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10 Cards in this Set
- Front
- Back
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increased activation of what 2 systems occurs due to Na deficit
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inc activation of Renin-Angtiotensin and SNS
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describe ADH
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-acts primarily to protect ECF osmolality and to a lesser extent ECF volume by conserving water through effects on distal tubule and collecting duct
-changes concentration of ECF solutes but does not alter solute excretion by influencing water excretion -synthesized in hypothalamus (supraoptic and paraventricular nuclei), stored in posterior pituitary (pars nervosa) -inc water reabsorption and urea permeability of inner medullary collecting duct for reabsorption -stimuli include inc effective osmolarity of ECF via osmoreceptorts (ant hypothalamus); dec blood volume- low pressure baroreceptors monitoring venous return and high pressure baroreceptors monitoring CO via SNS activation; nausea and vomiting, pain, surgery, emotion, exercise, stress, NE, barbiturates, anesthetics, angiontensin 2 -diabetes insipidus- impairs ADH release, associated with diuresis, mild hypernatremia, excessive thirst and polydipsia -SIADH- excessive ADH release-water retention, hypotonic volume expansion and hyponatremia |
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describe desire to drink
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-hypertonicity is more potent stimuli; change 2-3% will produce strong desire to drink
-dec in blood volume 10-15% required to produce same response -dipsogen- causes thirst |
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describe the JG apparatus
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-granular cells- differentiated smooth muscle cells in afferent arteriole- make, store and release renin
-macula densa cells- specialized tubular epithelial cells that sense changes in delivery and subsequent reabsorption of Na and or Cl in late cortical portion of thick ascending loop -mesangial cells- interstitial cells in contact with both granular and macula densa cells |
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list renin-angiotensin cascade
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angiotensinogen (liver) to angiotensin 1 via renin from JGA
1 to angiotensin 2 via ACE to 3 via peptidase -angiotensin 2 acts on zona glomerulosa to secrete aldosterone; brain for thirst and ADH, kidney, CV vasoconstriction, NE release |
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describe characteristics of various molecules in RAAS pathway
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-renin half life 40-120 min, no physiological effect other than activating angiotensin 1
-angiotensinogen is an alpha 2 plasma globulin produced primarily in liver -angiotensin 2- half life 1-3 min; acts on efferent arterioles to inc tubular Na and water reabsorption -aldosterone- effects on distal tubule and collecting duct, lag of 1-2 hours |
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describe characteristics of aldosterone
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-stimulates active reabsorption of Na
-water is passively reabsorbed with Na so there is little inc in plasma Na concentration; ECV expands isotonically -only 3% of total Na reabsorption is regulated by aldosterone -acts via- inc number of Na channels on apical membrane, stimulates Na/K/ATPase on basolateral membrane, stimulates Krebs cycle in mitochondria, inc phospholipase activity and FA synthesis in cytosol -enhances tubular secretion of H as Na is reabsorbed therefore aldosterone excess can lead to metabolic alkalosis which can be aggravated by K depletion -stimulates renal excretion of magnesium |
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what stimulates aldosterone secretion
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-adrenocorticotropic hormone (ACTH)- released via anterior pituitary, secreted in large amounts in trauma and stimulates aldosterone secretion
-inc plasma K concentration -angiotensin 2 |
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what stimulates renin? inhibit?
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-intrarenal baroreceptors- volume or pressure within afferent arterioles
-macula densa- dec delivery of Na and Cl. dec flow may be due to reduced GFR or inc fluid reabsorption by proximal tubule -renal sympathetic nerves- neurons have direct stimulatory effect on renin secretion via beta 1 adrenergic receptors on granular cells, indirectly stimulate renin release by reducing flow to macula dense via dec GFR and inc reabsorption of proximal na and water INHIBIT -atrial natriuretic peptide- cardiac atrial cells secrete ANP- inhibits secretion of renin and acts directly on adrenal cortex to inhibit aldosterone release. inc Na excretion on nephron. released by hypovolemia -angiotensin 2 |
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describe aldosterone diseases
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-conn's syndrome- chronic primary hyperaldosteronism- chronically elevated plasma levels of aldosterone causes hypernatremia, hypervolemia-hypertension, hypokalemia, alkalemia
-addison's disease- aldosterone deficiency- inc in serum K, Na loss may lead to hypovolemia |
