Metabolic Acid-Base Disorders Flashcards
DiBartola
Chapter 10 Metabolic Acid-Base Disorders
How may a metabolic acidosis occur?
loss ofHCO3
Addition of fixed acid
Or failure of renal excretion of fixed acid.
What are common causes of bicarb loss?
gastrointestinal tract (e.g., small bowel diarrhea),
Kidneys
(e.g., carbonic anhydrase inhibitors, proximal renal tubular acidosis)
What are examples of addition of fixed acids?
lactate, ethylene glycol, ketones, ureamia
What stimulates a respiratory response after an acute acid load
peripheral and central chemoreceptors increasing alveolar ventilation
Do dogs and cats have similar resp comp regarding metabolic acidosis?
No, evidence is limited but suggests cats do not compensate to the same extent
Chronic metabolic acidosis reduces HCO3 by two mechanisms - what are they?
Direct effect of buffering and
A reduction in renal HCO3 reabsorption that accompanies secondary hyperventilation.
How do kidneys respond to an acute acid load?
Mainly augmenting NH4 excretion (cats may not do this we don’t know) and resorbing HCO3.
What are the detrimental consequences of a metabolic acidosis
decreased cardiac output,
decreased arterial blood pressure, and decreased hepatic and renal blood flow
Decreased myocardial contractility.
Predisposition to arrhythmias
How does acidosis affect the oxyhaemoglobin dissociation curve?
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
How does acidosis affect K+ conc
Increases plasma conc if due to an organic acid –> due to transcellular shift
How does acidosis affect Ca2+?
Should increase iCal due to a reduction of albumin binding sites resulting in more free Ca
How is renal tubular acidosis characterised?
hyperchloremic metabolic acidosis caused by either decreased HCO3 reabsorption (proximal RTA) or defective acid excretion (distal RTA)
What is the hallmark of distal RTA
Increased urine pH
(>6.0) in the presence of acidosis
How may a Dx of RTA be diagnosed?
ammonium chloride tolerance test - admin PO ammonium chloride and continually measure urine pH
Why is proximal RTA usually thought of as ‘self limited’
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
What other resorption abnormalities usually accompany proximal RTA?
glucose,
phosphate, sodium, potassium, uric acid, and amino acids
How is proximal RTA Dx?
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%)
What breed is predisposed to fanconi?
Basenji
What co-morbidity may be associated with RTA
copper hepatopathy - RTA resolved with copper chelation.
Why do infused amino acids result in metabolic acidosis?
Due to resulting H+ and NH+ as it is converted to urea in the liver
Disorders associated with an increased anion gap
Pg 260
What is the process of ethylene glycol metabolism
ehtylene glycol –> glycoaldehyde (in the presens of alcohol dehydrogenase) –> glycolic acid –> glyocylic acid –> oxalate and a-hydroxy-b-ketoadipate
What aspect of ethylene glycol metabolism is primarily responsible for metabolic acidosis?
Glycolic acid
What causes renal damage?
glycoaldehyde, glycolic acid, and glyoxylic acids, and calcium oxalate crystals
What are some clinpath features of ethylene glycol
azotemia, isosthenuria, hypocalcemia, hyperphosphatemia,
and hyperglycemia. Calcium oxalate dihydrate and monohydrate (more specific) on UA
why is ethanol use?
Alcohol dehydrogenase has greater affinity for ethanol than EG.
Why does salicyate intoxication result in metabolic acidosis
Uncouples ox-phos in mitochondria –> results in build up of lactate, ketones, and others
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.)
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
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%
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.
How long you wait before judging the effect of administered bicarb?
at least 30 mins
What is the main goal in treating a metabolic acidosis?
Recognition and treatment of the cause
What is the aim of bicarb therapy?
To increase pH to 7.2 to ameliorate the consequences of acidosis
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
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
Metabolic Alkalosis
Pg 271
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.
What are the two types of metabolic alkalosis
Chloride responsive (due to volume depletion - very common) and chloride non-responsive
What is the adaptive respiratory response to metabolic alkalosis
alveolar hypoventilation. 0.55-0.7mmHg increase per 1mEq/L increase in HCO3
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.
What are the clinical signs associated with metabolic alkalosis?
underlying disease
Seizures reported in humans
hypokalaemia, hypocalcemia
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
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
What two conditions may result in chloride resistant metabolic alkalosis
Hyperaldosteronism, and hyperadrenocortisism
