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BiB Midterm 3 & Final > Renal Acid-Base > Flashcards

Renal Acid-Base Flashcards

1
Q

What are the values of pH, [H+], and [HCO3-] in Metabolic Acidosis?

A

pH < 7.38
[H+] > 42 nM
HCO3- < 24

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2
Q

What is the compensatory response in Metabolic Acidosis? What about Respiratory Acidosis?

A

Metabolic Acidosis: Decrease CO2- (hyperventilate)

Respiratory Acidosis: Increase HCO3-

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3
Q

What is the compensatory response in Metabolic Alkalosis? What about Respiratory Alkalosis?

A

Metabolic Alkalosis: Increase CO2 (hypoventilate)

Respiratory Alkalosis: Decrease HCO3-

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4
Q

What are the 3 ways in which we classify Metabolic Acidosis

A

Bicarbonate Loss
Failure to Excrete Acid (or Regenerate Bicarbonate)
Bicarbonate Consumption

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5
Q

What is the anion gap (AG)?

Provide the associated equation.

A

AG = The difference between Na+ and the sum of Cl- and HCO3- that represents the other plasma anions.

AG = [Na+] - ([Cl-]+ [HCO3-])

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6
Q

Which of the following will increase the Anion Gap?[Anion Gap Metabolic Acidosis (AGMA)]?:

Bicarbonate Loss
Bicarbonate Consumption
Failure to excrete acid/ regenerate bicarbonate

A

Bicarbonate Consumption

Failure to excrete acid/regenerate bicarbonate

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7
Q

Which of the following will increase the anion gap (AG) and WHY?
Hydrochloric acid
Carbonic Acid
Lactic Acid

A

Lactic Acid will increase the anion gap because it does not have a chloride or bicarbonate anion. When it gives off a protein it will lower the concentration of Cl- or HCO3- which will increase the AG. (High AG = Acidosis)

When hydrochloric or carbonic acid dissociate, they replace the Cl- or HCO3- that picks up the H+.

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8
Q

What are the types of acids/situations that can lead to Metabolic Acidosis? (There’s a mnemonic…)

A

GOLDMARK

Glycols, Oxoproline, L-Lactate, D-Lactate, Methanol, Aspirin, Renal Failure, Keto-acids

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9
Q

Briefly describe the pathophysiology of lactic acidosis. Does this affect the anion gap? If so how?

A

Lactic Acidosis - Increase in lactic acid production leads to a lower concentration of bicarbonate –> Acidosis

The anion gap is increased. (Bicarbonate consumption)

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10
Q

Briefly describe the pathophysiology of Renal Failure. Which stage affects the AG? How?

A

Increase in phosphate and sulfate anions increases unmeasured anions which decreases Cl- & HCO3- concentration which leads to acidosis.

The anion gap is increased in the early stages (HCO3- consumption)

In later stages kidneys cannot excrete acid (H+) which leads to NAGMA (?)

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11
Q

What are the two treatment options for lactic acidosis?

A

IV Bicarbonate

Treat underlying problem (ie. hypoperfusion)

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12
Q

What is the treatment options for renal failure?

A

Oral sodium bicarbonate

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13
Q

Briefly describe the pathophysiology of Diabetic Ketoacidosis (DKA).

Does it affect the anion gap (AG)? If so how?

A

In DKA, the body is not responding to insulin, which means the cells cannot absorb much glucose. This makes the cells use lipids (lipolysis) for energy. This generates beta hydroxybutyric acid and acetoacetic acid. In excess these lower Cl- and HCO3- leading to acidosis.

AG increases due to consumption of HCO3-…and Cl- (?)

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14
Q

Briefly describe the pathophysiology of Salicylate (ASA) Intoxication?

Does it affect the anion gap (AG)?

A

ASA (aspirin) Intoxication leads to build up of salicylic acid which decreases HCO3- and Cl- leading to acidosis.

This increases the AG. (Low Cl- and HCO3-)

ASA intoxication can also cause respiratory alkalosis (patient will over hyperventilate in response to ASA)

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15
Q

How can ASA Intoxication be treated?

A

Gastric Lavage, Charcoal
Urine alkalinization (Bicarbonate)
Dialysis if severe

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16
Q

AGMA should make you think of…

NAGMA should make you think of …

A

AGMA- GOLDMARK

NAGMA - Diarrhea or RTA (Renal Tubular Acidosis)

17
Q

What are the values of pH, [H+], and [HCO3-] in Metabolic ALKALOSIS?

A

pH < 7.38
[H+] = 38nM
[HCO3-] >24

18
Q

What are the two phases of metabolic alkalosis?

A

1) Generating Metabolic acidosis

2) Maintaining Metabolic acidosis

19
Q

What are the primary ways in which metabolic alkalosis can be generated? (2)

A
  1. Loss of H+ in the urine

2. Loss of H+ in the GI tract

20
Q

Which will lead to a loss of H+ in the GI tract? Vomiting or Diarrhea?

A

Vomiting

21
Q

What types of diuretics cause Metabolic Alkalosis and how?

A

Diuretics (Loop and Thiazide) increase sodium resorption at the collecting duct leading to an increase in H+ secretion. (Na+/H+ antiporter)

22
Q

What are the two Na+ dependent effects and Na+ independent effects of aldosterone?

A

Na Dependent: More Na+ resorb, More K+ and H+ secretion

Na Independent: More HCO3- resorb (HCO3-/Cl- pump) and More H+ secretion (H/+ ATPase pump)

23
Q

What are the 4 things that lead to metabolic alkalosis?

A
  1. Cl- Depletion - HCO3- cannot be excreted during alkalotic state (Beta- Intercalated cell)
  2. Low Plasma K+ - K+ will leave the ICF to the ECF which causes H+ to move from ECF to ICF.
  3. ECV volume decrease - RAAS activation causes increated H+ and K+ secretion
  4. High aldosterone - Increase Na+ and HCO3- resorb and H+ and K+ secretion
24
Q

What are the two ways in which aldosterone leads to H+ excretion?

A

H+ ATPase pump

Na+/H+ antiporter

25
Q

Which of the following can co-exist at the same time?
Metabolic acidosis and alkalosis
Respiratory acidosis and alkalosis

A

Metabolic acidosis and alkalosis
You can only have respiratory acidosis or alkalosis

So you can only have 3 of the diseases at a time. Not all 4!

26
Q

Insulin Deficiency or Decreased insulin responsiveness leads to an increase in serum ___. Why?

A

Glucose

Insulin facilitates cellular glucose absorption, without it glucose remains in the blood plasma/serum.

27
Q

A patient comes in with metabolic acidosis and respiratory alkalosis. This is an indicator of what type of AGMA?

A

Aspirin Overdose (Salicylic Acid AGMA)

Aspirin increases the AG with salicylic acid and also stimulates the respiration.

28
Q

High BUN and Creatinine levels are indicative of ____ failure. Why?

A

Renal Failure

This shows that the kidney is not properly filtering out Urea or creatinine (decreased GFR) which indicates Renal Failure.

29
Q

Describe how Renal/Kidney Failure can lead to AGMA and NAGMA.

A

AGMA - Kidney cannot secrete phosphates and sulfates which increases the unmeasured anions, therefore decreasing Cl- and HCO3- and increasing the anion gap.

NAGMA - Decreased ammonia production (NH3+) leads to more acidic urine which damages the kidney and leads to less H+ excretion.

30
Q

Why doesn’t the anion gap increase if you loose bicarbonate via diarrhea, vomiting, etc?

A

Because a primary loss of bicarbonate results in a compensatory increase in extracellular chloride (the anion gap is therefore unchanged).

Causes of HCO3- depletion: diarrhea, vomiting, renal tubular acidosis, and certain drugs

31
Q

How is metabolic alkalosis maintained? Explain how for each way. (4)

A
  1. Low ECV - Na+ Resorbtion occurs to maintain volume; causes HCO3- to also be resorbed
  2. Aldosterone - Promotes Na+ Resorb and K+ and H+ excretion

Low plasma K+: K+ goes into plasma from cells and H+ goes into cells (electroneutrality); plasma becomes more basic, cells become more acidic.

  1. Cl- Depletion: Less chloride will be filtered into the tubule, so beta intercalated cells cannot effectively excrete bicarb with the bicarb/Cl- antiporter.
32
Q

How is metabolic alkalosis maintained? Explain how for each way. (4)

A
  1. Low ECV - Na+ Resorption occurs to maintain volume; causes HCO3- to also be resorbed
  2. Aldosterone - Promotes Na+ Resorb and K+ and H+ excretion

Low plasma K+: K+ goes into plasma from cells and H+ goes into cells (electroneutrality); plasma becomes more basic, cells become more acidic.

  1. Cl- Depletion: Less chloride will be filtered into the tubule, so beta intercalated cells cannot effectively excrete bicarb with the bicarb/Cl- antiporter.
33
Q

To treat metabolic alkalosis with a low urine chloride, you give NaCl (to replace chlorine) and WHAT ELSE?

A

KCl to replace K+

BiB Midterm 3 & Final (10 decks)

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