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66 Cards in this Set

  • Front
  • Back
3 principal regulators of serum K+;
Epi Insulin Aldosterone;
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
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

(DCT Na blocking diuretics)
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 (like loop)(Defect in TAL)- Normal or in Ca2+, Normal to low Mg2+
Gitelman's (Like thiazide)(na/cl coT in DCT) - Low ser Mg, low urine Ca+B26
Types of Bartter's
Type I - NKCC2 - Na/2Cl/K CoT
Type II - ROMK - K passive
Type III - CIC_Kb - Cl passive
How do NSAIDs cause hyperkalemia?
Block Renin.
How does Heparin cause hyperkalemia?
Blocks production of aldosterone.
How does Beta2 stim affect [K+]?
Redistribution --> hypokalemia.
Hypokalemia /w low bP
BIG DAM - Bartters, Induced (drug), Gitelman's, Diuretics, Acidosis (tubular), hypoMagnesemia
Hypokalemia w/ hypertension
ALL - Aldosterone, Liddle's, Licorice
What is the capacity of the kidneys to excrete water
About 15% of the GFR
How does ADH work to increase water reabsorption?
Binds to V2 recopter of CD cells--> Increased insertion of AQP-2 into apical membrane (luminal side)
How does ADH work to increase BP
Binds V1 receptor --> smooth muscle contraction.
Which diuretics causes hyponatremia
Thiazides, Loops, Osmotics, (ADH)
Explain translocational hyponatremia
Another osmole (I.e. glucose) pulls water out of cells --> hyponatremia.
What osmoles can cause trans. Hyponatremia
Glucose, Glycine, Maltose, Mannitol
What cause psuedohyponatremia
Hyperlipid or Hyperparaprotein
Too much ADH --> hyperosmotic urine (esp from lung cancer/pulm infection, drug induced)
Osmotic Demyelination
Demyelination when hyponatremia is corrected too fast.
Where are high pressure vol receptors?
Carotid Sinus, Aortic Arch, L. Ventricle, JGA
Where are low pressure vol receptors?
Cardiac Atria, R ventricle, Pulm Vessicles
Proximal Tubule Cell: Impt actions
Na/H antiport, Na nutrient symport.
Thick Ascending Limb: Imp Actions
NaK2Cl symport, paracell. cation trans.
Distal Convoluted Tubule: Impt Actions
Ca/Na antiport, NaCl symport.
Aldosterone renal actions
Inrease Na abs, K & H exc
Atrial Natriuretic Petptide - Relased from cardiac atria. --> Vasodilator, Na excretor
Pressure Natriuresis
Backup mechanism - Hypertension --> na excretion. Hypotension --> na retention.
pH = 6.1 + log[HCO3-]/(.03Pco2)
Normal anion gap
12-14 w/ potassium 6-10 w/o potassium
Causes of high anion gap Acidosis
MUDTILES 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
Relevance of L Arginine, L Lysine, Hyperalimentation
Cause hyperchloremic acidosis.
Net Acid Excretion
NAE = (NH4+ + TA) - HCO3 TA = titrable acid
Type I - Distal - Decreased H+ (NH4) excretion --> acidosis (Alkaline urine)
Type II - Proximal - HCO3 wasting esp above threshold
Type III - Distal w/ HCO3 waste Type IV - Hyperkalemic ass. W/ Aldost deficiency.
Drugs that suppress ADH
"Make All Dicks Leak" - Methoxyflurane, Amphotericin B, Democlocycline, Lithium
How can Lithium polydipsia be prevented?
Give amiloride (diuretic) - blocks the ENaCl transporter that also uptakes Li.
Normal Compensation for increased HCO3
Approximately .6-.7 increase in pCO2
ECF Expansion causes (pH)
Decreased HCO3- -> dec pH
Aldosterone and PH
Stimuleates H+ secretion (by increasing Na reabsorption)
PTH blocks HCO3 reabs
Ang II and pH
Ang II stimultes HCO3 reabsorption
Hypokalemia and pH
Hypokalemia stimulates HCO3 reabs
Responsive alkaloses
Low urine chloride - Gastric fluid loss, Stool loss, diuretic therapy
Resistant Alkaloses
High urine chlored - Primary hyperaldosteronism, steroids, Bartter's, Gittelmans
Hypokalemic Metabolic Acidoses ??? Typo
Diuretic, Vomiting, Bartter's
What do loop diuretics block?
Na2ClK channel in Thick ascending loop of henle
Function of early distal tubule
Reabsorb Na, Cl. Impermeable to water.
Which are the K sparing diuretics?
Amiloride, Triamterene, Spironolactone (A&T close Na channels in principle cell, spironolactone blocks ADH)
Which diuretics are carbonic anhydrase inhibitors?
Acetazoliamide and Benzolamide - Block CA --> blocks Na-H antiporter in Proximal Tubule
What are the loop diuretics?
Bumetadine, Furesomide, ethacrynic acid
How do loop diuretics work?
Block the NaK2Cl transporter. Also increase Ca, k wasting.
How do thiazide diuretics work?
Block the NaCl transporter in the distal tubule. Also block Ca reabs.
CA diuretics do what to pH
Second function of CA diuretics.
Which ions do loop diuretics waste?
Ca, H, K
Thiazides and calcium?
Thiazides increase calcium reabs.