Metabolic Acidosis Flashcards

0
Q

GI causes of normal gap metabolic acidosis

A

(loss of bicarb)

  • Diarrhea
  • Drainage of panc/biliary sec
  • Small bowel fistula
  • Utero-enterostomy or obstruction of ileal conduit
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1
Q

Renal causes of normal gap metabolic acidosis

A
  • RTA
  • Carbonic anhydrase inhibition
  • Kidney failure
  • Mineralocorticoid def/resistance
  • Drugs
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2
Q

Causes of high anion gap metabolic acidosis?

A
  • Diabetic, fasting, or alcoholic ketoacidosis
  • Lactic acidosis
  • Toxic ingestions: methanol, ethylene glycol, diethylene glycol
  • Pyroglutamic acidosis
  • Toluene intox
  • Advanced kidney failure (reduced GFR)
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3
Q

What are the causes of acidosis with reduced GFR?

A

Decreased nephron function (causes the reduced GFR) causes a dec in the filtration of many acids, an increase in K+ reabs, and a decrease in sensitivity to aldosterone

  • K+ effects: hyperkalemia leads to a alkalemia of the intracellular space (switches with H+) which impairs NH4 generation
  • ECF volume expansion: due to kidney failure causes an inhibition fo aldosterone which reduces distal acidification
  • Can be normal or high gap

SUMMARY:

  • Can’t filter your acids
  • Hyperkalemia (NH4)
  • Aldosterone effects
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4
Q

Fanconi Syndrome

A

Looks like proximal RTA with glucosuria, aminoaciduria, phosphousturia, urocosuria (hypouricemia and hypophos)

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5
Q

Causes of type I distal RTA

A

Alpha interacalated cell:

  • H-ATPase or H-K ATPase defect
  • Cl-HCO3 co transporter mutation
  • CA-II def

Amphotericin (med) causing H+ backleak into apical membrane of alpha intercalated cell

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6
Q

Type I and II RTA effects on calicum

A

HYPOkalemia

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7
Q

Which causes worse acidemia, dRTA or pRTA?

A

dRTA

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8
Q

Causes of type IV (hyperkalemia distal) RTA

A

Aldo def

Resistance

DT dysfxn

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9
Q

Drugs that cause aldo def?

A

Heparin, ACE inhib, ARB

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10
Q

Ethylene glycol and methanol

A
  • Metabolized into acids by ADH (alcohol has a higher affinity) so it takes a while for the high gap acidosis to occur.
  • At first, before there is a big acidosis, see a high serum osmolal gap so you know they ingested something (measured=lab - expected =sodium, glucose, urea)
  • Ethylene glycol see calcium oxalate in the urine
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11
Q

Clinical manifestations of metabolic acidosis

A
  • Hyperkalemia (concomitant kidney failure, cell lysis, tissue injury)
  • Hemodynamic compromise
  • Chronic musculoskeletal manifestations
  • Hyperventilation (kaussmaul)
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12
Q

Order of compensation for metab acidosis

A
  1. ECF buffering
  2. ICF buffering
  3. Resp compensation
  4. Renal acid excretion (mostly inc ammonium)
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13
Q

Winter’s formula

A

1.5(bicarb)+8 +/- 2

ONLY used for metab acidosis, tells you if pCO2/resp is compensating correctly. If not, there is another acid/base disturbance

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14
Q

Delta/delta

A
  • Amt anion gap inc from normal=amt bicarb falls (because it is buffering the additional acid)
  • Mismatch means that there is more than one acid/base disturbance
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15
Q

Risks of giving NaHCO3 for acute metabolic acidosis

A
  • Hypernatremia and vol overload
  • Hyperkalemia (only if given as hypertonic bolus)
  • CO2 generation
  • CSF acidosis due to CO2 diffusion over BBB
  • Overshoot alkalosis
  • Mechanical ventilation can be used to raise pH

–>for acute, correct underlying problem is best. For chronic, replace bicarb and treat acidosis

16
Q

Lab manifestations of Cl depletion metab alk

A

Blood: high HCO3, and pCO2 (compensatory)

Low serum K

Elevated blood pH decreased urine pH