone bind its receptor?

binds MR in cytoplasm

What is aldosterone's receptor?

the mineralocorticoid receptor (a nuclear receptor)

How does the aldosterone-MR complex initiate cell changes?

1) MR-Ald releases HSP, 2) MR-Ald translocates to nucleus, 3) MR-Ald is phosphorylated, 4) MR-Ald forms a homodimer, 5) 2 MR-Ald binds to GRE in promoter regions

What are aldosterone's effects on its target cells?

1) increases Na/K ATPase, 2) increases Enac (epithelial sodium channel), 3) increases mitochondria

What are the major/minor glucocorticoids?

major: cortisol (hydrocortisone); minor: corticosterone

What are the synthetic glucocorticoids?

1) cortisone, 2) prednisone, 3) dexamethasone

What are the 5 stages of inflammation?

1) release of pro-inflammatory mediators, 2) erythema, 3) increased capillary permeability, clotting, and non-pitting edema/swelling, 4) leukocyte infiltration, 5) tissue remodeling and healing

How do glucocorticoids oppose inflammation?

1) stabilizes lysosomal membranes, 2) decreases capillary permeability (by inhibiting COX2), 3) opposis leukocyte infiltration (chemotaxis via stopping leukotrienes), 4) suppresses T-lymphocytes, 5) decreases IL-1 (decreases fever)

What are the immune effects of glucocorticoids?

1) decreased allergy inflammatory response, 2) decreased eosinophils & lymphocytes, 3) increased lymphoid atrophy, 4) increased RBCs

What systems do the glucocorticoids affect?

muscle, liver, adipose, immune/inflammation

What are the glucocorticoid effects on muscle?

muscle wasting & t2dm via inhibiting GLUT4 translocation

What are the glucocorticoid effects on the liver?

increases glycogen, increases gluconeogenesis, increases insulin

What are the effects of glucocorticoids in adipose?

lipolysis, but insulin overpowers to cause lipogenesis

What enzyme converts cortisone to cortisol?

11-beta-HSD

What is a Type 1 receptor?

the MR

What is a type 2 receptor?

Where and when is CRF released?

by PVN of hypothalamus under stress

What is the function of PC1?

splits POMC to ACTH and beta-lipotropin; in the anterior pituitary

What is the function of PC2?

splits PC1 products to MSH and inactivated ACTH; in the hypothalamus

What is MSH?

melanocyte stimulating hormone

What are the effects of MSH?

1) melanin formation and dispersion, 2) decreased food intake/water consumption, 3) increased blood flow to brain, 4) increased tissue respiration

From what pre-prohormone is ACTH derived?

POMC (proopiomelanocortin)

What are the feedback loops in CRF/ACTH/cortisol?

cortisol inhibits CRF and ACTH (short and long loops)

What percentage of the adrenal gland is the medulla?

10-20%

Where is the type 1 (MR) receptor present?

in the kidney tubule

What are the relative affinities of corticosterone and aldosterone for the type 1 (MR) receptor?

they are equal

What are the relative affinities of corticosterone and aldosterone for the type 2 (GR) receptor?

corticosterone has greater affinity

Why does cortisone have aldosterone effects at high concentrations?

if 11-beta-HSD is overwhelmed, cortisol is not converted to cortisone and cortisol can trigger aldosterone-like (HTN) effects

What enzymes must be present to synthesize aldosterone?

aldosterone synthase

What enzymes must be present to synthesize the glucocorticoids?

17-alpha, but NOT 17,20

What enzymes must be present to synthesize the adrenal androgens?

17-alpha, AND 17,20

What are the adrenal androgens and what role do they play?

weak androgens that play large role in fetal development

What do adrenal androgens cause in males?

precocious puberty and stunted growth

What do adrenal androgens cause in females?

masculinization

What causes primary aldosteronism?

zona glomerulosa tumor

What is the treatment for primary aldosteronism?

surgery then aldosterone replacement

What is another term for addison's disease?

hypoadrenalism

What is another term for cushing's disease?

hyperadrenalism

What are the causes of Cushing's?

1) too much CRF: dysfuntional HT; 2) too much ACTH: anterior pituitary adenoma; actopic ACTH tumor; 3) too much cortisol: cortical adenoma; glucocorticoid therapy

What are the treatments for Cushings?

1) surgery, 2) block steroidogenesis with ketoconazole, 3) block ACTH secretion (serotonin antagonists and GABA-TA inhibitors)

What are the symptoms of Cushings?

buffalo torso (upper body fat), moon face, acne, hirsuitism, hyperglycemia