Past qs Flashcards
ALT
who is it specific for
where is it found
cause of elevation in plasma
- liver specific in carnivores
- liver cells, RBC, cytoplasm
- small amt in heart- striated muscle cells and kidney
- increase caused by liver
- liver cell damage
- hepatic lipidosis
- chronic active hepatitis, cholangiohepatitis
- cirrosis
- bile obstruction
- other: pancreatitis, septicaemis, neoplasm
- drugs: barbiturates, gcc, salicylates, tetracyclines
- cu storage disorders
acute pancreatitis
- causes: inflammation, hypoxia, free radicals, cold temp, mechanical trauma -> membrane damage -> enxyme activation
- clinical signs: anorexia, depression, abdominal pain, vomit, exiccosis, diarrhea, heart fail signs, vasculitis, kidney fail, liver fail, dyspnoe, anemia, icterus, peritonitis, paralytic ileus, septicemia, DIC, organ fail, abcess in pancreas
- lab exams:
- haematology: rbc morph, count
- serum biochem: pancreatic enzymes in plasma, pancreatic function
- a-amylase: starch digestion test, p-nitrophenol method
- lipase: turbidimetric method
- a-amylase/creatinin ratio
- trypsin like immunoreactivity
- pancreatic specific lipase
- cytology, microbiology
lab findings in prehepatic jaundice
plasma, urine, faeces
causes for blood urea concentration increase
prerenal
- GI:
- increased protein intake
- increased bacterial production / dysbacteriosis
- rumen alkalosis / poor energy status
- internal bleeding
- protein catabolism
- starvation
- haemolysis
- hyperthyroidism
- fever
- (SIBO)
- perfusion
- strangulation of A. Renalis
- heart fail
- dehydration
- low BP
- shock
renal
- embolism inside kidney
- CKD - fibrosis
- hypoplasia
- polycystic kidney disease
- amyloidosis
- kidney tumor
- glomerular nephritis
- NSAIDs
postrenal
- obstruction of kidney pelvis, urether, urethra, bladder
- rupture
causes of blood urea decrease
- impaired liver function: decreased urea synth, increased NH3 level
- Haemodilution / hyperhydration
- decreased protein intake: starve, anorexia
lab findings in posthepatic jaundice
water deprevation test
- needed parameters: BW, Ht, creatinine, urea, TP, osmolality
- goal: to find cause of PU/PD - CDI, PDI or PP?
- how:
- empty bladder by catheter, check BW, urine test every hr
- withold water till 5% dehydration - approx 6 hrs
- measure SG
- result:
- PP: sg above 1025
- CDI or PDI: SG 1010 or below
- differentiate CDI and PDI: give ADH and check after 60 min
- if SG increase it was CDI
- if SG is still below 1010 its PDI
- contraindication: endocrine disturbance, dehydration, azotemia, liver dysfunction, preggo,
lab findings in hepatic jaundice
tests for tubular function
- specific gravity
- urinary sediment analysis
- fractional electrolyte clearance
- analysis of enzymuria
- urinary osmolality
- (water deprevation test)
what is icerus and what causes increased Br in plasma
- icterus=jaundice: visible yellow discoloration
- in plasma, fat, skin and mucous membranes
- first visible sight is mucous membrane of genital tract
- increased Br in plasma:
- prehepatic jaundice, haemolysis: immune mediated haemolytic anemia, babesiosis
- hepatic: liver cell damage, damaged intrahepatic structure, cirrosis
- posthepatic: cholestasis, obstruction, pancreatitis
causes of increased Br1 in serum
- excess production of Br1 due to increased RBC destruction
- acute haemolysis
- absorption of Hgb after massive haemorrhage or haematoma - absorption icterus
- transfusion of stored blood w/ many dying RBCs
- decreased uptake of Br1 from blood by liver cells
- impaired hepatic function
- acute haemolysis
- decreased rate of conjugation of Br1 by livercells
- impaired hepatic function
increased blood creatinine
prerenal
- muscle
- rhabdomyolysis
- rhabdomyosarcoma
- trauma
- myositis
- necrosis
- GI: increased protein intake
- perfusion:
- A. Renalis strangle
- heart fail
- dehydration, low BP, shock
renal
- embolism inside kidney
- CKD - fibrosis
- hypoplasia
- polycystic kidney disease
- amyloidosis
- kidney tumor
- glomerular nephritis
- NSAIDs
postrenal
- rupture of kidney, urether, bladder, urethra
- (obstruction do not cause!!)
ALKP
- location: every cell membrane, placenta, bone, liver, biliary epithelial cells, intestines, kidney tubular cells
- only hepatic and bone ALKP in blood
- tubular cell damage cause increase in urine
- liver ALKP heat stable, bone ALKP heat labile
- SIAP: steroid induced alkaline phosphatase, from liver
- bile duct obstruction enzyme
- pH optimum 10
- phosphotransferase: ex: P from alchohol to another
local and general consequences of distal ileus

causes of increased ALKP
- bone originated
- young dogs, newborn, preggo
- bone tumors: osteosarcoma
- osteomyelitis
- bone fractures, healing of fractures
- paraneoplastic: lymphoid, lung, hepatic tumours
- liver originated
- cholestasis, intra/extra hepatic bile obstruction
- bile acids
- acute hepatic necrosis
- liver cirrhosis
- cholangitis
- hepatic lipidosis
- drugs: barbiturates, salicylates
- increased SIAP: hyperadrenocorticism, chronic stress
causes of decreased urine pH
- metabolic and respiratory acidosis: increased h excretion
- vomiting: Na+ reabsorbed wih HCO3, less hco3 in urine
- hypokalaemia: increased h excretion (na/k)
- acidic drugs
- distalis renalis tubularis acidosis: low hco3 excretion
- abomasal displacement
- toxicosis with acidifying agents
inorganic compounds in urine
example of why they are in urine
alkaline urine
- struvite: urease + bacteria - UTI
- calcium-carbonate and calcium-phosphate: hypercalcuria - hyperparathyroidism
- amorphous phosphate: meat and grain diet
- ammonium-ureate/biurate: impaired hepatic function - PSS, dalmatian dog
acidic urine
- calcium oxalate: cat eating toxic plant
- uric acid: dalamtian dog
- cystine, tyrosine, leucine: metabolic disease
- bilirubin crystals: prehepatic and hepatic jaundice
- sulphonamides: sulphonamide therapy
bile acid measurements
- HPLC
- TBA: total bile acids, specific!
- spectrophotometric
- only blood serum!
- either after 12 hr straving
- or postprandial
causes of increased alpha amylase
- acute pancreatitis
- acute/subacute kidney fail
- FIP, other immune mediated diseases
- lymphoma, myeloma
- DM
- ileus
- gastric or intestinal perforation
- parotitis
- chronic enteritis
Rivalta test
- add 1-2 drops of native sample to 3% acetic acid solution
- coagulation, smoky appearance: exudate, coag of labile protein fibrinogen, globulin
- no coagulation, sample dissolved: transudate, stable proteins, albumin
- drops remain in reagent: sample has high amt of globulin, FIP
- globulins on surface of drop coagulates, making sample stay in a drop
- note!! urinanalysis need 20% salisylic acid, this coagulates all protein
EPI - what is it, causes, lab tests,
- decreased production of digestive enzymes or obstruction of the pancreatic duct
- causes:
- chronic necrotic or atrophic damage
- chronic inflammation, fibrosis
- inherited pancreatic acinar atrophy
- chronic necrotic or atrophic damage
- lab tests
- TLI-concentration: trypsinogen
- BT-PABA test: chymotrypsin
- dyed agar gel digestion and schwachmann film test
- chymotrypsine, elastase
- lipid absorption test: malabsorption/maldigestion
- faecal elastase test: elastase
- faecal smear: check undigested material in faeces
transudate fluid
parameters from body cavity fluids
- physical parameters: color, odour, consistency
- rivalta test
- coagulation ability
- specific gravity
- pH
- RBC count
- nucleated cell count
- TP concentration
- albumin/globulin ratio
- creatinine, ure concentration
- alpha amylase, lipase activity
- LDH activity
- triglycerol, cholesterol concentration
- cytology
types of body cavity fluids
- transudate(hydro-)
- exudate (pyo-)
- modified transudate
- blood
- chylus - lymph
- ( cavities: abdominal/peritoneal, thoracic/pleural, mediastinum included, pericardial cavity)
Talk about bile
- primary bile acids: cholic acid, chenodeoxycholic acid
- synthesized in liver from cholesterol
- stored and concentrated in gall bladder
- released to duodenum via bile duct
- primary bile acids are deconjugated by bacteria in intestines, form secondary bile acids
- litho-cholic acid, deoxy-cholic acid
- 90% of conjugated bile acids reabsorbed at terminal ileum
- transported back to liver via portal circulation
- 2-5% faecal loss
- function: detergent effect, key role in micelle formation and lipid digestion and anti-endotoxin effect
- emulgating big fat droplet to smaller drops with more surface
- neutralize effect of gram- bacteria toxins
- concentration in plasma increased after eating
- release is mediated by cholecystokinin-pancreozymin and secretin
specific gravity
methods
interpretation
methods
- urinometer: most accurate at 21 degrees, easy, cheap, but need alot of urine
- refractometer: easy, one drop urine is enough, not reliable if urine sample is not transparent
- test strip: not usefull
interpretation
- normal: up to 1030 g/l - large variation
- hyposthenuria: below 1008
- hyperadrenocorticism, decreased ADH prod, ADH resistance, renal tubular damage, PP
- may also be seen in: hypoadrenocorticism, liver disease, prolonged fluid therapy
- medullary washout
- isosthenuria: 1008-10012 g/l
- tubules cant concentrate/dilute filtrate
- severe tubular damage
- also in case of: medullary washout, CDI, PDI, PP
- hypersthenuria: above 1012 g/l (physiologic)
- decreased water intake, water loss, acute kidney failiure
- also in DM (rare)
always measure more than once as large variation is normal
glomerular function tests
- blood urea concentration in blood plasma
- creatinine concentration in blood plasma
- plasma urea / plasmacreatinine ratio
- creatinine clearance
- urinary total protein concentration
- urinary TP / creatinine ratio
- SDMA
what parameters change in portosystemic shunt and why
- decreased hepatic perfusion
- the shunt redirect part of the blood flow away from liver
- increased bile acids in blood
- absorbed bile acids bypass liver tissue
- decreased urea concentration in blood
- nh3 dont reach liver, no urea synthesis
- increased NH3 in blood
- microcytosis, hyperchromasia
- decreased MCV, decreased MCHC
how to measure TP/total creatinine ratio
what are the causes
list sampling and analysis of CSF
- sampling:
- Na K EDTA tubes!!
- check speed of dripping - intra cranial pressure
- important to check intracranial pressure first
- retina observation
- lumbosacral zona: more protein and cells
- optical zona
- physical examination
- color:
- red: fresh bleeding
- yellow: bleeding in the past
- opaque: highly inflamed/ neoplastic disease
- turbidity:
- slight: cell count 100-300
- severe: cell count 2000-3000
- coagulation: coagulative in highly inflammatory processes
- color:
- cell count
- total cell count: native sample
- normal count: 5-10 micro litre
- cytology
- protein content
- glucose concentration
- lactate concentration
- enzyme activity
body cavity fluids and causes for accumulation
- types of fluids: transudate, modified transudate, exudate, chylus, blood
- cause of accumulation
- increased vessel permeability - non inflammatory
- increased hydrostatic pressure
- right sided heart fail
- liver hypertension, failiure, cirrosis
- blockage of a blood vessel
- renal fibrosis
- decreased plasma coloid oncotic pressure
- decrease of plasma albumin
- protein intake
- malabsorption, maldigestion
- epi
- liver failiure: no synthesis
- high utilisation
- loss: ple, pln, gnp
- decrease of plasma albumin
- impended lymph flow
- hormonal effect
- aldosterone, ADH
- increased hydrostatic pressure
- increased permeability of vessels - inflammatory
- bacterial toxin
- viral effect
- parasitic toxins
- inflammatory mediators
- increased vessel permeability - non inflammatory
evaluation of bile acids
- determination (spectrophotometric)
- HPLC: test every single acids, separate
- TBA: total bile acid, specific
- RIA
- sample: SERUM only!
- normal range: 20micromol/l fasting, 40 after eating
- 12hrs after starving or 2 hrs after feeding
- increase
- liver injury, damage
- bile duct obstruction, biliary stasis
- portosystemic shunt