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60 Cards in this Set
- Front
- Back
range of osmolarity of urine that can be excreted by kidney
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50 mOsm/L to 1200-1400 mOsm/L
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action of ADH
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increase permeability of distal tubules and collecting ducts to water
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net consequence of ADH
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large amount of water reabsorbed, decreased urine V, but doesn't markedly change the rate of renal excretion of the solutes
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what is the osmolarity of fluid leaving the early distal tubule
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~100 mOsm/L regardless of ADH concentration (hypo-osmotic, plasma is 3 times more)
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why does severe dehydration occur by drinking seawater
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seawater has osmolarity around 1000-1200 mOsm/L, max kidney urine concentration ability is 1200 and the kidney has to get rid of more solutes than just the components of the seawater (at least 600 mOsm/day)
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components required for concentrated urine
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1)ADH 2) high osmolarity of renal medullary interstitial fluid
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vasa recta
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specialized peritubular capillaries of the renal medulla
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Major factors that contribute to the build-up of solute concentration in the renal medulla
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1) active Na+ transport and co-transport of other electrolytes out of thick ascending and loop of Henle 2) active transport of ions from collecting ducts 3) facilitated diffusion of urea into interstitium 4) diffusion of only small amount of water from medullary tubules into interstitium
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why is the osmolarity difference of the thick ascending loop max out around 200 mOsm/L
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paracellular diffusion of ions back into the tubule eventually counterbalances transport of ions out
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countercurrent multiplier
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repetative reabsorption of NaCl by the thick ascending loop of Henle and contiued inflow of new NaCl from the proximal tubule into the loop of Henle
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what preserves high medullary interstitial fluid osmolarity when water is reabsorbed (especially in presence of ADH)
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reabsorbed into the cortex where it is swept away by rapidly flowing peritubular capillaries
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what percent of renal medullary interstitium osmalarity is urea responsible for
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~40-50%
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how is urea reabsorbed
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passively in inner medullary collecting ducts
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what is the urea transporter UT-AI activated by
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ADH
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malnutrition and urea concentration ability
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low in medullary interstitium and considerable impairment of urine concentration ability
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how much of the filtered load of urea is usually excreted
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20-50%
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what determines rate of urea excretion
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1) concentration of urea in plasma 2) glomerular filtration rate (GFR)
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where is 40-50% of filtered urea reabsorbed
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proximal tubule
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what areas are fairly urea impermeable
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thick limb, distal tubule, and cortical collecting tubule
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how can urea circulate through the terminal parts of the tubular system
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secreted into thin loop of henle and is reabsorbed in collecting duct
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Two special features of vasa recta that preserves high solute concentrations
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1)medullary blood flow is low 2) serve as a countercurrent exchange minimizing washout
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what can increase blood flow in renal medulla and 'wash-out' solutes
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vasodilators, high arterial P
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reabsorption in porximal tubule
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~65% filtered electrolytes reabsored here, but water follows
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descending loop permeabilities
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water, less to NaCl and urea
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thin ascending limb permeabilities
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not to water; reabsorbs some NaCl and urea
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thick ascending limb permeabilities
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not to water; large amounts of NaCl, K+ actively transported into interstitium; 100 mOsm/L filtrate
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what does low Na+ concentration in body stimulate
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angiotensin II and aldosterone
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osmolar clearance
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volume of plasma cleared of solutes per minute
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osmolar clearance formula
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Cosm = Uosm x V / (Posm); Uosm is urine osmolarity, V is urine flow rate, and Posm is plasma osmolarity
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Free water clearance
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represents rate at which solute-free water is excreted by the kidneys; difference btwn water excretion (urine flow rate) and osmolar clearance
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what does a pos/neg free water clearance mean
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pos = excess water being excreted; neg = excess solutes being removed
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what can impair ability to concentrate urine
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1) inappropriate ADH secretion 2)impairment of countercurrent mechanism 3) inability of distal tubule, collecting tubule, and collecting ducts to respond to ADH
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another name for failure to produce ADH
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central' diabetes insipidus
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what can cause central diabetes insipidus
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head injuries, infections, congenital
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central diabetes insipidus treatment
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synthetic ADH called desmopressin
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what does desmopressin act on
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selectively on V2 receptors to increase water permeability in late distal and collecting tubules
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another name for inability of kidneys to respond to ADH
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nephrogenic' diabetes insipidus
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what can cause nephrogenic diabetes insipidus
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failure of countercurrent mechanism; failure of distal and collecting tubules to respond to ADH
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how do diuretics impair concentrating ability
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inhibit electrolyte reabsorption
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what drugs can impair kidney response to ADH
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lithium and tetracyclines
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plasma Na+ concentration
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140-145 mEq/L
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Plasma osmolarity rough calculation
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Posm = 2.1 x Plasma Na+ concentration
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why does urea exert little effective osmotic P under steady state conditions
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easily permeates most cell membranes
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Two primary systems involved in regulating concentration of Na+ and osmolarity of ECF
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1) osmoreceptor-ADH system 2) thirst mechanism
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where are osmoreceptor cells
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anterior hypothalamus near the supraoptic nuclei
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what occurs when osmoreceptor cells shrink
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causes them to fire relaying signals down stalk of pituitary gland to posterior pituitary
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magnocellular neurons in the hypothalamus that synthesize ADH
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supraoptic and paraventricular nuclei
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how rapidly can ADH be secreted
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rapidly; plasma ADH levels can increase several fold within minutes
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anteroventral region of the third ventricle contains
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subfornical organ on upper part, inferior is organum vasculosum, and in the middle s the median preoptic nucleus
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connections of the median preoptic nucleus
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supraoptic nucleu and BP control centers in the medulla
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what cardiovascular reflexes can control ADH secretion
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1)arterial baroreceptor reflexes 2) cardiopulmonary reflexes (aortic arch and carotid sinuses, cardiac atria)
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what nuclei are P refexes sent to from the glossopharyngeal and vagus nerves
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tractus solitaris
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what drugs stimulate ADH release
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nicotine, morphine; (alcohol inhibits)
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thirst center
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anteroventral wall of 3rd ventricle
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angiotensin II and thirst
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acts on organum casculosum
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how long is required for water to be absorbed once ingested
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30-60 minutes
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angiotensin II and aldosterone effect on sodium concentration
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little effect except under extreme conditions due to water reabsorption along with Na+
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Addisons and sodium concentration
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lack of aldosterone leads to sodium wasting, thirst mechaism compensates for volume loss, but not Na+ loss
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average industrial Na+ intake vs necessary intake
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100-200 mEq/day vs 10-20 mEq/day
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two primary stimuli for salt appetite
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1) decreased ECF Na+ concentration 2) decreased blood V or BP; similar neuronal mechanisms as thirst mechanism
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