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66 Cards in this Set
- Front
- Back
(164);
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(164);
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3 principal regulators of serum K+;
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Epi Insulin Aldosterone;
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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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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
(DCT Na blocking diuretics) |
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Pseudohypoaldosteronisms
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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 (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 |
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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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How do NSAIDs cause hyperkalemia?
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Block Renin.
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How does Heparin cause hyperkalemia?
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Blocks production of aldosterone.
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How does Beta2 stim affect [K+]?
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Redistribution --> hypokalemia.
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Hypokalemia /w low bP
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BIG DAM - Bartters, Induced (drug), Gitelman's, Diuretics, Acidosis (tubular), hypoMagnesemia
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Hypokalemia w/ hypertension
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ALL - Aldosterone, Liddle's, Licorice
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165
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165
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What is the capacity of the kidneys to excrete water
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About 15% of the GFR
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How does ADH work to increase water reabsorption?
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Binds to V2 recopter of CD cells--> Increased insertion of AQP-2 into apical membrane (luminal side)
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How does ADH work to increase BP
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Binds V1 receptor --> smooth muscle contraction.
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Which diuretics causes hyponatremia
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Thiazides, Loops, Osmotics, (ADH)
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Explain translocational hyponatremia
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Another osmole (I.e. glucose) pulls water out of cells --> hyponatremia.
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What osmoles can cause trans. Hyponatremia
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Glucose, Glycine, Maltose, Mannitol
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What cause psuedohyponatremia
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Hyperlipid or Hyperparaprotein
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SIADH
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Too much ADH --> hyperosmotic urine (esp from lung cancer/pulm infection, drug induced)
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Osmotic Demyelination
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Demyelination when hyponatremia is corrected too fast.
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166
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166
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Where are high pressure vol receptors?
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Carotid Sinus, Aortic Arch, L. Ventricle, JGA
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Where are low pressure vol receptors?
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Cardiac Atria, R ventricle, Pulm Vessicles
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Proximal Tubule Cell: Impt actions
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Na/H antiport, Na nutrient symport.
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Thick Ascending Limb: Imp Actions
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NaK2Cl symport, paracell. cation trans.
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Distal Convoluted Tubule: Impt Actions
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Ca/Na antiport, NaCl symport.
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Aldosterone renal actions
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Inrease Na abs, K & H exc
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ANP
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Atrial Natriuretic Petptide - Relased from cardiac atria. --> Vasodilator, Na excretor
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Pressure Natriuresis
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Backup mechanism - Hypertension --> na excretion. Hypotension --> na retention.
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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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MUDTILES Methanol Uremia Diabetic ketoacidosis Toluene Infection Lactic Acidosis Ethylene glycol Salicylates
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Causes of hyperchloremic metabolic acidosis(extrarenal)"
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HCl generating compounds - NH4Cl, HCl, Larginine, Llysine, Cl gas, Hyperalimentation GI HCO3 losses - Diarrhea, Ileus, Pancreatic/Biliary fistula, laxatives
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Relevance of L Arginine, L Lysine, Hyperalimentation
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Cause hyperchloremic acidosis.
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Net Acid Excretion
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NAE = (NH4+ + TA) - HCO3 TA = titrable acid
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RTA's
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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. |
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171
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171
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Drugs that suppress ADH
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"Make All Dicks Leak" - Methoxyflurane, Amphotericin B, Democlocycline, Lithium
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How can Lithium polydipsia be prevented?
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Give amiloride (diuretic) - blocks the ENaCl transporter that also uptakes Li.
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172
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172
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Normal Compensation for increased HCO3
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Approximately .6-.7 increase in pCO2
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ECF Expansion causes (pH)
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Decreased HCO3- -> dec pH
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Aldosterone and PH
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Stimuleates H+ secretion (by increasing Na reabsorption)
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PTH & PH
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PTH blocks HCO3 reabs
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Ang II and pH
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Ang II stimultes HCO3 reabsorption
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Hypokalemia and pH
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Hypokalemia stimulates HCO3 reabs
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Responsive alkaloses
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Low urine chloride - Gastric fluid loss, Stool loss, diuretic therapy
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Resistant Alkaloses
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High urine chlored - Primary hyperaldosteronism, steroids, Bartter's, Gittelmans
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Hypokalemic Metabolic Acidoses ??? Typo
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Diuretic, Vomiting, Bartter's
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173
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173
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What do loop diuretics block?
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Na2ClK channel in Thick ascending loop of henle
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Function of early distal tubule
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Reabsorb Na, Cl. Impermeable to water.
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Which are the K sparing diuretics?
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Amiloride, Triamterene, Spironolactone (A&T close Na channels in principle cell, spironolactone blocks ADH)
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Which diuretics are carbonic anhydrase inhibitors?
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Acetazoliamide and Benzolamide - Block CA --> blocks Na-H antiporter in Proximal Tubule
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What are the loop diuretics?
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Bumetadine, Furesomide, ethacrynic acid
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How do loop diuretics work?
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Block the NaK2Cl transporter. Also increase Ca, k wasting.
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How do thiazide diuretics work?
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Block the NaCl transporter in the distal tubule. Also block Ca reabs.
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CA diuretics do what to pH
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decrease
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Second function of CA diuretics.
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Glaucoma
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Which ions do loop diuretics waste?
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Ca, H, K
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Thiazides and calcium?
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Thiazides increase calcium reabs.
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