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16 Cards in this Set
- Front
- Back
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Formula for determining fractional excretion of sodium.
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FENa = UNa/PNa ÷ Ucreat /Pcreat
Urine Sodium = UNa Plasma Sodium = PNa |
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What is the best indication of a patient's sodium intake?
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24-hour urinary sodium excretion; what comes out in urine is almost exactly the same as how much you ingest (when in a steady-state)
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Which of the following would best indicate that a patient is hypovolemic?
Low plasma sodium Low urinary sodium High cardiac output Chest x-ray with small cardiac size Elevated plasma catecholamines |
Low urinary sodium concentration: under conditions of hypovolemia, mechanisms of renal sodium conservation are activated.
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In order to determine whether a patient's change in renal function is due to hypovolemia or aminoglycoside toxicity (which causes tubular dysfunction), which of the following tests would you recommend?
Plasma renin activity Plasma aldosterone level Fractional excretion of sodium Plasma sodium concentration Measurement of cardiac output |
Fractional Excretion of Sodium: to distingush:
FENa should be low (<1%) during hypovolemia; will exceed 1% when tubular injury occurs, since tubules have lost capacity for Na reabsorption |
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Where does the bulk of sodium reabsorption occur?
Where does the remainder of sodium reabsorption occur? |
Bulk of sodium reabsorption takes place in Proximal Tubule
Some in ascending limb Some in DCT Some in collecting duct These latter 3 do fine tuning! |
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How is sodium absorbed in the proximal tubule?
How does this differ in the early and late proximal tubule? |
Proximal tubule: Isosmotic absorption of solutes; 2/3 of sodium and H2O is absorbed here ISOSMOTICALLY
Early Prox Tubule: Linked to cotransport process with glucose, AAs, phosphate, and bicarb (these are all reabsorbed); countertransport of H+ Energy process that drives all this is Na/K ATPase, which allows outward movement of Na and inward movement of K; sets up energy to drive other processes (which facilitate entry of Na into cell) Late Prox Tubules: Na/H exchanger links with Cl- exchange; Na entry, |
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Fanconi Syndrome is a disorder of proximal tubular function. Which of the following would you NOT expect in the urine of a patient with Fanconi Syndrome:
Phosphate Glucose Bicarbonate Acid urine pH Amino Acids |
Acid urine pH; in Fanconi, can't reabsorb bicarbonate; bicarbonaturia would alkalinize the urine, an acid urine pH is not expected.
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Peritubular capillary forces in sodium reabsorption.
Decribe changes in states of volumetric contraction and expansion. |
Net vector of sodium back into peritubular capillaries
If you have forces favoring reabsorption of solute, then you'll reabsorb more Na in peritubular capillaries; happens in pts with volume contraction, higher colloid osmotic pressure, constriction of efferent arteriole (lower hydrostatic pressure); favors increased reabsorbed uptake of Na In volume expansion, filtration fraction decreases, colloid osmotic pressure decreases, capillary pressure is higher, so although still absorbing in peritubular capillary, it's not as much. |
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Describe solute reuptake in the thick ascending limb.
Relevant drug? Water permeability? |
Thick Ascending Limb: 25% of sodium reabsorption takes place
Done by Na/K/2Cl cotransporter; 1 Na in per 2 Cl- in; this is inhibited by Furosemide Also electrogenic bc inside of channel is positive, and Cl- is negative This is part of diluting segment; is not permeable to water! |
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Bartter's Syndrome is associated with an inherent defect in the function of the ascending limb of the loop of Henle.
Which of the following would NOT be an expected clinical feature: Hypokalemia High Urine Chloride Metabolic Aklalosis Elevated Renin-Angiotensin-Aldosterone Elevated Blood Pressure |
Elevated BP; due to defect in chloride transport in TAL, Bartter's syndrome is characterized by Na, K, and Cl loss in urine.
Resultant hypovolemia activates Renin-Ag system. Despite activation of Renin-Ag, systemic HTN does not occur. (Losing Na/K, bicarb goes up and get alkalosis) |
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Describe solute reuptake in the early distal tubule.
Relevant drug? Water permeability? |
Early Distal Tubule:
Load dependent Na/Cl cotransporter; inhibited by thiazide Diluting segment, so impermeable to water |
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Describe solute reuptake in the late distal tubule and collecting duct.
Relevant drug? Water permeability? |
Late Distal Tubule and Collecting Duct:
Epithelial Na-channel (ENaC) blocked by K-sparing diuretics (amiloride, triampterene) and INDUCIBLE by aldosterone |
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Use of diuretics is characterized by the "braking phenomenon"--a reduction in urinary sodium loss after the first few days of use.
Which of the following would NOT explain this phenomenon: Occupancy of drug receptors Stimulation of aldosterone and late distal sodium reabsorption Augmented Na reabsorption in early distal tubule Reduction in GFR and filtered load of sodium Augmented proximal reabsorption of sodium |
Occupation of drug receptors
Braking phenomenon is characteristic to all diuretics. Simply put, it means that if one segment of the nephron is blocked by diuretic action, the other segments compensate by augmenting sodium reabsorption. If a loop diuretic is adiministered, within days, the proximal and sital tubules, and collecting duct will increase Na reabsorption, through the other mechanisms described. |
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Describe the role of ANP in maintenance of blood volume.
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ANP:
When there's increased fluid volume, as in heart failure, there is decreased production of vasopression, aldosterine, renin; Results in inc'd salt and water excretion ALL OF THIS MEDIATED THROUGH ANP which blocks these hormonal systems; also acts as vasodilator to reduce systemic resistance and blocks Na+ reabsorption ANP leads to inc'd Na+ excretion Dec'd atrial volume-->ANP is decreased; activates symp NS to inc Na+ resorption in both proximal and distal tubules |
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What are the effects of AgII?
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Vasoconstriciton
Aldosterone secretion-->Inc'd tubular Na reabsorption |
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Mr. Aldrich is a 40 year-old man with severe hypertension. On examination he is found to have a blood pressure of 200/105 in the right arm. However, when blood pressure is measured in the right leg, it is 130/80 and radio-femoral “pulse delay” is noted.
What is the most likely diagnosis? |
Aortic Coarctation:
The characteristic clinical features of aortic coarct are hypertension, confined to the upper limbs, along with pulse delay. |
