Acid and Base disorders Flashcards
normal anion gap metabolic acidosis happens because of
renal or GI losses
bicarbonate kidney responds to metabolic acidosis by increasing renal ammonium excretion which can be estimated by looking at urinary anion gap
what is the urinary anion gap equation?
urine anion gap = (urine sodium + urine K) - urine chloride = a value
positive number - renal loss of bicarb - think RTA’s
negative number - GI loss of bicarbonate - think laxatives
negative urinary anion gap shows
significant amount of unmeasured positively charged cation or (ammonium) in urine
algorithm for metabolic acidosis
purpose behind a urinary anion gap?
helps differentiate beween GI and renal causes of hyperchloremic causes of metabolic acidosis
negative urinary anion gap indicates
urine anion gap = (urine sodium + urine K) - urine chloride
GI source of bicarbonate loss or extra renal source of bicarbonate loss
RTA type 4
impaired aldosterone at tubular level so see hyperkalemia and seen with DM2
hyperchloremic acidosis is caused by
loss of bases via the kidney (RTA) and loss of base via bowel (diarrhea) or gain of mineral acid (HCI infusion)
If acidosis is result of loss of base via the bowel then the kidneys respond by increasing ammonia excretion so net loss of H+ from the body and so urinary anion gap is decreased (increased NH4 with increased Cl and increased urinary cations decreases urinary AG)
if acidosis is lose of base via the kidney the problem is that the kidney cannot increase ammonia excretion and so the UAG is not increased.
changes in PCO2 and serum bicarb chart
if there’s chronic respiratory acidosis (4-5 days) kidneys will retain 4mEg/l bicarb for every
10 mmhg increase in pCO2.
So if a chronic COPDer has respiratory acidosis present for more than 4-5 days will see increase in serum bicarb
distal RTA can result in
non anion gap metabolic acidosis and marked hypokalemia and hypophosphatemia with inappropriately high urine pH.
causes of normal anion gap metabolic acidosis.
distal RTA is also known as
Type 1
in metabolic alkalosis, what should you look at to help you distinguish etiologies
urinary chloride.
Hypochloremic <15 in urine - body is low in chloride; it holds onto it. Body will responds to NaCl, KCL
vomiting, purging
volume depletion
prolonged NG suction
post hypercapnea
diarrhea causes what effect on urinary chloride?
causes this to be high because as you lose bicarb from GI system, the kidneys excrete chloride into urine to maintain the cation-anion balance
Bicarb is neg and chloride is negatively charged
metabolic alkalosis with hypokalemia is seen with
vomiting, diuretic use, and abnormal renal sodium handling from Gitelman, Bartter’s and Littleman syndrome.
Gitelman mimics lasix, Bartter’s mimics HCTZ
what does diuretic do with urinary chloride?
it forces the kidney to excrete chloride.
SO it will be high urinary chloride >25
but after drug wears off, the urine chloride will return to low lovels.
primary hyperaldosteronism presents with
hypertension, hypokalemia and metabolic alkalosis
nausea causes the urinary chloride to be
low.
Drugs that cause non anion gap metabolic acidosis are:
acetazolamide and topiramate (for seizures and migraine headaches) cause bicarbonate diuresis and resultant non anion gap metabolic acidosis.
Other agents can cause mild forms of RTA and anccompanying non anion gap metabolic acidosis and nephritis.
causes of hyperchloremic metabolic alkalosis
These don’t improve with chloride salts, they are volume expanded (not dehydrated), and H+ is lost but bicarbonate is not lost. Chloride is lost by kidneys and so HCO3 is reabsorbed in compensation.
See a urinary chloride >25
excess steroids (mineralcorticoids, prednisone), Cushing’s syndrome
diuretics - forcing the kidney to excrete Cl- during therapeutic window
recent high BP
licorice ingestion (acts like aldosterone and can develop HTN)
Liddle Syndrome (mimics aldosterone)
Low to normal BP
- hypomagesemia
- hypokalemia
- Bartter’s Syndrome
- Gitelman’s syndrome
most common causes of metabolic alkalosis with hypokalemia are:
vomiting and purging- see low urinary chloride. losing HCl or chloride when vomiting and so losing acid and so body will try to hold onto extra chloride.
diuretics -see high urinary chloride.
lactic acidosis can be caused by
metformin
NRTI’s
linezolid
lorazepam gtt
seizures
septic shock ** increased mortality
RTA 1
Classical type
Tubules are not secreting chloride or cannot excrete H+
so this causes chloride to go up in serum
Because the chloride is not in PH the urine is alkaline. so the bicarb drop in the serum. so the chloride is high the serum pH becomes acidic.
seen in Sjogrens SLE Amphotericin B and stones and obstruction with stones. When urine is more alkaline it can see calcium phosphate stones more.
what are the metabolic deficits in diarrhea?
see urine Chloride is HIGH
GI tract can have secretions lost from upper and lower GI. Upper GI is more acidic secretions (can be lost if vomiting) and lower GI secretes alkaline secretions (can be lost with diarrhea). Also remember chloride has a acid with it so if lost a lot of alkaline (bicarb) then too much acid in body.
So if pt has diarrhea it’s the lower GI (not upper GI) that is losing alkaline secretions. Thus since the Chloride is intact (Upper GI) and there’s a lot of H+ Chloride around.
Kidneys will compensate by losing a lot of Chloride in urine (and H+ will follow) to maintain the pH neutrality of body.
why do you see a non anion gap metabolic acidosis in ureterosigmoidostomy?
ureterosigmoidostomy - secretion of urine into bowel so creating an artifical diarrhea
same process of diarrhea -losing bicarbonate through lower GI tract .
why do we see non anion gap metabolic acidosis with large volume NS?
because you gave the patient a ton of acidic fluid with elevated Cl. If you want to slow it down give half NS. But if they are volume depleted and need volume expansion give NS.
Proximal RTA
RTA type 2
primary defect is reabsorption of bicarb HCO2
so see loss of serum K and loss of serum bicarbonate (and see serum pH drop because deficit in bicarbonate).
Urine pH is variable:
<5.5 when Cl is excreted and urine Cl helps to keep it acidic
>5.5 when not in steady state and not as much CL is excreted in urine so the urine pH is higher.
no kidney stones
-seen in falconi syndrome, multiple myeloma, acetazolamide, zonisamide, topiramate, osteomalacia
RTA 4 is with
defect: no aldosterone so no H and K excretion into urine.
- since no H is being excreted out will not see Cl- excreted into urine so urine pH> 5.5 (alkaline)
causes a non anion gap metabolic acidosis due to loss of aldosterone. Distal tubule Na reabsorption is controlled by aldosterone and linked with acid secretion. If there’s low aldosterone then the renal tubule has sodium wasting in urine and hydrogen retention in the serum.
seen with low hypoaldosteronism (addison’s dx) and DM2, renal insufficiency, spironolactone/eplerenone, trimethoprim
anion gap is
low in high albumin states
high anion gap in hypoalbumim states.
metabolic alkalosis is from
elevation in serum bicarb concentration
loss of acid or from administration or retention of bicarb
