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15 Cards in this Set
- Front
- Back
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3 principal regulators of serum K+
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Insulin
Epinephrine Aldosterone |
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Hyperkalemia and EKG
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1. High T wave
2. Prolonged PR, depressed ST 3. IV block 4. Vfib |
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Principal cell
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Cell in CCT
Na/K control (reg by ald) |
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Na channel blockers
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"Amiloride
Triamterene Trimethoprim Pentamidine" |
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Pseudohypoaldosteronism
(and types) |
"True Aldosterone Resistance
Type IA Dominant - defect in Mineralocorticoid receptor (Milder) Type IB Recessive - defect in ENaCl (Severe) Type II Dominant - unknown (defective chlorine shunt)" |
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Bartter's vs Gitelmans
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"BOTH: Hypokalemia, metabolic alkalosis, normal/low BP, Inc renin, res to Ang II
Bartter's (Defect in TAL)- Normal or in Ca2+, Normal to low Mg2+ Gitelman's (na/cl coT in DCT) - Low ser Mg, low urine Ca" |
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K+ in mineral vs organic acidosis
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"Mineral: Increase K+ because anions are held extracellularly (pulling K+ out)
Organic: No change. Organic anions are taken into cell" |
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Types of Bartter's
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"Type I - NKCC2 - Na/2Cl/K CoT
Type II - ROMK - K passive Type III - CIC_Kb - Cl passive" |
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(170)
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(170)
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Henderson-Hasselbach
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pH = 6.1 + log[HCO3-]/(.03Pco2)
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Normal anion gap
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"12-14 w/ potassium
6-10 w/o potassium" |
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Causes of high anion gap Acidosis
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"Methanol
Uremia Diabetic ketoacidosis Toluene Infection Lactic Acidosis Ethylene glycol Salicylates" |
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"Causes of hyperchloremic metabolic acidosis
(extrarenal)" |
HCl generating compounds
-NH4Cl, HCl, Larginine, Llysine, Cl gas, Hyperalimentation GI HCO3 losses -Diarrhea, Ileus, Pancreatic/Biliary fistula, laxatives |
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Net Acid Excretion
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"NAE = (NH4+ + TA) - HCO3
TA = titrable acid" |
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RTA's
(renal tubular acidosis) |
"Type I - Distal - Decreased H+ (NH4) excretion --> acidosis (Alkaline urine)
Type II - Proximal - HCO3 wasting esp above threshold Type III - Distal w/ HCO3 waste" |
