Metabolic Acidosis - Basok

Question 1

How are acids dealt with in the body?

Answer 1

Excretion:

Carbonic acids equilibrize to bicarbonate.

Noncarbonic acids form sulfur products excreted in the urine through the kidneys. Ex: phosphate (titratable).

Can excrete a small amount as pure protons (1%)

Ammonium production (can increase in response to acidosis and hypokalemia)

Buffers:

1. Extracellular Bicarbonate, ammonium (increased with hypokalemia)
2. Intracellular proteins, inorganic phosphate and HGB
3. Bone carbonate (loss induces osteopenia)

Question 2

Henderson Hesselbach Equation and the response to metabolic acidosis

Answer 2

[H+]= 24xpCO2 / [HCO3-]
pH = 6.10 + log ([HCO3] ÷ [0.03 x PCO2])

Fall of pCO2 by 1.2 mmHg per each reduction of HCO3- of 1 mEq

1. Start with pH.
2. Low bicarbonate means primary acidosis. Respiratory alkalosis would be secondary. Also cause of Kussmaul respirations.

If pCO2 is higher: it means concomitant acidosis.
If pCO2 is lower: concomitant alkalosis (due to respiratory (anxiety) or pulmonary embolism)

3. Calculate the anion gap

Question 3

Features and Mechanisms of Metabolic Acidosis

Answer 3

• Increased ventilation Kussmaul breathing
• Hypotension
• Pulmonary edema
• Cardiac standstill-don’t respond well to catecholamines if pH<7.2
• Calciuria with marked calcium
loss from bone

• Increased acid generation (ketoacidosis and lactic acidosis)
• Loss of bicarbonate (diarrhea or type 2 proximal renal tubular acidosis) or a bicarbonate precursor (ketoacid anion loss in ketoacidosis)
• Diminished renal acid excretion (renal failure or type 1 [distal] renal tubular acidosis)

Question 4

Types of Renal Tubular Acidosis

Answer 4

Type I
Distal tubular acidosis. Problem with H+ ATPase pump on intercalated cells. Idiopathic, can be related to other diseases like Sjogren’s syndrome or hereditary.

Type II
In proximal Convoluted Tubule. Part of Fanconi syndrome. bicarbonuria, amino aciduria, glucouria, tubular proteinuria, phosphaturia.

Type III doesn’t exist

Type IV
In juxtaglomerular apparatus. Low renin, low aldosterone. Low aldosterone–>hyperkalemia. Decrease in renal ammoniagenesis. NH3 not grabbing excess protons in urine. Easily correctible: correct increase in K (diurese K with thiazide, etc) Caused by destruction in JG apparatus. ACE-I would cause further hyperkalemia- give thiazide first.

Question 5

Correction of hypokalemia and acidosis with ammonium (in type II RTA)

Answer 5

Ammonia production from the metabolism of glutamine is increased in the presence of an acid load.

Glutamine-glutamate-alphaketoglutarate with ammonium secreted at proximal tubule cells into lumen. Picked up in ThAL via Na/K/2Cl swing instead of K. Diffuses into the collecting duct as NH3 and picks up an extra proton. Excreted as ammonium chloride.

Hypokalemia–>increased ammoniogenesis (because protons in cells and then in urine). Less ammoniogenesis with hyperkalemia.

Hypokalemia and liver cirrhosis–>ammonia accumulation because the liver can’t turn it into urea–>encephalopathy. Prone to hypokalemia because of vomiting or furosemide.
Use K sparing diuretic (aldactone) in order to correct.

Can be caused by a defect in carbonic anhydrase. Can be inhibited by diamox (acetazolamide).

Question 6

Calculation of anion gap

Answer 6

Plasma:

Anion gap= measured cations- measured anions = unmeasured anions-unmeasured cations

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

Normally between 8-12

Calculated to check for unknown anions (antifreeze, etc.) or reduced cations (hypomagnesemia or hypocalcemia).

Depends on albumin, need to account for hypoalbuminemmia: a fall of 2.5mEq of AG for each g of reduced albumin

Urine:

Calculated if plasma AG is normal to estimate ammonium in urine to check for RTA contrasted with diarrhea

UAG=[Na+]+[K+] - [Cl-]

If negative, diarrhea with normal working kidney and ammonium excreted in urine
If positive, no ammonium excreted in urine: RTA

Question 7

Differential Diagnoses for metabolic acidosis

Answer 7

High AG:

MUDPILES:
Methanol Ingestion (formic acid production causes blindness and death)
Uremia
Diabetic (DKA), or other ketoacidosis: alcoholic, starvation (treat with insulin and saline until pH and anion gap corrected-even if need to add glucose)
Peraldehyde/Propylene glycol
Infection, Iron, Isoniazid, Inborn errors of metabolism
Lactic acidosis: concealed sepsis or metformin (don’t give for Cr>1.5-malameformin-associated lactic acidosis) also ethanol. Type A (NADH activation): shock, acute severe hypoxia and anemia. Type B: cyanide, metformin, NRTI (AZT).
Ethylene glycol (crystal formation)
Salicylates (children for rheumatic fever/pericarditis)

Renal failure

Normal AG:

RTA
Carboanhydrase inhibitor (RTAII)
Hippurate (glue sniffing)
Hyperchloremic:
Diarrhea (lose bicarbonate)
Ileal conduit (fistula leads to diarrhea)