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Acid-Base and Nutrition > Acid-Base Disorders > Flashcards

Acid-Base Disorders Flashcards

1
Q

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

A

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

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2
Q

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

A

pH 7.35-7.45, pCO2, pO2, calculated bicarbonate

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3
Q

What are the clinical effects of severe acidemia?

A

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

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4
Q

What is the homeostatic response to acid/base loads?

A

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

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5
Q

How do the kidneys regulate pH?

A

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

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6
Q

What are the three components of net acid excretion?

A

titratable acids, ammonium, bicarbonate

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7
Q

What are titratable acids?

A

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

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8
Q

what are the sources of ammonium?

A

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

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9
Q

what approach do you take to acid-base disorders?

A

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

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10
Q

what are the features of metabolic acidosis?

A

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

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11
Q

what are the common etiologies of metabolic acidosis?

A

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)

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12
Q

What are the causes of high gap acidosis?

A

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

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13
Q

How do you treat lactic acidosis?

A

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

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14
Q

what are the causes of lactic acidosis?

A

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

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15
Q

What causes ketoacidosis?

A

most commonly type 1 diabetes, also alcoholics or starvation

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16
Q

what are the symptoms of salicylate poisoning?

A

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

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17
Q

How do salicylates cause acidosis?

A

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

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18
Q

How do you treat salicylate intoxication?

A

supportive care and dialysis if elevated level symptomatic

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19
Q

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

A

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

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20
Q

What is the delta delta gap?

A

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

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21
Q

What happens when AG is greater than change in HCO3?

A

high AG metabolic acidosis with primary metabolic acidosis

22
Q

What happens when change in HCO3 than change in AG?

A

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

23
Q

What are the causes of non-AG acidosis?

A

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

24
Q

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

A

NH4 excretion increases-> UAG decreases; form of RTA

25
Q

what is RTA? Causes?

A

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

26
Q

what are the features of Type 1 RTA?

A

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

27
Q

What are the causes of RTA 1?

A

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

28
Q

How do you treat type 1 RTA?

A

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

29
Q

What are the features of type 2 RTA?

A

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

30
Q

What are the causes of Type 2 RTA?

A

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

31
Q

What is Fanconi’s syndrome?

A

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

32
Q

How do you treat Type 2 RTA?

A

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

33
Q

What are the features of type 4 RTA?

A

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

34
Q

What are the causes of type 4 RTA?

A

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

35
Q

How do you treat Type 4 RTA?

A

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

36
Q

What are the clinical effects of alkalemia?

A

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

37
Q

What are the phases of alkalosis?

A

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

38
Q

What are some causes of generation of metabolic alkalosis?

A

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

39
Q

What mechanisms are responsible for metabolic alkalosis?

A

decreased renal perfusion, hypermineralocorticoidism, sever hypokalemia, elevated pCO2

40
Q

What causes impaired HCO# excretion that allows metabolic alkalosis?

A

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

41
Q

How do you differentiate causes of metabolic alkalosis?

A

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

42
Q

What are the causes of NaCl responsive metabolic alkalosis?

A

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

43
Q

What are the causes of NaCl resistant metabolic alkalosis?

A

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

44
Q

What are the unclassified causes of metabolic alkalosis?

A

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

45
Q

What are the features of Bartter’s syndrome?

A

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

46
Q

what are the features of Gitelman’s syndrome?

A

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

47
Q

What is milk alkali syndrome?

A

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

48
Q

What is the diagnostic approach to metabolic alkalosis?

A

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

49
Q

what is the treatment for chloride responsive alkalosis?

A

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

50
Q

What is the treatment for chloride resistant metabolic alkalosis?

A

diagnose cause and treat it

51
Q

What are special problems in metabolic alkalosis management?

A

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

Acid-Base and Nutrition (6 decks)

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