Anion gap equation and normal anion gap
Gap = Na - Cl - HCO3
normal anion gap: 10-12 meQ/L
If HCO3- changes, how will the lungs compensate?
^ HCO3 = ^ CO2
The compensation will occur in the SAME direction as the primary change!!
How will a chronic vs acute change in acid/base status affect the compensatory response?
- Larger compensatory response in chronic vs acute
- With chronic disorders, body has had more time to mount a response
What are the different types of acidosis?
- High anion gap
- Normal anion gap:
- Type II renal tubular acidosis (RTA): proximal
- Type I renal tubular acidosis (RTA): distal
What does an anion gap greater than 10-12 meq/L tell us?
It tells us that the acidosis is caused by an increase in acid production
Which disorders are associated with high anion gap acidosis?
*increased acid production OR decreased excretion of inorganic anions
- ketoacidosis
- lactate acidosis
- toxin ingestion: methanol, ethylene glycol
- renal failure: failure to excrete sulfate and phosphate
Which disorders are associated with normal anion gap: hyperchloremic acidosis?
*decreased bicarb in body and failure to excrete acid
- GI: diarrhea
- renal: CA inhibitors > decreased bicarb reabsorption
- administration of acid: HCL or TPN = total parenteral nutrition
- administration of large amounts of saline = dilute bicarb
Which disorders are associated with normal anion gap: RTA II?
- normal anion gap
- proximal tubule disease + decreased absorption of HC03-
- leads to low bicarb and spillage of bicarb immediately into urine if treat with bicarb*
- [normal person would reabsorb bicarb until normalized levels > then spill out into urine]
Which disorders are associated with normal anion gap: RTA I?
*normal anion gap
-distal tubule disease
-malfunctioning Na/H ATPase = inability to excrete H+
>H+ builds up into cells
How to treat RAS?
- Give bicarb
- Treat underlying disease: determine if bicarb or excess acid is the issue
Alkalosis can be caused by: ?
- increased bicarb
- decreased acid
- loss of chloride
What can loss of H+ be caused by?
-GI: vomit
–renal: excess MR = hyperaldosterone = less Na in tubule = negative lumen charge and more K and H into tubule to neutralize
—in response to hypokalemia: K from cells into blood, Na/H+ into cell from blood to balance
Define the relationship between chloride and bicarb?
> They go together; inversely proportional
> decrease bicarb, body will retain chloride (increase) and vice versa to main normal pH
What causes loss of chloride?
GI: stool and decreased absorption in gut
skin: sweat in CF
renal: diuretics; barters and gitelmans
**Lose Cl- = decreased volume = RAA + aldo > Ca/H+ loss
Name the two disease associated with chloride loss?
BARTER’S: BA = BABY like loop-to =loops
- kids: inherited
- inhibition of Na/K/2Cl- in the Loop of Henle
- causes decrease absorption of all three ions = loss of Cl-
- endogenous loop diuretic
GITELMAN’S:
- adults: inherited
- inhibits luminal Na/Cl- symporter in the DCT
- causes decreased absorption of both ions
- endogenous thiazide
The kidney should just be able to get rid of the excess base, but it doesn’t. What are the reasons for this?
- ECF depletion: keeps HCO3 around to avoid volume depletion
- Chloride depletion
- K+ depletion: counterbalances mvmt of K from cells to blood during severe hypokalemia
- Hypercapnea (increased PCO2): due to compensatory mechanisms > leads to keeping bicarb around to balance
What is the treatment for alkalosis?
Give chloride > decrease HCO3
How? intercalated cells in the distal nephron act to increase
bicarb excretion
Type A: H+ ATPase stimulation > H+ and HCO3 into tubule
Type B: increase Cl- stimulates HCO3/Cl antiporter on the basolateral side; more Cl- INTO cell, more bicarb OUT and into blood
What two categories can alkalosis be divided into for a differential?
chloride responsive: low chloride in urine; diuretics, vomit/diarrhea, CF
chloride resistant: high chloride in urine; MR excess states
Other ways to treat alkalosis?
- CA inhibitors: acetazolamide > decrease bicarb reabsorp
- volume repletion: NaCl administration
- K administration (for hypokalemic w/ Barter’s)
Clinical findings of alkalosis?
- HTN
- hypoventilation (increase in CO2)
- arrhythmia (pH >7.6)
What is MUDPILES?
Causes of high anion gap
M: methanol ingestion U: uric acid D: iabetic ketoacidosis P: ropylene glycol/antifreeze I: nfection L: actic acidosis E: thylene glycol S: alicylates
