Acid-Base Disorders

Question 1

Which values on a BMP are important in acid/base disorders? Normal values?

Answer 1

Na 140 mEq/L, K 4.1 mEq/L, Cl 108 mEq/L, CO2 24 mEq/L (bicarb), BUN 10 mg/dL, Creatinine 0.8 mg/dL

Question 2

Which values on a ABG are important in acid/base disorders? Normal values?

Answer 2

pH 7.35-7.45, pCO2, pO2, calculated bicarbonate

Question 3

What are the clinical effects of severe acidemia?

Answer 3

depr. cardiac funct., impaired response to catecholamines, arteriolar vasodilation (simultan. venoconstr.), systemic hypotension, pulm edema, insulin resistance, red. hepatic lactate uptake, accel. protein catabolism

Question 4

What is the homeostatic response to acid/base loads?

Answer 4

chemical buffering by extracellular and intracellular buffers, changes in alveolar ventilation to control pCO2, alterations in renal H excretion to regulate P[HCO3]

Question 5

How do the kidneys regulate pH?

Answer 5

regulate P[HCO3], formation of titratable acidity, excretion of NH4 in urine; whenever H is secreted from a renal cell into tubule fluid, an intracellular HCO3 is left behind and added to blood

Question 6

What are the three components of net acid excretion?

Answer 6

titratable acids, ammonium, bicarbonate

Question 7

What are titratable acids?

Answer 7

secreted H combines with urinary buffers (primarily inorganate P to form H2PO4 and HCO3)

Question 8

what are the sources of ammonium?

Answer 8

urinary acidification increased by excretion of urinary NH4, tubular cells synthesize NH4 from glutamine, excretion of NH4 leaves behind an intracellular HCO3

Question 9

what approach do you take to acid-base disorders?

Answer 9

det. electrolyte and ABG values, acidosis/ alkalosis, resp. or met, det. degree of compensation, calculate AG, if elevate Osm gap, if normal UAG

Question 10

what are the features of metabolic acidosis?

Answer 10

pH decreased due to decrease in serum HCO3 due to either net gain H or net loss of HCO3, lungs compensate inc. ventilation and dec. pCO2

Question 11

what are the common etiologies of metabolic acidosis?

Answer 11

addition of acid- endog (lactic acid) or exog. (ethylene glycol od), loss of bicarb- GI (diarrhea) or kidney (proximal tubule acidosis=RTA 2), inability to excrete normal daily acid production by kidneys (RTA 1)

Question 12

What are the causes of high gap acidosis?

Answer 12

MMUDPPILES: methanol, metformin, uremia, diabetic ketoacidosis, propylene glycol, pyroglutamic acid, isoniazid, lactic acid, ethylene glycol, salicylates

Question 13

How do you treat lactic acidosis?

Answer 13

correct underlying disorder, supportive care for shock: IV fluid (crystalloid or colloid), antibiotics, pressors

Question 14

what are the causes of lactic acidosis?

Answer 14

type A: tissue hypoperfusion or hypoxia, or B: drugs (metformin, linezolid, propofol, nucleosides), thiamine deficiency, liver failure, malignancy, and D-lactic acidosis

Question 15

What causes ketoacidosis?

Answer 15

most commonly type 1 diabetes, also alcoholics or starvation

Question 16

what are the symptoms of salicylate poisoning?

Answer 16

tinnitus, N/V, inc temp, lethargy/excitability, hyperventilation leading to resp. alkalosis, severe toxicity= met. acidosis and seizures

Question 17

How do salicylates cause acidosis?

Answer 17

stimulate respiratory center directly, early fall in PCO2 and respiratory alkalosis, AG metabolic acidosis due to accumulation of organic acids (lactic and keto)

Question 18

How do you treat salicylate intoxication?

Answer 18

supportive care and dialysis if elevated level symptomatic

Question 19

How do methanol and ethylene glycol cause acidosis? What is the treatment?

Answer 19

methanol-> formate + H+, ethylene glycol-> oxalate + H+; fomepizole and dialysis

Question 20

What is the delta delta gap?

Answer 20

used in high gap metabolic acidosis, decrease in bicarb is equal to the increase in AG

Question 21

What happens when AG is greater than change in HCO3?

Answer 21

high AG metabolic acidosis with primary metabolic acidosis

Question 22

What happens when change in HCO3 than change in AG?

Answer 22

either high AG metabolic acidosis with non-AG metabolic acidosis or high AG metabolic acidosis and chronic respiratory alkalosis with compensatory non-AG metabolic acidosis

Question 23

What are the causes of non-AG acidosis?

Answer 23

Renal or GI; separate based on history and on urinary anion gap

Question 24

How does urinary ammonium change with urinary anion gap? What does it mean if UAG doesn’t change?

Answer 24

NH4 excretion increases-> UAG decreases; form of RTA

Question 25

what is RTA? Causes?

Answer 25

net loss of bicarbonate by the kidneys; Distal RTA (1)- defect in H ion secretion in DT, Proximal (2) defect in PT reabsorption of HCO3, and 4 relative insufficiency of or lack of responsiveness to aldosterone by DT

Question 26

what are the features of Type 1 RTA?

Answer 26

distal defect->decreased H secretion, H builds in blood, K secreted instead of H, Hypercalciruia, renal stones

Question 27

What are the causes of RTA 1?

Answer 27

1- idiopathic or familial, 2- hereditary hypercalcemia, hyperthyroidism, vitamin D intoxification

Question 28

How do you treat type 1 RTA?

Answer 28

1-3 mmol/kg/day HCO3, sodium citrate better tolerated than NaHCO3, potassium citrate if hypokalemic

Question 29

What are the features of type 2 RTA?

Answer 29

HCO3 wasting, urine pH< 5.5, K low to normal

Question 30

What are the causes of Type 2 RTA?

Answer 30

Fanconi's syndrome, multiple myeloma, carbonic anhydrase inhibitors, heavy metal poisonings, amyloidosis

Question 31

What is Fanconi's syndrome?

Answer 31

generalized PT dysfunction, urinary loss of phosphorus, uric acid, glucose, AA

Question 32

How do you treat Type 2 RTA?

Answer 32

alkali therapy (5-15 mmol/kg/day HCO3), K supplementation, Vit. D replacement

Question 33

What are the features of type 4 RTA?

Answer 33

impaired function of Na/K/H (cation) exchange mechanism, decreased and K secretion-> plasma build up of H and K hyperkalemia, urine pH < 5.5

Question 34

What are the causes of type 4 RTA?

Answer 34

decreased renin- diabetic nephropathy, interstitial nephritis, drugs, tubulointerstitial disease

Question 35

How do you treat Type 4 RTA?

Answer 35

dietary Na restriction, NaHCO3, furosemide= loop diuretic to get rid of K

Question 36

What are the clinical effects of alkalemia?

Answer 36

cardiac arrhythmias, neuromuscular irritability, tissue hypoxia, cerebral and myocardial blood flow fall and respiratory depression can occur

Question 37

What are the phases of alkalosis?

Answer 37

generation- loss of H or gain of HCO3, maintenance- prevents kidney from excreting HCO3, Lungs compensate by decreasing ventilation and increasing pCO2

Question 38

What are some causes of generation of metabolic alkalosis?

Answer 38

loss of acid- vomiting, nasogastric suction, intestinal loss; excessive gain HCO3- oral or enteral intake, lactate or ketone metabolism; renal- persistent mineralocorticoid excess, K deficiency

Question 39

What mechanisms are responsible for metabolic alkalosis?

Answer 39

decreased renal perfusion, hypermineralocorticoidism, sever hypokalemia, elevated pCO2

Question 40

What causes impaired HCO# excretion that allows metabolic alkalosis?

Answer 40

ECircV depletion, Chloride depletion (decrease HCO3 secretion), Hypokalemia, Hyperaldosteronism

Question 41

How do you differentiate causes of metabolic alkalosis?

Answer 41

responsiveness to NaCl, urine Cl < 10mEq/L alkalosis will respond to NaCl, urine Cl > 20 mEq/L

Question 42

What are the causes of NaCl responsive metabolic alkalosis?

Answer 42

GI loss of H vomiting, gastric drainage or renal loss of H, diuretics, post-hypercapnia, poorly reabsorbable anion

Question 43

What are the causes of NaCl resistant metabolic alkalosis?

Answer 43

severe K depletion or excess mineralocorticoid activity- hyperaldosteronism, Bartter's and Gitelman's, Cushing's, Excess licorice intake

Question 44

What are the unclassified causes of metabolic alkalosis?

Answer 44

contraction, exogenous bicarbonate (blood transfusion), milk alkali syndrome, and hypercalcemia with decreased PTH

Question 45

What are the features of Bartter's syndrome?

Answer 45

metabolic alkalosis, hypokalemia, hypercalciuria, hypomagnesemia, normal BP, gene- loop-durietic sensitive Na/K/Cl cotransporter of thick ascending LOH or apical K channel

Question 46

what are the features of Gitelman's syndrome?

Answer 46

Metabolic alkalosis, hypokalemia, hypocalcuria, hypomagnesemia, normal BP, genes- thiazide sensitive NaCl cotransporter of distal tubule

Question 47

What is milk alkali syndrome?

Answer 47

seen in pts with long history of excessive ingestion of milk and antacids, hypercalcemia and vitamin D excess increase, renal insufficiency, develop nephrocalcinosis

Question 48

What is the diagnostic approach to metabolic alkalosis?

Answer 48

ABG and BMP (pH >7.4, HCO3 > 28, Pco2 > 40), assess compensation (winters), check if chloride responsive (UCl)

Question 49

what is the treatment for chloride responsive alkalosis?

Answer 49

normal saline (correct volume, replace deficient Cl), replete K deficits

Question 50

What is the treatment for chloride resistant metabolic alkalosis?

Answer 50

diagnose cause and treat it

Question 51

What are special problems in metabolic alkalosis management?

Answer 51

CHF- fluid overload with diuretics use acetazolamide (CA inhibitor), weak diuretic also causes bicarbnaturia; RF- hemodialysis or HCl drip