Batlle & Friends
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- (164);
- (164);
- 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) - Pseudohypoaldosteronisms
-
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
- 165
- 165
- 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
- SIADH
- Too much ADH --> hyperosmotic urine (esp from lung cancer/pulm infection, drug induced)
- Osmotic Demyelination
- Demyelination when hyponatremia is corrected too fast.
- 166
- 166
- 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
- ANP
- Atrial Natriuretic Petptide - Relased from cardiac atria. --> Vasodilator, Na excretor
- Pressure Natriuresis
- Backup mechanism - Hypertension --> na excretion. Hypotension --> na retention.
- (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
- 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
- RTA's
-
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. - 171
- 171
- 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.
- 172
- 172
- 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 & PH
- 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
- 173
- 173
- 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
- decrease
- Second function of CA diuretics.
- Glaucoma
- Which ions do loop diuretics waste?
- Ca, H, K
- Thiazides and calcium?
- Thiazides increase calcium reabs.