Approach to Metabolic Acidosis and Alkalosis Flashcards Preview

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Flashcards in Approach to Metabolic Acidosis and Alkalosis Deck (30):
1

Metabolic Acidosis

Metabolic acidosis is defined as a primary decrease in the bicarbonate concentration of the plasma.

2

What is the respiratory adaptation for metabolic acidosis?

Hyperventilation to reduce PCO2

3

What is [H+] at pH = 7.4?

[H+] = 80

4

How is the anion gap calculated?

AG = (Na+) - (HCO3‐ + Cl‐)

5

What are the top 3 most represented ions in the body?

1. Na+
2. Cl-
3. HCO3-

6

What is the normal range of the anion gap?

9-12 mEq

7

What are the causes of Increased Anion Gap Acidosis?

- Increased organic acid production
- Failure to excrete inorganic anions

8

How does generation of organic acid increase the anion gap?

Generation of organic acid will lead to the titration of the HCO3- which will decrease its levels by a proportionate
amount

9

What are the causes of Normal Anion Gap (Hyperchloremic) Acidosis?

• Gastrointestinal loss of bicarbonate
• Renal loss of bicarbonate
• Failure to excrete acid
• Administration of acid
• Administration of large amounts of saline (dilution)

10

How does Type II renal tubule acidosis cause acidosis?

Disease of the PT that leads to decreased filtration
of HCO3- but with complete reabsorption - HCO3- still
decreased because of decreased filtration

11

How does Type I renal tubule acidosis cause acidosis?

Disease of the DT that is due to several mechanisms:
1. Inability to excrete H+ ion - problem with H+ ATPase
2. Reuptake of H++ ions

12

Metabolic Alkalosis

Metabolic alkalosis is defined as a primary increase in the bicarbonate concentration of the plasma.

13

What is the respiratory adaptation for metabolic alkalosis?

Hypoventilation to increase PCO2

14

What are some causes of metabolic alkalosis?

• Net loss of H+ from ECF
• Net addition of HCO3‐ to ECF
• Chloride depletion (contraction)

15

What happens with HCl loss from the stomach?

If HCl is lost from the body because of vomiting or gastric drainage then there is a net gain of bicarbonate

16

What does aldosterone excess cause and how?

Metabolic alkalosis.

It causes hypokalemia which will shift K+ from inside the cells out of the cells to try and maintain equilibrium. H+ will be taken into the cells causing increased plasma pH

17

What can cause HCO3- gain?

• Exogenous alkali administration
– bicarbonate
– lactate
– citrate
– acetate

18

How does the GI have excess Cl- loss?

• Secretion of chloride into stool (villous adenoma)
• Failure of gut reabsorption of chloride (congenital chloridorrhea)

19

Bartter's syndrome

Genetic defect of the loop diuretic‐sensitive Na‐ K‐2Cl cotransporter in the loop of Henle ("endogenous loop diuretic")

20

Gitelman's syndrome

Genetic defect of the thiazide‐sensitive Na‐Cl cotransporter in the distal tubule ("endogenous thiazide")

21

What causes skin loss of Cl-?

Cystic fibrosis ‐‐ loss of chloride in excess of bicarbonate in sweat

22

What happens to ionized Ca2+ with increased pH?

Increased pH will increase the amount of Ca2+ bound to albumin - decreased ionized fraction

23

Metabolic Alkalosis Lab Findings

Elevated [HCO3‐], decreased [Cl‐], usually low [K+]

24

Chloride‐responsive type Metabolic alkalosis

Kidney is avidly reabsorbing chloride because of persistent volume (and chloride) depletion that developed during the generation of metabolic alkalosis.

25

Chloride‐resistant type (urine Cl‐ > 20 mmol/L) Metabolic alkalosis

Mineralocorticoid excess states ‐‐ can be either primary (low renin) of secondary (high renin) - hyperaldosteronism

26

What can be used for treatment of metabolic alkalosis?

• Potassium administration
• Acetazolamide
• Volume repletion
• Intravenous HCl or NH4Cl

27

A 70‐year‐old man presents with weakness.

• Blood chemistries reveal (inmmol/L): Na+145, K+3.0, Cl‐ 120, CO2 16; (in mg/dL): Urea nitrogen 30, Creatinine 1.2.
• Arterial blood gases (ABG) reveal: pH 7.35, PCO2 30 mmHg, HCO3‐ 16 mEq/L.

Q: What is the acid base disturbance?
A. Metabolic acidosis
B. Metabolic alkalosis
C. Mixed metabolic acidosis/metabolic alkalosis
D. No metabolic disturbance

A. Metabolic acidosis

28

A 70‐year‐old man presents with weakness.

• Blood chemistries reveal (inmmol/L): Na+145, K+3.0, Cl‐ 120, CO2 16; (in mg/dL): Urea nitrogen 30, Creatinine 1.2.
• Arterial blood gases (ABG) reveal: pH 7.35, PCO2 30 mmHg, HCO3‐ 16 mEq/L.

What is the nature of the metabolic acidosis?

A. High‐anion gap acidosis
B. Normal anion gap (hyperchloremic) acidosis

B. Normal anion gap (hyperchloremic) acidosis

145 - (120+16) = 9

29

A 30‐year‐old female presents with fatigue and weakness. She denies vomiting or diarrhea and takes no medications. Her physical examination is normal except for mild orthostatic hypotension. Blood chemistries reveal (in mmol/L): Na+ 138, K+ 2.9, Cl‐ 90, CO2 40. Arterial blood gases (ABG) reveal: pH 7.50; PCO2 53 mmHg; HCO3‐ 40 mEq/L. The urine pH is 7.5. Urine chemistries reveal (in mEq/L): Na+ 30 K+ 30 Cl‐ 5.

Q: What is the acid base disorder?

A. Metabolic acidosis
B. Metabolic alkalosis
C. Mixed metabolic acidosis/metabolic alkalosis
D. No metabolic disturbance

B. Metabolic alkalosis

30

A 30‐year‐old female presents with fatigue and weakness. She denies vomiting or diarrhea and takes no medications. Her physical examination is normal except for mild orthostatic hypotension. Blood chemistries reveal (in mmol/L): Na+ 138, K+ 2.9, Cl‐ 90, CO2 40. Arterial blood gases (ABG) reveal: pH 7.50; PCO2 53 mmHg; HCO3‐ 40 mEq/L. The urine pH is 7.5. Urine chemistries reveal (in mEq/L): Na+ 30 K+ 30 Cl‐ 5.

What is the likely diagnosis?

A. Diuretic intake
B. Bartter’s syndrome
C. Gitelman’s syndrome
D. Surreptitious vomiting
E. Hypokalemic periodic paralysis

D. Surreptitious vomiting

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