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80 Cards in this Set
- Front
- Back
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Percentage of body weight TBW/ICF/ECF
Exception |
60/40/20
Can only be used in normal physiologic condition |
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Measuring Plasma Na in lipidemic plasma causes -
Why? |
Pseudohyponatremia
Because there is reduced water content in plasma (normal 93%) and increased solids (lipids/proteins). |
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PNa =
Posm = |
PNa = NaH20 x plasma fraction (normal = .93)
Posm = 2Pna Under normal conditions - if urea or BUN are elevated use Posm = 2PNa + (glucose/18) + BUN (2.8) |
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Fluid shifts
+ hypertonic NaCl + isotonic NaCl (IV fluids) + hypotonic fluid (water) Patient Case Study - What could cause acute hyponatremia with cerebral edema? |
Hypertonic NaCl: increases ECF osmolarity, causing ICF fluid to shift to ECF (ECF expands, cells shrink)
Isotonic saline: ECF volume increases, no change in osmolarity, no fluid shift Hypotonic fluid: Decrease ECF osmolarity, fluid shifts from ECF to ICF, ICF expands, cells swell. May cause edema Patient Case: Acute hyponatremia with cerebral edema after running marathon and drinking 10 L of water. |
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Glomerular Filtration Barrier composed of:
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Fenestrated endothelium, trilaminar basement membrane which negative charge, podocyte foot processes making slit diaphragms
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Normal GFR
Normal Urine Flow |
180 L/day or 125 mL/min
2 L/day |
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Clearance =
GFR = RPF = RBF = Filtration Fraction = Filtered Load = |
C = UV/P
GFR = Cin or Ccr = Kf ((Pgc-Pbc) - PIgc) RPF = Cpah RBF = RPF/1-Hct FF = GFR/RPF FL = GFR x Px |
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How can you increase GFR
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Increase Pgc by dilating afferent arteriole or constricting efferent arteriole or decrease plasma protein concentration
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Do Starling forces change across glomerular capillary?
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The hydrostatic force does not change but the plasma protein concentration (oncotic pressure) increases as fluids and solutes are filtered and proteins are left behind.
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Autoregulation
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As BP varies, GFR and RPF are kept constant. This is caused by afferent arteriole sensing stretch and constricting (myogenic reflex).
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Tubuloglomerular Feedback
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Juxtaglomerular apparatus has macula densa cells that sense NaCl concentration and distal flow rate. If the flow rate is too high (NaCl high), afferent arteriole constriction reducing GFR. If the flow rate is too low, dilate afferent arteriole to increase GFR.
TG feedback is probably mediated by adenosine causing vasoconstriction through A1 receptor. Modulation of set point by NO, PGs, angiotensin II. |
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JGA activation of Renin Angiotensin System
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JG cells synthesize renin when stimulated by sympathetic NS, decreased ECF volume, decreased NaCl/flow at macula densa, decreased renal perfusion pressure.
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Glomerulotubular Balance
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Increased GFR causes increased PT reabsorption. Cilia mechanosensation senses flow.
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Secondary Hyperparathyroidism in Renal Disease
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Kidneys can't return calcium to blood or hydroxylate Vitamin D. You need active Vit D to absorb calcium. Calcium concentration falls, PTH increases which causes bone resorption. Phosphorus binds to calcium further decreasing available calcium and complexes can be deposited in soft tissue.
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Tubular Transport in Early Proximal Tubule
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Na+ glucose/amino acid/lactate cotransporter - uptake of ~100% in PT
Na+ K+ ATPase on basolateral membrane controlling Na+ gradient Na+ uptake causes -Vte Na+ H+ exchanger - uptake of Na+ and H+ secreted, coupled to HCO3 reabsorption. H+ + HCO3 made into CO2 and H2O. CO2 goes back into cell to make HCO3 which is then reabsorbed. 3HCO3 made for 1 Na. |
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Acetazolamide
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Carbonic anhydrase inhibitor working in proximal tubule to block HCO3 reabsorption.
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Tubular Transport in Late Proximal Tubule
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Cl concentration has increased as Cl is not reabsorbed in early PT.
Transcellular pathway: Na+ H+ exchanger coupled to Cl/A- exchanger, Na and Cl uptake. Paracellular pathway: + Vte driving Na+ across TJs into blood. Cl gradient forms facoring diffusion of Cl from lumen to interstitium. |
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Water Reabsorption in Proximal Tubule
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Leaky TJs - isosmotic water reabsorption down gradient made by solute reabsorption
2/3 transcellular (aquaporins) 1/3 paracellular 67% of water and Na reabsorption in PT |
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Does inulin concentration increase or decrease along the proximal tubule?
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Increase, because water and solutes are being reabsorbed and inulin is left behind.
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Tubular Transport in Thick ascending limb
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Na+ K+ 2 Cl - cotransporter
K+ channels on apical and basolateral surface. +Vte drives reabsorption of Ca2+, Mg2+ Diluting segment - water impermeable |
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Furosemide
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Loop diuretic blocking Na+ K+ 2Cl - cotransport in TAL.
Enhances cation - Ca2+ and Mg2+ K+ - excretion |
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Early Distal Tubule Transport
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Apical NaCl cotransporter
Basolateral Cl - channel Low water permeability (does not respond to ADH) |
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Late Distal Tubule/Cortical Collecting Duct
Principal Cells Intercalated Cells |
Principal Cells: Na reabsorption and K+ secretion (enhanced by aldosterone). Na+ uptake through ENAC. Na+ K+ ATPase basolateral. K+ can go across apical or basolateral channel but favors apical channel/secretion because of -Vte.
-Vte is created by Na reabsorption Water permeability is low but in late distal tubule can be regulated by ADH. Intercalated cells regulated acid/base balance. |
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Medullary Collecting Duct
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ENAC reabsorbs Na
No apical K+ channel because K+ homeostasis is complete. Low water and urea permeability increased with ADH. |
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Thiazides
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Inhibit NaCl co transport in distal tubule
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K+ Sparing Diuretics
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Amiloride: blocks ENAC channels in collecting duct, decreasing -Vte, decreasing driving force for K+ secretion thereby decreasing K+ excretion.
Spironolactone binds to mineralcorticoid receptor blocking aldosterones action -blocking Na reabsorption and K+ secretion. |
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Liddle's Disease
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Monogenetic hereditary hypertension caused by mutation increasing # and activity of ENAC. Treat with amiloride.
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Fractional Excretion
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FE = (UxPcr/UcrPx)
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Net Transport Rate
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Tx = (GFR x Px) - (Ux x V) = filtered load - amount excreted
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What does it mean if a substance has a +Tx or a -Tx?
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+Tx is filtered and absorbed
-Tx is filtered and secreted |
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Positive Na Balance
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Suddenly increase Na+ intake, urinary output rises but doesn't equal intake for about 3 days.
PNa does not change during this time. Body weight increases (ECF expansion). |
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Negative Na Balance
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Suddenly decrease Na+ intake and urinary output of Na is more than intake for a few days. Pna constant, body weight decreases.
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Increased Na+ Intake
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Increase Posm, ADH release, increase thirst and water reabsorption. ECF expansion .
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High ECV
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High ECF volume, increased renal perfusion pressure, increased RPF (a lot), GFR, decreasing FF. Increased hydrostatic pressure, decreased oncotic pressure leading to increased reabsorption.
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Low ECV
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Low ECF caused by hemorrhage, CHF (low CO) decreased renal perfusion pressure, decreased RPF (a lot), decreased GFR, leading to increased filtration fraction. Oncotic pressure increases and hydrostatic pressure decreases thereby increasing reabsorption.
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Sympathetic Nervous System with low ECV
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Decreases GFR and RPF (a lot) increasing FF through efferent arteriole constriction. Increase PT reabsorption.
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ANP/Urodilation
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Increased ECV stimules ANP to increase RBF and GFR and inhibits aldosterone and renin.
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Hypervolemia
Reabsorption in nephron segments |
Decreased reabsorption in PT (50%) but increased reabsorption in TAL (30) and DCT (12). Deliver 8% to collecting duct and excrete 6%.
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Hypovolemia
Reabsorption in nephron segments |
Increase PT reabsorption (80%) and decrease in TAL (14) and DCT (4) but only 2% delivered to collecting duct and 0% excreted.
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Congestive Heart Failure - Problems with volume control
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ANP is not released from failing heart. Leading to increased CVP and edema.
Even though there is increased ECF there is decreased plasma volume (low CO, increasing Na reabsorption) therefore decreased ECV and CO. |
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Hyperosmotic Plasma Response
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Increased Posm triggers osmoreceptors for pituitary to release ADH - increased water reabsorption and antidiuresis. Increased water will return Posm to normal.
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Hyposmotic Plasma Response
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Decreased Posm will decrease thirst, osmoreceptors stop ADH release, water diuresis will bring Posm back to normal.
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Diabetes Insipidus
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Either no ADH produced (central) or kidney unresponsive to ADH (nephrogenic). This causes high Pna with excretion or large amounts of dilute urine.
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Antidiuretic Hormone (ADH aka Vasopressin)
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Increased Posm causes ADH release leading to increased water reabsorption. In pathophysiologic condition of decreased ECV, ADH can cause vasoconstriction which is why it is AKA vasopressin. ADH does not cause vasoconstriction in steady state. ADH decreases urine flow rate, increases water reabsorption, increases urine osmolarity.
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Measure Clearance using water excretion
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V = Cosm + CH20
V = urine output CH20 = solute free water Cosm = osmolarity clearance Cosm = UosmV/Posm |
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Water Diuresis
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No ADH, TAL and DCT reabsorb NaCl but not water. Dilute urine to 50-60 mOsm. Increase CH20 excretion.
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Antidiuresis
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Increased Posm increases ADH increasing Uosm and decreasing water excretion.
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Aquaporins
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Renal water channels in both apical and basolateral membranes. ADH binds to V2 receptors increasing aquaporin synthesis and expression on apical side
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Syndrome of Inappropriate ADH (SIADH)
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High ADH levels when there shouldn't be based on normal/low Posm. Retain water, decreasing Pna/Posm, increased Uosm.
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Kidney Countercurrent Multiplier
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Ascending limb actively transports Na into interstitium but water stays behind (water impermeable). Descending limb is water permeable and so its osmolality equilibrates with the interstitium. This causes an osmotic gradient from low in cortex to high in medulla.
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Countercurrent Exchanger
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Vasa recta maintain medullary gradient using passive countercurrent exchange. Descending vessel: as osmolarity increases - water moves out, solute enters. Ascending vessel: as osmolarity decreases -water diffuses in, solute diffuses out.
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Osmolality and Volume of Blood leaving Vasa Recta
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Increase osmolarity and volume because of fluid uptake while ascending.
Plasma protein concentrates on the way down as water leaves, and on way up they promote uptake of water. |
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Where is the equilibrium point in vasa recta?
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Its past the loop at the beginning of the ascending vessel.
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Blood osmolarity of descending vasa recta?
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As the interstitial osmolarity increases, water moves out and solute moves into the descending vessel. However, the blood osmolarity is still lower than that of the interstitium because of the flow rate.
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Where is urea permeable?
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Urea is permeable in the inner medulla - in the loop of henle (goes into lumen and is recycled) and in the medullary collecting duct (ADH needed) where it moves into interstitium. Urea is NOT permeable in the cortex and outer medulla
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What happens to urea in the PT?
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Urea is freely filtered and reabsorbed by passive transport based on its concentration gradient. It's concentration increases as water/solutes are absorbed, and therefore its gradient increases allowing absorption in late PT.
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What happens to BUN/Pcr ration in dehydrated patients?
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Increased because with antidiuresus there is low urine flow, increased urea concentration and reabsorption. However CrCl is independent of flow rate and doesn't change.
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What makes up the interstitial osmotic gradient?
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NaCl and urea. In inner medulla, 600 mOsm NaCl and 600 mOsm urea make up the 1200 mOsm.
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NaCl transport in loop of henle
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Descending loop has high water permeability and low NaCl permeability (water reabsorbed)
Ascending loop has low water permeability and high NaCl permeability so NaCl moves passively into the interstitium. |
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Hyperaldosteronism
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Hypertension and hypokalemia (increases Na reabsorption and K+ secretion)
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What would happen to patient with gastroenteritis who was vomiting but could drink water?
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Hypovolemia and hyponatremia: loss of hypertonic solution decreases Pna and volume. Volume wins out and ADH is released causing water reabsorption. Low volume concentrated urine output. Hypokalemia caused by aldosterone increasing Na reabsorption and K+ secretion. Alkalosis caused by loss of gastric HCl. Azotemia (increased BUN) because ADH also increases urea permeability and reabsorption.
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Metabolic Acidosis
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Low pH, low HCO3, low PCO2 (resp compensation)
Causes without anion gap: diarrhea (lose base) Causes with anion gap: diabetic ketoacidosis or lactic acidosis |
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Buffering systems
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ECF: HCO3 (immediate)
Respiratory: hyperventilate (acidosis) or hypoventilate (alkalosis) - min to hrs ICF: negative proteins/Hb (hrs) Renal NAE - increased NH4 excretion in acidosis (hrs to days) |
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How do you get rid of volatile acids? Nonvolatile Acids?
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Volatile acids like CO2 are excreted by lungs. Nonvolatile acids are excreted by the kidney (lactic acid, sulfuric acid)
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Metabolic Alkalosis
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high pH, high HCO3, high PCO2 (resp compensation)
Causes: vomiting lose HCl |
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Respiratory Acidosis
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low pH, high HCO3, high PCO2
Causes: lung disease |
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Respiratory Alkalosis
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high pH, low HCO3, low PCO2
Causes: hyperventilation |
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Anion Gap
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Unmeasured anions like negative plasma proteins (ketoacids, lactic acid).
Na - (HCO3 + Cl = 8-16 Use in metabolic acidosis. |
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Winter's Formula
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PCO2 = 1.5[HCO3] + 8
Should be within 2 of the PCO2, if not here is not appropriate compensation. Use in metabolic acidosis. |
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HCO3 reabsorption
How to increase? |
85-90% in PT coupled with H+ secretion using NHE.
Increase HCO3 reabsorption by increasing GFR or plasma HCO3 or PT reabsorption. Decreased ECF Volume , respiratory acidosis (high PCO2), high PCl (electroneutrality), aldosterone. |
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Titratable Acid Excretion
How to increase? |
H+ into lumen can titrate HPO4 to H2PO3. For each H+ secreted, release HCO3 into blood. Increased TA excretion means increased HCO3 reabsorption.
Increased buffer leads to increased H+ secretion. |
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Which buffer (phosphate or creatinine) is more effective at buffering in acidic urine?
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Creatinine is more effective because it's pK = 4.97 and urine can be decreased down to 4.4. Phosphate's pK is 6.8.
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Ammonia Excretion
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NH4 made from glutamine in PT cells (HCO3 made at same time) and secreted into lumen. NH3 more concentrated in medulla and diffuses into collecting duct where it is protonated to NH4, trapped, and excreted.
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Where do you adjust K+ secretion and reabsorption?
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Distal tubule and CCD.
A constant fraction of filtered load is reabsorbed, secretion influenced by aldosterone and diet. |
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What is the range of K+ excretion?
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1% (as low as possible) to 200% with high K+ diet.
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Which cell in collecting duct used for K+ reabsorption? K+ secretion?
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Intercalated cells used for K+ reabsorption and principal cells for K+ secretion.
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How can you increase K+ secretion?
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Increase flow rate (lower concentration at any given point in lumen, higher driving force/gradient), aldosterone, high K+ diet/high Pk, Alkalosis.
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How can you maintain K+ balance in water diuresis and antidiuresis?
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In water diuresis, increased flow increases K+ secretion but lack of ADH decreases K+ secretion.
In antidiuresis, ADH increases K+ secretion but low flow rate decreases K+ secretion. ADH prevents coupling of water and k+ balance. |
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Phosphate transport
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Freely filtered - reabsorbed 100% until Tm. Even a small increase in plasma concentrate gets to Tm and leads to excretion.
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PTH
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Increases bone resorption, Calcium and phosphate release. Increases calcium reabsorption in kidney (decreased in PT and increased in TAL and DCT) and decreases phosphate reabsorption in kidney.
Increases Vit D activation which then increases Ca reabsorption in kidney and GI Ca and P absorption. |
