Midterm II Flashcards
1
Q
What faeces tests are useful for EPI determination/diagnosis?
A
Dyed agar-gel digestion and Schwachmann-filmtest- uncharged x-ray film contains gelatin + pH increaser + feces and incubate. After 30-60 minutes if x-ray film becomes transparent there is digestive enzymes in the feces. You can also stain agar and be prepared so it has a stable pH value of 8, pour into petri dish. Place piece of fecal sample into middle of dish after 30-60minutes we can see a wide digested circle around sample if feces contains enough digestive enzymes.
Smears to detect nutrients. Giemsa- undigested fibers.
Lugol- undigested starch particles
Sudan III- undigested lipid particles
2
Q
How can urine specific gravity be measured? When is the urine hypo normo and hyperstenuric?
A
refers to urine osmolality
indicator of concentrating ability (tubular function). SG is the ratio of the weight of the liquid to an equal volume of distilled water. SG of urine is always greater than distilled water. SG increases with increasing concentration of dissolved ions (osmolality), glucose, proteins, lipids and contrast materials.
urinometer – best method
refractometer – problem if lot of glucose or if urine is not homogenous
test strip – not so good test
-Hyposthenuria: SG<1.008 Temporary hyposthenuria can be normal with an increase in water uptake but if it is persistent then it can be pathological. causes: Hyperadrenocorticism, liver disease, prolonged fluid therapy.
-Isothenuria: SG 1.008-1.012. Temporary can be normal due to increased water uptake, Persistent can be pathological. Indicator for severe tubular damage.
-Hypersthenuria: SG >1.012 (Normal). as major function of tubules is to concentrate the primary glomerular filtrate. Can be pathological if 1) decreased water intake 2) substantial water loss 3) acute kidney failure. SG may be increased in diabetes mellitus due to increased glucose concentration.
SG is important in polyuria and polydipsia.
3
Q
What is ALT?
A
Alanine Aminotransferase. In cytoplasm of liver and red blood cells. better sensitivity and specific than AST . Converts alpha-keto-glutaric acid to L-glutamic acid and L-alanine to pyruvic acid. Carnivore liver specific. normal ca >60 IU/l Increase: liver cell damage chronic active hepatitis cirrhosis bile duct obstruction liver neoplasm pancreatitis septicaemia copper storage disorder drugs – barbiturates, glycocorticoids, salicylates
4
Q
Proximal and distal ileus
A
PROXIMAL ILEUS foreign body in stomach or prox. duodenal part. vomit that contains HCl early on metabolic alkalosis later metabolic acidosis dehydration anaerobic glycolysis
DISTAL ILEUS foreign body in jejunum and more distal parts animal don’t eat/empty stomach dehydration anaerobic glycolysis lactic acid formation metabolic acidosis alkaline vomit
5
Q
List and group the liver enzymes. What information is gained about the liver in case of enzyme deviations
A
PARENCHYMAL ENZYMES aspartate aminotransferase AST alanine aminotransferase ALT glutamate dehydrogenase GLDH sorbite dehydrogenase SDH
BILE DUCT OBSTRUCTION ENZYMES
cholestatic: ap-alkaline phosphatase ALKP
gamma glutamyl-transferase GGT
measured by kinetic spectrophotometry
not parameters for liver function but damage
6
Q
What is AST, where is it found? Where can we see it‘s elevation in the plasma? In what species is it useful?
A
AST – ASPARTATE AMINOTRANSFERASE in mitochondria of liver, muscle, red blood cell converts alpha-keto-glutaric acid to L-glutamic acid & L-aspartate to oxalic acetic acid herbivore liver specific normal dog >30 IU/l Increase: hepatitis fatty liver neoplasm hemolysis muscular injury training myocarditis herbivores: hepatopathy ca: severe parenchymal damage
7
Q
What is AP?
A
ALKP – AP-ALKALINE PHOSPHATASE
in cytoplasm, produced by different organs (biliary epithelial cells, hepatocytes, bone)
only hepatic (heat-atable) & bone (heat-labile) appears in blood
optimal pH 10
phosphotransferases – phosphate-esters are translocated to alcohol or phenol
hydroxyl group to another
normal ca/ru >200 IU/l (not used in cat because of its short half-life)
Increase: hepatitis
cholestasis
acute hepatic necrosis
cirrhosis
neoplasm
internal/external biliary obstruction
steroid induced hyperadrenocorticism (SIAP)
drugs – barbiturates, glycocorticoids, salicylates
8
Q
What is GGT?
A
GGT – GAMMA GLUTAMYL-TRANSFERASE
produced by different organs, liver origin appears in blood
L-alpha-AA can be better attached to reduced glutathione & transported through
membranes
normal ca >10 IU/l (good parameter for cat & eq)
Increase: hepatitis
cholestasis
acute hepatic necrosis
cirrhosis
neoplasm
internal/external biliary obstruction
steroid induced hyperadrenocorticism (SIAP)
drugs – barbiturates, glycocorticoids, salicylates
9
Q
Detecting protein from urine?
A
PROTEINURIA
very low, measured by ultrasensitive protein measurement
proteinuria (mainly albuminuria) is an essential indicator for glomerular dysfunction
increased cc – proteinuria febrilis
proteinuria/day <20 mg/kg bw/day
test strip – AA of proteins cause a colour change on test strip blue-greenish. Most sensitive to albumin.
sulfosalicylic test – 4-5 drops of acid to 1-2ml of sample. Sample becomes more opaque if more coagulated precipitates are formed due to higher protein cc. More sensitive than tests strips, but not specific.
gmellin (heller) test – Showing bile pigment metabolites and protein content of the urine. ccHNO3 layered underneath the urine in a TT. white ring of denaturated proteins.
Spectrophotometric method- methods can be grouped 1) colour intensity of a complex formed by direct reaction of urinary proteins with dye-reagent. 2) have to concentrate the protein(less practical) .
Urine protein: Creatinine protein
Determination of Bence-Jones proteins
10
Q
List the laboratory tests which allow us to evaluate the impairment of glomerulus-function.
A
1) Blood Urea (BUN=blood urea nitrogen) concentration in blood plasma
2) Creatinine concentration in blood plasma
3) Plasma urea (mmol/L) / Plasma creatinine (μmol/L)
4) Creatinine clearance
5) Urinary Total Protein conc.
6) Urinary Total Protein / Urinary creatinine ratio
7) others: Radioisotopic methods, C-inulin clearance, H-tetraethyl-ammonium-chloride clearance.
11
Q
What are the causes of increased blood urea concentration?
A
-PRERENAL decreased perfusion (shock, dehydration) increased nitrogen/protein intake energy deficiency in rumen- ruminal microorganisms can not produce enough protein so catabolised protein (NH3) is absorbed intestinal protein catabolism intestinal or gastric bleeding hemolysis fever liver function Decreased blood perfusion in kidneys (Addisons) -RENAL reabsorption uremia (tubular obstruction) retention uremia (glomeruli problem) -POSTRENAL inhibition of urine flow reabsorption uremia (lower urinary tract rapture, obstruction)
12
Q
What are the causes of increased blood creatinine concentration?
A
state of muscles (acute trama/injury, necrosis, cachexia) kidney glomerulus function: -prerenal decreased perfusion nitrogen/protein intake energy deficiency intestinal protein catabolis intestinal or gastric bleeding hemolysis fever liver function -renal neoplastic process retention uremia -Post renal inhibition of urine flow reabsorption uremia (lower urinary tract rupture)
13
Q
What is proteinuria? How can it be evaluated?
A
Normally, primary ultrafiltrate contains 20-30% proteins and it is reabsorbed by tubules almost completely, thus protein content of normal urine is very low. measured by ultrasensitive protein measurement
proteinuria (mainly albuminuria) is an essential indicator for glomerular dysfunction
increased cc – proteinuria febrilis
proteinuria/day <20 mg/kg bw/day
test strip – not good, react mainly with albumin
sulfo test – denaturation of proteins, becomes whitish
gmellin (heller) test – white ring of denaturated proteins
14
Q
What info is provided by the urine TP/creatinine ratio? Where can it be used
A
When high total protein cc is measured in urine, we measure this ratio as it is not influenced by SG of urine
physiological value <0.8, if 1-5 the proteinuria is prerenal cause, if >5 renal disease
15
Q
Water deprivation test - What is the goal of this test, its method and interpretation.
A
preformed very rarely! used to evaluate the causes of polyuria and polydipsia.
used to detect diabetes insipidus.
needed parameters – bw, Ht, creatinine, urea, TP, osmolality
empty bladder, weigh patient and urine sampling repeat every hour
water is withheld until bw is decreased by 5% from basal weight-usually 6 hour deprivation is needed. Urine specific gravity should be measured at this time.
Results: 1) 1050-1080g/l: psychogenous polydysia
2) 1001-1007g/l: tubular cell damage or decreased ADH function. Give ADH IM or Intranasally and check SG after 60 minutes, a) 1050-1080g/l: Central diabetes insipidus (decreased ADH production). b) 1001-1007g/l: peripheral (renal) diabetes insipidus (decreased effect of ADH on damaged tubular cells)
16
Q
What is the goal of Enzymuria Evaluation? Goal and how is it performed/tested?
A
for tubular function tubular cells contain ALKP & GGT Their release into URUNE is increased in acute/peracute tubular damage. Values must be referred to the creatinine levels in order to exclude misdiagnosis caused by high enzyme level in concentrated urine. Alkaline phosphatase (U/l)/ Creatinine (umol/L): normal=0.02 Gamma-Glutamyl transferase (U/I)/Creatinine (umol/L): normal=0.01
17
Q
List the causes of abnormal urine pH (increased, decreased).
A
ca – acidic (65.5-7.5)
herbivores – alkaline (7-8.5)
postprandial alkalization (kidney compensation)
food changes pH slightly within physiological range
test strip – only whole numbers
test paper
Increase-Alkaline: 1) Feeding in carnivores results in alkalisation of urine. highly acidic gastric juice is released in the stomach after feeding resulting in slight metabolic alkalosis.
2)Urinary tract infection (UTI) caused by urease producing bacteria. ureases enzyme breaks down urea to ammonia-increasing pH.
3) Metabolic and respiratory alkalosis result in decreased H+ excretion (increased alkaline intake, increased loss of C02)
4) proximal renal tubular acidosis causes an increased HCO3- excretion to urine
5) long storage tome causes urea decompensation to ammonia (pH increase), can also occur in urinary tract obstruction.
Decrease-Acidic: 1) Metabolic and respiratory acidosis- increase of H+ excretion in the kidney (HCO3 loss due to diarrhoea, ileus, muscle weakness)
2) vomiting, Na+ is reabsorbed with HCO3-, due to decreased HCO3- excretion in urine pH becomes more acidic
3) hypokalaemia there is increased H+ excretion in exchange to reabsorbed K+
4) treatment with acidic drugs
5) distalis renalis tubularis acidosis
6) abomasal displacement
7) toxicosis with acidifying substances (metaldehyde)
18
Q
What can be seen in the physiological urine sediment? List the pathological abnormalities in the urine sediment.
A
Organic sediment: Blood cells(WBCs and RBCs) abnormal in haematuria: renal or urinary tact disease, obstruction, trauma
Cells from the lower urogenital tract: abnormal- inflammation or infection of urinary tract
Viral inclusion bodies: distemper
Microbes : bacteria
Mucin
Casts(cylinders): Abnormal- increase- acute tubular disease or renal tubular damage, haemorrhage(RBC cast), inflammation(WBC cast)
Inorganic sediment: small amount of struvite or different calcium- crystals may be found in normal urine. Larger number lead to stone formation.
Mostly in alkalic urine:
Struvite: UTI
Calcium Carbonate: hypercaluria
Calcium-Phosphate: hypercalcuria
Amorphous Phosphate: Meat and grain diet
Ammonium-ureate/biurate: severe impairment of hepatic function in Dalmatian dogs
Mostly in acidic urine:
Calcium oxalate: toxic plant consumption
Uric acid: Dalmations
Cystine, Tyrosin, Leucine: metabolic disease
Bilirubin: prehepatic and hepatic jaundice
Sulphonamides: sulphonamide therapy
19
Q
How can the presence of blood or haemoglobin be shown in the urine? How can the two be distinguished from each other
A
Haematuria is the presence of blood(intact RBC) in urine. Haemoglobinuria and Myoglobinuria is presence of free dissolved haemoglobin and myoglobin in urine. If presence is seen by naked eye colour of urine- pink, red, brownish.
benzidine test – sample into reagent, check pseudoperoxidase activity. Not specific test.
test strips: speckled appearance of test pad-haematuria, diffuse colour- haemogloburia or myoglobinuria.
Urine sediment analysis: RBCs can be seen microscopically.
Haematuria can be differentiated by centrifuging the sample, since RBCs sediment, the supernant clears up, in haemoglobinuria and myoglobinuria the urine supernant remains reddish. While in haemoglobinuria usually concurrent reddish discolouration of plasma and anaemia are also observed, in myoglobinuria the plasma is clear and muscle damage indicator enzyme activities are elevated.
Causes of haematuria:
lower urinary tract infection, trauma, genital tract injury, tumor or inflammation
Causes of hemoglobinuria:
intravascular haemolysis
long term stasis of blood in urinary bladder
Causes of myoglobinuria
excessive muscle trauma or exercise, burns
DISTINGUISH HEMOGLOBULINURIA FROM MYOGLOBULINURIA
creatine-kinase test
lactate dehydrogenase test
aspartate aminotransferase test
20
Q
How can the presence of pus be shown in the urine? What are the causes?
A
pus: an accumulation of neutrophil granulocytes, some tissue cells and microbes. Pus in urine-pyuria. microscope – sediment evaluation donne test – reagent makes sample more viscous if pus is present (and so bubbles elevate slower). (-, +, ++, +++) Positive result may occur in males if sperm is present. Causes: Kidney pelvis inflammation cystitis (inflammation in urine bladder) inflammation of penis/vagina: endometritis (females) prostatitis (males)
21
Q
Hapatocellular enzymes in dogs
A
ALT, GLDH
22
Q
What is TLI? Describe its usefulness in the diagnosis of EPI
A
TRYPSIN LIKE IMMUNOREACTIVITY
Tests for pancreatitis and EPI
most specific method.
Determined by radioimmunoassay (RIA) and ELISA
antibodies are produced against one part of trypsinogen. Antibodies marked by radioisoptopes are bound to trypsinogen in sample. marked trypsinogen cause increased radioactivity that can be measured.
trypsinogen goes to duodenum & is activated by enterokinase to trypsin this can get into blood stream and the cc will be 15 times more than normal.
If TLI-cc is less than 2.5 ug/L the probability of EPI of decreased enzyme synthesis origin is reliable. if EPI is caused by obstruction of the pancreatic duct, TLI level is normal or high.
23
Q
Describe the Gmelin-Test.
A
C.c. HNO3 has to be carefully layered under urine in a test tube, and the width of the differently coloured layers at the meeting of the two fluid phases has to be evaluated. Differently coloured layers from the highest layer: condensed material on the surface of the glass tube - acidic urea yellow - urine itself white (opaque) – protein purple - indicane (indol-sulphate) green – biliverdin brown - urobilinogen (UBG) HNO3
24
Q
List the most important findings in the blood and urine for prehepatic icterus.
A
Blood: Br I ↑↑ Br II ↑ UBG ↑↑ Free Haemoglobin ↑ Haptoglobin cc. ↓ Ht ↓ Reticulocyte count↑↑↑ Coag. parameters (PT, APTT, TT) ↔↑(DIC) enzyme activities: ALT, LDH↑ substrate cc: Urea↑ Urine: UBG↑↑ Br↑ Hb↑↑↑
25
List the most important findings in the blood and urine for hepatic icterus.
```
Blood: Br I ↑
Br II ↑↑
UBG ↑
Free Haemoglobin↔ ↑
Haptoglobin cc. ↔
Ht ↔↓
Reticulocyte count ↔↓
Coag. parameters (PT, APTT, TT) (no change after vitamin K administration)
enzyme activities: ALT, AST, GLDH↑
substrate cc: Urea↓ , NH3, Bile Acids↑
Urine: UBG↑
Br↑↑
```
26
List the most important findings in the blood and urine for posthepatic icterus.
```
Blood: Br I ↔↑
Br II ↑↑↑
Free Haemoglobin↔
Haptoglobin cc. ↔
Ht ↔
Reticulocyte count ↔
Coag. parameters (PT, APTT, TT) (improves after vitamin K administration)
enzyme activities: ALKP, GGT↑
substrate cc: Bile acids↑
Urine: UBG↓
Br↑↑↑
```
27
Bile acids. How to measure them and when is their concentration elevated in the serum/blood?
```
Bile acids (cholic acid, chenodeoxycholic acid) are synthesized in the liver from cholesterol.
Measurement: HPLC, RIA or total bile acids (TBA)
There are two ways of sampling: 1) after 12 hours starvation, 2) after eating, postprandial value - postprandial value can be 10 times (dog), 5-6 times (cat) more than the value measured after starvation. Na-EDTA or -citrate can be used as an anticoagulant, because heparin disturbs the measurement. Normal value (fasting): 6 µmol/l (carnivores) 20-30 µmol/l (other animals).
```
```
Increased:Liver injury, hepatic cell damage - increased outflow of bile acids from the damaged hepatocytes to the blood,
bile duct obstruction or bile endothelial cell damage - decreased secretion of bile acids to the bile, increased outflow to the plasma instead,
decrease in liver function, therefore decreased uptake of the absorbed bile acids (note: increased urobilinogen level !)
biliary stasis (cholangiohepatitis cirrhosis, hepatic or pancreatic neoplasm, pancreatitis)
portosystemic shunt (absorbed bile acids bypass liver tissue)
```
28
What method is used in blood ammonia concentration measurement? In which diseases is blood ammonia concentration increased?
produced in intestine by bacteria, absorbed & detoxified in liver by urea cycle
cc measurement = liver function test
starve animal 24 hours, avoid air contamination when sampling,
spectrophotometry or refractometry
normal dog 26.4-70.5 micromol/l
Ammonia checkers
Ammonia tolerance test: after 24 hours of starvation and pretreatmen tof neomycin, take basal blood sample and give NH4CL in 5% water solution, blood samples taken every 30-40 minutes. if liver function is normal, ammonia cc is <120umol/L in dogs and <175 umol /L in cats.
INCREASED AMMONIA CONCENTRATION
impaired liver function – decreased urea production, liver cirrhosis, portosystemic
shunt, liver lipidosis, hepatitis, toxic damage
ruminal alkalosis/ammonia toxicosis
ru/eq/rabbit – intestinal overgrowth of NH 3 -producing bacteria
congenital enzymopathies: decreased activity
29
What are the causes of proteinuria vera and proteinuria spuria?
```
True proteinuria (proteinuria vera):
proteins from or through kidney
kidney disease
sudden protein catabolism (fever, hemolysis, exercise, starvation, onset
of glucocorticoid treatment)
```
```
False proteinuria (proteinuria spuria)
proteins from lower urinary tract or genital tract
lower urinary tract infection
tumors
prostatic testicular inflammation
```
30
Rivalta test- goal, how to perform, interpretation
Prepare 3% acetic-acid solution. One-two drops of native samples (NOT CENTRIFUGED) dripped into the solution. If there is coagulation(labile proteins-fibrinogen, globulins) there will be a smoky appearance, this result is exudative. (+/++/+++)
If coagulation is not observed but sample is dissolved in the solution the result is transudate(stabile proteins-albumin) stabile proteins do not show coagulation with weak acids (-).
If sample contains a lot of globulins the sample goes honey like in case of FIP after adding some drops of sample into solution the smoky appearance of coagulation is not visible., but sample does not dissolve in solution but remains forming one drop. In this case globulins are coagulated on the surface.
31
When does alpha-amylase activity increase?
```
acute pancreatitis
acute, subacute kidney failure
FIP & other immune-mediated diseases
lymphoma, myeloma
diabetes mellitus
ileus
gastric or intestinal perforation
parotitis
chronic enteritis
```
32
EPI. What is it, how to test it? (Laboratory diagnosis of EPI)
```
Exocrine pancreatic insufficiency
Develop due to chronic necrotic or atrophic damage to the pancreas., or inherited
disease.
Features:
- decreased production of digestive enzymes or enzymes do not get out from organ to
intestines.
- Maldigestion
- pancreatogenous dyspepsia
- weightloss
- overeating & vomit
- coprophagia
- allotriophagia
- Large amount undigested food in intestines cause bacterial overgrowth
- Intermittent chronic diarrhea
- bacterial enteritis
- frequent flatulence
- undigested fat on surface of feces
- vitamin deficiency
- skin an fur problems
- mild anemia.
Laboratory examinations:
- TLI concentration
- BT-PABA test
- Dyes agar-gel digestion and schwamann filmtest
- Lipid absorption test
- Fecal elastase test
```
33
Biochemical parameters for examination of free fluids.
- outlook physical parameters (colour, odour, consistency)
- Rivalta-test
- coagulation ability
- specific gravity
- pH
- nucleated cell count
- total protein concentration
- albumin/globulin ratio
- creatinine, urea concentration
- alpha-amylase, lipase activity
- LDH activity
- triglycerol, cholesterol concentration
- cytological analysis
34
What is the lipid absorption test, and which disorders can it confirm or eliminate
perform this test in order to determine whether there is existing lipid malabsorption, maldigestion , especially in EPI or chronic small bowel disease . When there is fast lipid intake in normal conditions, plasma triglycerol (TG) concentration rises to twice as the normal value (normal for dogs: 1 mmol/l).
If the result is increased TG concentration and lipaemia, we can suspect that the original problem is exocrine pancreatic insufficiency (EPI). If the result is no change in TG concentration and lipaemia is not seen, we can suspect intestinal absorption defect
35
Laboratory diagnosis of pancreatitis
urine amylase: ↑ urine creatinin: ↑ pancreatitis plasma amylase:↑
plasma creatinin:↔(↑)
36
ALT-level in blood
normal ca >60 IU/l
37
Causes for high or low blood-creatinine concentration.
```
high: inflammation of muscles
muscle trauma
Increase meat intake
Low/normal: cachexia
chronic muscle atrophy
```
38
Urea conc. in blood
```
from liver urea cycle (detoxified NH 3 absorbed from intestines)
nontoxic but osmotically active
filtrated through glomeruli
reabsorbed from tubules
normal 8-10 mmol/l
```
39
Urinalysis- Main test
Urinalysis is a basic diagnostic tool like haematology and biochemical profile of the blood. Urinalysis is the physical, chemical, and microscopic examination of urine.
Free catch sample - use a clean or sterile container and avoid contamination of the sample with hair, dust or mud etc, catch urine middle stream for most reliable results.
40
Liver function test
PT, APTT, TT (not specific)
Albumin (not very sensitive)
Bilirubin (not specific)
Bile acids (best liver test, sensitive but not very specific) Ammonia (conversion of ammonia to urea occur in liver)
41
Proteinuria: causes and types
Causes of proteinuria Proteinuria may be caused by glomerulonephropathy, tubular transport defect, inflammation, infection or marked haematuria within the urogenital tract. Considering the causes of proteinuria it is important to distinguish true or real proteinuria and false proteinuria.
1. Real Proteinuria i.i. nephrongenic (proteinuria vera)
a. Selective proteinuria
b. Non-selective proteinuria
2. Pseudo-Proteinuria (spuria)
42
Local and general consequence of distal ileus
local anaerobic glycolysis & lactic acidosis →tissue necrosis & inflammatory processes
fluid accumulation prox to intestinal block
bacterial overgrowth due to content accumulation
gram – release endotoxins (absorbed → endotoxaemia, shock)
gram + release exotoxins (absorbed→ bacteraemia, sepsis)
Ht (PCV) increased
glomerular filtration rate & renal function decreased
hypokalaemia
hyperkapnia, hypoxaemia cause respiratory acidosis
painful abdominal cavity→ stress & adrenaline effect
bacteria & intestinal hypoxia → can cause pancreatitis & liver damage
43
Causes of increased ALKP in the blood
```
hepatitis
cholestasis
acute hepatic necrosis
cirrhosis
neoplasm
internal/external biliary obstruction
steroid induced hyperadrenocorticism (SIAP)
drugs – barbiturates, glycocorticoids, salicylates
```
44
Causes of decreased urine pH
metabolic/respiratory acidosis
distal tubular defect (decreased HCO 3 excretion)
fanconi syndrome
hyperkalaemia + metabolic alkalosis (paradox aciduria)
toxicosis
acidotic substances (eg. ammoniumchloride)
abomasal displacement
45
Inorganic components of urine and one example of why they would be found in urine.
a small amount of struvite and calcium crystals can be found in urine but are increased when there are a large number it can lead to stone formation. Urinary Tract Infection (UTI) can also cause an increase of these in the urine.
46
Causes of increased alpha amylase
```
acute pancreatitis
acute, subacute kidney failure
FIP & other immune-mediated diseases
lymphoma, myeloma
diabetes mellitus
ileus
gastric or intestinal perforation
parotitis
chronic enteritis
```
47
Which laboratory tests allow us to confirm acute pancreatis?
hematological analysis – polycythaemia, degradation of RBCs, anemia, leukocytosis,
neutrophilia (left shift), leukomoid reaction
serum biochemistry – determine increase of activity or cc of pancreatic enzymes in
blood
alpha-amylase, lipase, pancreas specific lipase,
trypsin-like immunoreactivity
determine glucose cc (decreased insulin production)
kidney, liver parameters & TP, albumin cc should be measured in order to diagnose
effects of complications
48
What is icterus? What can be the causes of increased plasma bilirubin concentration?
(JAUNDICE)
prehepatic – hemolysis (by blood parasites, bacteria, anemia) check PCV
hepatic – liver cell damage (Br I can’t be taken up or most of produced Br I get out)
posthepatic – cholestasis (obstruction of bile vessels &/or duct, complication in acute
pancreatitis)
strongly connected to each other
INCREASED BR I IN SERUM
excess production of Br I due to increased RBC destruction
defective uptake of Br I by liver enzymes
defective conjugation of Br I by liver cells
INCREASED BR II IN SERUM
defective excretion of Br II by liver cells
obstruction of bile canaliculi within liver
obstruction of bile canaliculi due to blockage or compression of bile duct
rapture of biliary vessels, duct or gall ladder
49
List the laboratory tests which allow us to evaluate the impairment of tubular-function!(Tubular dysfunction test.)
```
Specific gravity of urine
Urine osmolality
Water deprivation test
Fractional electrolyte clearance
Urine sediment
Analysis of Enzymuria
```
50
The signs of Br and UBG at the three types of jaundice
```
Prehepatic(haemolysis)- Blood:
Br I ↑↑
Br II ↑
UBG ↑↑
Urine:
UBG↑↑
Br ↑
Hepatic (Liver damage)-
Blood:
Br I ↑
Br II ↑↑
UBG ↑
Urine:
UBG↑
Br ↑↑
Posthepatic (bile duct obstruction)-
Blood:
Br I ↔(↑)
Br II ↑↑↑
UBG -
Urine:
UBG↓or no
Br ↑↑↑
```
51
Ruminal pH. List the causes of acidosis and alkalosis
Normal pH:
range between 6.3–7 (slightly acidic)
cows fed grain can have slightly lower, those fed hay or green slightly higher pH Abnormal pH:
Elevated pH (Rumen alkalosis) -Simple indigestion or reduced feed intake for greater than 2 days -Urea indigestion -Putrefaction of ruminal content from prolonged rumen stasis - Saliva contamination
Lowered pH 5.5.-6 (Rumen acidosis) -Grain overfeeding -Chronic ruminal acidosis
52
Preheaptic icterus.
prehepatic – hemolysis (by blood parasites, bacteria, anemia) check PCV
increase in the quantities of unconjugated bilirubin (indirect-reacting) in the serum (unable to pass the renal filter), stercobilin in the stool, (imparting a darker colour to the stool), and urinary urobilinogen. Increased urinary urobilinogen may be partly because of secondary liver damage (less re-excreted into the bile and hence lost to the serum and urine) in addition to the increased quantity of bile pigments metabolized owing to erythrocyte haemolysis. If secondary liver damage is extensive from haemosiderosis or bile pigment overload, some bilirubin glucuronide may be regurgitated and lost to the urine
53
Laboratory tests for diagnosis of acute pancreatitis.
hematological analysis – polycythaemia, degradation of RBCs, anemia, leukocytosis,
neutrophilia (left shift), leukomoid reaction. Serum biochemistry – determine increase of activity or cc of pancreatic enzymes in:
blood
alpha-amylase, lipase, pancreas specific lipase,
trypsin-like immunoreactivity
determine glucose cc (decreased insulin production)
kidney, liver parameters & TP, albumin cc should be measured in order to diagnose effects of complications.
54
Bile acids. How to measure them, and what causes increased levels in the blood?
synthesized from cholesterol in liver
excreted into intestines conjugated to taurine or glycine
reabsorbed in jejunum & ileum
role in micelle formation & lipid absorption
needed for absorption of fat-soluble vitamins
concentration in plasma increased
normal less than 10 micromol/l
```
MEASUREMENT OF BILE ACIDS
spectrophotometry or radioimmunoassay
sampling either after 12 hours starvation or postprandial (after eating, higher value)
above 40 micromol/l liver damage
grey scale betw 20-40 micromol/l
Increase:
impaired liver function
cholestasis
portosystemic shunt
```
55
Causes of exudate and cytological picture.
Causes:
Developtment:
- Increased permeability of vessels due to inflammatory causes (bacterial, viral,
parasitic, inflammatory)
- Increased migration of phagocytes
- Increased proliferation of mesothelial cells
- Increased production of inflammatory proteins
Septic:
- Trauma of pleural, peritoneal, pericardial wall
- Internal perforation of organs
- Hematogenous of lymphatic spreading of bacteria
Cytology
Neutrophils, macrophages and reactive mesothelial cells are seen.
Cells might show nuclear degeneration (karyolysis, karyohexis, sometimes
karyopinosis)
Visible bacterias in the IC phagycytosed form.
If bacteria can be seen out of cell – process worsening.
If only bacterias out of cell – bacterial contamination
56
Alkaline phosphatase
Alkaline phosphatase
Location:
- Every cell membrane
- Produced by different organs (placenta, bones, liver, intestines, kidneys, tubular
epithelial cells)
- Only hepatic and bone ALKP appear in blood.
- Not liver specific in cats
- Increased activity in urine in case of tubular cell damage.
It has several isoenzymes.
Function:
not active enzyme since its optimum is pH 10.
Causes of decreased ALKP in blood:
- Severe cirrhosis
Causes of increased ALKP in blood:
Bone originated:
- Young dogs
- Pregnant animals
- Bone tumors
- Osteomyelitis
- Bone fractures
- Healing of fractures
Paraneoplastic processes:
- Lymphoid tumors
- Lung tumors
- Hepatic tumors
Liver originated:
- Cholestasis
- Bile acids
- Acute hepatic necrosis
- Liver cirrhosis
- Intra or extrahepatic biliary obstruction
- Chlangioheptaitis
- Hepatic lipidosis
- Barbiturates
- Salycilates
In connection with increased SIAP
- Hyperadrenocorticism
- Iatrogenous
- Endogenous
- Chronic stress
57
Causes of transudate and cytological picture.
Causes:
* Increased vessel permeability due to:
- increased hydrostatic pressure of the blood
- Decreased plasma colloid oncotic pressure
- Impeded lymphatic flow
- Hormonal effects
Cytology:
-Basic cell types are small lymphocytes.
More RBC and WBC in cavities in case of heart disease.
In case of long term stasis, increase in neutrophils and macrophages.
58
What is ileus? What is the difference between prox. and dist. ileus?
ILEUS
spasm or foreign body block of intestines
cause local alterations – changes of circulation, electrolyte/acid-base/water balance
cause systemic alterations
proximal ileus – stomach, prox duodenum
distal ileus – jejunum & more distally
```
PROXIMAL ILEUS
vomit that contains HCl
early on metabolic alkalosis
later metabolic acidosis
dehydration
anaerobic glycolysis
```
```
DISTAL ILEUS
animal don’t eat/empty stomach
dehydration
anaerobic glycolysis
lactic acid formation
metabolic acidosis
alkaline vomit.
```
59
What causes increase urea concentration in the blood?
```
-PRERENAL
decreased perfusion (shock, dehydration)
increased nitrogen/protein intake
energy deficiency in rumen- ruminal microorganisms can not produce enough protein so catabolised protein (NH3) is absorbed
intestinal protein catabolism
intestinal or gastric bleeding
hemolysis
fever
liver function
Decreased blood perfusion in kidneys (Addisons)
-RENAL
reabsorption uremia (tubular obstruction)
retention uremia (glomeruli problem)
-POSTRENAL
inhibition of urine flow
reabsorption uremia (lower urinary tract
rupture, obstruction)
```
60
Describe Gmelin test.
C.c. HNO3 has to be carefully layered under urine in a test tube, and the width of the differently coloured layers at the meeting of the two fluid phases has to be evaluated. Differently coloured layers from the highest layer:
- condensed material on the surface of the glass tube - acidic urea
- yellow - urine itself
- white (opaque) – protein
- purple - indicane (indol-sulphate)
- green – biliverdin
- brown - urobilinogen (UBG)
- HNO3
61
ALT - what animal is specific, where is it found, causes of elevation in plasma
ALANINE AMINOTRANSFERASE
in cytoplasm of liver & red blood cells
better sensitivity & specificy than AST
converts alpha-keto-glutaric acid to L-glutamic acid & L-alanine to pyruvic acid
carnivore liver specific
normal ca >60 IU/l
Increase: liver cell damage
chronic active hepatitis
cirrhosis
bile duct obstruction
liver neoplasm
pancreatitis
septicaemia
copper storage disorder
drugs – barbiturates, glycocorticoids, salicylates
62
Why/how can the presence of bacteria be shown in urine?
Urine sediment analysis. For sediment evaluation a constant amount(!) of fresh (re-warmed if stored in refrigerator) urine sample should be centrifuged in a conical centrifuge tube gently (1000-2000 rpm for 5 min). The supernatant is decanted (one quick movement) and can be further used for the above biochemistry evaluations. The sediment is rehomogenised by the remaining droplet of urine in the apex of the tube. One droplet of resuspended sediment is poured on a glass slide, a coverslip is placed on the droplet – the sample prepared like this is called a native sample. Native samples are evaluated firs on low power (magnification 100x), then using magnification 400x. A smear can also be performed using a droplet of resuspended sediment, dried at room temperature and fixed and stained by routinely used haematological stains. The stained smear allows us to use 1000x (immersion oil) magnification to assess cell quality e.g. neoplastic cells and presence of bacteria – this is called cytological evaluation of urine sediment and is especially useful for the less experienced evaluator. We classify sediments to organic and inorganic components
63
Acute pancreatitis
damage of pancreas that causes outflow of enzymes from acinar cells to tissues.
Clinical signs_ Anorexia, depressions, severe abdominal pain, severe vomiting, exsiccosis, diarrhea, signs of heart failure, vasculitis, kidney failure, liver failure, DIC, abscess formation in pancreas.
Lab examinations:
-Haematological
Cytological
-Serum biochemical
-Microbiological
64
Urea plasma levels (when is it increased/decreased)
```
-PRERENAL
decreased perfusion (shock, dehydration)
increased nitrogen/protein intake
energy deficiency in rumen- ruminal microorganisms can not produce enough protein so catabolised protein (NH3) is absorbed
intestinal protein catabolism
intestinal or gastric bleeding
hemolysis
fever
liver function
Decreased blood perfusion in kidneys (Addisons)
-RENAL
reabsorption uremia (tubular obstruction)
retention uremia (glomeruli problem)
-POSTRENAL
inhibition of urine flow
reabsorption uremia (lower urinary tract
rapture, obstruction)
Decrease: liver failure
portosystemic shunt
polyuria-polydypsia
decreased protein intake
anabolic steroids
```
65
Pseudoproteinuria
proteins from lower urinary tract or genital tract
lower urinary tract infection
tumors
prostatic testicular inflammation
66
Test glomerular function
General blood parameters of kidney function (plasma or serum urea and creatinine level) show increased concentration, if 75% of nephrons are inactive.
-Blood urea (BUN=blood urea nitrogen) concentration in blood plasma: Urea colour test
Enzymatic urea method
-Creatinine concentration in blood: Jaffe method
Enzymatic method
-Plasma urea(mmol/L)/ plasma creatinine (μmol/L)
-Creatinine clearance
-Urinary TP cc
Urinary TP/ urinary creatinine ratio
67
Enzymuria (disease, causes of increased Br in plasma)
Tubular cells contain enzymes (ALKP, GGT). Their release into the urine is increased in case of acute/peracute tubular damage.
- ALKP, GGT
- Release into urinve increased in case of acute/peracute tubular damage
- ALKP U/l / creatinine umol/l :Normal 0.02
- GGT U/l creatinine umol/l Normal 0.01
68
Ammonia in blood and diseases
- In carnivores to diagnose severe decrease of liver function, portosystemic shunt
- In ruminants as consequence of ruminal alkalosis, severe systemic alkalosis due to
hyperammoniuaemia
- Horse, rabbit pathologic breakdown of ingesta in the colon or cecum or in case of
liver failure.
- Before taking blood samples for ammonia measurements, animal should starve for
24h. EDTA as anticoagulant.
Basis of ammonia measurement method
- Light refraction based method
- Ammonia tolerance test
69
Test tubular function
1. Specific gravity analysis of urine
2. Fractional electrolyte clearance % test
3. Analysis of enzymuria: high enz. level in conc. urine, ALKP, GGT
4. Urinary sediment analysis
5. Water deprivation test
6. Tubular clearance examination
70
What is AP, where is it found, what animal and when is increase seen proteinuria, causes.
Alkaline phosphatase
Location:
- Every cell membrane
- Produced by different organs (placenta, bones, liver, intestines, kidneys, tubular
epithelial cells)
- Only hepatic and bone ALKP appear in blood.
- Not liver specific in cats
- Increased activity in urine in case of tubular cell damage.
It has several isoenzymes.
Function:
not active enzyme since its optimum is pH 10.
Causes of decreased ALKP in blood:
- Severe cirrhosis
Causes of increased ALKP in blood:
Bone originated:
- Young dogs
- Pregnant animals
- Bone tumors
- Osteomyelitis
- Bone fractures
- Healing of fractures
Paraneoplastic processes:
- Lymphoid tumors
- Lung tumors
- Hepatic tumors
Liver originated:
- Cholestasis
- Bile acids
- Acute hepatic necrosis
- Liver cirrhosis
- Intra or extrahepatic biliary obstruction
- Chlangioheptaitis
- Hepatic lipidosis
- Barbiturates
- Salycilates
In connection with increased SIAP
- Hyperadrenocorticism
- Iatrogenous
- Endogenous
- Chronic stressad
71
Urine and pH changes.
ca – acidic (6.2-6.8)
herbivores – alkaline (7-8.5)
postprandial alkalization (kidney compensation)
food changes pH slightly within physiological range
test strip – only whole numbers
test paper
Alkaline: lower urinary tract bacterial infection
metabolic/respiratory alkalosis
proximal tubular acidosis (defect HCO 3 excretion)
alkalizing substances (eg. drug)
Acidic: metabolic/respiratory acidosis
distal tubular defect (decreased HCO 3 excretion)
fanconi syndrome
hyperkalaemia + metabolic alkalosis (paradox aciduria)
toxicosis
acidotic substances (eg. ammoniumchloride)
72
Laboratory findings in posthepatic jaundice (plasma, urine, faeces).
```
Plasma:
- Increased BrII, BrI
- coagulation parameters
- ALKP
- GGT
- bile acids
Urine:
- Increase Br
- No UGB produced
Feces:
- No stercobilin produced
- Clay colored feces
- acholic
```
73
What is AP, where is it found, what animal and when is increase seen.
Alkaline Phosphatase
Location:
- Every cell membrane
- Produced by different organs (placenta, bones, liver, intestines, kidneys, tubular
epithelial cells)
- Only hepatic and bone ALKP appear in blood.
- Not liver specific in cats
- Increased activity in urine in case of tubular cell damage.
It has several isoenzymes.
Function:
not active enzyme since its optimum is pH 10.
Causes of decreased ALKP in blood:
- Severe cirrhosis
Causes of increased ALKP in blood:
Bone originated:
- Young dogs
- Pregnant animals
- Bone tumors
- Osteomyelitis
- Bone fractures
- Healing of fractures
Paraneoplastic processes:
- Lymphoid tumors
- Lung tumors
- Hepatic tumors
Liver originated:
- Cholestasis
- Bile acids
- Acute hepatic necrosis
- Liver cirrhosis
- Intra or extrahepatic biliary obstruction
- Chlangioheptaitis
- Hepatic lipidosis
- Barbiturates
- Salycilates
In connection with increased SIAP
- Hyperadrenocorticism
- Iatrogenous
- Endogenous
- Chronic stress
74
Proteinuria, causes.
very low, measured by ultrasensitive protein measurement
proteinuria (mainly albuminuria) is an essential indicator for glomerular dysfunction
increased cc – proteinuria febrilis
proteinuria/day <20 mg/kg bw/day
test strip – not good, react mainly with albumin
sulfo test – denaturation of proteins, becomes whitish
gmellin (heller) test – white ring of denaturated proteins.
```
True proteinuria (proteinuria vera):
proteins from or through kidney
kidney disease
sudden protein catabolism (fever, hemolysis, exercise, starvation, onset
of glucocorticoid treatment)
```
```
False proteinuria (proteinuria spuria)
proteins from lower urinary tract or genital tract
lower urinary tract infection
tumors
prostatic testicular inflammation
```
75
What is AST, where is it found and when is it elevated in the blood plasma?
ASPARTATE AMINOTRANSFERASE
```
in mitochondria of liver, muscle, red blood cell
converts alpha-keto-glutaric acid to L-glutamic acid & L-aspartate to oxalic acetic acid
herbivore liver specific
normal dog >30 IU/l
Increase: hepatitis
fatty liver
neoplasm
hemolysis
muscular injury
training
myocarditis
herbivores: hepatopathy
ca: severe parenchymal damage
```
76
What causes elevated amylase in the blood?
```
acute pancreatitis
acute, subacute kidney failure
FIP & other immune-mediated diseases
lymphoma, myeloma
diabetes mellitus
ileus
gastric or intestinal perforation
parotitis
chronic enteritis
```
77
What is AP/ALP, where is it found and which disorders?
Alkaline Phosphatase
in cytoplasm, produced by different organs (biliary epithelial cells, hepatocytes, bone)
only hepatic (heat-atable) & bone (heat-labile) appears in blood
optimal pH 10
phosphotransferases – phosphate-esters are translocated to alcohol or phenol
hydroxyl group to another
normal ca/ru >200 IU/l (not used in cat because of its short half-life)
Increase: hepatitis
cholestasis
acute hepatic necrosis
cirrhosis
neoplasm
internal/external biliary obstruction
steroid induced hyperadrenocorticism (SIAP)
drugs – barbiturates, glycocorticoids, salicylates
78
What causes elevated lipase concentration in blood?
```
LIPASE
more specific than alpha-amylase
measured with kinetic spectrophotometry
excreted by kidneys (60-80%)
also produced in intestines
turbidimetric method
normal <150-300 IU/l
```
```
INCREASED LIPASE ACTIVITY
acute pancreatitis
acute, subacute kidney failure
ileus
gastric or intestinal perforation
chronic enteritis
```
79
Laboratory features of transudates? What causes transudates?
Causes:
* Increased vessel permeability due to:
- increased hydrostatic pressure of the blood
- Decreased plasma colloid oncotic pressure
- Impeded lymphatic flow
- Hormonal effects
Cytology:
-Basic cell types are small lymphocytes.
More RBC and WBC in cavities in case of heart disease.
In case of long term stasis, increase in neutrophils and macrophages
80
Causes for increase ALKP and consequences of distal ileum
```
Bone originated:
- Young dogs
- Pregnant animals
- Bone tumors
- Osteomyelitis
- Bone fractures
- Healing of fractures
Paraneoplastic processes:
```
- Lymphoid tumors
- Lung tumors
- Hepatic tumors
Liver originated:
- Cholestasis
- Bile acids
- Acute hepatic necrosis
- Liver cirrhosis
- Intra or extrahepatic biliary obstruction
- Chlangioheptaitis
- Hepatic lipidosis
- Barbiturates
- Salycilates
In connection with increased SIAP
- Hyperadrenocorticism
- Iatrogenous
- Endogenous
- Chronic stress
81
Tests for acute pancreatitis
- Haematological (polycythaemia (due to dehydration) degradation of red blood cells (membrane damage due to high activated enzyme level in the blood, schysiscytosis, acanthocytosis), anaemia (in chronic sever cases), leukocytosis (or leukopenia in case of abscess), neutrophilia (or -penia), left shift, leukemoid reaction)
- Serum biochemical (Determination of pancreatic enzymes in the plasma: alpha-amylase activity, lipase activity, phospholipase-a2 activity, trypsinogene - /trypsine/ concentration (RIA or ELISA methods), elastase concentration (RIA or ELISA methods), Best is: pancreas specific lipase (PSL) (ELISA method)
- Cytological
- Microbiological
82
How to differentiate hematuria from hemoglubinuria?
Haematuria is the presence of blood (intact red blood cells) in the urine. Haemoglobinuria and myoglobinuria is the presence of free dissolved haemoglobin and myoglobin, respectively in urine.
haematuria can be differentiated by centrifuging the sample, since red blood cells sediment, the supernatant clears up after centrifugation. In haemoglobinuria and myoglobinuria the urine supernatant remains reddish. While in haemoglobinuria usually concurrent reddish discolouration of plasma and anaemia are also observed, in myoglobinuria the plasma is clear and muscle damage indicator enzyme activities are elevated (CK, LDH)
83
Causes of Increased flotation in ruminal fluid
Very active fluid.
High fermentation, lots of gas produced.
-Causes of stable froth: frothy bloat, hoflund disease, treatment with acetylcholine for
ruminal atonia.
- smaller particles sink, larger particles float on bubbles of fermentation.
(-rapid sedimentation: inactive fluidlack of fermentative gases:ruminal acidosis,
anorexia, idigestible feed)
84
How to determine the reductibility of ruminal fluids
Redox potential – constant in rumen.
Dehydrogenation activity – color reagents.
Methylene blue reduction test – color reduced to colorless. Reducing ability of the
anaerobid rumen flora.
TTC – test – Reduced from colorless to color (red).
Nitrite reduction test – capability of ruminal bacteria to reduce the nitrites and nitrates.
85
Inrease and decrease of pH in rumen
```
Increase
-Rumen alkalosis
- Simple indigestion or reduced feed intake over more than 2 days
- Urea indigestion
- Putrefaction of ruminal content from prolonged rumen stasis
- Saliva contamination
Decrease:
- Rumen acidosis
- Grain overfeeding
- Chronic ruminal acidois
```
86
Distinguish Hemoglobinuria from Myoglobulinuria
creatine-kinase test
lactate dehydrogenase test
aspartate aminotransferase test
87
Bile acids- how to measure? when are they elevated in the blood?
Diaso method, HPLC, RIA, total bile acid - spectrophotometry
Elevated in blood, Br1:
- Excess production of Br 1 due to increased RBC destruction. (acute hemolysis,
absorption of hemoglobin following massive internal haemorrhage, or after big
hematoma formation, transfusion of stored blook, which contain many dyeing or dead
RBC’s)
- Decreased uptake of Br 1 from the blood by liver cells (impaired hepatic function,
acute hemolysis)
- Decreased rate of conjugation of Br 1 by the liver cells (impaired hepatic function)
Elevated in blood, Br2:
- A few days after severe acute intravascular hemolysis.
- Decreased excretion of Br 2 by the liver cells (impaired hepatic function)
- Obstruction of bile canaliculi within the liver, often due to inflammatory causing
swelling of cells, or connective tissue proliferation (impaired hepatic function)
- Obstruction of bile canaliculi due to blockage or compression of the bile duct
(rupture of the biliary vessels, duct or gall bladder)
88
Water deprivation test
used in case of pu/pd but you have to first rule out DM, pyometra, and kidney failure.
The animal also can't be pregnant, have known kidney or liver disease or be in a
general bad state, since it then would be dangerous to withhold water. The test is done
to confirm diabetes insepidus, and if it is ADH dependent (central) or not (peripheral),
after all other things have been ruled out.
Do not give water to the animal until you reach 5% bw loss.
Test used to evaluate causes of polyuria and polydipsia.
In hospitalized patients:
Need:
- bw, Ht, creatinin, urea, TP, osmolality.
Empty bladder with catheter. Take bw, and measure urine samples every hour.
Usually 6h needed to reach 5% decrease in bw. Then urine specific gravity should be
measured.
Check for diabetes insipidus:
Starv the animal, give only dry food. Empty urine bladder with catheter and take urine
sample every 3h. Measure specific gravity of the sample. If it reaches 1020-1030 g/l,
not necessary to continue- normal tubular function.
If not, give ADH – specific gravity should increase after 60min – central diabetes
insipidus proven, if not; renal diabetes insipidus can be suspected.
Home:
Do not give eater for 6-12h. Collect urine before and during this period. Measure
specific gravity, evaluate the result in the ame way as for hospitalized animals.
89
Ehrlich test
- Determine UBG
- Put some drops of ehrlich reagent into 2ml urine sample
Normal:
- Color: from above: mild reddish. From side: no color change
Abnormal:
- Color from above: intense red. From side: mild or intense red.
90
Ammonia tolerance test
After 24h starvation and pretreatment with neomycin, we take a basal blood sample
and give NH4Cl in 5% water solution. Then take blood samples after 30 and 45 min
after treatment. If liver function is normal: <120umol/l in dogs, <175 umol/l in cats.
91
Trypsin like immunoreactivity
determined by radioimmunoassay (RIA)
trypsinogen goes to duodenum & is activated by enterokinase to trypsin
normal 2.5-5 microg/l (in pancreatitis 15 x higher)
92
BT-PABA test
for exocrine pancreatic insufficiency
BT-PABA given orally
pancreatic chymotrypsin splits BT from PABA & PABA is absorbed
plasma or urine samples can be used
93
when to measure ammonia concentration
ca – severe decrease of liver function, portosystemic shunt
ru – ruminal alkalosis, decomposition of ruminal fluid, severe systemic alkalosis
eq + rabbit – pathologic breakdown of ingest in colon & cecum, liver failure
94
Protein synthesing ability of liver
measure TP, albumin, fibrinogen cc, hemostatic parameters, urea cc
albumin cc <20 g/l – expect edema
albumin cc <11 g/l – edema
95
Change in lipid metabolism due to impaired liver function
decreased total cholesterol cc (due to decreased esterification ability &
apolipoprotein synthesis)
increased FFA cc in energy requirement (due to decreased FFA utilization)
lipid accumulation in liver (due to decreased beta-oxidation & apolipoprotein
synthesis)
96
Hepatic enzymes
parenchymal: aspartate aminotransferase AST
alanine aminotransferase ALT
glutamate dehydrogenase GLDH
sorbite dehydrogenase SDH
cholestatic: ap-alkaline phosphatase ALKP
gamma glutamyl-transferase GGT
measured by kinetic spectrophotometry
not parameters for liver function but damage
97
Muscle enzymes to check by side of with AST
done to rule out muscle damage
lactate dehydrogenase LDH – long half-life, able to check old damage
creatine kinase CK – shorter half-life, muscle & brain isoenzymes
98
Clinical signs of kidney malfunction
change in body weight, condition, general status, fur skin
edema, ascites
appetite (smaller dogs have higher metabolism & therefore higher demand)
water intake – dog general 20-40 ml/kg bw/day
urine output – 20-30% of water intake
99
Creatinine clearance
for glomerular function
when glomerular filtration rate decreases by ¼ creatinine cc increases by 100-150%
C=urinary creatinine x urine volume in 24 hours
plasma creatinine
normal dog 2.4-5
100
Fractional electrolyte clearance
```
for tubular function
Na + <1
K + <24
Cl - <1.3
inorganic phosphate dog <39
```
101
Clinical signs and lab diagnose of acute kidney failure
oliguria, anuria, fatigueness, recumbence
Urinalysis: sediment – casts, tubular epithelial cells, neutrophils, RBCs
upper layer – protein ++/+++
glucose +/-
GGT & ALKP increase
increase of specific gravity
```
Blood test:
-increase
Ht , K+ , urea
creatinine
inorganic phosphate
TP
amylase
lipase
plasma osmolality
-Increase/normal
Na+ , Ca2+
-decrease
pH
, RBC damage
```
102
Urine smell
urea – normal
| ketoacidosis, ammonia (urease + bacteria), sweet/rotting (pus), B1, penicillin
103
Pus in urine (pyuria)
```
microscope – sediment evaluation
donne test – reagent makes sample more viscous if pus is present
Causes: kidney pelvis inflammation
cystitis
inflammation of penis/vagina
endometritis
prostatitis
```
104
Glucose concentration in urine
```
test strip (GOD-POD)
10 mmol/l
Glycosuria glycaemia
kidney problems
(also check blood parameters)
```
105
Sediment evaluation
unstained under microscope first then stain
Organic sediment: RBCs, WBCs (small amount accepted)
epithelia cells (small amount accepted)
tubular epithels
cylinder, casts (from kidney, only hyaline acceptable)
neoplasm
bacteria/fungi/parasites
Inorganic sediment: struvite crystal – Mg+NH 4 +P, like high pH, dissolve pH 6)
Ca-phosphate stones
Ca-carbonate stones
ammonium-urate crystals – high pH, Dalmatians
Ca-oxalate stones
type 1 – toxicosis
type 2 – low pH
ureate crystals – low pH
tyrosine crystals – low pH, congenital or liver defect
creatine crystals – low pH, congenital
106
List sampling and analysis CSF
In case of appearance of Central Nervous signs take CSF samples. Two spaces used: Occipital zona, Lumbosacral zone.Lumbosacral contains more proteins and cells. Samples must be taken to Na(K)2EDTA containing tubes.
1) Physical examination -colour: (red: fresh bleeding, yellow: bleeding in the past, opaque: highly inflammatory
- Coagulation(coagulates in highly inflammatory processes)
2) Preparation of sample: native samples centrifuged then upper layer is aspirated by pipette. sediment is resuspended. suspension must be pipetted onto a glass slide, and must be incubated at room temp. airdry, stain. Major cell types are small lymphocytes, macrophages and some epithelial cells.
3) Protein content examination: carbolic acid: +,++,+++ in case of CNS inflammation, there is increased globulin cc - smokey grey colour occurs, as a result of globulin coagulation after the administration of reagent.
4) Glucose cc examination: cc of glucose in CSF is 60-80% of the plasma glucose cc in case of inflammation glucose cc decreases.
5) Lactate cc: normal value in CSF <2.2mmol/L , increased lactate cc: bacterial meningitis, subarachnoidal bleeding
6) Enzyme activity examinations: AST,CK-B (creatinine kinase), LDH, the activity of these enzymes increases as a result of CNS injury
107
Body cavity fluids and cause of accumulation
Increased permeability of vessels due to the underlining non inflammatory causes:
- increase of hydrostatic pressure of blood: right sided heart failure, blockage of blood vessel
- decrease of plasma colloid oncotic pressure: decrease of plasma albumin-EPI, liver failure, utilisation, loss
- impeded lymphatic flow
- hormonal effects (aldosterone, ADH)
```
Increased permeability of vessels due to inflammatory causes:
-Bacterial toxins
-viral infections
parasitic toxins
-inflammatory mediators
```
108
explain chloride in ruminal fluid
In healthy ruminant the ruminal chloride concentration is low (15-20 mmol/l). Its main source is the diet and the saliva which passes into the rumen. In case of gastric torsion or in other cases of pylorus obstruction the hydrogen chloride will pass into the rumen (reflux phenomenon) and can increase chloride up to 30-100 mmol/l.
109
everything important about struvite crystals
(coffin-like) (tripplephosphate, magnesium-ammonium-phosphate): presence of urease positive bacteria in UTI (urinary tract infection).
110
important about calcium oxolate crystals formation in urine
monohydrate (needle-like) (e.g. ethylene glycol poisoning, consumption of toxic plants in cats e.g. Dieffenbachia, Philodendron), dihydrate (envelope-like) (e.g. long term feeding of high-oxalate diet: fruits, some vegetables)
111
increase and decrease bile acid production
Causes of increased bile acid level in the blood:
liver injury, hepatic cell damage - increased outflow of bile acids from the damaged hepatocytes to the blood, bile duct obstruction or bile endothelial cell damage - decreased secretion of bile acids to the bile, increased outflow to the plasma instead, decrease in liver function, therefore decreased uptake of the absorbed bile acids (note: increased urobilinogen level !) biliary stasis (cholangiohepatitis cirrhosis, hepatic or pancreatic neoplasm, pancreatitis) portosystemic shunt (absorbed bile acids bypass liver tissue)
Causes of decreased bile acid level in the blood:
decreased absorption from the intestines - intestinal wall damage or surgical removal of the ileum or lymphangiectasia severe liver cirrhosis (or other cause of severe liver cell damage) - decreased synthesis of bile acids
112
Different body cavity fluids
- Transudate (hydro-)
- Exudate (pyo-)
- Modified transudate
- Blood
- Chylus (lymph)
113
Body cavity fluid analysis
organoleptic examination Rivalta-test analysis of total and nucleated cell count (by using automatic cell counters or haemocytometer) centrifuging (2000 rounds/min. for 5-10 minutes) by centrifuge or by cytospin separating upper layer for further biochemical analysis separation of sediment for cytological analysis method 1) After aspirating upper layer 100-200 µl must be remained in the tube, then the sediment must be resuspended by this fluid and aspirating 50-100 µl and flushing it carefully onto a glass slide then smear must be performed. This method is used for CSF, bronchoalveolar lavage, other few cell containing fluids. method 2) After centrifuging the sample 50-100 µl sediment can be directly aspirated by pipette. Then the aspirate is flushed onto the slide and smeared. If the fluid is bloody (contaminated by lots of red blood cells) sample must be aspirated from the "buffy coat" (nucleated cell) layer. (This method is used for blood containing or many cells containing fluids.
114
Parameters determined from BCF
- outlook physical parameters (colour, odour, consistency)
- Rivalta-test
- coagulation ability
- specific gravity
- pH
- red blood cell count
- nucleated cell count
- total protein concentration
- albumin/globulin ratio
- creatinine, urea concentration
- alpha-amylase, lipase activity
- LDH activity
- triglycerol, cholesterol concentration
- cytological analysis
