Clinical Approach to Acid-Base Disorders (Selby) Flashcards
What enzyme is responsible for producing bicarbonate in the Bicarbonate Buffer System?
Where is it located?
Carbonic Anhydrase
- located in both lung alveoli and tubular epithelial cells
What are the 4 major acid-base disturbances and what are they characterized by?
Metabolic ACIDosis = low serum HCO3
Metabolic ALKAlosis = high serum HCO3
Respiratory ACIDosis = high PCO2
Respiratory ALKAlosis = low PCO2
How is each of the 4 metabolic disturbances compensated for?
Metabolic Acidosis –> Respiratory Alkalosis
- dec. HCO3 –> dec. PCO2 (inc. RR)
Metabolic Alkalosis –> Respiratory Acidosis
- inc. HCO3 –> inc. PCO2 (dec. RR)
Respiratory Acidosis –> Metabolic Alkalosis
- inc. PCO2 –> inc. HCO3 (inc. reabsorption)
Respiratory Alkalosis –> Metabolic Acidosis
- dec. PCO2 –> dec. HCO3 (dec. reabsorption)
How does HCO3 change during Acute/Chronic Respiratory Acidosis and Acute/Chronic Alkalosis?
Respiratory Acidosis
- A: inc. 1 mEq/L for every 10 mmHg inc in pCO2
- C: inc. 3.5 mEq/L for every 10 mmHg inc in pCO2
Respiratory Alkalosis
- A: dec. 2 mEq/L for every 10 mmHg dec in pCO2
- C: dec. 5 mEq/L for every 10 mmHg dec in pCO2
Acid-Base Stepwise Approach
What are the 4 steps in the approach to pts. with metabolic disturbances?
- determine if acidosis or alkalosis is present
- determine if disturbance is metabolic/respiratory
- if metabolic acidosis –> calculate anion gap
- hypoalbuminemia –> osmolar gap
- HAGMA –> osmolar gap and delta-delta gap
- calculate appropriate compensation
- compensation appropriate - simple disorder
- compensation inappropriate - mixed
What are these normal value ranges:
- pH in the body
- HCO3
- PCO2
- Anion Gap
- Osmolality Gap
- 7.35 - 7.44
- acidosis: pH < 7.35
- alkalosis: pH > 7.44
- 24 mEq/L
- 40 mmHg
- 12
- 10 mOsm/kg
How is the Anion Gap calculated and what does it help differentiate?
AG = Na - (HCO3 + Cl)
- normal AG = 12 +/- 2
- clinically used to differentiate HAGMA vs NAGMA
How is the Osmolar Gap calculated?
What is it useful for screening for?
- calculate serum osmolality (normal = 275-290)
- 2 (Na) + (Glucose/18) + (BUN/2.8)
- calculate osmolar gap
- measured serum - calculated serum osmolality
- normal gap < 10 mOsm/kg
- > 10 mOsm/kg = additional solutes in blood
useful for alcohol ingestion screening –> if AG > 20, be highly suspicious of alcohol ingestion
How is the Delta-Delta Gap calculated?
Why is it performed and what does measuring HCO3 mean?
- used in pts. with HAGMA to determine if coexistent NAGMA or metabolic alkalosis present
- Delta Gap = calculated AG - normal AG (12)
- Delta HCO3 = normal HCO3 (24) - delta gap
- HCO3 close to 16 = no additional disturbances
- HCO3 > 16 = metabolic alkalosis with HAGMA
- HCO3 < 16 = NAGMA with HAGMA
HAGMA differential diagnosis
What does the GOLD MARK mneumonic mean?
G - glycols (ethylene and propylene)
O - oxoproline (acetaminophen toxicity)
L - L lactic acidosis (NORMAL)
D- D lactic acidosis (BACTERIA) must request this
M - methanol
A - aspirin
R- renal failure
K - ketoacidosis (alcohol, diabetes, starvation)
How is Acetaminophen Toxicity diagnosed in pts with HAGMA and how is it treated?
Dx: urinary organic acid screen
Tx: discontinue drug, IVF, N-acetylcysteine
What is the differential diagnosis for Increased Osmolar Gap and why are they important to look for?
MEDIE
M - methanol
E - ethanol
D - diethylene glycol (diuretics - mannitol)
I - isopropyl alcohol (RUBBING ALCOHOL)
NOT ASSOCIATED WITH METABOLIC ACIDOSIS
E - Ethylene Glycol (ANTIFREEZE)
important because these will KILL YOU if not treated
What does Alcohol Dehydrogenase convert Methanol and Ethylene Glycol into and what clinical issues does this lead to?
Methanol –> Formic Acid = BLINDNESS
Ethylene Glycol –> Oxalic Acid = RENAL FAILURE
- crystalize in the urine
What are the two major causes of Normal Anion Gap Metabolic Acidosis (NAGMA)?
Diarrhea and Renal Tubular Acidosis
What is Renal Tubular Acidosis and when can it NOT be diagnosed?
What are the 3 classifications of RTA?
- condition where net acid excretion by the kidneys is impaired that CANNOT be diagnosed in the setting of Acute Kidney Injury (AKI)
RTA Type 1 (Distal)
- dec. net H secretion in distal tubules and CDs
RTA Type 2 (Proximal)
- dec. HCO3 reabsorption in proximal tubules
RTA Type 3 (Hyperkalemic RTA) = MOST COMMON
- dec. aldosterone secretion or resistance
- dec. net H/K secretion in collecting duct (CD)
How is the Urine Anion Gap calculated and what is it used to differentiate between?
UAG = (UrineNa + UrineK) - UrineCl
- (-) = appropriate distal nephron urine acid. (Type 2)
- (+) = inappropriate distal nephron (Type 1 or 4)
- differentiates renal from non-renal causes of NAGMA and is a marker of NH4Cl excretion
Proximal RTA (Type 2)
How does it clinically manifest and what are two ways it is diagnosed?
C: NAGMA with or without proximal tubular dysfunction and HYPOkalemia (mild compared to Type 1)
Dx: Urine pH can be high or low (pH < 5.5 when in new steady state) and UAG that is NEGATIVE
Distal RTA (Type 1)
What is it, what does it lead to, and what are two conditions that can lead to it other than inherited? (S/T)
- due to dec. net H ion secretion in the distal nephron (H/K ATPase or H ATPase defects) or gradient defect allowing H ions to flow back into tubular cells
- Amphotericin/fungal infections
- lack of net H ion secretion prevents urinary acidification and excretion of ammonium
- can be seen in pts. with Sjogren’s Syndrome and pts. that sniff GLUE (due to Toluene)
Distal RTA (Type 1)
How does it clinically manifest and what are 3 ways it is diagnosed?
C: nephrolithiasis (kidney stones) and nephrocalcinosis (calcium deposits in parenchyma)
Dx: NAGMA, unable to acidify urine pH < 5.5, HYPOkalemia (SEVERE), (+) UAG
Hyperkalemic RTA (Type 4)
What is it and what two things usually cause it?
- distal nephron dysfunction from impaired renal excretion of H and K causing NAGMA and HYPERkalemia
- deficient circulating aldosterone
- aldosterone resistance in collecting ducts
- either above case results in impaired Na reabsorption by principle cells
Hyperkalemic RTA (Type 4)
How does it clinically manifest and what are two ways it is diagnosed?
C: NAGMA with HYPERKALEMIA (usually asymptomatic though)
- most pts. in 50-70s with Hx of diabetes/CKD
Dx: variable urine pH (usually > 5.5) and (+) UAG
What are 5 common causes of Metabolic Alkalosis? (H/V/D/VD/ME)
Hypokalemia Vomiting or Nasogastric Tube Suction Diuretics (thiazide or loop diuretics) Volume Depletion (contraction alkalosis) Mineralocorticoid Excess
**factors that stimulate Na reabsorption, secondarily inc. H secretion (simulating HCO3 reabsorption leading to metabolic alkalosis)
Bartter Syndrome
What is it caused by, what are its 4 clinical manifestations, and how does pathophysiologically develop?
- caused by Auto Recessive disease in PRENATAL/NEONATAL pts (usually death)
C: hypokalemia, metabolic alkalosis (saline NON-responsive), low BP, HYPERcalciuria and nephrocalcinosis
PP: inactivating mutations of Thick-Ascending Loop transporters
- NaCl loss –> volume depletion –> 2nd hyperaldosteronism
What are these types of Bartter Syndrome caused by:
Type 1 (N) Type 2 (R) Type 3 (C) Type 4 (B)
What is their net result similar to?
- NKCC2 mutation
- ROMK mutation
- CLC-Kb mutation
- Barttin mutation
net result is similar to LOOP DIURETIC use
