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
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
1) What is the normal pH range?
2) What is the pH range for acidosis?
3) What is the pH range for alkalosis
4) What is the normal HCO3 level?
5) What is the normal PCO2 level?
6) What is the normal Anion Gap
7) 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
What is the treatment for Pyroglutamic (5-oxoproline) acidosis?
1) Discontinue Acetaminophen
2) IVF
3) N-acetylcysteine
What is the differential diagnosis of increased osmolar gap?
ME DIE:
1) Methanol
2) Ethanol
3) Diethylene glycol
4) Isopropyl alcohol (rubbing alcohol)
5) Ethylene glycol
If a patient has a high anion gap and high osmolar gap but does not have metabolic acidosis, what is the most likely cause?
Isopropyl alcohol
What are the most important differentials for Normal Anion Gap Metabolic Acidosis (NAGMA)?
1) Diarrhea
2) Renal tubular acidosis
Renal Tubular Acidosis is a condition in which?
It cannot be diagnosed in setting of?
1) Net acid excretion by the kidneys is impaired
2) AKI
In the setting of RTA, secretion of what is impaired?
Reabsorption of what is impaired?
1) H+ ion
2) HCO3-
RTA type 1 (a.k.a. Distal RTA) results from?
Decreased net H+ ion secretion in distal tubules and collecting duct
RTA type 2 (a.k.a. Proximal RTA) results from?
Decreased HCO3- reabsorption in the proximal tubule
RTA type 4 (a.k.a. Hyperkalemic RTA) results from?
What does this lead to?
1) Decreased aldosterone secretion or aldosterone resistance
2) Decreased net H+ and K+ secretion in collecting duct
What is the most common RTA, often seen in DM2 or CKD?
RTA type 4 (Hyperkalemic RTA)
What is the urine anion gap in type 1 RTA?
Type 2?
Type 4?
1) Positive
2) Negative
3) Positive
Urine Anion Gap (UAG) is clinically used to differentiate?
Renal from non-renal causes of NAGMA
The Urine Anion Gap is a marker of?
NH4Cl (ammonium chloride) excretion
If the UAG is negative then it indicates?
If it is positive?
1) Appropriate distal nephron urinary acidification
2) Inappropriate distal nephron urinary acidification
What is the relationship between H+ and HCO3-?
H+ secretion leads to HCO3- reabsorption
What is the most common cause of proximal RTA (Type 2) in children?
In adults?
1) Cystinosis
2) Multiple myeloma from Fanconi syndrome
What are the clinical manifestation of proximal RTA?
1) NAGMA
2) Hypokalemia
How is proximal RTA diagnosed?
1) Urine pH less than 5.5 when in steady state
2) UAG is negative
Are proximal RTA patients able to acidify their urine?
Are Distal RTA (type 1)?
1) Yes
2) No
Distal RTA is commonly seen with systemic diseases like?
What can also cause it especially if it contains Toluene?
1) Sjögren’s Syndrome
2) Glue sniffing
What are the clinical manifestation of Distal RTA?
Nephrolithiasis or nephrocalcinosis
How is distal RTA diagnosis?
1) NAGMA
2) Unable to acidify urine pH < 5.5
3) Hypokalemia
4) UAG is positive
How does Type 4 RTA result in hyperkalemia?
Impaired Na+ reabsorption by principal cells
What populations is Hyperkalemic RTA more commonly seen in?
1) 50-70 years old
2) DM or CKD
How is Hyperkalemic RTA diagnosed?
1) Urine pH greater than 5.5
2) UAG is positive
In terms of ion levels, acidosis is associated with?
Alkalosis is associated with?
1) Hyperkalemia
2) Hypokalemia
What are the differentials for metabolic alkalosis?
1) Hypokalemia
2) Vomiting or Nasogastric tube suctioning
3) Diuretics (thiazide and loop diuretics)
4) Volume depletion
5) Mineralocorticoid excess
What factors in terms of reabsorption and secretion lead to metabolic alkalosis?
1) Na+ reabsorption
2) H+ secretion
3) HCO3- reabsorption
Bartter syndrome which is a rare autosomal recessive disease that typically affects prenatal or neonatal patients causes what clinical manifestations?
1) Hypokalemia
2) Metabolic alkalosis
3) Low blood pressure
4) Hypercalciuria
5) Nephrocalcinosis
Bartter Syndrome is caused by inactivating mutations of?
This causes NaCl loss and volume depletion leading to?
1) Thick-ascending loop (TAL) transporters
2) Secondary Hyperaldosteronism
The net result of Bartter syndrome is similar to?
Loop diuretic use
Gitelman Syndrome which is a rare autosomal recessive disease that typically is seen in late childhood or adulthood causes what clinical manifestations?
1) Hypokalemia
2) Metabolic alkalosis
3) Low blood pressure
4) Hypocalciuria
5) Hypomagnesemia
What is the distinguishing factor between Bartter Syndrome and Gitelman Syndrome?
1) Bartter Syndrome = Hypercalciuria
2) Gitelman Syndrome = Hypocalciuria
Gitelman Syndrome is caused by inactivating mutations of?
Na-Cl cotransporter (NCCT)
The net result of Gitelman Syndrome is similar to?
Thiazide diuretic use
Liddle Syndrome which is a rare autosomal recessive disease that typically presents at a young age causes what clinical manifestations?
1) Resistant Hypertension
2) Hypokalemia
3) Metabolic alkalosis
Liddle Syndrome is caused by mutations of what in the collecting duct of nephron?
Epithelial Na+ channel (ENaC)
How is Liddle syndrome diagnosed?
1) Genetic testing
2) Low Aldosterone and renin levels
How is Liddle syndrome treated?
1) Amiloride or Triamterene (block sodium channel)
2) Low salt diet
What causes respiratory alkalosis?
Anything that increases respiratory rate or tidal volume
What causes respiratory acidosis?
1) Anything that lowers respiratory rate/tidal volume, increases dead space, or worsens airway obstruction
2) Inadequate ventilator settings
3) Increases in CO2 production
