Renal Clinical Medicine Part 1: Acid-base disorders (M. Selby) Flashcards
What is the most important extracellular buffering system in the body?
The bicarbonate buffer system (HCO3- and CO2)
In the bicarbonate buffer system, if the HCO3 increases then what happens to the pH?
If the PCO2 increases?
1) pH increases
2) pH decreases
What is the enzyme involved in the bicarbonate buffer system?
Where is it found?
1) Carbonic anhydrase
2) Lung alveoli and renal tubular epithelial cells
How do the lungs alter the bicarbonate buffer system?
1) Increases in RR = increased CO2 blown off
2) Decreased RR = decreases CO2 blown off
If HCO3 is not reabsorbed by kidney then?
If large amounts of H+ are secreted into the tubular lumen by renal epithelial cells then?
1) It will be excreted and removes base from ECF
2) This removes acid from ECF
Low serum HCO3- results in?
High serum HCO3-?
1) Metabolic Acidosis
2) Metabolic Alkalosis
High PCO2 results in?
Low PCO2 results in?
1) Respiratory Acidosis
2) Respiratory Alkalosis
How is a metabolic acidosis (low HCO3-) compensated?
What causes this?
1) Respiratory Alkalosis (low PCO2)
2) Increase in RR
How is a metabolic alkalosis (high HCO3-) compensated?
What causes this?
1) Respiratory Acidosis (high PCO2)
2) Decrease in RR
How is respiratory acidosis (high PCO2) compensated?
What causes this?
1) Metabolic alkalosis (high HCO3-)
2) Increased kidney reabsorption and generation of new HCO3-
How is respiratory alkalosis (low PCO2) compensated?
What causes this?
1) Metabolic acidosis (low HCO3)
2) Decreased kidney reabsorption and generation of new HCO3-
For every 10 mmHg increase in pCO2, what happens to HCO3 in Acute Respiratory Acidosis?
What happens to HCO3 in Chronic Respiratory Acidosis?
1) HCO3 increases by 1
2) HCO3 increased by 3.5
For every 10 mmHg decrease in pCO2, what happens to HCO3 in Acute Respiratory Alkalosis?
What happens to HCO3 in Chronic Respiratory Alkalosis?
1) HCO3 decreases by 2
2) HCO3 decreases by 5
What is the Acid-Base Stepwise Approach?
1) Determine if acidosis or alkalosis is present
2) Determine if the primary disturbances is metabolic or respiratory
3) If metabolic acidosis is present, calculate the anion gap
-If Hypoalbuminemia calculate corrected Anion Gap)
-If HAGMA calculate osmolar gap and maybe delta-
delta gap
4) Calculate appropriate compensation for primary acid-base disorder
If high anion gap metabolic acidosis is present, why do you want to calculate the osmolar gap?
To screen for possible alcohol ingestion
What is present if the primary acid-base disorder has appropriate compensation?
If it has inappropriate compensation?
1) Simple acid-base disorder
2) Mixed acid-base disorder
What is the normal pH range?
What is the pH range for acidosis?
What is the pH range for alkalosis
What is the normal HCO3 level?
What is the normal PCO2 level?
What is the normal Anion Gap
What is the normal Osmolality Gap?
1) 7.35-7.44
2) Less than 7.35
3) More than 7.44
4) 24 mEq/L
5) 40 mmHg
6) 12
7) 10 mosm/kg
What protein is included as an anion?
Albumin
Why are anions important?
Because they are accompanied by protons (H+ ions), which are buffered by HCO3-
What is the anion gap clinically used for?
Differentiate etiologies of metabolic acidosis, either HAGMA or NAGMA
How is the anion gap calculated?
Anion gap = Na - (HCO3 + Cl)
If anion gap is greater than 20 what should you be highly suspicious for?
Alcohol ingestion
What is the Delta-Delta Gap used for?
Used in patients with HAGMA to determine if there is a coexistent NAGMA or metabolic alkalosis present
In the following scenario:
Delta gap = calculated AG – normal AG (12) = 20 – 12 = 8
Delta HCO3 = normal HCO3 (24) – Delta gap = 24 – 8 = 16
1) If the measured HCO3 was close ~16, then?
2) If the measured HCO3 was > 16, then?
3) If the measured HCO3 was < 16, then?
1) No additional acid-base disorder present
2) Metabolic alkalosis is present in addition to the HAGMA
3) Non-gap metabolic acidosis is present in addition to the HAGMA
What is the HAGMA differential diagnosis?
GOLD MARK:
1) Glycols (ethylene and propylene)
2) Oxoproline (aka Pyroglutamic acid, related to Acetaminophen toxicity)
3) L-Lactic acidosis
4) D-Lactic acidosis (caused by bacteria, seen in short bowel syndromes)
5) Methanol
6) Aspirin
7) Renal failure
8) Ketoacidosis (Alcoholic, Diabetic, Starvation)
Pyroglutamic (5-oxoproline) acidosis is seen more in what population?
How is it diagnosed?
It is a result of?
1) Women who are malnourished or critically ill
2) Urinary organic acid screen
3) Acetaminophen toxicity (depletes Glutathione so gamma-glutamylcysteine turns into 5-Oxoproline and not Glutathione)