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15 Cards in this Set

  • Front
  • Back
3 principal regulators of serum K+
Insulin
Epinephrine
Aldosterone
Hyperkalemia and EKG
1. High T wave
2. Prolonged PR, depressed ST
3. IV block
4. Vfib
Principal cell
Cell in CCT
Na/K control (reg by ald)
Na channel blockers
"Amiloride
Triamterene
Trimethoprim
Pentamidine"
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)"
Bartter's vs Gitelmans
"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"
K+ in mineral vs organic acidosis
"Mineral: Increase K+ because anions are held extracellularly (pulling K+ out)
Organic: No change. Organic anions are taken into cell"
Types of Bartter's
"Type I - NKCC2 - Na/2Cl/K CoT
Type II - ROMK - K passive
Type III - CIC_Kb - Cl passive"
(170)
(170)
Henderson-Hasselbach
pH = 6.1 + log[HCO3-]/(.03Pco2)
Normal anion gap
"12-14 w/ potassium
6-10 w/o potassium"
Causes of high anion gap Acidosis
"Methanol
Uremia
Diabetic ketoacidosis
Toluene
Infection
Lactic Acidosis
Ethylene glycol
Salicylates"
"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
Net Acid Excretion
"NAE = (NH4+ + TA) - HCO3
TA = titrable acid"
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"