Smith 4 - Samples and Lab Tests Flashcards
hyponatremia
indication of relative water excess
- vomiting, D+, excess sweat, adrenal insufficiency
- third space sequestration
hypernatremia
indication of relative water defecit
hypertonic dehydration
feed and water deprivation
isotonic dehydration
balanced loss of water and electrolytes - early stages of acute diarrhea or heavy sweating
hypotonic dehydration
hyponatremia indicating loss of ions
-subacute or chronic diarrhea
major intracellular cation
potassium
hypokalemia effects
- affects resting membrane potential
- muscle weakness, impaired urine concentration ability, arrhythmias
Cl tends to vary ____ with bicarb
inversely
increased Cl without increased Na occurs in
hyperchloremic metabolic acidosis, renal tubular acidosis
decreased Cl without Na is seen in
metabolic alkalosis, compensation for primary respiratory acidosis
ionized ca
50-60% of total calcium
physiologically active
doesn’t change with albumin concentration
alkalosis ___ ionized ca
reduces; increases protein binding
level of Ca causing recumbency
<6mg/dl – <4 is fatal
common cause of hyperCa in horses
chronic renal insufficency
metabolic disorders
change in bicarb concentration
-compensated by respiration
primary respiratory imbalances
changes in alveolar ventilation
-compensated by kidneys
causes of metabolic acidosis
rumen overload, ketosis, preg tox, hypovolaemic shock, acute D+, strangulating colic, strangulating abomasal torsion, peritonitis, ruptured bladder, excess exercise in horses
causes of metabolic alkalosis
fluid sequestration in abomasum, gastric reflux, massive sweat loss, Cl or K depletion, furosemide, pyloric stenosis
paradoxic acidurea
metabolic acidosis
-renal H excretion is linked to bicarb, so it cannot be excreted
causes of respiratory acidosis
pulmonary dz, airway obstruction, laryngeal edema, aspiration pneumonia, pneumonia, pleuritis, pneumothorax, asthma, CNS resp depression/Dz, drugs
causes of respiratory alkalosis
hypoxemia, pulmonary dz, CHF, severe anemia, CNS resp stimulation, hyperventilation, gram negative sepsis, excitement/fear/pain
primary a-b disturbances
bicarb and PCO2 always change in the same direction
anion gap
(Na + K) - (Cl + Bicarb)
normal 12-17mmol/L
causes of decreased anion gap + hyperCl + hypoK
GI losses, renal tubular acidosis
decreased anion gap +hyperCl + hyperK
Addisons dz or renal failure
high anion gap
accumulation of lactic acid
strong ion difference
(Na, K, Ca, Mg) - (Cl, SO4, Lactate, acetoacetate, BHB)
SDH
liver specific in all LA
- hepatocellular damage and leakage
- active and ongoing liver damage
CK is found in
cytoplasm of myocytes
CK isoenzymes
CK1BB - brain
CK2MB - cardiac muscle
CK3MM - skeletal muscle
CKMt - mitochondria
serum CK levels represent which isoenzyme
CK3 MM
Which organ damage produces higher levels of AST
muscle necrosis»_space; liver
GGT is found mostly in
biliary tract
elevated GGT indicates
liver damage / biliary obstruction
ALP is a marker for
intra or extra hepatic biliary obstruction
-periportal liver damage and biliary obstruction
icterus in fasting horses is due to an increase in
unconjugated bilirubin
increase in unconjugated bilirubin
indirect
- increased production
- hemolytic anemia
- hepatic uptake is diminished / liver failure
- anorexia
increase in conjugated bilirubin
direct
- liver failure
- cholestasis
- bile duct obstruction
- NI
bilirubin in hemolytic anemia is
indirect / unconjugated
urine crystals in horses
calcium carbonate
urine crystals in foals
calcium oxalate
urine crystals in feedlot cattle
struvite
MgNH4PO4-6H2O
polychromasia
- regeneration in ruminants
- doesnt occur in horses
cytologic signs of lead toxicity
- howell jolly bodies
- basophilic stippling
cytologic signs of oxidative damage
- heinz bodies
- eccentrocytes
anemia of inflammation
mild to moderate non-regenerative
Endotoxemia causes neutrophils to
redistribute from circulating into the marginal pool and tissues
bovine leukemia virus causes
persistent lymphocytosis
most common leukemia in horses
lymphocytic
most common cause of PLE in ruminants
johnes - MAP
gold standard assay for platelet function
aggregometry
high levels of Ig_ production can hinder platelet function
IgM
hinders platelet function via protein coating of platelet surfaces
PT
one stage prothrombin time
- measure intrinsic (TF) and common coag pathways
- add Ca-thromboplastin reagent to plasma, time to fibrin clot formation
prolonged PT = deficiency of
-fibrinogen <100
-common factors II, V, X
-tissue factor VII
>25% increase is significant
means >20% decrease in coag factor activity
Vit K is needed for coag factors
II, VII, IX, and X
Vit K inhibition causes
- deficient carboxylation
- inability to bind endothelium
- -> PIVKAs
PTT
measures intrinsic + common pathways
-add Ca to plasma with partial thromboplastin reagent, time to clot formation
prolonged PTT = deficiency of
factors XII, XI, IX, and VIII, and PK (prekallikrein)
most important inhibitor of coagulation
antithrombin (ATIII)
heparin
necessary cofactor for ATIII
causes of low fibrinogen
acute severe DIC
acute hepatic necrosis
severe hepatic fibrosis
hereditary in goats
teg can detect:
hyper coagulable states
increased fibrinolysis
neutrophil circulatory half life
10 hours
platelet life span
7-10 days
erythrocyte life span
5 months
how to assess for regeneration in anemic horses
bone marrow evaluation