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Urinary & Renal > Acid-Base > Flashcards

Acid-Base Flashcards

1
Q

name 3 things that generate H+ in the body

A

oxidation of amino acids; typical diet generates fixed acid; incomplete oxidation of fats and carbs

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2
Q

when might there be a net H+ load generated from the metabolism of carbs and fats?

A

hypoxia, diabetic ketoacidosis (DKA)

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3
Q

dietary HCO3- comes from the metabolism of?

A

organic acids in fruits and vegetables

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4
Q

how does the body eliminate dietary alkali?

A

converts citrate to bicarb in the liver, which is buffered by non-toxic endogenous organic acids produced by the liver. Together they are filtered freely by the kidneys, with the majority being excreted

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5
Q

why excrete alkali in the form of organic acids? (3 reasons)

A

attenuate free citrate to decrease calcium chelation (and hypocalcemia), keep urine pH sufficiently acidic to prevent stone formation, some citrate does chelate calcium and prevents hypercalcemia and calcium stones

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6
Q

the ideal urine pH to prevent stone formation is?

A

pH of 6 (stones form above 6.3)

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7
Q

the kidney maintains HCO3- at ___ and ventilation maintains PCO2 at ___, resulting in a normal pH of ____

A

24 mEq/L; 40 mmHg; 7.40

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8
Q

bicarb reabsorption occurs in the ____ indirectly via ____ exchange

A

proximal tubule; Na+/H+ exchange

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9
Q

___ facilitates the reabsorption of bicarb by recycling into and out of the lumen

A

H+

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10
Q

the amount of fixed acid that can be excreted at H+ is limited by?

A

finite activity of the H+ ATPase and limited permeability of the tubular epithelium that results in a maximally acidic urine of pH 4.5

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11
Q

the H+ ATPase is found on the ___ membrane of ____ cells

A

luminal; intercalated

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12
Q

urine pH of >5.5 is suggesive of?

A

decreased H+ ATPase function or renal tubular acidosis from H+ back leak into a disrupted epithelium

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13
Q

the majority of H+ is excreted through what two urinary buffers?

A

titratable acid and NH4+

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14
Q

dibasic phosphate acts as a buffer for protons at the?

A

proximal tubule (Na/H exchange) and distal tubule (H+ ATPase, intercalated cells in collecting duct)

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15
Q

dibasic phosphate accounts for ___ of the dailty fixed H+ excretion

A

half (30-50 mEq)

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16
Q

ammonium is synthesized in the ____ by ____ and transported into the interstitium by?

A

proximal tubular cells; deamination of glutamine; exchange with K+ on the NaK2Cl carrier of the thick ascending limb

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17
Q

for every H+ released into the urine (with titratable acid or ammonium), what happens?

A

an HCO3- is released into systemic circulation

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18
Q

equation for net acid excretion

A

(H2PO4 + NH4) - (HCO3 + OA)

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19
Q

normal sodium range

A

135-145 mEq/L

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20
Q

normal potassium range

A

3.5-5 mEq/L

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21
Q

normal chloride range

A

100-111

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22
Q

normal bicarb/total CO2

A

24

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23
Q

normal values for arterial pH

A

7.37-7.43

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24
Q

normal values for pCO2

A

36-44 mmHg

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25
Q

definition of metabolic acidosis

A

acidosis due to primary fall in serum bicarb concentration

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26
Q

causes of metabolic acidosis

A

loss of bicarb (diarrhea, proximal renal tubular acidosis), decreased excretion of acid (distal renal tubular acidosis), endogenous generation of excess acid (lactic/keto-acidosis), and ingestion of excess acid (salicylate toxicity, ethylene glycol poisoning)

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27
Q

definition of respiratory acidosis

A

acidosis due to primary increase in pCO2 due to ineffective alveolar ventilation

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28
Q

definition of metabolic alkalosis

A

alkalosis from primary increase in serum bicarb concentration

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29
Q

causes of metabolic alkalosis

A

loss of acid (vomiting, hyperaldosteronism) or retention of administered bicarb

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30
Q

definition of respiratory alkalosis

A

alkalosis from a primary decrease in pCO2

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31
Q

what detects metabolic disturbances and triggers respiratory compensation?

A

chemoreceptors in the medullary respiratory center

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32
Q

what detects respiratory disturbances and triggers renal compensation?

A

kidney proximal tubular cells (which alter reabsorption of HCO3-)

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33
Q

what is the secondary respiratory response to metabolic acidosis?

A

increased minute ventilation to blow off CO2 and increase pH

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34
Q

what is the secondary renal response to respiratory acidosis?

A

increased reabsorption of HCO3- in the proximal tubules

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35
Q

which is faster: respiratory or renal compensation?

A

respiratory is immediate, but renal takes time (divided into acute and chronic)

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36
Q

acute metabolic compensation occurs within ____ while chronic metabolic compensation takes about ____

A

hours; 3-5 days

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37
Q

in metabolic acidosis, every 1 mEq/L decrease in [HCO3-] should result in ____ in pCO2

A

1.2 mmHg decrease

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38
Q

in metabolic alkalosis, every 1 mEq/L increase in [HCO3-] should result in ____ in pCO2

A

0.7 mmHg increase

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39
Q

in respiratory acidosis, every 10 mmHg increase in pCO2 should result in _____ in [HCO3-]

A

1 mEq/L increase (acute), 4 mEq/L increase (chronic)

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40
Q

in respiratory alkalosis, every 10 mmHg decrease in pCO2 should result in ____ in [HCO3-]

A

2 mEq/L decrease (acute), 4 mEq/L decrease

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41
Q

how to calculate anion gap

A

Na - (Cl+HCO3)

42
Q

what is a normal anion gap?

A

8-12 mEq/L

43
Q

an increased anion gap is suggestive of?

A

the presence of unmeasured acid (such as lactate or ingested acid) causing decreased serum bicarb

44
Q

a normal anion gap means that?

A

chloride ion is rising to replace loss of bicarb (or increase in H+)

45
Q

name two things that decrease the anion gap

A

hypoalbuminemia, cationic light chains

46
Q

what is the mnemonic for increased anion gap metabolic acidosis?

A

GOLDMARK

47
Q

what do each of the letters stand for in “GOLDMARK”?

A

Glycols, Oxyproline, L-lactate, D-lactate, Methanol poisoning, Aspirin toxicity, Renal failure (advanced), Ketoacidosis (diabetic or alcoholic)

48
Q

what is the most common form of increased anion gap metabolic acidosis?

A

lactic acidosis

49
Q

what is lactic acidosis?

A

serum lactate >4; type A occurs when tissue hypoperfusion is present, while type B occurs in the absence of hypoperfusion

50
Q

tx for lactic acidosis

A

reverse underlying cause; treat with bicarb therapy (target pH 7.2) in patients with pH less than 7.1 or with CV compromise

51
Q

who gets D-lactic acidosis?

A

patients with short-bowel syndrome

52
Q

symptoms of D-lactic acidosis

A

intermittent confusion, slurred speech, ataxia

53
Q

tx for D-lactic acidosis

A

ABX directed toward bowel flora (metronidazole, neomycin) and restriction of dietary carbs

54
Q

DKA results in an increased anion gap because?

A

insulin deficiency, increased catecholamines, and glucagon result in incomplete oxidation of fatty acids, leading to acetoacetate and beta-hydroxybutyrate

55
Q

how do you detect the presence of ketoacids?

A

nitroprusside assay or direct measure

56
Q

what is the main weakness of the nitroprusside assay?

A

doesn’t detect the predominant ketoacid beta-hydroxybutyrate and thus can be falsely negative in severe ketoacidosis

57
Q

tx of DKA

A

INSULIN + normal saline

58
Q

signs of alcoholic ketoacidosis

A

nausea, vomiting, hypovolemia after periods of poor caloric intake which cause mobilization of fatty acids (onnly in setting of chronic alcohol intake, not acute)

59
Q

tx for alcoholic ketoacidosis

A

IV glucose (or resumption of eating), normal saline if hypovolemic

60
Q

ethylene glycol and methanol poisoning are associated with what unique finding

A

osmolal gap greater than 10 (from elevated levels of parent alcohol)

61
Q

simultaneous ingestion of ___ with methanol or ethylene glycol may delay onset of symptoms due to inhibition of alcohol dehydrogenase

A

ethanol

62
Q

clinical signs of methanol or ethylene glycol poisoning

A

inebriation early, to obtundation, seizures, coma, cardiovascular collapse

63
Q

complication of ethylene glycol toxicity

A

calcium oxalate precipitation (AKI, kidney stones, hypocalcemia, and nephrocalcinosis)

64
Q

complications of methanol toxicity

A

impaired vision that can progress to blindess (from formic acid); abdominal pain and pancreatitis; secondary parkinsonism (putaminal injury)

65
Q

why might a patient with ethylene glycol/methanol poisoning present with a normal osmolal gap?

A

if they present after all of the parent alcohol has been metabolized

66
Q

tx for ethylene glycol or methanol poisoning

A

CLINICAL DX; supportive measures to optimize ventilation and organ perfusion; fomepizole (alcohol dehydrogenase inhibitor) once dx suspected; hemodialysis in severe cases

67
Q

in adults, salicylate toxicity typically presents with primary ____, but can result in _____ with more severe intoxication or as the primary disorder in children

A

respiratory alkalosis; increased anion gap metabolic acidosis

68
Q

what causes the anion gap in salicylate toxicity?

A

salicylate anion + lactic and ketoacidosis

69
Q

clinical manifestations of salicylate toxicity are due to _____ and include?

A

intracellular toxicity (not acid-base abnormalities); tinnitis, confusion, tachypnea, ?low-grade fever

70
Q

direct gastric mucosal toxicity from salicylate (aspirin) may cause?

A

metabolic alkalosis from nausea, vomiting, medullary chemoreceptor stimulation

71
Q

complications of salicylate toxicity

A

neurologic dysfunction (mental status changes, cerebral edema, herniation); acute lung injury and pulmonary edema (chronic exposure especially)

72
Q

how does salicylate toxicity cause neurologic problems?

A

diffuses across BBB and into cells in undissociated form, acidifying brain cells, causing neuroglycopenia

73
Q

tx of salicylate toxicity

A

judicious volume expansion, sodium bicarb tx to maintain arterial pH of 7.45-7.6 and urine pH >7.5 (to excrete salicylic acid), hemodialysis in severe cases

74
Q

chronic acetaminophen therapy (especially in patients with malnutrition) may result in?

A

pyroglutamic acidosis (increases anion gap)

75
Q

tx of pyroglutamic acidosis (also called oxyproline)

A

discontinue acetaminophen; volume expansion with normal saline and glucose, possibly N-acetylcysteine

76
Q

when does acute/chronic kidney disease cause an increased anion gap metabolic acidosis?

A

when it is severe enough to decrease GFR below 15 mL/min (due to retention of sulfates, phosphates, and organic acids)

77
Q

how to normal functioning kidneys respond to acidemia?

A

by increasing ammonium excretion about 6-fold (to 3mEq/kg/day), which takes about 3-5 days to occur

78
Q

major causes of normal anion gap metabolic acidosis

A

diarrhea, RTA, milder kidney disease, ureteral diversion, euvolemic DKA, toluene toxicity

79
Q

the urine ammonium level in a patient with diarrhea will be (lower/higher) than a patient with kidney dz

A

higher

80
Q

this causes renal tubular acidosis with increased serum potassium and low urine pH

A

decreased effective aldosterone (drugs that block Enac, calcineurin inhibitors, aldosterone antag, pseudohypoaldosteronism)

81
Q

this causes renal tubular acidosis with increased serum potassium and high urine pH

A

tubulointerstitial injury (urinary tract obstruction, chronic interstitial nephritis, sickle cell)

82
Q

this causes renal tubular acidosis with decreased serum potassium and high urine pH

A

hypokalemic distal RTA (type 1)

83
Q

this causes RTA with decreased serum potassium and low urine pH

A

proximal RTA (type 2)

84
Q

name three drugs that block ENaC channels and cause hyperkalemic RTA (with low pH)

A

amiloride, triamterene, pentamidine

85
Q

signs of type 2 RTA (proximal)

A

caused by decreased bicarb reabsorption, originally causing bicarbonaturia but urine pH is below 5.5 once steady state is reached; associated with Fanconi syndrome (protein, phosphate, and glycose in urine too), mild hypokalemia from secondary hypoaldosteronism, vitamin D deficiency and osteomalacia

86
Q

signs of type 1 RTA (distal)

A

defect in distal urinary acidification results in impaired excretion of hydrogen ions and thus urine pH >6, potassium wasting (hypokalemia), calcium-phosphate kidney stones from high pH

87
Q

signs of type 4 RTA (hyperkalemic distal)

A

hyporenin/hypoaldosterone often secondary to meds such as NSAIDs, ACE inhibitors, ARBs; urine pH less than 5.5, metabolic acidosis from impaired generation of ammonia in setting of hyperkalemia

88
Q

voltage-dependent hyperkalemic distal RTA

A

associated with tubulointerstitial injury involving collecting duct which impairs urinary acidification (sickle cell, urinary obstruction) and results in high urine pH

89
Q

which of the hyperkalemic distal RTAs can be corrected by treating the hyperkalemia?

A

type 4 hyperkalemic RTA

90
Q

tx for voltage-dependent hyperkalemic RTA

A

relief of obstruction, potassium restriction, alkali therapy

91
Q

what are the 3 distinct forms of metabolic alkalosis

A
  1. true hypovolemia (saline responsive), 2. decreased EABV with increased ECF (CHF, liver failure, nephrosis), 3. saline resistant (increased ECF, increased EABV, HTN)
92
Q

treatment of saline responsive metabolic alkalosis (hypovolemia)

A

normal saline

93
Q

treatment of low EABV/high ECF metabolic alkalosis

A

amelioration of underlying cause; acetazolamide can be used if severe (carbonic anhydrase inhibitor)

94
Q

respiratory acidosis is due ____ and presents with?

A

decreased effective ventilation; impaired mentation (+/- asterixis), decreased contractility, cardiac arrhythmia, or increased cerebral blood flow & cerebral edema

95
Q

tx of respiratory acidosis

A

correct hypoxia first using supplemental oxygen; ventilate if pH goes below 7.2

96
Q

name 4 important causes of respiratory alkalosis

A

salicylate poisoning, sepsis, liver failure, and pregnancy

97
Q

mental status changes, tachypnea, and respiratory alkalosis with concomitant increased anion gap metabolic acidosis

A

salicylate poisoning

98
Q

respiratory alkalosis is known to decrease _______

A

cerebral blood flow

99
Q

stepwise approach to acid-base problem

A

look at pH to identify acidosis/alkalosis, then look at bicarb and pCO2 to determine metabolic or respiratory, then calculate anion gap, if increased then calculate osmolal gap, then determine if proper compensatory response or mixed disorder,

100
Q

an osmolal gap greater than ___ is abnormal

A

> 10

101
Q

name things that cause an increased anion gap and an osmolar gap

A

methanol, (di)ethylene glycol, propylene glycol, formaldehyde, DKA, AKA, lactic acidosis

102
Q

name things that cause an increased osmolar gap without metabolic acidosis

A

isopropyl alcohol poisoning, mannitol, dextran-40

Urinary & Renal (22 decks)

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