Haematology and Biochem Flashcards
albumins and globulins
albumin = most abundant, driver of oncotic pressure
- produced at constant rate by liver
- carries ion molecules
globulins = larger molecules, inflammatory cytokines and immunoglobulins
- produced by liver - acute phase proteins (inflammation) and coagulation proteins
- lymphocytes - immunoglobulins
hyperproteinemia
high albumin - dehydration
high globulin - dehydration, inflammation, neoplasia
hypoproteinemia
hypoalbuminemia -
reduce production - liver disease or inflammation
increased losses - renal disease (protein losing nephropathy, movement from blood into body cavity effusion
hypoglobulinemia -
rare
dehydration masking concurrent hypoalbuminemia
if actual hypoglobulinemia - immunodeficiency
panhypoproteinemia -
protein losing enteropathy - lymphoma, IBD, lymphangiectasia
protein losing dermatopathy - severe burns
liver markers - enzymes
Hepatocellular -
SDH - liver only - large animal
ALT - liver and muscle but mostly liver - not in large animal
GLDH - liver - more stable than SDH
Hepatobilliary -
ALP - biliary, bone, intestine, steroid - steroid only present in dogs
GGT - biliary only - small increases significant
liver markers - other
bile acids - specific to liver disease
bilirubin
cholesterol
albumin
glucose
coagulation factors
bile acid stimulation
produced by hepatocytes then degraded in gut and reuptaken to liver for processing
tests ability of liver to reuptake - good test of liver function
increase –> reduced liver function, portosystemic shunt, cholestasis
bilirubin
increased -
pre hepatic causes - excessive haem breakdown - haemolysis, fasting - unconjugate increased
hepatic causes - reduced ability to conjugate - toxic insult, lepto - conjugated and unconjugated both increased
post hepatic - gallstones, mucocoele, pancreatitis in cats - unconjugated increases first then both
cholesterol
produced by liver but also uptake from food and release from fat
increased -
cholestasis - increased bilirubin, GGT, ALT
starvation/anorexia - also increased triglycerides
recent meal - also increased triglycerides
neprhotic syndrome
decreased -
reduced intestinal absorption - GI disease, hypoadrenocorticism
hypoglycemia
diabetic ketoacidosis
starvation
insulinoma
artefact - wrong blood tube - should use fluoride oxalate
coagulation factors
synthesised by liver - liver failure –> increased coagulation times
muscular enzymes
creatinine kinase - muscle only - short half life
AST - muscle and liver - long half life
ALT - muscle and liver - more specific to liver
pancreatic markers
pancreatic lipase -
increased in pancreatitis and when GFR is reduced
amylase -
pancreatitis or reduced GFR
tli -
decreased in exocrine pancreatic insufficiency or up with pancreatitis or incomplete starvation
renal physiology
glomerulus - electrolytes out of blood, proteins stay in blood, RAAS
proximal tubule - resorption of electrolytes, vitamin D activation
loop of henle -
ascending - water absorption
descending - NaCl absorption
created medullary gradient to concentrate urine
distal tubule and collecting duct -
small amounts of electrolytes absorbed
reabsorbs water to concentrate urine
glomerular filtration rate
speed at which fluid is filtered out of blood into bowmans capsule
controlled by -
hydrostatic pressure - rate at which blood moves in and out of the glomerular capillaries and rate filtered fluid moves through renal tubules
oncotic pressure - amount of albumin in peripheral blood
hydrostatic changes -
increased inflow - high CO, high blood pressure
decreased inflow - low CO, water loss
increased flow through tubules - excretion of osmoactive substances (glucose, mannotol), diurectics, loss of medullt tonicity (psyhod=genic polydipsia, diabetes insipidus, liver failure)
decreased flow through tubules - injury to glomerulus, injury to tubules, urolithiasis
oncotic changes -
hypoalbuminemia - loss or decreased production
hyperalbuminemia - dehydration
renal biomarkers
urea -
produced by liver in protein metabolism and excreted by kidneys
concentration dependant on production (liver failure, high protein diet, increased with GI bleeding) and rate of excretion (renal damage)
creatinine -
released by muscles at constant rate and excreted by kidneys
concentration dependant on production (mucle mass or wasting) and rate of excretion (Renal damage)
azotemia
increase in creatinine, urea and SDMA
pre-renal - problem with renal blood supply or increased urea production in liver
renal - problem with kidney itself
post-renal - obstruction of urine outflow
evaluation -
USG - low likely renal, high assess bladder size, CRT and dehydration
enlarged bladder and history of anuria - post renal
dehydration and normal CRT - pre renal
uremia
clinical signs associated with azotemia -
lethargy/depression
mucosal ulceration
vomiting/diarrhoea
respiratory signs - uremic pneumonitis, metastatic calcification
hypertension
hypokalemia myopathy - plantigrade stance (Cats)
hyperkalemia bradycardia - AKI and urinary obstruction
non-regenerative anemia
differences between AKI and CKD - electrolytes
Sodium - drops in both
chloride - follows sodium - if increasing independently then Fanconi’s syndrome
potassium -
increased in AKI
increased in CKD in dogs and horses, decreased in cats
calcium -
increased in AKI
increased then drops in CKD
drops in urinary obstruction
prosphate - increases in both
magnesium - increases in both
alabama rot
cutaneous and renal glomerular vasculopathy (CRGV)
skin lesions
acute renal failure
differences between AKI and CKD - signs
collapse - more acute
alabama rot - acute
non regenerative anemia - chronic
weight loss - chronic
severity of azotemia - more severe in acute
PUPD
anuria
sodium
most abundant electrolyte
maintains osmotic pressure
increase -
diabetes insipidus - free water loss
water deprivation
salt poisoning
ayperaldosteronism
decrease -
loss from GIT - diarrhoea vomiting
kidney failure - diabetes mellitus, medullary washout
addisons
cavity effusion
perspiration - horses
chloride
second most abundant
usually moves with sodium
greater chloride loss than sodium -
vomiting
pyloric outflow obstruction - GDV, LDA, foreign body
greater sodium loss -
proximal small intestinal diarrhoea - pancreatitis
renal tubular injury - fanconi’s
cushings
can use corrected chloride to work out if moving in same direction
potassium
regulates pH and cell electrochemical gradient - exchanged for H+ when blood pH altered
increases -
acidosis
reduced renal excretion - CKD, AKI, urinary obstruction, addisons
artefact - hemolysis, delayed serum separation
decreases -
alkalosis
decreased intake - anorexia in horses
perspiration - horses
metabolic and respiratory acidosis
metabolic - acids or bases building up in tissues
respiratory - affected by ability to exhale CO2