AcidBasePathoFall2012

Poor tissue perfusion tissue hypoxia anaerobic

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Poor tissue perfusion  tissue hypoxia anaerobic metabolism Medications Nucleoside-analog reverse transcriptase inhibitors (NRTIs) Metformin Propylene glycol (solvent for some IV medications) Propofol
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Metabolic Acidosis Normal anion gap/hyperchloremic states GI bicarbonate loss Diarrhea Drugs Cholestyramine  diarrhea Magnesium oxide  diarrhea Acid ingestion Rapid infusion of NaCl
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Metabolic Acidosis Normal anion gap/hyperchloremic states Renal tubular acidosis (RTA) Inability of kidneys to appropriately regulate acid-base homeostasis: 3 types Distal (Type I) Proximal (Type II) Distal (Type IV)
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Metabolic Acidosis Normal anion gap/hyperchloremic states Distal (Type I) RTA Impaired H+ secretion from distal tubule Cannot excrete enough H+ to maintain acid-base balance Hypokalemia Causes (FYI) Ca2+, multiple myeloma, SLE, sickle-cell dz, renal transplant rejection, toluene ingestion
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Metabolic Acidosis Normal anion gap/hyperchloremic states Distal (Type IV) RTA Hyporeninemic hypoaldosteronism Impaired ammoniagenesis Hypoaldosteronism  hyperkalemia Causes (FYI): Nephropathy due to HIV, diabetes or sickle cell disease
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Metabolic Acidosis Normal anion gap/hyperchloremic states Proximal (type II) RTA Insufficient proximal bicarbonate reabsorption Bicarbonate is lost in urine Leads to Na+ wasting and secondary hyperaldosteronism Hypokalemia Is chronic and non-progressive Causes (FYI): Defects in proximal tubular bicarabonate reabsorption Amyloidosis, multiple myeloma, exposure to lead, mercury or expired tetracycline antibiotics Carbonic anhydrase inhibitors
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Metabolic Acidosis Clinical presentation Chronic metabolic acidosis Relatively asymptomatic Osteomalacia and osteopenia in adults Severe, acute acidosis (pH < 7.2) N/V, loss of appetitie Kussmaul respirations = deep rapid breaths Occurs as body attempts to compensate Vasodilation Flushing, tachycardia, CO  hypotension, organ blood flow & CO, bradycardia Confusion, lethargy, stupor, coma Hyperkalemia, hyperglycemia
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Metabolic Acidosis Respiratory Compensation Mechanism: Hyperventilation  Increased CO2 excretion Occurs immediately
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PQ is a 45 y/o M with the following ABG: pH 7.5, PaCO2 = 47, HCO3- = 36 Na = 146, Cl = 102, HCO3- = 36 What is his acid-base disorder? 1. Metabolic alkalosis, compensated 2. Metabolic alkalosis, not compensated 3. Respiratory alkalosis, compensated 4. Respiratory alkalosis, not compensated
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Compensation of Metabolic Alkalosis PaCO2 (in mmHg) should increase by 0.4-0.6 times the rise in plasma HCO3- (in mEq/L)
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appropriate? 1.
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Poor tissue perfusion tissue hypoxia anaerobic metabolism...

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