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65 Cards in this Set

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  • Back
How much fixed acid does a person on a typical Western diet typically generate per day
1 mmol of fixed acid per Kg of body weight
Intracellular buffers
most important one
Hemoglobin - most important
negatively charged proteins
phosphates and carbonates in bone
In a more acidic environment (such as weight lifting), what does hemoglobin do help buffer the lactic acid
As hemoglobin releases more oxygen (remember acidic environment promotes O2 release) the histidine residue can bind H more freely. This allows the bicarb to go into the area and buffer the acid
What can happen if bone is buffering fixed acid
osteoporosis and calcium oxalate kidney stones can develop due to released calcium from the phosphate and carbonate
Why is HCO3/CO2 buffer ineffective at buffering volatile acid
CO2 is part of the system - Increased CO2 would lead to increased H2CO3
There is also no carbonic anhydrase found in the ECF
What stimulates the Na/H exchanger in the PCT
ATN II
How is "new" bicarb generated
whenever the H that was secreted from the Na/H exchanger combines with a titratable acid or NH3 and is excreted into the urine
define titratable acidity
the amount of base that is added to increase the pH back to 7.4 (plasma)
What is the normal amount of titratable acid excreted in urine
Can this be regulated
titratable acidity accounts for a constant 36 mmols of fixed acid excretion daily (HPO4)
This is NOT regulated and only changes in extreme circumstances such as ketoacidosis
What situation would increase the amount of titratable acidity and allow more "new" bicarb to be added to the blood
increased filtration of ketoacids or creatinine
3 mechanisms that H can be excreted by the kidney
1. combine with titratable acids
2. combine with ammonia
3. excreted as free H
Is ammonia a titratable acid
No
Examples of titratable acids
phosphoric acid
sulfuric acid
ketoacids
The most important mechanism of fixed acid secretion
amount of ammonium secretion in the PCT
What is the formula for Net Acid Excretion
Urine(NH4 + H2PO4 - HCO3) x L urine/day
DDX of disorders that would produce excess excretion of acid (more fixed acid excretion than production)
decrease plasma volume
primary/secondary hyperaldosteronism
chloride depletion
hypokalmia
give two examples of disorders that would cause increased amount of fixed acid - decreased excretion of acid
Hypoaldosteronism
hyperkalemia
Why does chloride depletion lead to hypokalmic metabolic alkalosis
Because Na reabsorption must find a way to continue even when there is a deficiency of tubular chloride - H and K are secreted in exchange for Na reabsorption
Why is administering NaHCO3 to a patient with lactic acidosis during CPR not a good solution to correct their pH
Because the added HCO3 will combine with H (from lactic acid) and create CO2 - this person needs CPR and is probably not breathing, cannot expel the generated CO2
where is ECF bicarb generated
from hepatic oxidation of dietary citrate and acetate
what does the consumption of citrus fruit do to blood and urine
alkalinize - generates bicarb
Why do high protein diets increase the risk of developing osteopenia and calcium oxalate kidney stones
increased amount of ketogenic amino acids --> increased ketoacids and therefore decrease pH leading to release of calcium from bones
differentiate the time difference for the different buffers (plasma bicarb, interstitial, and intracellular) for fixed acid load
plasma bicarb - within seconds
insterstitial bicarb - within 30 minutes
intracellular - over several hours
What would you conclude from increased vs. decreased bicarb in the urine
increased urine bicarb - alkalosis
decreased urine bicarb - acidosis
*the kidney regulates the amount of bicarb excretion
Which cells reabsorb bicarb in the distal nephron
Is there luminal carbonic anhydrase found there
Type-A intercalated cells reabsorb bicarb driven by basolateral HCO3/Cl exchanger
No luminal carbonic anhydrase is found there
Type-B interacalated cells
secretes bicarb into the urine - important for correct metabolic alkalosis
What effect will loop and thiazide diuretics have on H and K secretion in the CCDs
decreased volume - increased RAAS - increased H and K secretion
most prevalent titratable acid in tubular fluid
HPO4
Why is ammonia better than titratable acids for regulation of fixed acids
unlimited source of glutamine
much higher pKa than HPO4/H2PO4 buffer system
What does the metabolism of glutamine yeild
two NH4 in the urine and two bicarb
why does a-ketoglutarate yield two "new" bicarb in the blood
metabolism of a-ketoglutarate generates two bicarb in the process
a-ketoglutarate --> malate + HCO3 --> glucose + HCO3
Total CO2
Venous HCO3 + (PCO2 x 0.03)
what is the general rule of thumb for the simple acid-base disorders
PCO2 and HCO3 go in the same direction
differentiate body compensation during acute vs. chronic respiratory acidosis
acute - carbonic anhydrase intracellular makes bicarb and H, the H binds to hemoglobin while the bicarb increases the extracellular pH
chronic - the kidney excretes H as well as generating bicarb via intracellular carbonic anhydrase
why does low plasma bicarb not establish the diagnosis of metabolic acidosis
because the compensation for respiratory alkalosis also lowers the plasma bicarb level
Anion Gap
normal value
Na - (HCO3 + Cl)
12 +/- 4
Delta gap
normal value
(change in anion-gap) - (change in venous bicarb)
0 +/- 6
what does a delta gap >+6 or <-6 signify
that there is a >90% that a second acid-base disturbance exists in the presence of anion-gap metabolic acidosis
what are the cardiovascular manifestation during acute respiratory alkalosis
1.bhypocalcemia due to increased negative charges on albumin: tetany, paresthesias, atrail/ventricular tachyarrhythmias
2. alkalosis and hypokalemia sensitize the heart to digoxin and prolongeg the QT interval on ECG
what are the cardiovascular manifestations during acute respiratory acidosis
decreased BP, tachycardia, and increased cardiac output due to the vasodilatory capacity of CO2
DDX of anion-gap metabolic acidosis (7)
KUSMALE:
advanced kidney failure
ketaoacidosis
salicylate (aspirin) toxicity
ethylene glycol poisoning
methanol poisoning
pyroglutamic acidosis (acetomenophen)
lactic acidosis
in what situation is there an anion-gap metabolic acidosis and respiratory alkalosis
aspirin toxicity
what is the osmolar gap and what two situations is there an increased osmolar gap and anion-gap metabolic acidosis
osmolar gap is the difference between the calculated and measured plasma osmolality
1. ethylene glycol poisoning
2. methanol poisoning
what is the serum electrolyte profile for anion-gap metabolic acidosis (Na, bicarb, Chloride)
Na = normal
HCO3 = decreased
Cl = normal
*unmeasured anion = increased
differentiate chloride-sensitive and chloride-resistant metabolic alkalosis
chloride-sensitive - decreased ECF volume causes secondary activation of RAAS (vomiting, NG suctioning, loop diuretics)
chloride-resistant - ECF volume expansion secondary to hyperaldosteronism (primary, secondary, SAME, licorice)
differentiate the urinary chloride in chloride-sensitive metabolic alkalosis, loop diuretics vs. vomiting/NG suctioning
loop diuretics - urinary chloride > 20 mEq/L
vomiting - urinary chloride < 10 mEq/L
treatment for chloride-sensitive metabolic alkalosis, why is it not the same for chloride-resistant
administration of isotonic NaCl solution raises serum Cl (which is depleted), this lower serum bicarb along with raising ECF volume and suppressing aldosterone secretion
isotonic saline administration would worsen chloride-resistant because there is already ECF volume expansion and chloride is not deficient
two common causes for hypokalemic metabolic acidosis
diarrhea
renal tubular acidosis (types 1 and 2)
urine anion gap
urine[(Na + K) - Cl]
differentiate causes for a positive and negative urine anion gap
positive - decreased urinary H excretion is responsible for non anion-gap acidosis (Na main ion) - RTA type 1 and 4, hypoaldosteronism
negative - some other than decreased H excretion is responsible for acidosis (increased urinary excretion of NH4 increases) - Diarrhea
what is a urine anion-gap useful for detecting
the cause of non anion-gap metabolic acidosis
what is the urinary chloride excretion in chloride-resistant metabolic alkalosis
> 20 mEq/L
*same as loop diuretics in chloride-sensitive but ECF volume will be different in the two
what is the mechanism responsible and related causes for types 1,2, and 4 renal tubular acidosis
type 1 - decreased tubular H secretion by type-A intercalated cells (autoimmune or amphotericin B)
type 2 - decreased PCT reabsorption of filtered bicarb (CA inhibitors, multiple myeloma, out-dated tetracyclines)
type 4 - decreased JG cell renin secretion secondary to decreased prostaglandin synthesis (DM, chronic interstitial nephritis, NSAIDs)
differentiate the serum Na and K found type 1 and 4 RTA
type 1 - decreased K and normal Na
type 4 - decreased Na and increased K secondary to hyporenic hypoaldosteronism
differentiate cause for decreased H secretion in type 1 RTA autoimmune vs. amphotericin B
autoimmune - decreased H secretion by H ATPase
amphotericin - increased H reabsorption in a-intercalated cell
cause for increased anion-gap during metabolic acidosis
accumulation of an acid accompanied by an anion other than Cl consumes plasma HCO3, the fall in HCO3 concentration is balanced by an equal rise in the concentration of the non-Cl anion
what would cause a decreased in the anion-gap
hypoalbuminemia - since 80% of the normal anion-gap is attributable to albumin
why could critically ill patients receiving therapeutic doses of acetaminophen fall into anion-gap metabolic acidosis
the oxidative stress from the illness as well as the acetaminophen causes intracellular glutathione depletion - leads to increased produdction of pyroglutamic acid (unmeasured anion)
what are the two types of non anion-gap metabolic acidosis and what are their respective causes
hypokalmic - loss of bicarb and K from stool or urine (diarrhea, type 1 and 2 RTA, or carbonic anhydrase inhibitors)
hyperkalemic - Type 4 RTA (hyporeninemic hypoaldosteronism), spironolactone, adrenal insufficiency
a clinical syndrome characterized by non anion-gap metabolic acidosis and impaired renal urinary acidification
renal tubular acidosis
differentiate urinary pH in the different types of RTA
type 1 - pH > 5.5
type 2 - pH < 5.3
type 4 - pH < 5.5
which RTA is associated with increased calcium kidney stones
type 1 RTA
*calcium loss from bone as well as more alkalized urine pH
how many "new" bicarb are generated total from metabolism of glutamine --> glucose
4
two from NH3 and two from metabolism of a-ketoglutarate
what causes decreased contractility in metabolic acidosis
excess H competes with Ca for binding sites on the contractile proteins
shortcut delta gap equation
Na - Cl - 37