Acid and Base disorders

Question 1

normal anion gap metabolic acidosis happens because of

Answer 1

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

Question 2

what is the urinary anion gap equation?

Answer 2

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

Question 3

negative urinary anion gap shows

Answer 3

significant amount of unmeasured positively charged cation or (ammonium) in urine

Question 4

algorithm for metabolic acidosis

Answer 4

Question 5

purpose behind a urinary anion gap?

Answer 5

helps differentiate beween GI and renal causes of hyperchloremic causes of metabolic acidosis

Question 6

negative urinary anion gap indicates

urine anion gap = (urine sodium + urine K) - urine chloride

Answer 6

GI source of bicarbonate loss or extra renal source of bicarbonate loss

Question 7

RTA type 4

Answer 7

impaired aldosterone at tubular level so see hyperkalemia and seen with DM2

Question 8

hyperchloremic acidosis is caused by

Answer 8

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.

Question 9

changes in PCO2 and serum bicarb chart

Answer 9

Question 10

if there’s chronic respiratory acidosis (4-5 days) kidneys will retain 4mEg/l bicarb for every

Answer 10

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

Question 11

distal RTA can result in

Answer 11

non anion gap metabolic acidosis and marked hypokalemia and hypophosphatemia with inappropriately high urine pH.

Question 12

causes of normal anion gap metabolic acidosis.

Answer 12

Question 13

distal RTA is also known as

Answer 13

Type 1

Question 14

in metabolic alkalosis, what should you look at to help you distinguish etiologies

Answer 14

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

Question 15

diarrhea causes what effect on urinary chloride?

Answer 15

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

Question 16

metabolic alkalosis with hypokalemia is seen with

Answer 16

vomiting, diuretic use, and abnormal renal sodium handling from Gitelman, Bartter’s and Littleman syndrome.

Gitelman mimics lasix, Bartter’s mimics HCTZ

Question 17

what does diuretic do with urinary chloride?

Answer 17

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.

Question 18

primary hyperaldosteronism presents with

Answer 18

hypertension, hypokalemia and metabolic alkalosis

Question 19

nausea causes the urinary chloride to be

Answer 19

low.

Question 20

Drugs that cause non anion gap metabolic acidosis are:

Answer 20

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.

Question 21

causes of hyperchloremic metabolic alkalosis

Answer 21

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

Question 22

most common causes of metabolic alkalosis with hypokalemia are:

Answer 22

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.

Question 23

lactic acidosis can be caused by

Answer 23

metformin

NRTI’s

linezolid

lorazepam gtt

seizures

septic shock ** increased mortality

Question 24

RTA 1

Classical type

Answer 24

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.

Question 25

what are the metabolic deficits in diarrhea?

Answer 25

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.

Question 26

why do you see a non anion gap metabolic acidosis in ureterosigmoidostomy?

Answer 26

ureterosigmoidostomy - secretion of urine into bowel so creating an artifical diarrhea

same process of diarrhea -losing bicarbonate through lower GI tract .

Question 27

why do we see non anion gap metabolic acidosis with large volume NS?

Answer 27

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.

Question 28

Proximal RTA

RTA type 2

Answer 28

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

Question 29

RTA 4 is with

Answer 29

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

Question 30

anion gap is

Answer 30

low in high albumin states

high anion gap in hypoalbumim states.

Question 31

metabolic alkalosis is from

Answer 31

elevation in serum bicarb concentration

loss of acid or from administration or retention of bicarb