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MHD > Acid Base > Flashcards

Acid Base Flashcards

1
Q

What is the anion gap used for?

A

The Anion Gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions.

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2
Q

What is the tx for metabolic acidosis?

A
  • Treat underlying cause(s)
  • Bicarbonate (especially w/ nl AG acidosis) – Na or K bicarbonate (or bicarbonate former) depending on etiology and electrolyte values.
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3
Q

Explain the lab abnormalities seen w/each of these labs w/metabolic alkalosis:

  • ABG
  • Lytes
  • BUN
  • Hct
  • Urine [Cl-]
A
  • ABG: increased pH, [HCO3-], and PCO2
  • Electrolytes: elevated [HCO3-], decreased [Cl-], usually low [K+], slight increase in anion gap (increased negative charges on albumin, increased lactate due to increased intracellular pH)
  • BUN: frequently increased (volume depletion)
  • Hematocrit: frequently increased (volume depletion)
  • Urine [Cl-]: very helpful in differential diagnosis (value < 10 mmol/L indicates volume/chloride depletion)
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4
Q

How is metabolic alkalosis treated?

A
  • Potassium administration
  • Acetazolamide
  • Volume repletion
  • Intravenous HCl or NH4Cl (rarely done)
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5
Q

Why does a loss of HCl from the body lead to a metabolic alkalosis? (explain)

A
  • HCl is normally titrated by pancreatic sodium bicarbonate
    HCl + NaHCO3 –> NaCl + CO2 + H2O
  • However, if HCl is lost from the body (was normally there) because of vomiting or gastric drainage, there is a net gain of bicarbonate
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6
Q

Once metabolic alkalosis has occurred, its maintenance must indicate a failure of the kidneys to excrete the excess bicarbonate.
Explain the 2 way how this can occur. (Which mech must it be in the absence of renal failure?)

A
  • Decreased filtered load of bicarbonate (due to a decrease in GFR)
  • Increase in tubular bicarbonate reabsorption or decrease in bicarbonate secretion (must be this is absence of renal failure)
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7
Q

How can Cl- be lost thru the skin?

A

Cystic fibrosis – loss of chloride in excess of bicarbonate in sweat.

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8
Q

What can 2 overall causes lead to a high-AG metabolic acidosis? (give eg’s of each)

A

Overproduction of an endogenous organic acid
(H+A-), where A- is the acid anion (e.g., with lactic acidosis A- = lactate)
- Ketoacidosis; Toxin ingestion; Methanol (formate); Ethylene glycol (glyoxylate, oxylate)

Failure to excrete inorganic anions
- Renal failure (phosphate; sulfate);

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9
Q

How does K+ administration work to treat metabolic alkalosis?

A

K+ moves into cell, H+ moves out, and that will titrate some of the bicarb

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10
Q

What is the Henderson-Hasselbalch equation?

*What is the abbreviated version that is useful to us?

A

pH = pKa + log[HCO3-]/[H2CO3]

[H+] = 24 x PCO2 / [HCO3-]

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11
Q

Define contraction alkalosis.

A

Refers to the increase in blood pH that occurs as a result of fluid losses (volume contraction). Na+ flows to distal sites where it is collected in exchange for H+

  • May be due to compensatory mechs related to V loss, leading to aldo release and H+ secretion. Also Na/H exchange at PCT.
  • The change in pH is especially pronounced with acidic fluid losses caused by problems like vomiting.
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12
Q

What channel is present on the luminal membrane of beta-intercalated cells?
What channel is on the basolateral membrane?

A
  • Luminal: HCO3-/Cl- antiport (bicarb excreted!)

- Basolateral: H+ pump (H+ reabsorbed!)

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13
Q

What types of collecting duct cells have H+ pumps and Na+/H+ pumps?
What side of the cell?

A

Alpha-intercalated cell

Luminal

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14
Q

What are 2 ways by which Cl- could be lost in the stool?

give the names of the 2 dz’s a/w each mechanism

A
  • Secretion of chloride into stool (villous adenoma)

- Failure of gut reabsorption of chloride (congenital chloridorrhea)

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15
Q

How do you derive pH from H+?

A

pH = -log[H+]

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16
Q

Why does overproduction of an endogenous organic acid lead to an AG metabolic acidosis?

A

H+ added to the blood, leading to acidosis. There is increased anion being added to the blood as well, so anion gap increases.

17
Q

What are some of the sx of metabolic alkalosis?

Physical signs?

A

None, but sometimes cramps

  • HTN (primary mineralocorticoid excess), hypoventilation, tetany, increased DTRs, cardiac arrhythmias
18
Q

For every pH change of ___, there will be a doubling or a halving of the [H+].

A

0.3

19
Q

What are the 3 overall causes of metabolic alkalosis?

A
  1. Net loss of H+ from ECF
  2. Net addition of HCO3- to ECF
  3. Chloride depletion (leads to increased bicarb)
20
Q

Would CA inhibitors lead to an AG or non-AG metabolic acidosis?

A

non-AG (loss of bicarb but compensatory increase in Cl-)

21
Q

Why does failure to excrete inorganic anions lead to an AG metabolic acidosis?

A

Excess H+ is being buffered by phosphate/sulfate in the blood. If you can’t excrete them, acid builds up, leading to acidosis. There is an anion gap due to the leftover anions.

22
Q

What ion deficit is in the definition of metabolic acidosis and alkalosis?

What adaptation is seen?

A

HCO3- (bicarb)

  • Increase or decrease in CO2 (respiratory) to maintain near-nl pH
23
Q

How can Cl- be lost in the kidney?

A

Diuretics: you lose Cl-, but this is what macula densa senses.

24
Q

In chloride-resistant metabolic alkalosis, what are the 2 general conditions that can cause it?

A

Consider mineralocorticoid excess states – can be either primary (low renin) of secondary (high renin).

25
Q 
Which RTA has a urine pH > 5.5? (basic)
Which RTA is a/w stones?
Which RTA is hyperchloremic?
Which RTA is hyperkalemic?
What is the plasma bicarb level for each?
A
  • I
  • I
  • I, II, IV
  • IV
    I: <10meq/L II: 12-20meq/L IV: >17meq/L
26
Q

How can administration of huge amounts of nl saline lead to a metabolic acidosis? Is it AG or non-AG?

A

Dilutional acidosis: increasing Cl-, bicarb has to go down to maintain electrical neutrality
- Non-AG

27
Q

Bicarb is primarily reasborbed at the ___________. What other ion is part of it’s transport?

A

PCT
(Comes in as CO2)
Apical membrane: cotransport w/Na+

28
Q

Name the 3 mechanisms by which the kidney excretes acid.

Which is most important?

A
  1. Free hydrogen ion (H+) excretion (lowers urine pH); least important
  2. Titratable acid excretion: secreted H+ combines with poorly reabsorbable anions such as PO43-
  3. Excretion of ammonium ion (NH4+). The kidney generates ammonia (NH3) which combines with secreted H+ and is excreted as ammonium (NH4+) ion; This is most important
29
Q

What’s the formula for anion gap?

What is the nl range?

A

Anion Gap = Na+ - (Cl- + HCO3-)
Unmeasured anions - unmeasured cations = AG

10-12 meq/L

30
Q

What are the 3 major causes of H+ loss?

A
  1. GI loss
  2. Renal loss
  3. Shift into cells
31
Q

Name the primary defect behind the 3 types of RTA, and where in the nephron they occur?

A

I: Impaired ability to excrete H+ in the DCT
II: Impaired HCO3- reabsorption in the PCT
IV: Decreased secretion of or effect of aldosterone

32
Q

How could cellular ionic homeostatic changes account for a metabolic alkalosis? (explain)

A

Shift of K+ out of cells into the extracellular fluid (ECF) in exchange for H+ (“loss” of H+ into the cells)
- Helps us avoid severe hypokalemia

33
Q

In metabolic alkalosis, what is the predicted CO2 compensation for each numerical gain of bicarb?

A

HCO3- x 0.7

34
Q

How does acetazolamide work to treat metabolic alkalosis?

A

Leads to bicarb loss in urine

35
Q

What’s another name for non-AG metabolic acidosis?

What are some causes of this?

A

Hyperchloremic

  • GI loss of bicarb (diarrhea)
  • Renal loss of bicarb
  • Failure to excrete acid
  • Administration of acid (HCl, NH3Cl)
  • Administration of large amounts of saline
36
Q

How could HCO3- be gained exogenously?

Would this lead to an alkalosis or acidosis?

A
  • Addition of alkali (which are converted to bicarb in the blood): bicarb itself, lactate, citrate, acetate

(not their acidic forms!)

37
Q

In metabolic acidosis, what is the predicted CO2 compensation for each numerical loss of bicarb?

A

HCO3- x 1.2

38
Q

Which is the mech behind RTAs type 1, 2, and 4?

A

1: Defect in the luminal H+/ATPase of the DCT
2: Impairment in proximal HCO3- reabsorption
4: Aldosterone deficiency or resistance

MHD (20 decks)

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