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Renal > Acid Base Integration > Flashcards

Acid Base Integration Flashcards

1
Q

What is the largest soruce of acid in the body?

A

the CO2 produced from metabolism of CHO, amino acids, and fat

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2
Q

What are the processes involved that prevent large changes in blood pH in response to an acute load?

A

extra cellular and intracellular buffers that act to neutralize excess H+ and thus prevent changes in pH induced acid load

alveolar ventilation increases to eliminate CO2 rapidly and more efficiently

the plasma HCO3- concentration is held within narrow limits by regulation of renal H+ excretion

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3
Q

What are some of the reactions that produce metabolic sources of acids and bases?

A

reactions producing CO2 - complete oxidation of neutral carbohydrates and fat

reactions producing nonvolatile acids - oxidation of sulfur-containing amino acids

reactions producing bases - oxidation of anionic amino acids

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4
Q

What is the Henderson-Hasselbach equation for predicting acid/base balance in the body?

A

pH = 6.1 + log([HCO3-]/(0.03 x pCO2))

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5
Q

What is the immediate compensation for changes in HCl load?

A

extracellular buffering of the excess H+ by HCO3- present in the blood

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6
Q

What is the response after several minutes to HCl changes in the blood?

A

respiratory compensation begins, resulting in hyperventilation, a decrease in the PCO2, and therefore an increase in the pH toward normal

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7
Q

What is the defense against an acid load after 2 to 4 hours?

A

intracellular buffers (primarily proteins and organic phosphates) and bone provide further buffering, as H+ ions enter the cells in exchange for intracellular K+ and Na+

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8
Q

What is the body’s response to an acid load after a day and lasts up to 4 to 6 days?

A

renal excretion of the acid load

returns plasma HCO3- towards normal levels

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9
Q

What are some of the mechanisms that cells use to maintain intracellular pH?

A

most important are the Na+/H+ exchanger and a Cl-/HCO3- exchanger (Na+ dependent and independent)

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10
Q

How does a cell respond to metabolic acidosis?

A

addition of hydrogen ions stimulates the Na+/H+ exchanger to extrude H+

at the same time, the decrease in pH inhibits the HCO3- and the Cl- exchanger

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11
Q

How does a cell respond to metabolic alkalosis?

A

increased OH- stimulates the export of HCO3- by combining OH- with CO2 and activating the HCO3-/Cl- exchanger

higher pH inhibits the activity of the Na+/H+ exchanger

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12
Q

How does the kidney respond to acidemia?

A

increased H+ secretion

increaed HCO3- reabsorption

happens primarily in the proximal tubule and the collecting duct

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13
Q

How does the kidney respond to alkalemia?

A

decreased H+ secretion

decreased HCO3- reabsorption

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14
Q

How does ECF volume affect HCO3- reabsoprtion in the kidney?

A

ECF expansion inhibits HCO3- reabsorption

ECF contraction augments HCO3- reabsorption

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15
Q

How does aldosterone affect H+ secretion?

A

directly stimulates H+ secretion by intercalated cells by stimulating synthesis and insertion of ATPase pumps in the apical cell membrane

indirectly stimuates H+ secretion via stimulating sodium reabsorption by principal cells

Na+ reabsoprtion produces a lumen-negative transepithelial voltage, which favors alpha-intercalated cell H+ secretion

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16
Q

What facilitates the major fraction of proximal tubular HCO3- reabsorption?

A

H+ secretion via the Na+/H+ antiporter located in the apical membrane of the cells

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17
Q

factors that increase kidney H+ secretion

A

low blood pH

high blood pCO2

endothelin (proximal tubule)

ECF volume contraction (proximal tubule)

angiotensin II (PCT and DCT)

aldosterone (DCT and CCD)

hypokalemia (proximal tubule)

PTH (chronic, TAL and DCT)

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18
Q

factors that decrease kidney H+ secretion

A

high blood pH

low blood pCO2

ECF volume expansion (proxmial tubule)

low aldosterone level (DCT and CCD)

hyperkalemia (proximal tubule)

PTH (acute, proximal tubule)

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19
Q

How does parathyroid hormone, angiotensin II, and hypokalemia affect HCO3 reabsorption?

A

inhibits

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20
Q

How should bicarb behave in pure anion gap acidosis?

A

it should decrease the same amount that the anion increases above normal value

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21
Q

defense mechanisms for metabolic alkalosis

A

hypoventilation (increased pCO2)

decreased renal net acid excretion which leads to decrease in blood HCO3-

22
Q

defense mechanisms for metabolic acidosis

A

hyperventilation (increased pCO2)

increased renal net acid excretion, which leads to an increase in blood HCO3-

23
Q

defense mechanisms for respiratory acidosis

A

increased renal net acid excretion which leads to increased blood HCO3-

24
Q

defense mechanisms for respiratory alkalosis

A

decreased renal net acid excretion which leads to a decrease in blood HCO3-

25
Q

causes of hyperchloremic (normal anion gap) metabolic acidosis

A

bicarbonate wastage - diarrhea, urnary tract diversions to intestine

impaired renal H+ secretion and reduced NH4+ excretion - distal renal tubular acidosis and aldosterone deficiency

impaired NH3 formation and reduced NH4+ excretion - advanced chronic kidney disease (GFR < 20 mL/min) and hyperkalemia

administration of chloride containing acid (rare)

26
Q

expected compensatory chang ein pCO2 or HCO3 in metabolic acidosis

A

decrease in pCO2 = 1.2 x (delta HCO3-)

delta HCO3- = (24-observed HCO3-)

27
Q

expected compensatory chang ein pCO2 or HCO3 in metabolic alkalosis

A

increase in pCO2 = 0.6 x (delta HCO3-)

delta HCO3 = (measured HCO3- - 24)

28
Q

expected compensatory chang ein pCO2 or HCO3 in chronic respiratory acidosis

A

increase in HCO3- = 0.4 x (delta pCO2)

delta pCO2 = (measured pCO2 - 40)

29
Q

expected compensatory chang ein pCO2 or HCO3 in chronic respiratory alkalosis

A

decrease in HCO3 = 0.5 x (delta pCO2)

delta pCO2 = (40 - measured pCO2)

30
Q

What are two ways that H+ can build up in the circulation?

A

as inorganic acid - HCL

as organic acid - lactic acid

31
Q

pathogenesis of lactic acidosis

A

increased lactic acid generation - tissue hypoxia

decreased utilization of lactic acid - liver failure

32
Q

general types of acidosis of primary renal origin

A

renal insufficiency

distal RTA (classic or type I)

proximal RTA (bicarbonate wastage or type II)

distal RTA with bicarbonate wastage (type III)

hyperkalemic RTA associated with aldosterone deficiency (type IV)

hyperkalemic forms of distal RTA not primarily caused by aldosterone deficiency

33
Q

features of urinary acidification in proximal tubular acidosis

A

bicarbonate wastage at normal or high plasma HCO3- concentrations

reduced renal HCO3 threshold (15-20 mEq/L)

intact ability to lower urine pH < 5.5 during acidosis

34
Q

How does type I RTA differ from type II RTA in terms of NH4+ secretion and urine pH?

A

type I pH > 5.5 and NH4+ excretion is reduced

type II pH <5.5 and NH4+ excretion is normal

35
Q

clinical features of proximal RTA

A

bicarbonaturia which increases K+ excretion (hypokalemia)

glycosuria

phsphaturia

hyperuricosuria

aminoaciduria

no nephrocalcinosis or kidney stones

rickets

36
Q

clinical symptoms of distal RTA syndrome

A

hyperchloremic metabolic acidosis

hypokalemia

nephrocalcinosis

kidney stones

inability to lower urinary pH below 5.5 despite acidemia

fractional bicarbonate excretion less than 5-10%

37
Q

What does a large negative urine anion gap mean?

A

NH4 is abundant in the urine

appropriate in the presence of metabolic acidosis

38
Q

What does a positive urine anion gap reflect?

A

NH4 is low in the urine, which is an abnormal finding in the presence of acidosis and therefore a clue that the patient has distal RTA, a disease with metabolic acidosis because NH4+ is excreted in the urine in low amounts

39
Q

common causes of metabolic acidosis with increased plasma anion gap

A

ketoacidosis

renal failure

methanol

ethylene glycol

salicylates

40
Q

What is the limiting factor in the response to metabolic alkalosis?

A

the development of hypoxemia

pCO2 rarely exceeds 55 mmHg

41
Q

What is the renal compensatory response to metabolic alkalosis?

A

excretion of HCO3- by reducing its reabsorption along the nephron

42
Q

What is the renal response in the setting of decreased ECV?

A

HCO3- does not occur due to the low volume

if the underlying cause is corected, pH is eventually returned to normal by increased excretion

43
Q

causes of metabolic alkalosis

A

loss of hydrogen ions - gastrointestinal loss through vomiting or renal loss through loop or thiazide-type diuretics, minaralocorticoid excess, and tubular disorders

administration of NaHCO3

44
Q

What is the urine chloride in chloride responsive mtabolic alkalosis?

A

less than 15 mEq/L

caused by fluid H+ ion losses

45
Q

urine chloride in chloride-resistant metabolic alkalosis

A

>30 mEq/L

caused by diuretics, primary hyperaldosteronism, or Barter’s syndrome

46
Q

How much does pCO2 change with a 1.0 mEq/L increase in HCO3-?

A

0.6 mmHg

47
Q

What is the pathophysiological process following metabolic alkalosis (maintenance phase)?

A

decreased GFR

enhanced proximal bicarbonate reabsorption, which leads to volume and potassium depletion

increased distal tubular bicarbonate reabsorption leads to mineralocorticoid excess and hypokalemia

48
Q

What is the pathophysiological process following metabolic alkalosis (recovery phase)?

A

Cl- administratino (usually 0.9% NaCl) to reexpand volume and corect chloride deficit

Kcl administration if hypokalemia is present

49
Q

What is the expected compensation for a 1 mmHg rise in blood Pco2?

A

0.4 mEq/L increase in blood HCO3-

50
Q

How much does pCO2 decrease for each mmEq/L decrease in HCO3-?

A

1.2 mmHg

Renal (28 decks)

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