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Year 2 Renal > Acid base I > Flashcards

Acid base I Flashcards

1
Q

what are the clinical decision making steps to assessing acid base disorders?

A
  1. history
  2. pH: acidemic or alkalemic?
  3. metabolic or respiratory?
  4. anion gap?
  5. appropriate compensation?
  6. if metabolic acidosis, is it a mixed disorder?
  7. diagnosis?
  8. treatment?
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2
Q

what is the pH range compatible with life?

A

6.80 - 7.80

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3
Q

can a respiratory acid base disorder be both alkalosis and acidosis?

A

no

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4
Q

what is the range of normal blood pH?

A

7.35 - 7.45

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5
Q

what is the conceptual cause of metabolic alkalosis?

A

increased serum HCO3-

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6
Q

what maintains metabolic alkalosis?

A

condition resulting in inability to secrete HCO3- by the kidneys

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7
Q

what value indicates a primary metabolic alkalosis?

A

over 40 mmol / L [HCO3-]

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8
Q

what is the compensatory mechanism for metabolic alkalosis?

A

respiratory acidosis - hypoventilation, increased pCO2

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9
Q

what are the etiologies of metabolic alkalosis?

A
  • GI proton loss
  • renal proton loss
  • intracellular shift of hydrogen
  • alkali administration
  • contraction alkalosis
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10
Q

what should be considered the normal value for bicarb?

A

25 mmol / L

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11
Q

although contraction alkalosis can be caused by diuretics, it is maintained by ___________

A

hyperaldosteronism

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12
Q

what is the mechanism for contraction alkalosis?

A
  • diuretics trigger secretion of H+ and K+ with loss of volume
  • to counteract this hypovolemia, aldosterone is released which promotes Na+/H2O/HCO3- and secretion of K+/H+
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13
Q

what are two major reasons why metabolic alkalosis can be maintained?

A
  • chloride depletion (also decreases bicarb secretion)

- hypokalemia

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14
Q

which two drugs can cause renal hydrogen loss leading to metabolic alkalosis?

A
  • loop diuretics

- thiazide diuretics

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15
Q

what are the treatment options for metabolic alkalosis?

A
  • correct underlying cause and maintainers

- correct electrolyte abnormalities (NaCl or KCl resuscitation)

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16
Q

what are maintainers of metabolic alkalosis?

A
  • hypovolemia
  • hypokalemia
  • reduced GFR
  • chloride depletion
  • aldosterone excess
17
Q

what drug interferes with bicarb reabsorption?

A

acetazolamide

18
Q

what value of [HCO3-] indicates a primary metabolic ACIDOSIS?

A

under 15 mmol/L

19
Q

what is the compensation for metabolic acidosis?

A

respiratory alkalosis - hyperventilation, decreased pCO2

20
Q

usually an increase in the anion gap is caused by an increase in the unmeasured _____________ (cations / anions)?

A

unmeasured anions

21
Q

what is the concept behind anion gap? what is its purpose?

A
  • the total number of cations and anions must be equal to maintain neutrality
  • however, the ions measured by the lab (Na, Cl, HCO3) are NOT equal
  • purpose: differentiates different causes of metabolic acidosis (high vs normal / non-anion gap)
22
Q

what are the scenarios that lead to a normal anion gap metabolic acidosis?

A
  1. loss of substantial amounts of measured anion HCO3-, leading to a hyperchloremic state
    - sum total of measured anions remains the SAME, and in turn the anion gap remains the same, but hyperchloremic
  2. defective renal acidification resulting in failure to excrete normal quantities of metabolically produced acid
    - hyperchloremic state occurs because conjugate base is excreted as sodium salt and sodium chloride is retained
23
Q

what are the causes of high anion gap metabolic acidosis?

A 
Methanol 
Uremia (chronic renal failure) 
Diabetic ketoacidosis (most common reason) 
Propylene glycol 
Infection / Iron / Isoniazid 
Lactic acidosis 
Ethylene glycol 
Salicylates (aspirin)
24
Q

diabetic ketoacidosis is a triad of:

A
  • hyperglycemia
  • high anion gap metabolic acidosis
  • ketonemia
25
Q

what is the serum osmolal gap?

A

measured serum osmolal - calculated serum osmolal

26
Q

what are two common causes of an increased serum osmolal gap?

A
  • methanol intoxication

- ethylene glycol intoxication

27
Q

what are the signs and symptoms of methanol toxicity?

A
  • CNS / retinal injury
  • pancreatitis
  • high anion gap
  • increased serum osmolal gap
28
Q

ethylene glycol is metabolized to ______ and _________

are these measured or unmeasured compounds?

A

oxalate, hippurate (unmeasured anions)

29
Q

what are the signs and symptoms of ethylene glycol poisoning?

A
  • neuro / cardiopulmonary collapse
  • calcium oxalate crystals in urine
  • high anion gap
  • increased serum osmolal gap
30
Q

what are the early symptoms of salicylate (aspirin) poisoning?

A

EARLY:

  • tinnitus
  • vertigo
  • nausea
  • vomiting
  • diarrhea

LATE:

  • altered mental status
  • hyperpyrexia
  • noncardiac pulmonary edema
  • coma
31
Q

how do you characterize the acid-base progression in aspirin poisoning? what is the net effect?

A
  • initially: respiratory alkalosis
  • later: high anion gap metabolic acidosis

NET EFFECT: mixed disorder - primary respiratory alkalosis + primary metabolic acidosis

32
Q

what explains the early respiratory alkalosis in aspirin poisoning?

A

salicylates stimulate the respiratory center directly, resulting in an early fall in pCO2

33
Q

what explains the late high anion gap metabolic acidosis seen in aspirin poisoning?

A

accumulation of organic acids, including lactic acid and ketoacids

34
Q

what is the management for aspirin poisoning?

A
  • GIVE BICARBONATE IMMEDIATELY

- activated charcoal if caught early

35
Q

what level of serum salicylate concentration is associated with increased morbidity and mortality? this is an absolute indication for what treatment?

A
  • 100 mg/dL

- hemodialysis

Year 2 Renal (38 decks)

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