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90 Cards in this Set
- Front
- Back
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what do mineralcorticoids effect
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electrolytes (minerals)
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zona glomerulosa
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thin layer of cells under capsule; secrete aldosterone (contain aldosterone synthase)
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what controls hormone secretion of zona glomerulosa
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angiotensin II and potassium
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zona fasiculata
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middle and widest layer-secretes glucocorticoids and small amounts of adrenal androgens and estogens
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What controls secretion of zona dasiculata cells
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ACTH
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zona reticularis
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deep layer of cortex-secretes adrenal androgens (DHEA and androstenedione) and small amounts of estrogens and some glucocorticoids
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what regulates secretion of zona reticularis cells
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ACTH and possibly other pituitary hormones (cortical androgen-stimulating hormone)
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what are adrenocortical hormones derived from and where do they obtain it
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cholesterol; most provided by LDLs in plasma
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how does cholesterol enter cells
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LDLs attached to coated pits and are endocytized
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what is transport of cholesterol into adrenal cells regulated by
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ACTH and angiotensin II increases LDL receptors and enzyme activity for appropriate cells
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what occurs to cholesterol once it enters the cells
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cleaved by cholesterol desmolase to form pregenolone in mitochondria (rate limiting step of all adrenal steroids)
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cortisol structure
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keto-oxygen on carbon 3 and is hydroxylated at carbons 11 and 21
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aldosterone structure
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oxygen bound at carbon 18
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aldosterone info
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mineralcorticoid; 90% of all mineralcorticoid activity
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desoxycorticosterone info
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mineralcorticoid; 1/30 as potent as aldosterone, small quantities secreted
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corticosterone info
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slight mineralcorticoid activity; glucocorticoid-4% total glucocorticoid activity, much less potent than cortisol
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9a-Flurocortisol info
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mineralcorticoid; synthetic and slightly more potent than aldosterone
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cortisol info
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very slight mineralcorticoid activity, but large amount secreted; very potent glucocorticoid, about 95% glucocorticoid activity
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cortisone info
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synthetic; slight mineralcorticoid activity; almost as potent as cortisol as glucocorticoid
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prednisone info
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synthetic; 4 times as potent as cortisol
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methylprednisone info
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synthetic; 5 times as potent as cortisol
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Dexamethasone info
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synthetic; 30 times as potent as cortisol; almost 0 mineralcorticoid activity
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what does cortisol bind in plasma
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90-95% bound to cortisol-binding globulin or transcortin, also some albumin
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what does degree of cortisol binding affect
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slows elimination of cortisol from plasma and gives uniform distribution; half-life of 60-90 minutes
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what does aldosterone bind in plasma
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40% free form; shorter half life of 20 minutes
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where are adrenal steroids degraded and by-products
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liver and mostly conjugated to glucouronic acid, some sulfates
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what happens to by-products of degraded adrenal steroids
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25% excreted in bile and then feces; remaining enter circulation and filtered by kidneys into urine
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what occurs in liver diseases
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depress rate of adrenocortical hormone inactivation
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what occurs in kidney diseases
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reduce excretion of inactivate conjugates
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normal aldosterone concentration in blood and secretory rate
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6 ng/ 100 ml; 150 ug/day (.15 mg/day)
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normal cortisol concentration in blood and secretory rate
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12 ug/100 ml; 15-20 mg/day
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what does mineralcorticoid deficiency cause
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severe renal sodium chloride wasting and hyperkalemia
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how quickly does mineralcorticoid deficiency become fatal
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3 days to 2 weeks without salt therapy or mineralcorticoid injection
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aldosterone vs cortisol mineralcorticoid activity
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aldosterone is 3000 times more potent, but cortisol concentration is 2000 times aldosterone
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how much can aldosterone decrease sodium loss
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as little as a few milliequivalents per day
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how much sodium can be lost with no aldosterone
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10-20 g per day into urine (1/10 to 1/5 total body sodium)
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what occurs when extracellular fluid volume increases 5-15% above normal
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arterial P increases 15-25 mmHg; called aldosterone escape
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what occurs when potassium in plasma falls 1/2 normal
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severe muscle weakness
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what occurs when potassium rises 60-100% above normal
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serious cardiac toxicity-weakness of heart contraction and dvlp of arrhythmia
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how does aldosterone affect hydrogen ions
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excess causes increased tubular H+ secretion and mild alkalosis
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how does aldosterone affect sweat glands and salivary glands (and colon)?
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same as it does on renal tubules; important to conserve salt in hot environments
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Aldosterone mechanism of action step 1
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diffuses across membrane to interior of tubular epithelial cells
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Aldosterone mechanism of action step 2
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combines with highly specific cytoplasmic receptor protein
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Aldosterone mechanism of action step 3
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aldosterone-receptor complex diffuses into nucleus…finally inducing one or more specific portions of DNA to form mRNA
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Aldosterone mechanism of action step 4
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mRNA diffuses to cytoplasm and creates proteins via ribosomes
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what are the proteins/enzymes formed via aldosterone induction
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Na/K ATP in basolateral membrane, part of pump; epithelium Na channel proteins in luminal membrane
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how long does it take for new enzymes/proteins induced by aldosterone take to become effective
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45 minutes and reaches max after several hours
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possible nongenomic actions of aldosterone/steroid hormones
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second messenger systems
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most important regulators of aldosterone in order
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1) K+ increases 2) renin-angiotensin system 3) Na+ increases 4) ACTH-doesn't control rate of secretion
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best known metabolic effect of glucocorticoids
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stimulate gluconeogenesis by liver as much as 6 to 10 fold
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Two effects of cortisol that cause gluconeogenesis
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1) increases enzymes required to convert aas into glucose in liver cells 2) mobilization of aas from extrahepatic tissues (maily from muscle)
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What is the benefit of the liver soting more glucose due to cortisol stimulated gluconeogenesis
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allows other glycolytic hormones (ephinephrine, glucagon) to mobilize glucose in times of need
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suggested mechanism of cortisol decreasing glucose utilization in most body cells
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depress oxidation of NADH to form NAD+; NADH is required to allow glycolysis
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proposed mechanism of why insulin is not as effective with elevated glucocorticoids
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glucocorticoids cause mobilization of lipids and may impair insulin actions on tissues; similar to excess GH effects
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what can occur with great excess of cortisol
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muscles extremely weak, immunity fxns of lymphoid tissue decreased drastically
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what is required for deposition and maintenance of triglycerides in adipose cells
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alpha-glycerpphosphatase
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what occurs in the absence of alpha-glycerpphosphatase
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mobilization of fatty acids
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how long does it take for cortisol to shift metabilic systems in cells
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several hours (in contrast to rapid change in insulin)
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What stresses can cause increase in cortisol
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1) trauma 2) infection 3) intense heat or cold 4) injection of norephinephrine and other sympathomimetic drugs 5) surgery 6) injection of necrotizing substances under skin 7) restaining 8) debilitating diseases
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How does cortisol block inflammation (5)
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1) stabilizes lysosomal membranes 2) decreases capillary permeability 3) decreases migration of WBCs 4) suppresses immune system 5) attenuates fever
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what diseases are characterized by severe local inflammation that harm body due to inflammation
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rheumatoid arthritis, rheumatic fever, acute glomerulonephritis
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what WBCs does cortisol decrease in blood
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eosinophils and lymphocytes
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how does a large dose of cortisol affect immunity
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atrophy of all lymphoid tissue-decreases T cells and antibodies; level of immunity for almost all forgein invaders decreased
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cortisol and RBCs
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increases cause increase in RBCs-unknown mechanism
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ACTH alternate names and fxn
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corticotropon, adrenocorticotropon; stimulates glucocorticoid and enhances adrenal androgen production
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ACTH structure
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large polypeptide with 39 aas
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what controls ACTH
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CRF from hypothalamus
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where are the cell bodies that secrete CRF
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paraventricular nucleus of hypothalamus-receives nervous connections from limbic system and lower brain stem
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principle affect of ACTH
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activate adenylyl cyclase in cell membrane which induces cAMP formation in cytoplasm (reaches max effect in 3 mins)
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most important of all ACTH-stimulated steps for controlling adrenocortical secretion
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activation of protein kinase A-causes initial converion of cholesterol to pregnenolone
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how does mental stress affect cortisol secretion
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increased activity in limbic system, especially in amygdala and hippocampus
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Daily cycle of ACTH and CRF
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high in morning, low at night
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proopiomelanocortin (POMC)
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precursor to ACTH and several other peptides including melanocyte stimulating hormone (MSH), B-lipotropin, B-endorphin…
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Where is POMC actively transcribed
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corticotroph cells of anterior pituitary, POMC neurons in arculate nucleus of hypothalamus, cells of dermis, lymphoid tissue
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prohormone convertase 1 causes POMC to make…
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N-terminal peptide, joining peptide, ACTH, B-endorphin, B-lipotropin; expressed in corticotroph cells
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prohormone convertase 2 in the hypothalamus make what from POMC
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alpha, beta, and gamma-MSH
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what does alpha-MSH play a major role in
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appetite
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ACTH affect on melanocytes
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1/30 as potent as MSH, but much greater quantites…therefore ACTH is likely more important than MSH in determining amount of melanin in skin
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What do androgens cause in females
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growth of pubic and axillary hair
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what causes addison's in 80%
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autoimmunity against cortices
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lack of aldosterone causes…
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decreased extracellular fluid V, hyponatremia, hyperkalemia, and mild acidosis
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glucose/metabolism issues in glucocorticoid deficiency
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glucose issues btwn meals since can't synthesize glucose by gluconeogenesis, also lack of mobilization of proteins and fats from tissues
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Effects of Cushing's are caused from excess…
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cortisol and androgen secretion
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cushing's disease
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when cushings is secondary to excess secretion of ACTH by anterior pituitary
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primary overproducation of cortisol is present in what percent cushings
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20-25%; high cortisol, low ACTH levels
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why do 80 % cushings patients have hypertension
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mineralcorticoid affects of cortisol
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metyrapone, ketoconazole, aminoglutethimide are drugs that
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block steroidogenesis; can be useful in cushings
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serotonin antagonists and GABA-transaminase inhibitors are drugs that
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inhibit ACTH secretion
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Conn's syndrome
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primary aldosteronism; small tumore in zona glomerulosa that secretes large amount of aldosterone
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diagnostic criteria for primary aldosteronism
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decreased plasma renin concentration
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