NSG 533 EXAM 1
• Type B lactic acidosis: Results from a mitochondrial defect in oxygen utilization
• PLUMSEEDS: ParaldehydeLactic acidosis
Uremia Methanol Salicylates Ethanol Ethylene glycolDKA
Starvation
• Anion gap: (Na) - (Cl + HCO3)
• Reference range for anion gap without K: 12 +/- 2
• Serum potassium falls about 0.3 mEq/L for each ...: 0.1 increase in pH(alkalosis)
• Serum potassium rises about 0.3 mEq/L for each ...: 0.1 decrease in pH inrespiratory
acidosis and 0.7 mEq/L in metabolic acidosis
• Cause of pre-renal AKI: Decreased renal perfusion
• 4 causes of intra-renal AKI: 1. Vascular
2. Glomerular
3. Tubular
4. Interstitial
• Most common cause of AKI: Tubular
• 2 major causes of acute tubular necrosis: 1. Ischemic
2. Nephrotoxic
• Cause of post-renal AKI: Obstruction anywhere along the GU tract can causeblockage of
urine flow and kidney failure
• Relationship of creatinine with GFR: As GFR decreases, creatinine levels willincrease
• Hemolytic jaundice: basic defect: Excessive production of bilirubin
• Hemolytic jaundice: elevation of serum bilirubin: Mild
• Hemolytic jaundice: type of bilirubin in plasma: Unconjugated
• Hemolytic jaundice: bilirubin in urine: Absent
• Hemolytic jaundice: urobilinogen in urine: Increased
• Hemolytic jaundice: bilirubin in feces: Increased
• Hemolytic jaundice: red cell survival: Decreased
• Hemolytic jaundice: liver function tests: Normal
, • Hemolytic jaundice: bile ducts: Normal
• Hepatocellular jaundice: basic defect: Defective uptake, conjugation, and/orexcretion of
bilirubin
• Hepatocellular jaundice: elevation of serum bilirubin: Severe
• Hepatocellular jaundice: type of bilirubin in plasma: Conjugated and uncon-jugated
• Hepatocellular jaundice: bilirubin in urine: Present (if the defect is in biliaryexcretion)
• Hepatocellular jaundice: urobilinogen in urine: Variable depending on thestage of the
disease
• Hepatocellular jaundice: bilirubin in feces: Variable
• Hepatocellular jaundice: red cell survival: Normal
• Hepatocellular jaundice: liver function tests: Abnormal
• Hepatocellular jaundice: bile ducts: Normal
• Obstructive jaundice: basic defect: Obstruction of bile ducts
• Obstructive jaundice: elevation of serum bilirubin: Severe
• Obstructive jaundice: type of bilirubin in plasma: Conjugated
• Obstructive jaundice: bilirubin in urine: Present
• Obstructive jaundice: urobilinogen in urine: Decreased (absent)
• Obstructive jaundice: bilirubin in feces: Decreased
• Obstructive jaundice: red cell survival: Normal
• 5 essential components of pathophysiology: 1. Etiology (causative mecha-nisms)
1. Epidemiology (risk factors and distribution in populations)
2. Pathogenesis (disease mechanisms)
3. Clinical manifestations (signs, symptoms, and diagnostic criteria)
4. Outcomes (cure, remission, chronicity, or death)
• 7 general mechanisms of cell injury: 1. ATP depletion
2. Mitochondrial damage
3. Accumulation of oxygen and oxygen-derived free radicals
4. Membrane damage (depletion of ATP)
5. Protein folding defects
6. DNA damage defects
7. Calcium level alterations
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