metabolic alkalosis - columbia university€¦ · to produce alkalosis, but, it is insufficient...
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Metabolic AlkalosisHigh pH HighHCO3 High pCO2
Development of Metabolic Alkalosis
Generation of Excess HCO33HCO3 Ingestion or Acid Loss
Maintenance of Excess HCO3Maintenance of Excess HCO3Increased renal H+ secretion
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Metabolic AlkalosisGeneration of Excess HCO3
HCO3 Ingestion
HCO3 Generation from metabolizeable anions e.g. lactate, citrate or β-OH butyrate
Metabolic Alkalosis
Acid Loss
vomiting ; upper GI suction
Generation of excess HCO3 is often necessary
to produce alkalosis, BUT, it is insufficient since
the kidney’s ability to excrete HCO3 is very large
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Maintenance of Metabolic Alkalosis
The higher level of HCO3 is maintained by increased renal H+ secretion
1. Decreased Filtration Rate2. Volume Depletion increases Proximal
HCO3 Reabsorption by a. High Filtration Fractiona. High Filtration Fractionb. AII stimulates Na:H exchanger
3. High aldosterone increases collectingduct H+ secretion and HCO3 generation
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Potassium
Intracellular Extracellular
[K] = 110 mEq / L[Na] = 10 mEq / L
[K] = 4 mEq / L[Na] = 140 mEq / L
Total Body K 4400 mEq 50 mEq
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K
4
Time, hrs
Disposal of an ingested K Load occurs by re-distributionand by urinary excretion
K
Acidosis
4Alkalosis
Time, hrs
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K
Diabetes
4Insulin
Time, hrs
K
β blockers
4Epinephrin
Time, hrs
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PCT DCT
ThAL CDThAL
K is Freely Filtered s ee y te ed
> 95% of Filtered K is reabsorbed in the Proximal Tubule and Thick Ascending Limb
What appears in the Urine is secreted by the Distal Tubule and Collecting Duct
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K Secretion in Collecting Duct
NaK
ENaC
KNa
K
ENaC Epithelial Na ChannelK K channel
H,K ATPase
Driving Forces for K Secretionin Collecting Duct
KK
-100 mV
0
Concentration GradientTrans-epithelial Membrane Potential
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0.3
0.35N
Hi K diet
0 05
0.1
0.15
0.2
0.25
Low K diet
0
0.05
0 5 10 15 20 25 30 35
Tubule Flow rate, nanoL/min
Regulation of K Secretion
Na ENaCK
Na
K
Aldosteroneincreases activity of K channelincreases activity of Na channelincreases Na,K ATPase
KK
Urine Flow Ratebrings in low K tubular fluid
Acid Base balance affects Cell K
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Approach to the patient withHypo- or Hyperkalemia
1. Redistribution Acid/Base status, insulin, catecholeamines
2. Intake dietary;; Intravenous
3. Renal Excretion Aldosterone, Urine Flow Rate, Acid/Base statusRenal FailureInterstitial Disease
4. Non-Renal Loss Gastro-intestinalSweat
HypokalemiaRedistribution
Alkalosis; Glucose/insulin; Catecholeamines
Increased ExcretionHyperaldosteronism
primary: (including Cushing’s Syndrome)secondary: CHF, volume depletion, cirrhosis
Increased Urine Flow Rate DiureticsAlkalosisDrugs Amphotericin B
Extra-renal Loss Sweating; Diarrhea; Vomiting
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Clinical Manifestations of HypokalemiaMuscle Weakness eventually paralysis;
occasionally rhabdomyolysis
RT aKiMembrane Potential ΔΨ = - ln
F aKo
C di th iCardiac arrythmias
Clinical Manifestations of Hypokalemia
Effects on Renal FunctionInhibition of concentrationIncreased HCO3 reabsorptionIncreased NH3 production
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Hyperkalemia
RedistributionAcidosis; Diabetes β-blockers; β
Increased IntakeOral or I.V. (with Renal Failure)
Decreased ExcretionLow AldosteroneDecreased Flow RateAcidosisDrugs
Hyperkalemia
Decreased Excretion-Hypoaldosteronism
primary: Addison’s Diseasesecondary: Hyporeninemic Hypoaldosteronsim
ACE inhibitors-Decreased Urine Flow Rate
Acute Renal Failure with oliguriag-Acidosis-Drugs K sparing diuretics
NSAIDsHeparin
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Clinical Manifestations of Hyperkalemia
Cardiac Arrythmia
Hyperkalemia can induce acidosis by inhibiting NH3 production in the nephron
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