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135 Cards in this Set
- Front
- Back
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what is the CO and blood flow to the kidneys?
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25% CO, 1.25L / min
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what is used to measure GFR?
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creatinine, inulin...amount of creatinine filtered is equal to the amount excreted
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what are the determinants of GFR?
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size, electrical charge (negative charge is repelled), filtration decreasing with increasing size
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what specific forces cause ultra-filtration?
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starling forces of hydrostatic and osmotic pressures
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what factors affect Pgc or hydrostatic pressure in glomerular capillary.
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changes in afferent arterioles resistance...changes in efferent arteriole resistance. changes in renal arterial pressure
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what is the equation for renal blood flow?
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Q = deltaP / R
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what is used to measure RPF?
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para aminohippuric acid
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clearance ratio of <1 means?
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filtration and reabsorption
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clearance ratio of >1 means
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filtration and secretion
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what is autoregulation and what maintains it?
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it is the process of which RBF and GFR are maintained constant...maintained by myogenic mechanism and tubuloglomerular feedback
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what are the steps of the tubuloglomerular feedback mechanism?
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signal to inc GFR. this inc Na,Cl,K into macula densa. ATP goes to extraglomerular mesangial cell and to granular and VSM cells. causes renin release to decrease. afferent arteriole vasoconstrict..get larger effect on efferent arterioles of glomerulus, then GFR decreases
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what are steps of autoregulation via myogenic mech (short version)?
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depends on stretch activated Ca channels in SM.
an increase in pressure -->(myo mech) increase resistance --> reduce RBF and GFR |
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what is reabsorbed at the PT?
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67% Of filtered H2O, Na,Cl,K through Na-K ATPase. virtually all glc, AA
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How are ions/glc transported along the first half of proximal tubule?
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through coupling of the NHE3 on apical membrane with Na/K atpase on basolateral leading to Na into basolateral side.
there are also glc transporters |
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how are ions transported along 2nd half of PT?
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they enter via Na=H, Cl-anion antiporter on transcellular side.
paracellular takes advantage of inc [Cl] in first half to favor diffusion of Cl to interstitial space |
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loop of henle reabosrbs how much filtrate and how does it absorb Na?
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25% of filtrate. Na enters via Na-K-Cl symporter
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loop of henle reabsorbs how much filtrate and what ions?
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25% of filtrate and 15% of filtered H2O
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what does the descending thin limb reabsorb and what is the ion it doesn't absorb?
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water via AQP1 channel, Ca, and HC03. Doesn't reabsorb NaCL
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what does the thin ascending limb do and do not absorb?
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it is impermeable to H2O and reabsorbs NaCl by passive mechanism
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thick ascending limb reabsorbs via what mechanism?
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Na-K Atpase
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what does the DT and CD reabsorb and what %?
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8% of NaCl and 8-17% of H2O
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early segment of DT reabsorbs what and is impermeable to what?
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reabsorbs Na,CL,Ca by Na-Cl symporter and is impermeable to H2O
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Late segment of DT and collecting duct have what cells reabsorbing what?
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principle cells reabsorb NaCl, H2O, secrete K
intercalated cells reabsorb K, secrete H or HCO3 |
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angioII does what where?
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inc NaCl and H2O re absorption. acts on DT, TAL, DT/CD
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Aldosterone does what where?
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inc NaCL H2O re absorption (but not H2O in TAL)
stimulates secretion of K in DT, CD |
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ANP does what?
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released from atria in response to stretch of low-pressure sensors.
dilates arterioles -> inc GFR inhibits Nacl reabsorption in CD directly reduces plasma aldosterone by inhibiting renin release inhibits secretion of ADH |
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dopaine does what?
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Directly inhibits re absorption of NaCl and water in proximal tubule
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ADH does what
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regulates reasbsorption of h2o in kidneys. inc reabosption of h2o in CD
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positive h2o balance means
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intake exceeds loss
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neg h2o balance means
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intake less than loss
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normal values of urine osmolality
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50 - 1200 mOsm/ Kg h2o
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normal values of urine volume
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urine volume vary 18 - .5L / Day
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plasma osmolality
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measure number of solute particles in 1kg of h2o
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major determinant of osmolality in ECF
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Na, cl, hco3
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major determinant of osmolality in ECF
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k+
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how do kidney regulate body fluid osmolality?
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alternating volume and [urine] excreted
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what are external regulatory factors of regulating osmolality?
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sensory receptors, ADH -> causes dec excretion of h2o from kidneys
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countercourrent mechanism -
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inflow runs parallel to, counter to and in close proxmitity to the outflow for some distance
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countercurrent mechanism depends on
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maintaing gradient of inc osmolality along medullary pyramids
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countercurrent mechanism gradient is produced by
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the operation of the loops of henle as a countercurrent multiplier
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countercurrent mechanism is maintained by
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the operation of the vasa recta as countercurrent exchanger to help maintain salt balance
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role of urea in countercurrent mech is
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exert an osmotic effect on descending limb of loop of henle, promote h2o osmosis, inc the [NaCl] in the tubule and help passive re absorption of Nacl in ascending limb of LH
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Counter current multiplication happen in
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loop of henle
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Counter current multiplication allows urine
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to be concentrated / diluted and maintain plasma osmolality with kidneys ability to separate h2o from solute
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producing a dilute urine
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means low [Nacl and urea], approx 10% of GFR
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concentrate urine
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high [urine ] and non reabsorbed solutes..similar [] to that of inersititum
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effect circulating volumne
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volume of arterial blood (vascular ECF) effectively perfusing tissue
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baroreceptors
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respond to pressure changes and result in sympathetic nerve output and ADH secretion
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what are the 3 signals for RAA for secretion
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dec in arterial blood pressure as detected by baroreceptors
dec in Nacl in ultra-filtrate detected by macula densa, sympathetic NS activity acting through B1 adrenergic receptors, renin activates RAS by cleaving angiotensinogen |
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ANP released in response
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to stretch of low pressure sensors
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ANP effects
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inc GFR, inhibits Nacl re absorption in CD, reduces plasma aldosterone by inhibiting renin release, inhibits secretion of ADH
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% location of K+ body
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98% located inside cells, average is 150 mEq / L
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catecholamines
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stimulate re absorption of Nacl
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k regulated by 2 mechanisms
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regulate [k+] in ECF maintain the amt of K+ constant by renal excretion
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what happens with k+ regulation after a meal?
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after a meal by rapid uptake of K+ into cells. regulation within hours -> absorbed by GI tract -> excreted by kidneys
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what 3 hormones cause uptake into cell
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epinephrine, aldosterone, insulin
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what are 2 mech of K+ uptake
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acute stimulation of K+ uptake by an inc turnover rate of existing transpoter, chronic inc in k+ uptake is mediated by an inc in the quanity of na,k, atpase
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insulin effects
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stimulates uptake of k+ into cells and most important hormone to shift k+ into cells
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aldosterone effects
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promotes uptake k+ into cells. alters [k+] by acting on both uptake and excretion
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how does acidosis increase plasma [k+]CF from cell l
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inhibiting transporters that accumulate k+ inside cells -> reduced pH bc of reciprocal movement h+ into cells, k+ out
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how do organic acids cause less hyperkalemia
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organic anions may stimulate insulin secretion which moves k+ into cells. this movement may counteract the direct effect of the acidosis which moves k+ out of the cells
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metabolic alkalosis and respiratory alkalosis both dec plasma __
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k+
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what are 2 ways causing plasma osmolality imbalances for diabeetus pts?
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plasma [k+] often is elevated bc the lack of insulin and inc in plasma [glc ] inc plasma osmolality
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how can cell death cause hyperkalemia?
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the addition of intracellular K+ to ECF from cell lysis
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what ion is released from skeletal muscle during exercise?
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k+
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kidneys excrete ____ of k+ ingested in diet
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90-95%... 5-10-% of ingested are lost in excretion of shit and sweat
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key factor of determining urinary k+ excretion is the secretion of k+ by cells of ___ and ___
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DT and CD
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physio factors that keep k+ balance constant
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plasma, aldosterone, ADH
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Cellular mech of k+ secretion by principal cells in DT and CD
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Na / k atpase, electro chem gradient tof k+ across apcial membrane, permeability of apical membrane to k+ in going from inside to outside
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effect of aldosterone on secretion of k+ by principal cells in CD
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Inc k, k atpase in basolateral membrane. inc expression of enac, SGK1 -> inc Enac and k channels. inc CAP1, inc permeability of apical membrane to k+
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effect of ADH on k secretion by DT and cortical collecting duct
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inc electrochem gradient, inc permeability of apical membrane dec flow of h2o, urine flow helps keep constant balance
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cellular mech whereby an inc flow rate of tubule fluid stimulates secretion of k by principal cells in CD
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inc flow bends cilia, cause Ca secretion and stimulates Na entry
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what are 2 ways which glucocorticoids work?
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inc GFR -> inc flow rate -> inc urinary excretion of k+.
stimulate SGK1 -> inc urinary excretion of K+ |
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hypokalaemia is when [k+] in ECF is _____
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less than 3.5 mEq / L
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hyperkalemia is when [k+] _____
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exceeds 5 mEq / L
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pseudohyperkalemia
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lysis of RBC releases k+ into plasma and artificially elecvates k+ in plasma
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what are effects of hyper/ hypo kalemia on resting membrane potential?
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hyper - less negative, inactive fast Na channels, dec excitability.high t wave
hypo - hyperpolarize, reduce excitability, low t-wave |
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hypocalcemia condition and effects
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low ionized [ca]. closer to resting potential and inc excitability
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hypercalcemia
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inc ionized ca. decrease excitability
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calcitriol
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carrier mediated transport mech that GI tract absorbs Ca
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what hormones regulate distribution of ca between bone and ECF?
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PTH, calcitriol, calcitonoin regulate ca between bone and ECF
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calcitriol inc plasma [ca] by 3 ways
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inc the expression of key ca transport and binding proteins in the kidney
inc ca absorption by GI tract and facilitates action of PTH on bone |
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calcitriol
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hypocalcemia stimulates secretion of PTH -> stimulates production of vitamin D3
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inc plasma [ca] effects
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stimulates absorption of ca from GI tract reabsorption. facilitates action of PTH On bone. inc the expression of key ca transport and binding proteins in kidneys
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calcitonin
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dec plasma [ca] by stimulating bone formation
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acidosis
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inc plasma ionized ca, inc [h+] displaced to the bound Ca
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alkalosis
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dec plasma ionized ca
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hypoalbumineriea
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inc ionized ca+
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hyperalbumineriea
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dec ionized ca
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___% OF PLASMA CA IS FILTERED
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55%
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what are the cellular mech for reabsorption of ca by transcellular and cellular pathways in DT, PT, TAL
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DT - Has a transporter
PT- Transcellular TAL - paracellular |
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% location of phosphate in bone, ICF, ECF and normal []
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Bone - 86%, ICF - 14%, ECF .03%. normal [Pi] = 4mg / dL. approx 10% of PI is protein bound
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Pi homeostatsis depends on 2 factors?
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the amt of PI in the body, distribution of PI between ICF, ECF compartments - renal Pi excretion is primary mech by which body regulates PI balance and Pi homeostasis
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what hormones influence phosphate balance and effects?
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PTH, Calcitriol, stimulate release of Pi (and Ca) from bone. calcitonin inc bone fromation and dec plasma Pi
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what part of nephron reabsorbs primarily Pi?
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PT
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3 effects of pH fluctuation of pH on body
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influence enzyme activity, changes in excitability of nerve and muscle cells, influence K+ levels in body
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acidosis
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when addition of acid exceeds excretion
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alkalosis
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if excretion of acid exceeds addition
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3 mech to compensate A/B disorders
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intra/extra cellular buffering, alterations in ventilation rate of lungs, adjustments in renal net acid secretion
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hco3 is an important buffer of ECF and is regulated by ____ and __-
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lungs and kidneys
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____ greatly accelerates the rate limiting steps of co2 + h2o <-> h2co3
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carbonic anhydrase
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co2 is termed ______bc has potential to generate h+ after hydration with h2o
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volatile acid
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______ is acid not derived from hydration of co2
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nonvolatile acid
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metabolism of dietary AA yields _____
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non-volatile acid
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how much nonvolqatile acid is added to the body each day?
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.7 - 1mEq / kg body weight
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to excrete sufficient amount of aci
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h+ is excreted with urinary buffer called titratable acids...
synthesis and excretion of ammonium |
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3 methods of acid excretion
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reabsorbing filtered load of hco3, excreting an amt of acid equal to amt of non-volatile acid, secretion of ammonium NH4
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What mech are used for reabosption of hco3 by PT?
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Na-H antiporter...Na gradient. H-ATPase.
within cell -> H, HCO3 formed. -basolateral... HCO3 -> peritubular fluid by 1Na with 3HCO3 with Cl-HCO3 antiporters |
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loop of henle is similar to PT with only isoforms dif and addition
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K-HCO3 symproter on basoleteral membrane
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cellular mech for reabsoprtion and secretion of HCO3 by intercalced cells of C-alpha intercalated cells
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predominant. apical: h-atpase, HK atpase.
basolateral: CL, HCO3 antiporter |
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cellular mech for reabsoprtion and secretion of HCO3 by intercalced cells of beta intercalated cells
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this is hco3 secreting cell.
apical: CL, hco3 antiporter. basolateral: h-atpase |
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CD has apical membrane impermeable to ___
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H+
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net acid excretion must equal _____ to keep body pH constant
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nonvolatile acid production
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what % of hco3 is reabosrbed in PT, TAL, DT, CCD?
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PT 80%, TAL 10%, DT 6%, CCD 4%
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acid base disorders pH
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pH of ECF varies when either [hco3] or Pco2 is altered
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effect of cortisol in short term acidosis
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inc transcripition and translation of transporter
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2 ways of forming new hco3
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excretion of h+ with non-hco2 urinary buffers, production, transport, excretion of NH4+ by nephron
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(RTA) renal tubule acidosis is a condition in which ______ and caused by
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excretion by kidneys is impaired, can be caused by a defect in H+ secretion
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metabolic acidosis is compensated ?
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buffering of h+, respiratory compensation. ventilatory rate inc due to dec pH and this reduce pco2. renal compensation . renal net acid excretion in inc
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metabolic acidosis values
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hc03 < 24 mEq / L
pco2 < 40 mm Hg |
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metabolic alkalosis is compensated by
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buffering predominantly in ECF compartment, respiratory compensation - ventilatory rate is reduced, renal compensation - inc in the excretion by reducing its reabsorption along the nephron
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metabolic alkalosis values
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hc03 > 24 meq / L
pco2 > 40 mm hg |
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respiratory acidosis compensated by
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elevated pco2 and reduced ECF pH.
compensated by buffering almost entirely in ICF compartment, renal compensation with inc reabsorption of hco3 and excretion of titrable acid and NH4,inc net acid excretion and generate new hco3 |
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respiratory acidosis values
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pco2 > 40 mm Hg, [Hco3] > 24meq / L
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respiratory alkalosis
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reduced pco2 and inc ECF pH
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respiratory alkalosis compensated by
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buffering in ICF, renal compensation - inhibit reabsorption of hco3 by nephron and reduced excretion of titratable acid and NH4
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metabolic alkalosis is seen with wat kind of urine
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acidic urine
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Renal failure def
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progressive deterioration in renal function as evidenced by an inc in blood urea nitrogen, serum [creatinine] decline in urinary creatinine clearance and development of uremic symptoms
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azotemia
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biochem abnormality that refers to elevated BUN and serum [creatinine]
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dec reneal reserve means
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can't live under renal stress but can in normal life
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superficial nephrons responsible for
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excretory and regulatory
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juxtamedullary nephrons responsible for
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dilution and concentration
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GFR equals?
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(Urinary [creatinine] x urine flow rate) / plasma [creatinine]
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renal clearance is
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the rate at which all of substance X is removed from plasma in urine (volume / unit time)
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filtration fraction is
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the fraction of plasma filtered by the glomerulus and passing into the tubules. GFR / RBF
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