Acidosis/Alkalosis Flashcards

1
Q

4 Causes of Hyperchlroemic Acidosis

A
  • Impaired renal acid excretion (renal failure, distal renal tubule acidosis)
  • Renal bicarb loss (CA inhibitors, proximal renal tubule acidosis)
  • GI bicarb loss (diarrhea, pancreatic drainage, ureteral diversion)
  • Acid gain (tpa, ammonium Cl ingestion)
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2
Q

8 Causes of High Anion Gap Acidosis

A
  • M - methanol ingestion (formate and lactate)
  • U -uremia (renal failure –> phosphate, sulfate, organic acids)
  • D diabetic ketoacidosis (beta- hydroxybutyrate or acetoacetate)
  • P - propylene glycol, paraldehyde
  • I - infection, iron, isonazid, inborn errors
  • L - lactic acidosis
  • E - ethylene glycol ingestion (ocylate, glycolate)
  • S - salicylates (aspirin –> ketoacids, lactate, salicylate)
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3
Q

Anion Gap Equation

A

AG = [Na] - [Cl-] - [bicarb]

normal is 10 +/- 2

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4
Q

Urinary Anion Gap Equation (+ what does it tell us?)

A

UAG = [Na] + [K] - [Cl] (no bicarb in urine normally)

  • UAG <0 - non-renal cause of acidosis b/c make up for acidosis by ammonium production in kidney (+ charge so negative anion gap)
  • UAG > 0 - renal cause of acidosis b/c no ammonium present
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5
Q

What kind of acidosis is present in chronic kidney disease?

A

BOTH

it can start as hypercholermic acidosis and later become high anion gap

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6
Q

Winter’s Formula

A
  • Predicts the respiratory comp for metabolic acidosis

PCO2 = 1.5 x [bicarb] + 8 +/-2

  • If actual meas PCO2 is > prediction by formula… compensatory
  • If actual meas PCO2 is < prediction by formula … primary respiratory acidosis
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7
Q

What is the risk of chronic metabolic acidosis?

A
  • Bone disease/rickets/growth fail in kids

- Osteoporosis in adults

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8
Q

Type I RTA

A

Classic distal RTA

  • Defective distal nephron H+ pumps or back leak of H+ into tubular lumen
  • Can be… impaired H-ATPase, bicarb/Cl exchanger, carbonic anhydrase
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9
Q

Type II RTA

A

Proximal RTA

  • If congenital defect or proximal tube damage –> impaired H+ secretion –> lower threshold for bicarb reclamation (start spilling bicarb into urine at much lower threshold)
  • Can be part of Fanconi Syndrome (mult prox tube defects - glycosuria, phosphate wasting, aminoaciduria and hypouricemia)
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10
Q

Type IV RTA

A

Hyperkalemic distal RTA

  • Either aldosterone def/resistance
  • OR voltage-dep defect in H+ excretion; if dec Na+ reabsorption then this dec gradient for H+ secretion
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11
Q

What 2 things must occur for metabolic alkalosis to take place?

A
  • Generation (acid loss of alkali gain)

- Maintenance (why is alkalosis not being corrected by body?)

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12
Q

Generation of Metabolic Alkalosis

A
  • Acid Loss
    - In kidney - diuretics, mineralocorticoid excess, Cushing’s (steroid), severe K+ depletion, Bartter’s, Gitelman’s, Liddle’s
    - In GI - vomiting, nasogastric drainage, chloride diarrhea
  • Alkali Gain
    - Bicarb admin
    - Milk-alkali syndrome
    - Infusion of organic anions that are metabolized to bicarb (ex- citrate in blood transfusion; lactate; acetate)
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13
Q

Maintenance of Metabolic Alkalosis

A
  • Dec GFR –> less bicarb filtered load; from either dec EABV or renal insufficiency
  • Inc proximal tube bicarb reclamation; from dec EABV or chloride depletion
  • Inc H+ excretion; from mineralocorticoid excess or hypokalemia
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14
Q

2 Classes of Metabolic Alkalosis Tx

A

1- Responds to saline (vol or Cl- depletion)

- This will enhance EABV and Cl- delivery to dec proximal bicarb reclamation
- Can also give KCl in saline if hypokalemia is severe and contributing
- Also give if GI losses or diuretic use

2- Resistant to saline (PT NOT VOL OR CL- DEPLETED)

- So due to mineralocorticoid excess; give aldosterone antagonist instead
- Also due to severe hypokalemia (Barrters, Gitelmans, Liddles); give K-sparing diuretic instead
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