Acid/Base Flashcards

1
Q

What is the effect of alkalosis on K status?

A

High pH causes a shift of K+ into cells from the ECF, creating a greater driving force for K+ secretion; high pH also de-inhibits apical K+ channels, allowing greater flux from cells to the tubule lumen

Alkalosis produces hypokalemia

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2
Q

Acetazolamide

A

Blocks carbonic anhydrase

Weak diuretic action, as distal parts of the nephron compensate for decreased proximal reabsorption of Na+

Causes wasting of bicarbonate in the urine; may cause metabolic acidosis, or be used to treat metabolic alkalosis

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3
Q

How much nonvolatile acid is produced each day?

A

60 mEq / day (sulfuric acid, phosphoric acid)

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4
Q

Effect of hypokalemia on plasma pH

A

Low ECF K+ causes a shift of H+ into cells; in the tubular cells, this means that more H+ is available for secretion, causing an alkalosis

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5
Q

Effect of hyperkalemia on plasma pH

A

Increased ECF K+ causes a shift of H+ out of cells; in the tubular cells, this means that less H+ is availabe for secretion and so H+ is inappropriately retained in the ECF, producing an acidosis

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6
Q

Respiratory Alkalosis - Compensation

A

Decrease in HCO3-

Acutely, HCO3- drops by 2 mEq/L for every 10 mmHg decrease in PCO2

Chronically, HCO3- drops by 4 mEq for every 10 mmHg decrease in PCO2

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7
Q

Respiratory acidosis - Compensation

A

Increased synthesis of bicarbonate

Acutely, bicarbonate increases by 1 mEq/L for every 10 mmHg increase in PCO2

Chronically, HCO3- increases by 4 mEq/L for every 10 mmHg increase in PCO2

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8
Q

Post-hypercapnea

A

Development of metabolic alkalosis in a patient with chronic respiratory acidosis who has received mechanical ventilation; pCO2 is rapidly lowered but compensatory HCO3- remains high

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9
Q

Effect of mineralocorticoids on acid/base status

A

Mineralocorticoids act on the H+ ATPase on the apical membrane of the intercalated cell in the distal tubule, stimulating it to secrete H+ into the tubule lumen, which is accompanied by bicarbonate resorption

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10
Q

2 types of metabolic alkalosis

A

Chloride (saline) responsive

Chlorine (saline) unresponsive

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11
Q

Chloride responsive metabolic alkalosis

A

Urine Cl < 20mEq/L

Low urine chloride reflects Cl- depletion as a major maintenance factor for metabolic alkalosis

Usually associated with intravascular volume depletion

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12
Q

Choride unresponsive metabolic alkalosis

A

Urine Cl > 20 mEq/L

Caused by hyperaldosteronism and Cushing’s syndrome; metabolic alkalosis is generated and maintained by renal H+ loss rather than Cl- depletion

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13
Q

What is the effect of Chloride on metabolic alkalosis?

A

Chloride depletion results in the resorption of bicarbonate by the kidney, maintaining metabolic alkalosis

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14
Q

Metabolic alkalosis - Compensation

A

Decreased ventilation with increased retention of CO2

PCO2 increases from 40 by 0.25-1x the increase in HCO3- over 24

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15
Q

Treatment of metabolic alkalosis

A

Mechanical hypoventilation with maintenance of oxygenation

Chloride responsive - infusion of NaCl (saline)

Chloride resistant - spironolactone to block mineralocorticoid effect

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16
Q

Normal serum anion gap

A

Na - Cl - HCO3- = 9 +/- 3

17
Q

Causes of metabolic acidosis - 2 categories

A
  1. Loss of bicarbonate - Renal vs. extra-renal

2. Addition of acid

18
Q

Renal Tubular Acidosis - 2 types

A

Proximal renal tubular acidosis - failure of proximal tubule to reabsorb filtered HCO3-

Distal renal tubular acidosis - decreased free H+ excretion

19
Q

Loss of bicarbonate - 2 mechanisms

A

Renal - urine pH > 5.3 suggests failure of kidney to reabsorb filtered HCO3- or to excrete free H+

Extra-renal - urine pH < 5.3 suggests that the kidney is functioning normally; HCO3- loss is likely GI in origin (diarrhea)

20
Q

Urine anion gap

A

Urine Na + K - Cl

Indirectly assesses whether NH4+ is increased in response to metabolic acidosis; if NH4+ production is increased the Cl- should also increase to maintain electroneutrality; as Cl- increases, urine AG becomes negative

Negative AG suggests that NH4+ production by the kidney is occurring and that the non-anion gap metabolic acidosis is due to GI loss of HCO3-

Positive AG suggests that NH4+ production is impaired and that an RTA is present

21
Q

Causes of anion gap metabolic acidosis

A
Methanol
Uremia
DKA
Propylene glycol
Isoniazid
Lactate
Ethylene glycol
Salicylate