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
anuria
urine production <2ml/kg/day
causes:
* obstructive dz
* toxic nephrosis
pollakiuria
increased frequency of urination, decreased amounts but normal daily volume
causes:
* bladder inflam
* bladder mass lesion
* pregnancy
* behavioral
artifacts due to delayed urinalysis
increased bacteria
more alkaline
cloudy (crystals fall out of soln)
colorless urine cause
very dilute urine
dark yellow urine cause
concentrated, bilirubinuria
red- brown urine cause
hematauria, hemaglobinuria, myoglobin, metHgb
green urine cause
bilirubin
cloudy urine causes
lots of causes- look at sediment
* Increased cells (RBC, WBC)
* Numerous crystals
* Bacteria
* Lipiduria (lipids often rise to the surface)
* Mucus (especially in horses)
* Semen
* Fecal contamination
stong ammonia urine odor
consider bacterial UTI
(bacteria split urea to ammonia)
acetone odor of urine
indicates ketones
ketosis
urine specific gravity
high SG= reduced volume of urine being produced (conservation)
low SG= increased volume (waste)
Dog/cat/LA specific gravity that shows sufficient kidney function
Canine: >1.030
Feline: >1.035
Large animals: >1.025
urine pH is affected by:
carnivores: acidic
ruminants: alkaline
post prandial alkaline tide: after eating carnivores = more alkaline
age: older= more alkaline
bacteria: more alkaline
acidic urine pH causes
Increased protein metabolism
Metabolic or respiratory acidosis
Paradoxical aciduria
alkaline urine pH causes
Low protein diet
Metabolic/respiratory alkalosis
Bacterial cystitis
Prolonged storage at room temp
protein in urine
Always interpret in light of specific gravity
Normal urine contains no protein
Trace protein can occur in very concentrated urine
Dipstick is qualitative
Many false positives
* Alkaline urine
* Increased contact time
Physiologic causes:
* Convulsions, excess muscular exertion
* Very high protein diet
Pathologic causes:
* Prerenal: Hgb, Mgb
* Renal: Glomerular disease, Tubular disease
* Post renal: Hemorrhage, Inflammation
urine protein/creatinine ratio
< 0.2 normal in health
0.2 - 0.5 borderline
0.5 - 3.0 tubular disease (globulins)
> 3.0 glomerular disease (albumin)
NOT useful if
* Pyuria
* Hemorrhage
* Hemoglobin
* Myoglobin
glucose in urine
Glucosuria + Hyperglycemia
* Diabetes mellitus (ketone +)
* Enterotoxemia
* Epinephrine or steroids
Glucosuria + normoglycemia
* Transient - epinephrine
* Persistent - tubular dysfunction
False Positives (peroxidases)
False Negatives (Vit C, tetracyclines)
ketones in urine
Uncontrolled diabetes mellitus
Ovine pregnancy toxemia
Bovine ketosis
Starvation
urine hemoprotein
Hematuria (intact RBCs)
* Red urine color clears on centrifugation
Hemoglobinuria:
* Red plasma color
Myoglobinuria:
* Normal plasma color
Hemoglobinuria & myoglobinuria
* Does not clear on centrifugation
* Very dilute urine may cause lysis of RBCs
urine hemoprotein
Hematuria (intact RBCs)
* Red urine color clears on centrifugation
Hemoglobinuria:
* Red plasma color
Myoglobinuria:
* Normal plasma color
Hemoglobinuria & myoglobinuria
* Does not clear on centrifugation
* Very dilute urine may cause lysis of RBCs
urine bilirubin
Positive:
* Male dogs (usually 1+)
* Hepatobiliary disease/cholestasis
* Urine color may cause false positive
False negative
* UV light (converts to biliverdin)
* Vitamin C (inhibits reaction)
* Aged samples (hydrolyzes to unconjugated)
urine sediment RBCs
urine sediment WBC
Calcium oxalate monohydrate
(ethylene glycol, deadly)
Calcium carbonate
incidental in horses
Calcium oxalate dihydrate
incidental
Ammonia biurate
liver failure
bilirubin
cholestasis
Triple phosphate
incidental
urine sediment casts
more than 2-3 per view (10x)
tubular injury
Renal dz vs insufficiency vs failure
Renal dz: something isnt right (not always failure)
renal insufficiency: reduction in renal function but not yet azotemia (loss of ~66% of nephrons)
* LOSE ABILITY TO CONCENTRATE URINE
renal failure: reduction in renal function leading to azotemia, loss/dysfunction of >75% nephrons
azotemia
increases in blood urea and/or creatinine
classification: (need specific gravity to differentiate)
* pre renal
* renal
* post renal
uremia
increases in blood urea and/or creatinine + clinical signs of renal dysfunction…anorexia, vomiting, diarrheal etc
Isosthenuria
[urine sg] = [plasma sg]
Sp. Gr. = 1.008-1.012
Normal hydration
Hyposthenuria
[urine sg] < [plasma sg]
Sp. Gr. =1.001-1.007
Working to excrete excess free water
Over-hydrated
Hypersthenuria
[urine sg] > [plasma sg]
Sp. Gr. > 1.012
Working to conserve free water
Under-hydrated
Adequately vs inadequately
Glomerular Filtration Rate
volume of plasma cleared of a specific substance per minute
best indicator of renal function
Actual measurement of GFR difficult
Estimated by: urea (BUN), creatinine, SDMA, SPG
increased urea causes
Decreased GFR
* Dehydration/hypovolemia (prerenal)
* Glomerular disease (renal)
* Outflow obstruction (postrenal)
Increased protein digestion
* GI hemorrhage, high protein diets
Increased protein catabolism
* Fever, burns, corticosteroids, starvation
Must lose 75% of renal function before urea increases
decreased urea causes
Diuresis / increased plasma volume
Decreased hepatic function
increased/decreased creatinine
similar to urea but more specific for kidney
Decreased GFR
* Dehydration/hypovolemia (prerenal)
* Glomerular disease (renal)
* Outflow obstruction (postrenal)
Decreased values: Diuresis
SDMA
Symmetric dimethylarginine: Methylated form of the amino acid arginine
Increases suggest impaired GFR
Detects as little as 25% loss of function
prerenal azotemia
Decreased GFR
Increased Cr and or urea
Adequate urine concentration
Causes:
Any cause of dehydration / hypovolemia
renal azotemia
Decreased GFR
Increased urea and or creatinine
Isosthenuria or inadequately concentrated urine
Indicates > 75% loss of functioning nephrons
Renal dysfunction/failure (acute / chronic)
renal azotemia
Decreased GFR
Increased urea and or creatinine
Isosthenuria or inadequately concentrated urine
Indicates > 75% loss of functioning nephrons
Renal dysfunction/failure (acute / chronic)
renal azotemia
Decreased GFR
Increased urea and or creatinine
Isosthenuria or inadequately concentrated urine
Indicates > 75% loss of functioning nephrons
Renal dysfunction/failure (acute / chronic)
postrenal azotemia
Occurs due to obstruction of urine outflow> decreased GFR
Increased Urea and creatinine
Urine SG variable
Hematuria, casts and renal cells on sediment exam depending on lesion location or duration
Clinical signs of oliguria, anuria, straining to urinate
The classic accompanying electrolyte pattern:
↓Na, ↓Cl, ↑K, ↑P (urinary bladder rupture)
early pre-azotemic renal insufficiency
1/4 - 2/3 nephrons lost
Not azotemic
Maybe increase Pr : Cr ratio
Increased SDMA
USPG can be adequality concentrated
later pre-azotemic renal insufficiency
2/3 -3/4 nephrons lost
Not azotemic
Maybe increase Pr : Cr ratio
Increased SDMA
USPG can not be adequately concentrated
cats renal failure differences
cats may develop azotemia before SPG goes up
glomerulotubular imbalance
looks like pre-renal azotemia
acute renal failure
rapid (hours to days)
causes:
* nephrotoxin
* infectious dz
* ischemia/infarct
* UTI
urine volume: oliguric to anuric
prognosis: immediately life threatening but reversible
kidneys enlarged
