Physio Exam 3 Renal 4 Flash Cards

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Title: Physio Exam 3 Renal 4
Description: Physio Exam 3 Renal 4
Number of Cards: 48
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Author: dethlovemag9
Created: 2011-11-29
Tags: 3 4 exam physio renal
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    • Question
    • Answer
    • Side 3
    • Thick ascending limb is known as
    • Diluting segment because H2O is impermeable but NaCl is reabsorbed
    • Na+ reabsorption in the thick ascending limb is load dependent meaning
    • Amount of Na pumped by NKCC2 is load dependent. The more Na the more reabsorbed.
    • The NKCC2 pump utilizes
    • Na gradient
    • What maintains the [K] in the thick dascending tubule?
    • H channels on apical membrane
    • In the thick ascending tubule Na is also absorbed via
    • H secretion
    • As compared to the proximal tubule, thick ascending limb's reabsorption of HC03 is
    • smaller
    • Cation paracellular diffusion (Na, K, Ca, Mg) in the thick ascending tubule due to
    • the positive electrical gradient established
    • Loop diuretics inhibit NKCC2 as a consequence
    • consequence more NaCl loads delivered to distal part of nephron so as a consequence impair Na and water reabsorption of collecting tubules=diauresis
    • Barttter's Syndrome affects the thick ascending limb, what this occurs due to mutation in NKCC2
    • Mutation in the NKCC2, ROMK, or ClC-Kb channels cause an inhibition of NaCl
      and K reabsorbtion in the TAL via the NKCC2 pump. This results in an increase
      in Na+ delivered to the distal tubule and conducting duct, resulting in salt depletion
      and polyuria, triggering the renin-angiotensin-aldosterone pathway. Hyperaldosteronism
      causes hypokalemic metabolic alkalosis.
    • Bartters Syndrome can also be caused by a mutation in K channel leading to
    • same consequences as the mutation of NKCC2, in this case, mutation prevents back lead of K so NKCC2 function is compromised
    • Another Bartter's Syndrome mutation occurs in Cl channel mutation, leading to
    • elevation in intracellular Cl, NKCC2 is inhibited because it relies in the Cl gradient
    • Transport characteristic of the early distal tubule
    • Cortical diluting segment (Early distal tubule is impermeable to H20. This segment is the diluting segment because tubule is impermeable to water yet, NaCl is reabsorbed.)
      Electroneutral Na+ Reabsorption
    • Early Distal Tubule is the site of action of
    • thiazide diuretica
    • Electroneutral Na reabsorption in the early distal tubule is achieved by
    • Na/Cl symporter, Na and Cl into cell depending on Na gradient established by Na/K basolateral pump
    • Transport by the late distal tubule and collecting tubule
    • The collecting tubule sees the appearance of principal cells and intercalated cells
    • Principal cells job
    • Na+ Reabsorption (ENaCs)
      K+ Secretion
      Variable H20 Reabsorption (AQPs)
    • K secretion from principal cells is induced by
    • Aldosterone
    • Variable H2O reabsorption is induced by
    • ADH-.AQP
    • Intercalated cells job
    • Secrete either H+ or HCO3-
      Acid/Base balance
      Reabsorb and regulate K+
    • Hyperkalemia (elevated K) effect on action potential
    • elevation
      of Resting Membrane Potential and inactivation of fast Na+ channels,
    • Hypokalemia effect on Resting membrane potential
    • moves the RMP further
      from threshold. In the heart, alterations in
      K+ can also cause abnormalities in
      repolarization.
    • Cardiac arrhythmias are produced with
      both
    • hypo- and hyperkalemia
    • in terms of K balance The kidneys have the ability to
    • remove a lot of K
    • Immediate regulation of K balance
    • : Alter the internal K+ balance by altering the distribution of K+ between ICF and ECF. Minute to minute
    • Long term regulation of K balance
    • Alter the external K+ balance by altering the urinary excretion of K+. Effective
      after about 6 hours
    • Homeostatic regulatory mechanisms of internal K balance
    • Insulin
      Aldosterone
      Epinephrine
    • Insulin
    • Stimulates K+ uptake into muscle,
      liver, bone via stimulation of
      Na/K ATPase, NKCC1, NaCl
      symporters. In contrast, diabetes
      mellitus produces hyperkalemia
    • Aldosterone
    • Similar to insulin, induces K+ uptake
      but takes longer (60 minutes)
    • Epinephrine:
    • Epinephrine release stimulated by
      elevated plasma K+ as well as
      β2 agonists induce cell uptake
      similar to insulin. α agonists can
      produce the opposite, resulting
      in hyperkalemia.
    • Abnormal Plasma K can be caused by
    • Acid-base
      Osmolarity
      Exercise
      Cell Lysis
    • whats used to buffer acid-base shifts?
    • : The cellular H+/K+
    • Metabolic
      Acidosis can produce
    • hyperkalemia
    • Metabolic Alkalemia can produce
    • hypokalemia
    • acid base shifts leading to abnormal K production also involve direct inhbition of
    • Na/K Atapse and NKCC1
    • Hyperosmolarity causes
    • Hyperkalemia. As water leaves
      cells, ICF becomes hyperosmolar
      and K+ diffusion gradient increases
      as intracellular [K+] increases
    • Minor hyperkalemia can be caused by
    • increased muscle activity, but this minor hyperkalemia is important for local control of blood flow
    • . Rhadomyolysis and
      tumor lysis syndrome (cell lysis) can cause
    • : High cellular K+ can produce hyper-
      kalemia.
    • The regulatory event of external K balance is
    • regulated K+
      secretion by
      principal cells
      in the late
      distal tubule
      and collecting
      duct. Only place where K is regulated.
    • Regulated secretion of K by principal cells depends on
    • 1)Concentration gradient across the principal cell established
      by Na/K ATPase (If Na/K activity goes up, more Na out, K in, concentration gradient and K would be secreted through K channel at greater levels)
      2)The electrical gradient
      generated by the reabsorbtion of Na thru E-Na channels (If Na reabso stimulated, intracel more positive, K out of cell into lumen of nephron
      )
      3)The K+ permeability of the
      apical membrane
    • Hyperkalemia effect on principal cells
    • stimulates Na/K ATPase
      increases apical K+ permeability
      increases tubular flow rate
      increases aldosterone secretion
    • Hypokalemia effect on principal cells
    • inhibits Na/K ATPase
      reduces apical K+ permeability
      reduces tubular flow rate
      reduces aldosterone secretion
      increase reabsorbtion via the H+/K+
      exchanger in intercalated cells
    • Chronic Hyperkalemia effect on principal cells
    • increase Na/K ATPase
      increase ENaC
      increase Serum Gluccocorticoid-
      stimulated Kinase
      increase Channel Activating
      protease
      increase K+ channel permeability
      increases mitochondrial activity
      to support energy expenditure
    • Aldosterone stimulated by
    • Ang II or by hyperkalemia
    • ECF volume or diuresis effect on tubular flow rate
    • Increases Na+ load delivered
      to distal tubules and collecting
      duct and elevates principal cell
      [Na+], enhancing electrical gradient
      and stimulating Na+/K+ ATPase
      2)Bending primary cilium of
      principal cell activates Ca++
      entry via PKD1/PKD2 calcium
      channel, which activates K+
      channels (Maxi-K, ROMK)
    • Long standing chronic
      Metabolic Acidosis such
      as seen with diabetic
      ketoacidosis can result in
    • increased excretion
      of K+. Plasma levels in
      these patients can be
      elevated because of a shift
      in cellular K+ subsequent
      to acidosis; however total
      body K+ is reduced as
      excretion is stimulated.
    • Long standing chronic metabolic acidosis patients can be treated with insulin but this may lead to
    • serious hypokalemia
      and potential cardiac
      arrhythmias, so plasma
      K+ must be monitored
      during treatment
    • Short term metabolic acidosis effects
    • ; INHIBITION of Na/K Atpase and decrease in K permeability, secretion of K in principal cells decreased hence, so K in blood up, causing slight hyperkalemia
    • Long term, acid load for longer time, shift of acid into cell which exchanges
    • with K and pump K out of cell, K/h exchange increased, as a result, aldosterone is released. In the proximal tubule due to inhibition of Na/K Atpase, decrease in NaCl and H2O reabsorption hence tubule flow rate increases and extracellular fluid volume would decrease, more water excreted..aldosterone goes up at collecting tubule and distal tubule and K secretion would increase, so we would be depleting intracellular stores developing into hypokalemia.