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Metabolic Acid-Base Disorders Flashcards

1
Q

DiBartola

A

Chapter 10 Metabolic Acid-Base Disorders

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2
Q

How may a metabolic acidosis occur?

A

loss ofHCO3
Addition of fixed acid
Or failure of renal excretion of fixed acid.

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3
Q

What are common causes of bicarb loss?

A

gastrointestinal tract (e.g., small bowel diarrhea),
Kidneys
(e.g., carbonic anhydrase inhibitors, proximal renal tubular acidosis)

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4
Q

What are examples of addition of fixed acids?

A

lactate, ethylene glycol, ketones, ureamia

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5
Q

What stimulates a respiratory response after an acute acid load

A

peripheral and central chemoreceptors increasing alveolar ventilation

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6
Q

Do dogs and cats have similar resp comp regarding metabolic acidosis?

A

No, evidence is limited but suggests cats do not compensate to the same extent

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7
Q

Chronic metabolic acidosis reduces HCO3 by two mechanisms - what are they?

A

Direct effect of buffering and
A reduction in renal HCO3 reabsorption that accompanies secondary hyperventilation.

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8
Q

How do kidneys respond to an acute acid load?

A

Mainly augmenting NH4 excretion (cats may not do this we don’t know) and resorbing HCO3.

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9
Q

What are the detrimental consequences of a metabolic acidosis

A

decreased cardiac output,
decreased arterial blood pressure, and decreased hepatic and renal blood flow
Decreased myocardial contractility.
Predisposition to arrhythmias

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10
Q

How does acidosis affect the oxyhaemoglobin dissociation curve?

A

shifts right, –> enhancing O2
release from hemoglobin, but this effect is offset by a decrease in red cell 2,3-diphosphoglycerate, after 6 to 8 hours of acidosis and shifts the curve
back to the left

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11
Q

How does acidosis affect K+ conc

A

Increases plasma conc if due to an organic acid –> due to transcellular shift

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12
Q

How does acidosis affect Ca2+?

A

Should increase iCal due to a reduction of albumin binding sites resulting in more free Ca

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13
Q

How is renal tubular acidosis characterised?

A

hyperchloremic metabolic acidosis caused by either decreased HCO3 reabsorption (proximal RTA) or defective acid excretion (distal RTA)

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14
Q

What is the hallmark of distal RTA

A

Increased urine pH
(>6.0) in the presence of acidosis

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15
Q

How may a Dx of RTA be diagnosed?

A

ammonium chloride tolerance test - admin PO ammonium chloride and continually measure urine pH

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16
Q

Why is proximal RTA usually thought of as ‘self limited’

A

As HCO3 is unable to be resorbed proximally - it can be in the distal tubules and usually allows bicarb to be maintained at a new slightly lower setpoint

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17
Q

What other resorption abnormalities usually accompany proximal RTA?

A

glucose,
phosphate, sodium, potassium, uric acid, and amino acids

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18
Q

How is proximal RTA Dx?

A

acid urine pH (<5.5 to 6.0) in the presence of
hyperchloremic metabolic acidosis and a normal GFR but an when HCO3 increased to normal –> increased urine pH (>6.0) and increased urinary fractional excretion of HCO3 (>15%)

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19
Q

What breed is predisposed to fanconi?

20
Q

What co-morbidity may be associated with RTA

A

copper hepatopathy - RTA resolved with copper chelation.

21
Q

Why do infused amino acids result in metabolic acidosis?

A

Due to resulting H+ and NH+ as it is converted to urea in the liver

22
Q

Disorders associated with an increased anion gap

23
Q

What is the process of ethylene glycol metabolism

A

ehtylene glycol –> glycoaldehyde (in the presens of alcohol dehydrogenase) –> glycolic acid –> glyocylic acid –> oxalate and a-hydroxy-b-ketoadipate

24
Q

What aspect of ethylene glycol metabolism is primarily responsible for metabolic acidosis?

A

Glycolic acid

25
What causes renal damage?
glycoaldehyde, glycolic acid, and glyoxylic acids, and calcium oxalate crystals
26
What are some clinpath features of ethylene glycol
azotemia, isosthenuria, hypocalcemia, hyperphosphatemia, and hyperglycemia. Calcium oxalate dihydrate and monohydrate (more specific) on UA
27
why is ethanol use?
Alcohol dehydrogenase has greater affinity for ethanol than EG.
28
Why does salicyate intoxication result in metabolic acidosis
Uncouples ox-phos in mitochondria --> results in build up of lactate, ketones, and others
29
What products are detected in urine ketone strip?
Acetoacetate and acetone OMG (This problem can be overcome by adding a few drops of hydrogen peroxide to urine, which nonenzymatically converts b-hydroxybutyrate to acetoacetate.)
30
How may volume status affect the anion gap of a presenting patient with DKA?
Patients with severe volume depletion have an increased anion gap because of retention of ketoanions, whereas those without volume depletion have hyperchloremia as a result of increased urinary excretion of the sodium and potassium salts of ketoanions and retention of chloride
31
What results in an increased anion gap metabolic acidosis in renal disease
retention of phosphates, sulfates and organic anions - this usually only happens when GFR reduces to 10-20%
32
Whats the difference between type A and Type B lactic acidosis
Type A (hypoxic) - mitochondrial function is normal but O2 delivery to tissues is inadequate Type B (non-hypoxic) - there is adequate O2 delivery to tissues but defective mitochondrial oxidative function and abnormal carbohydrate metabolism.
33
How long you wait before judging the effect of administered bicarb?
at least 30 mins
34
What is the main goal in treating a metabolic acidosis?
Recognition and treatment of the cause
35
What is the aim of bicarb therapy?
To increase pH to 7.2 to ameliorate the consequences of acidosis
36
Why are bicarb dosing guidelines difficult to create
Bc compensatory CO2 will change with admin. Vd changes with time --> 15min to ECF and 2-4 hrs to bone and intracellular
37
What are the complications of bicarb admin?
- volume overload caused by administered sodium, - tetany resulting from decreased serum ionized calcium concentration caused by increased binding of calcium to plasma proteins, - decreased O2 delivery to tissues because of increased affinity of hemoglobin for O2, - paradoxical CNS acidosis as hyperventilation abates and CO2 diffuses into CSF, - late development of alkalosis as metabolism of organic anions (e.g., ketoanions, lactate) - hypokalemia as potassium ions enter and H+ ions exit intracellular fluid in response to alkalinization of ECF
38
Metabolic Alkalosis
Pg 271
39
How may a metabolic alkalosis be caused?
loss of chloride rich fluid from the body via either the gastrointestinal tract or kidneys or by chronic administration of alkali. Most cases of metabolic alkalosis in small animal practice are caused either by vomiting of stomach contents or by administration of diuretics.
40
What are the two types of metabolic alkalosis
Chloride responsive (due to volume depletion - very common) and chloride non-responsive
41
What is the adaptive respiratory response to metabolic alkalosis
alveolar hypoventilation. 0.55-0.7mmHg increase per 1mEq/L increase in HCO3
42
As renal HCO3 excretion of bicarb is rapid, why may a metabolic alkalosis persist?
Metabolic alkalosis persists only if renal excretion of HCO3 is impaired. if GFR is decreased (i.e., decreased filtered load of HCO3  ), a continued high rate of alkali administration, or some stimulus for the kidneys to retain sodium in the presence of a relative chloride deficit.
43
What are the clinical signs associated with metabolic alkalosis?
underlying disease Seizures reported in humans hypokalaemia, hypocalcemia
44
Why may an increased anion gap occur in metabolic alkalosis
increased numbers of negative charges on proteins and partially the result of the increase in plasma protein concentration that occurs as a consequence of ECFV depletion
45
Why may diuretics cause a metabolic alkalosis
disproportional loss of chloride. Also result in sodium loss --> sodium avidity in the tubules --> more H+ and K+ excreted
46
What two conditions may result in chloride resistant metabolic alkalosis
Hyperaldosteronism, and hyperadrenocortisism

Acid/Base and Electrolytes (12 decks)

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