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M2 Renal/FEK > Acid Base > Flashcards

Acid Base Flashcards

1
Q

Metabolism of carbohydrates, phospholipids, and proteins results in:

A 
Carbohydrates = Carbonic Acid, Lactic Acid*
Phospholipids = carbonic acid, phosphoric acid*
Proteins = carbonic acid, sulfuric acid*, and HCl*
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2
Q

3 types of buffers in the body

A

HCO3
Phosphate
Proteins (albumin)

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3
Q

How does bicarb serve as a buffer?

A

present in 5x10^6 times greater conc. than H+ concentration

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4
Q

How does phosphate serve as a buffer? where is it normally stored?
What happens if there is chronic acidosis?

A

stored mostly in the mineral matrix of bone; therefore buffering of acids by phosphate (acidosis) can force the body to release phosphate from the skeleton as a buffer, leading to bone mineral loss over time.

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5
Q

How does albumin serve as a buffer?

What happens during acidemia? alkalemia?

A
  • Negatively charged; contains exposed amine groups that complexes with Na, Ca, Mg (main extracellular cations)
  • With significant acidemia, albumin binds H+ and releases Ca, resulting in incr. free Ca.
  • During periods of alkalemia, Ca is bound to albumin and symptomatic hypocalcemia can develop.
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6
Q

How to calculate anion gap?

What is NOT measured routinely in an AG?

A

Anion Gap = Na – (Cl + HCO3)

Albumin, sulfate, and phosphate are (-) charged and are not measured during a routine metabolic panel

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7
Q

What is the normal AG? What is it primarily attributed to?

A

normal AG = 12mEq/L; primarily due to albumin

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8
Q

How does albumin affect the AG?

A

hypoalbuminemia causes decr. AG (1 g/dL decr. albumin = AG decr. by 2.5)

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9
Q

What happens if the AG increases?

A

presence of an non-HCl acid load ie lactic acid, ketoacid, acetic acid; even if HCO3/CO2 is normal!!.

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10
Q

What causes increased AG?

A 
o	Methanol
o	Uremia
o	DKA
o	Paraldehyde
o	INH
o	Lactic acidosis
o	Ethylene glycol
o	Salicylates
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11
Q

Calculation for osmolar gap?

A

2xNa + glucose/18 + BUN/2.8 + 1/amount ingested

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12
Q

What does it mean if the calculated osmolar gap is greater than the expected osmolar gap?

A

there is an unmeasured osmole present!

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13
Q

What are some toxins that can can incr. osmolar gap with acidosis?

A
  • Etylene glycol
  • Methanol
  • Ketoacidosis
  • Uremia
  • Paraldehyde
  • Lactic acidosis
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14
Q

What are some toxins that can can incr. osmolar gap w/o acidosis?

A
  • Ethanol
  • Isopropanol
  • Mannitol
  • Diethyl ether
  • Severe hyperlipidemia
  • Hyperproteinemia
  • Severe Li+ toxicity
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15
Q

AG = 16 and HCO3 = 10
what is the ∆AG and ∆HCO3?
What does this mean?

A

Δ[anion gap] = 16 – 12 = 4
Δ[HCO3-] = 24 – 10 = 14

[HCO3-] has changed more than AG (ΔAG-Δbicarb = -10)

  • both a hyperchloremic acidosis and a incr. AG acidosis are present
  • the concurrent hyperchloremic acidosis makes the overall acidosis WORSE than the gap acidosis alone
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16
Q

AG = 20 and HCO3 = 20
what is the ∆AG and ∆HCO3?
What does this mean?

A

Δ[anion gap] = 20 – 12 = 8
Δ[HCO3-] = 20 - 24 = 4

[HCO3-] has changed less than AG (ΔAG-Δbicarb = +4)

  • both a metabolic alkalosis and a AG acidosis are present
  • the concurrent metabolic alkalosis makes the acidosis IMPROVED compared to the gap acidosis alone;
17
Q

AG = 16 and HCO3 = 30
what is the ∆AG and ∆HCO3?
What does this mean?

A

Δ[anion gap] = 16 – 12 = 4
Δ[HCO3-] = 24 – 30 = -6

Anion[HCO3 (ΔAG – Δbicarb = +10)
Again, both a metabolic alkalosis and a incr. AG acidosis are present
This time the metabolic alkalosis is the dominant process, but they co-exist, nonetheless!

18
Q

How to calculate ∆∆?

What is the normal ∆∆ you should expect?

What if it is not proportional?

A

Delta-Delta Gap (∆∆) = ∆AG - ∆HCO3

for every incr 1 mEq in AG = decr 1 mEq/L HCO3
ie expected AG = 12, expected HCO3 = 24

if ∆AG ≠ ∆HCO3, then an additional acid-base d/o is may be present.

Note: ∆anion gap and ∆HCO3 are not mutually exclusive.

If there is incr. AG, measure ∆∆ to determine if there is an concurrent metabolic disorder.

19
Q

What does it mean if:
ΔAG > Δbicarb
ΔAG < Δbicarb
ΔAG = Δbicarb

A

ΔAG > Δbicarb = metabolic alkalosis (AG rise is more than the fall in HCO3) + AG acidosis. Need less HCO3 to buffer it, which is why it’s greater in presence.

ΔAG < Δbicarb = hyperchloremic metabolic acidosis (AG rise is less than the fall in HCO3) + AG acidosis - bicarb has changed less because a lot of HCO3 is req’d to buffer it

ΔAG = Δbicarb, incr. AG acidosis is the sole metabolic disorder.

20
Q

Urinary AG calculation?

When do you calculate it?

A

Urine Anion Gap (UAG) = Urinary ([Na+] + [K-]) – [Cl-]

when the pH is abnormal.

21
Q

How does kidneys excrete acid?

A

as NH4Cl

NH3 is volatile and is difficult to measure accurately because it can diffuse freely across membranes, but in the distal tubule, NH3 is “trapped” by H+ as NH4 for excretion.

NH4+ is polar and lipid-insouble and since Cl- must accompany NH4 for electroneutrality, urine Cl can be used to infer urinary acid excretion

22
Q

Metabolic acidosis = if UAG is +, what does this mean? If UAG is -??

Metabolic alkalosis = if UAG is +, what does this mean? If UAG is -??

A

Acidosis
(–) UAG = appropriate renal response/excretion of acid

(+) UAG = renal disorder (ie distal renal tubular acidosis)

Alkalosis
(–) UAG = renal d/o (incr. CL excretion)
(+) UAG = appropriate renal response (less Cl excretion)

Remember: Urine Anion Gap (UAG) = Urinary ([Na+] + [K-]) – [Cl-]

23
Q

How do kidneys compensate for respiratory acidosis?

Respiratory Alkalosis?

A

renal compensation: incr. HCO3 production and retention to restore pH towards normal

resp. acidosis
- acute: limited response (min-hours); rate: incr. 1 mEq HCO3 for every 10mmHg CO2
- chronic: more robust (2-3days); rate: incr. 3-4 mEq for every 10mmHg CO2

resp. alkalosis:
- Acute: decr. 2 mEq/L HCO3 = decr. 10 mmHg pCO2
- Chronic: decr. 4 mEq/L HCO3 = decr. 10 mmHg pCO2

24
Q

What characterizes metabolic acidosis?

how is it compensated?

A

decr. HCO3
decr. pH
incr. AG and/or Hyperchloremic Acidosis*

compensation: respiratory

25
Q

What causes Hyperchloremic acidosis?

A

HCO3 loss via gut - - incr. Cl intake (occurs at the expense of HCO3)
- examples: saline resuscitation or hyperailmentation, as evidenced by history and review of IV fluids

H+ retention via kidneys - distal renal tubular acidosis -> impaired H+ excretion -> incr HCl

26
Q

how does aspirin OD usually present?

What is the mxn behind this?

A

1˚ respiratory alkalosis with an incr. AG acidosis

salicyclate produces an incr. AG metabolic acidosis; the body responds by incr. minute ventilation, thus lowering pCO2.

Aspirin also directly stimulates the respiratory center, furthering lowering pCO2 and causing a superimposed respiratory alkalosis.

27
Q

Type I RTA

cause?
Labs?
Urine pH? UAG?
trmt?

A

RTA I (distal) - ICCs are unable to secrete H+ or H+ leaks back into the cell from the lumen

causes: autoimmune, small things (ie Ca excess, drugs (ifosfamide, amphotericin, lithium, toluene)

Serum Labs:
decr. HCO3 (5.5
(+) UAG

Trmt:
HCO3

28
Q

Type II RTA

cause?
Labs?
Urine pH? UAG?
trmt?

A

RTA II (proximal): defect in HCO3 reabsorption in PCT -> bicarbonaturia

Causes: “best one to have”; caused by large things “amyloidosis, light chain myeloma, PNH, heavy metals, drugs (ifosfamide, tenovfir, aminoglycosides, Ca inhibitors)

Labs

decr. HCO3 (12-18mEq/L)
decr. K - due to incr Na/bicarbonate delivery to principal cells and incr Na delivery, which incr K secretion

Urine
pH = <5.5 - distal acidification mechanisms are still intact
(–) UAG, steady state

Trmt:
HCO3

29
Q

Type IV RTA

cause?
Labs?
Urine pH? UAG?
trmt?

A

Type IV RTA - hypOaldosteronism or aldosterone resistance (via ACEi/ARB): net effect: limited H,K excretion

Serum Labs
- decr. HCO3
Should be suspected in any case of hyperchloremic acidosis with hyperkalemia with normal or near-normal creatinine

Urine
decr. K (despite hyperkalemia)

Trmt:
hypOaldosteronism: fludrocortisone
HCO3 supplements
K restriction

30
Q

Hyperchloremic acidosis - what is it?

A

NORMAL AG, but the ratios of Cl and HCO3 has changed (usually due to HCO3 loss via gut or H+ retention via kidneys)

31
Q

Osmolar gap - what is normal?

What if it deviates from normal?

A

10-15 mOsms/L

if measured&raquo_space; calculated, then there is an unmeasured osmole pressent.

32
Q

2 types of metabolic acidosis. what are they and what does it mean?

A

AG acidosis - non-HCl acid (ie lactic acid, ketoacids)

Hyperchloremic acidosis - HCl retention or HCO3 loss (ratio of HCO3/HCl changes, but AG does not change), ie RTA I, II, IV, diarrhea

33
Q

Volume depletion does what to acid/base balance?

A

results in contraction ALKALOSIS because it results in RAAS activation ->
AII stimulates Na/HCO3 uptake in PCT
Aldosterone stimulates Na uptake, H/K secretion in CD

M2 Renal/FEK (20 decks)

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