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65 Cards in this Set
- Front
- Back
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How much fixed acid does a person on a typical Western diet typically generate per day
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1 mmol of fixed acid per Kg of body weight
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Intracellular buffers
most important one |
Hemoglobin - most important
negatively charged proteins phosphates and carbonates in bone |
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In a more acidic environment (such as weight lifting), what does hemoglobin do help buffer the lactic acid
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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
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What can happen if bone is buffering fixed acid
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osteoporosis and calcium oxalate kidney stones can develop due to released calcium from the phosphate and carbonate
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Why is HCO3/CO2 buffer ineffective at buffering volatile acid
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CO2 is part of the system - Increased CO2 would lead to increased H2CO3
There is also no carbonic anhydrase found in the ECF |
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What stimulates the Na/H exchanger in the PCT
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ATN II
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How is "new" bicarb generated
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whenever the H that was secreted from the Na/H exchanger combines with a titratable acid or NH3 and is excreted into the urine
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define titratable acidity
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the amount of base that is added to increase the pH back to 7.4 (plasma)
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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 |
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What situation would increase the amount of titratable acidity and allow more "new" bicarb to be added to the blood
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increased filtration of ketoacids or creatinine
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3 mechanisms that H can be excreted by the kidney
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1. combine with titratable acids
2. combine with ammonia 3. excreted as free H |
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Is ammonia a titratable acid
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No
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Examples of titratable acids
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phosphoric acid
sulfuric acid ketoacids |
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The most important mechanism of fixed acid secretion
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amount of ammonium secretion in the PCT
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What is the formula for Net Acid Excretion
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Urine(NH4 + H2PO4 - HCO3) x L urine/day
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DDX of disorders that would produce excess excretion of acid (more fixed acid excretion than production)
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decrease plasma volume
primary/secondary hyperaldosteronism chloride depletion hypokalmia |
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give two examples of disorders that would cause increased amount of fixed acid - decreased excretion of acid
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Hypoaldosteronism
hyperkalemia |
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Why does chloride depletion lead to hypokalmic metabolic alkalosis
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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
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Why is administering NaHCO3 to a patient with lactic acidosis during CPR not a good solution to correct their pH
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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
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where is ECF bicarb generated
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from hepatic oxidation of dietary citrate and acetate
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what does the consumption of citrus fruit do to blood and urine
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alkalinize - generates bicarb
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Why do high protein diets increase the risk of developing osteopenia and calcium oxalate kidney stones
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increased amount of ketogenic amino acids --> increased ketoacids and therefore decrease pH leading to release of calcium from bones
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differentiate the time difference for the different buffers (plasma bicarb, interstitial, and intracellular) for fixed acid load
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plasma bicarb - within seconds
insterstitial bicarb - within 30 minutes intracellular - over several hours |
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What would you conclude from increased vs. decreased bicarb in the urine
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increased urine bicarb - alkalosis
decreased urine bicarb - acidosis *the kidney regulates the amount of bicarb excretion |
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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 |
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Type-B interacalated cells
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secretes bicarb into the urine - important for correct metabolic alkalosis
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What effect will loop and thiazide diuretics have on H and K secretion in the CCDs
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decreased volume - increased RAAS - increased H and K secretion
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most prevalent titratable acid in tubular fluid
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HPO4
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Why is ammonia better than titratable acids for regulation of fixed acids
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unlimited source of glutamine
much higher pKa than HPO4/H2PO4 buffer system |
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What does the metabolism of glutamine yeild
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two NH4 in the urine and two bicarb
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why does a-ketoglutarate yield two "new" bicarb in the blood
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metabolism of a-ketoglutarate generates two bicarb in the process
a-ketoglutarate --> malate + HCO3 --> glucose + HCO3 |
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Total CO2
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Venous HCO3 + (PCO2 x 0.03)
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what is the general rule of thumb for the simple acid-base disorders
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PCO2 and HCO3 go in the same direction
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differentiate body compensation during acute vs. chronic respiratory acidosis
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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 |
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why does low plasma bicarb not establish the diagnosis of metabolic acidosis
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because the compensation for respiratory alkalosis also lowers the plasma bicarb level
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Anion Gap
normal value |
Na - (HCO3 + Cl)
12 +/- 4 |
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Delta gap
normal value |
(change in anion-gap) - (change in venous bicarb)
0 +/- 6 |
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what does a delta gap >+6 or <-6 signify
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that there is a >90% that a second acid-base disturbance exists in the presence of anion-gap metabolic acidosis
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what are the cardiovascular manifestation during acute respiratory alkalosis
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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 |
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what are the cardiovascular manifestations during acute respiratory acidosis
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decreased BP, tachycardia, and increased cardiac output due to the vasodilatory capacity of CO2
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DDX of anion-gap metabolic acidosis (7)
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KUSMALE:
advanced kidney failure ketaoacidosis salicylate (aspirin) toxicity ethylene glycol poisoning methanol poisoning pyroglutamic acidosis (acetomenophen) lactic acidosis |
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in what situation is there an anion-gap metabolic acidosis and respiratory alkalosis
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aspirin toxicity
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what is the osmolar gap and what two situations is there an increased osmolar gap and anion-gap metabolic acidosis
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osmolar gap is the difference between the calculated and measured plasma osmolality
1. ethylene glycol poisoning 2. methanol poisoning |
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what is the serum electrolyte profile for anion-gap metabolic acidosis (Na, bicarb, Chloride)
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Na = normal
HCO3 = decreased Cl = normal *unmeasured anion = increased |
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differentiate chloride-sensitive and chloride-resistant metabolic alkalosis
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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) |
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differentiate the urinary chloride in chloride-sensitive metabolic alkalosis, loop diuretics vs. vomiting/NG suctioning
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loop diuretics - urinary chloride > 20 mEq/L
vomiting - urinary chloride < 10 mEq/L |
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treatment for chloride-sensitive metabolic alkalosis, why is it not the same for chloride-resistant
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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 |
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two common causes for hypokalemic metabolic acidosis
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diarrhea
renal tubular acidosis (types 1 and 2) |
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urine anion gap
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urine[(Na + K) - Cl]
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differentiate causes for a positive and negative urine anion gap
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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 |
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what is a urine anion-gap useful for detecting
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the cause of non anion-gap metabolic acidosis
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what is the urinary chloride excretion in chloride-resistant metabolic alkalosis
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> 20 mEq/L
*same as loop diuretics in chloride-sensitive but ECF volume will be different in the two |
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what is the mechanism responsible and related causes for types 1,2, and 4 renal tubular acidosis
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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) |
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differentiate the serum Na and K found type 1 and 4 RTA
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type 1 - decreased K and normal Na
type 4 - decreased Na and increased K secondary to hyporenic hypoaldosteronism |
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differentiate cause for decreased H secretion in type 1 RTA autoimmune vs. amphotericin B
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autoimmune - decreased H secretion by H ATPase
amphotericin - increased H reabsorption in a-intercalated cell |
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cause for increased anion-gap during metabolic acidosis
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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
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what would cause a decreased in the anion-gap
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hypoalbuminemia - since 80% of the normal anion-gap is attributable to albumin
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why could critically ill patients receiving therapeutic doses of acetaminophen fall into anion-gap metabolic acidosis
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the oxidative stress from the illness as well as the acetaminophen causes intracellular glutathione depletion - leads to increased produdction of pyroglutamic acid (unmeasured anion)
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what are the two types of non anion-gap metabolic acidosis and what are their respective causes
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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 |
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a clinical syndrome characterized by non anion-gap metabolic acidosis and impaired renal urinary acidification
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renal tubular acidosis
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differentiate urinary pH in the different types of RTA
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type 1 - pH > 5.5
type 2 - pH < 5.3 type 4 - pH < 5.5 |
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which RTA is associated with increased calcium kidney stones
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type 1 RTA
*calcium loss from bone as well as more alkalized urine pH |
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how many "new" bicarb are generated total from metabolism of glutamine --> glucose
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4
two from NH3 and two from metabolism of a-ketoglutarate |
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what causes decreased contractility in metabolic acidosis
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excess H competes with Ca for binding sites on the contractile proteins
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shortcut delta gap equation
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Na - Cl - 37
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