Acid-Base Balance Flashcards Preview

Renal > Acid-Base Balance > Flashcards

Flashcards in Acid-Base Balance Deck (39)
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1
Q

two types of acid in the body

A

volatile and non-volatile

2
Q

volatile acid

A

CO2

3
Q

non-voltatile acids (fixed acids)

A

Sulfuric acid

Phosphoric acid

4
Q

Fixed acids overproduced in dz or ingested

A

ketoacids, lactic acid, salicylic acid

5
Q

major extracellular buffer

A

HCO3-

6
Q

minor extracellular buffer (most important as a urinary buffer)

A

H2PO4-

7
Q

excretion of H+ as H2PO4-

A

titratable acid

8
Q

major intracellular buffer

A

hemoglobin

9
Q

deoxyhemoglobin vs oxyhemoglobin - which is the better buffer?

A

deoxyhemoglobin

10
Q

pH = pKa + log[A-]/[HA]

A

Henderson-Hasselbalch

11
Q

pH = pKa + log ([HCO3-] / 0.03 x PaCO2)

A

pH arterial blood

12
Q

PCO2 = 1.5[HCO3-] + 8 ± 2

A

Winter’s formula

13
Q

used to measure the appropriateness of the compensatory response and to evaluate for a mixed acid/base disorder.

A

winter’s formula

14
Q

If measured PCO2 is higher than expected →

A

additional primary respiratory acidosis

15
Q

If measured PCO2 is lower than expected –>

A

additional primary respiratory alkalosis

16
Q

Serum anion gap =

A

[Na+] – ([HCO3-] + [Cl-])

Sodium - (bicarb + chloride)

17
Q

mnemonic for ↑ Serum anion gap metabolic acidosis (aka “gap acidosis”)

A

MUDPILERS

18
Q

M in mudpilers

A

Methanol (formate), Metformin

19
Q

U in mudpilers

A

Uremia—advanced (chronic) renal failure—vs. early renal failure, which may cause normal anion gap metabolic acidosis

20
Q

D in mudpilers

A

Diabetic ketoacidosis (β-hydroxybutyrate, acetoacetate)

21
Q

P in mudpilers

A

Paraldehyde, Phenformin

22
Q

I in mudpilers

A

Iron, Isoniazid

23
Q

L in mudpilers

A

Lactic acidosis—shock, hypoxia, poor tissue perfusion; carbon monoxide, cyanide

24
Q

E in mudpilers

A

Ethanol ketoacidosis (β-hydroxybutyrate, acetoacetate), Ethylene glycol (glycolate, oxalate)

25
Q

R in mudpilers

A

Rhabdomyolysis

26
Q

S in mudpilers

A

Salicylates—with concomitant respiratory alkalosis; prolonged Starvation ketoacidosis (β-hydroxybutyrate, acetoacetate)

27
Q

Mneumonic for Normal anion gap metabolic acidosis (aka, hyperchloremic metabolic acidosis, “non-gap acidosis”)

A

“FUSED CARS”:

28
Q

F in fused cars

A

Fistula (small bowel, pancreatic) → loss of HCO3-

29
Q

U in fused cars

A

Ureterogastric conduits (eg, urine-diverting colostomy) → loss of HCO3-

30
Q

S in fused cars

A

Saline administration (ie, saline worsens metabolic acidosis!) → gain of Cl-

31
Q

E in fused cars

A

Endocrine—eg, hyperparathyroidism (a cause of type 2 renal tubular acidosis), Addison’s disease (aldosterone deficiency)

32
Q

D in fused cars

A

Diarrhea → loss of HCO3-

33
Q

C in fused cars

A

Carbonic anhydrase inhibitors (eg, acetazolamide)(most common cause of type 2 renal tubular acidosis in adults) → loss of HCO3-

34
Q

A in fused cars

A

Acid infusion (eg, NH4Cl; hyperalimentation with TPN (total parenteral nutrition) if arginine HCl or lysine HCl are used as amino acids) → gain of Cl-

35
Q

R in fused cars

A
  • type 1 (↓ distal tubule H+ secretion): hypokalemia, urine pH>5.5
  • type 2 (↓ proximal tubule HCO3- reabsorption): hypokalemia, urine pH<5.5.
36
Q

S in fused cars

A

Spironolactone - blocks aldosterone receptors

37
Q

Normal anion gap metabolic acidosis is caused by

A

loss of HCO3- or gain of Cl-, both of which usually result in hyperchloremic metabolic acidosis:

38
Q

gain of Cl- is usually compensated by

A

loss of HCO3- → hyperchloremic metabolic acidosis

39
Q
  • loss of HCO3- is usually compensated by
A

Cl- retention → hyperchloremic metabolic acidosis