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20 Cards in this Set
- Front
- Back
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Adrenal gland Location, Blood Supply
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On top of the kidney
Blood Supply - Superior, middle and inferior suprarenal arteries in and one suprarenal vein out Right suprarenal vein dumps directly into IVC, Left suprarenal vein drains into left renal vein Capsular artery dips into zona glomerulosa forms subcapsular plexus, then reforms down in zona fasciculata, then forms deep plexus/sinusoid and ends in zona reticularis at base Long medullary arterioles go all the way down to the medulla and form a medullary plexus for drainage |
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Derivative of all cortex hormones
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Cholesterol - source for all
Cholesterol to Pregnenolone (via P450 Scc) and produce NADPH Pregnalone to Progesterone (3 B-dehydrogenase) to Deoxycorticosterone (via 21-hydroxylase) to Corticosterone (via 11-hydroxylase) to Aldosterone (via P450 Aldosterone Synthase Pregnenolone to 17-Hydroxyprogesterone (via 17-Hydroxylase) to Deoxycortisol (via 21- Hydroxylase) to Cortisol (via 11-Hydroxylase) Pregnelone to 17Hydroxyprogesterone (17 Hydroxylase) to DHEA (via LYASE) to testosterone via 17 B hydroxylase |
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Hormone deficiency in:
a) 21-hydroxylase b) 17- Hydroxylase c) 11-hydroxylase |
a) 21-hydroxylase - Build up of progesterone, lack of aldosterone synthesis and cortisol (from deoxycortisol). Shunted to ANDROGENS
b) 17- Hydroxylase - Build up of Pregnenolone. Shunt to ALDOSTERONE, deficient androgens and cortisol c) 11-hydroxylase - Build up of deoxycorticosterone, Deoxycortisol. Lack of cortisol and aldosterone, SHUNT to androgens |
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Rate limiting step for:
a) Aldosterone production b) Cortisol c) Testosterone/DHEA |
P450 Scc conversion of cholesterol to pregnenolone is rate limiting step for ALL cortex hormones
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Zona Glomerulosa, Stimulation, Product, Role
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Stimulation: Low blood pressure leads to lower BP in afferent arteriole and lower Na+ delivered to macula densa. This induces JG apparatus to secrete renin which is converted to angiotensinogin to Ag I then AgII (via ACE in lungs).
AgII binds Gq receptor in zona glomerulosa which increases Calcium influx and release from intracellular stores. This induces cholesterol to pregnenolone to corticosterone (via 11-deoxycorticosterone) to aldosterone IN THE MITOCHONDRIA Role: Aldosterone induces Kidney to reabsorb Na+ (and water follows) and excrete K+ in Cortical collecting duct but inducing expression of more Na/K ATPase on basolateral side to absorb more back and also induces more passive Na+ channels in lumen to absorb more Na+ Increases Blood volume, Na+ reabsorption and K+ excretion Also ZG sense hyperkalemia so high levels will close Gq K channel as if AgII was bound, aldosterone is made |
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Cortisol effect on Cortical collecting duct
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While most action by aldosterone (more Na+ channels on apical side and more Na/K pumps on basolateral side
Cortisol converted to cortisone at kidney |
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Zona Fasciculata, Stimulation, Inducers, Feedback, Product, Primary Physiologic Role
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Stimulation: Hypothalamic-pituitary-adrenal axis. Stress in cortex induces hypothalmus to synthesize and release corticotropin releasing hormone (CRH). CRH carried to anterior pituitary binds Ga receptor, Calcium up inside, ACTH released.
Inducers: hypothalamus CRH release due to a) Hypoglycemia b) Stress (infection, trauma, surgery) c) Sleep/wake cycle ACTH binds MELANOCORTIN-2 receptor to induce Gs, to PKA to cAMP up leading to cholesterol to pregnenolone to cortisol in MITOCHONDRIA and secretion Feeback: ACTH inhibits hypothalamic CRH secretion (short loop), cortisol inhibits pituitary (ACTH) and hypothalamus (CRH) via long loop Role: Cortisol induces: Muscle - protein degredation, protein synthesis, lowered glucose utilization and insulin resistance Liver - gluconeogenesis, glycogen storage Fat - lipolysis, lowered glucose utilization and insulin resistance Net effect - spares glucose for brain Increases breakdown of fat and muscle to increase blood sugar to go to liver and promote glycogen storage HIGH cortisol actually increases abdominal lipogenesis though |
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Other effects of cortisol in long term use at medical dosage (steroids) and side effects
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Less muscle mass
Less bone formation and more resorption - osteopenia Less connective tissue - collagen striae Modulates wakefulness and emotional tone Inhibits inflammatory and immune response GFR - less ADH |
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When is ACTH release highest/when to test?
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Early in morning at right before 8AM ACTH peaks and shortly after Cortisol peaks
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Cortisol effect on immune system at medical dosage
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Less B cells, T cells
Lower cell mediated immunity Lower cytokine production Less PMN migration Lower capillary permeability ANTI-INFLAMMATORY at high dose |
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Zona Reticularis Products
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Androgens, not too important in men but a large source of testosterone for women
Stimulated by ACTH |
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Adrenal Medulla Hormone biosynthesis
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Cytoplasm:
Tyrosine to DOPA (tyrosine Hydroxylase) DOPA to Dopamine (DOPA decarboxylase) Secretory granule Dopamine to Norepi (DBH) Norepi to Epi (Phenylethanolamine N-methytransferase - PNMT!!, also RATE LIMITING IN GRANULE) - most are released as epi, some nor epi Catecholamine production dependent on glucocorticoids, blood flow from cortex filters through venous plexus to here so gets exposure RATE LIMITING STEP IN CYTOPLASM IS activation of TYROSINE HYDROXYLASE via cholinergic SNS stimulation |
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Adrenal medulla stimulation
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Preganglionic SNS neuron releases Ach onto chromaffin cell (modified postganglionic SNS neuron)
Epinephrine released to blood to tissue |
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Signs of Aldosterone Deficiency, Excess
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Deficiency - salt craving, natriuresis, hyponatremia, ACIDOSIS, dehydration, orthostatic HTN
Excess - Sodium retention, POTASSIUM DEPLETION, hypokalemic, ALKALOSIS, Expansion of ECV, HTN |
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Cortisol deficiency Disease, Signs
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Addison's disease, mostly due to autoimmune destruction
Signs: Weakness, fatigue, anorexia and weight loss. Nausea and vomiting, Hypotension and shock, hypoglycemia, HYPERPIGMENTATION IF PRIMARY |
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Hyperpigmentation in which cortex hormone deficiency and why
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Cortisol deficiency/Addison's disease IF PRIMARY (destruction of adrenal cortex tissue)
As cortisol decreases, pituitary secretes more ACTH to compensate. ACTH from bigger gene Proopiomelanocortin which also has B-MSH (melanocyte stimulating hormone) and B endorphin These will be higher than normal so get hyperpigmentation |
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Cortisol Excess disease, signs, Causes
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Cushing's Syndrome, HIGH ACTH, HIGH cortisol, HIGH Adrenal androgens
Signs: Truncal Obesity, "moon facies", Hirsutism, easy bruisability, slow wound healing, gonadal dysfunction, psychological disturbances, osteoporosis, hypertension Causes: adrenal hyperplasia (primary), Exogeenous corticosteroids (anti-inflammatory), ACTH secreting tumor (unlike others will have high ACTH) |
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Role of 11-hydroxydehydrogenase
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Convertes cortisol to cortisone to nactivate at plasma membrane and stop cross reactivity between glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
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Main cause of congenital adrenal hyperplasia, signs
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21-hydroxylase deficiency
Still have increased ACTH b/c pituitary trying to increase cortisol. Since 21-Hydroxylase not there, CANT make cortisol BUT DO make androgens instead in ZR and leads to signs Signs: Sex organ dysfunction and pseudohermaphroditism |
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Cortisol vs Insulin roles
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Cortisol - provides glucose during fasting states/stress by causing lipolysis, protein degredation and less synthesis, glycogen stoorage promotion . Excess promotes lipogenesis in abdominal region
Insulin - reduces glucose after meals, ALSO promotes glycogen synthesis but mostly contradicts cortisol |
