GUA - Batlle
Terms
undefined, object
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- 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"