More clin path Flashcards
base
accepts proton
carbonate (HCO3-) = weak base
acid
donates proton
carbonic acid (H2CO3) = weak acid
Acidemia
Blood pH < 7.35
can be from acidosis
Alkalemia
Blood pH > 7.45
can be from alkalosis
normal blood pH
7.35 – 7.45
metabolic component of regulation of blood pH
Kidneys
* excrete H+
* retain HCO3-
* hours to days
blood buffers
* titrate H+
* seconds
respiratory of pH homeostasis
Lungs exhale CO2
minutes
bicarbonate buffer system
lungs and kidney manipulate H+
kidneys manipulate HCO3-
lungs manipulate CO2
blood gas pH testing gives info on:
give info on:
metabolic: pH and bicarb (HCO3-)
respiratory: pH, partial pressure of CO2 (pCO2)
biochemistry acid base testing
gives you metabolic indicators
* Total Carbon Dioxide (TCO2)
* Anion Gap (AG)
* Sodium vs. Chloride
urinalysis acid/base testing
metabolic indicators: urine pH
blood gas sample requirements
Heparinized whole blood
* Blood gas syringe
* Anaerobic
Rapid processing
must know Patient’s body temperature
“no fail” method to characterize acid-base status
- classify the pH (acidemia/alkalemia)
- classify the metabolic process (HCO3-)
- classify the respiratory process
- identify the primary process (match the -emia and -osis)
- identify the compesentory process (mismatch -emia and -osis)
respiratory acidosis
too much CO2
1. (-) Respiratory center
2. Upper airway obstruction
3. Pleural cavity disease
4. Respiratory muscles paralysis
5. Alveolar disease
6. Vascular disorders
Total CO2
Estimate of HCO3- (not pCO2)
Metabolic acid-base status
Increased TCO2 = metabolic alkalosis
Decreased TCO2 = metabolic acidosis
Causes:
1. Titration
2. Loss / secretional
TOTAL CO2 = HCO3- NOT pCO2
titrational metabolic acidosis
KLUE:
1. Ketones
2. lactate
3. uremic acids
4. ethylene glycol
increased anion gap
loss/secretional metabolic acidosis
loss of HCO3-
diarrhea
NOT increased anion gap
metabolic acidosis causes
increased total CO2
titrational: KLUE (ketones, lactate, uremic acid, ethylene glycol)
loss/secretional: loss of HCO3- (diarrhea)
calculating anion gap
UA + (HCO3 + Cl) = UC + (K + Na)
UA – UC = (Na + K) – (TCO2 + Cl)
AG = (Na + K) – (TCO2 + Cl)
increased anion gap
titrational metabolic acidosis
KLUE (ketones, lactate, uremic acid, ethylene glycol)
as anion gap goes up, bicarb (TCO2) goes down = titrational metabolic acidosis
Keto-acids
KLUE (titrational metabolic acidosis)
increases anion gap
Ketone bodies
* Acetone (waste)
* Acetoacetate (keto-acid)
* β-hydroxybutyrate
Fasting
* Adipose > Fatty acids > Liver > Ketone bodies
* Mobile lipid energy
* Muscle, Kidney
Definitions
* Ketosis
* Ketoacidosis
* Diabetic ketoacidosis
lactic acid
KLUE (titrational metabolic acidosis)
increases anion gap
Tissue hypoxia
* Aerobic to anaerobic metabolism
* Regenerate NAD for glycolysis
Lactic acidosis
* Ischemia
* Shock
* Severe anemia
* Cardiopulmonary failure
* Strenuous exercise
* Dehydration
Uremic acids
KLUE (titrational metabolic acidosis)
increases anion gap
Failure to excrete acids
* Phosphates
* Sulfates
* Citrate
Uremic acidosis
* Decreased renal blood flow (dehydration)
* Decreased renal function
* Urinary tract obstruction/rupture
Definitions
* Azotemia (increased urea, creatinine)
* Uremia
ethylene glycol
KLUE (titrational metabolic acidosis)
increases anion gap
Antifreeze (Glycolic acid, Glyoxylic acid, Oxalic acid)
Calcium-oxalate complexes
* Acute renal failure
* Calcium-oxalate crystals (monohydrate)
H+ shifting with metabolic acidosis
extra H+ ions diffuse into cell
to balance charges, K+ moves out
K+ is elevated in plasma
metabolic alkalosis
TCO2 (HCO3-) increased
Cl- decreased
Anion gap = normal
Diseases/conditions:
* Stomach/Abomasum loss of HCl (vomiting, LDA, GDV)
* Primary respiratory acidosis -> (Met compensation)
* Hypokalemia
* HCO3- administration
H+ shifting with metabolic alkalosis
decreased H+
H+ diffuses out of cell
K+ moves into cell
decreased K+ in plasma (hypokalemia)
Normal urine pH
herbivore= alkaline >7
carnivore= acidic <7
normally mimics metabolic acid/base status in serum (TCO2)
TCO2 and urine pH mismatch
can reflect prior acid/base status
paradoxical aciduria
artifacts:
* urease producing bacteria (alkaline)
* delayed urinalysis (alkaline)
TCO2 and urine pH mismatch
can reflect prior acid/base status
paradoxical aciduria
artifacts:
* urease producing bacteria (alkaline)
* delayed urinalysis (alkaline)
Diuresis
non pathologic increased urine production
causes:
* increased water consumption,
* diuretic therapy
* fluid or steroid admin
polyuria
pathologic increased urine production
causes:
* acute/chronic renal dz
* diabetes mellitus
* diabetes insipidus
* chushings dz
* pyometra
oliguria
decreased urine production (<1ml/kg/hr in hydrated animal)
pathologic causes: dehydration, fever, acute renal failure, shock
non pathologic: increased ambient temp, increased panting