MT 2

Question 1

What faeces tests are useful for EPI determination/diagnosis?

Answer 1

1. Faecal elastase test (by ELISA method)
   - Determine whether the faecal sample contains elastase or not. In case of EPI; no elastase
2. Examining undigested particles in faecal sample.
   Three faecal smears should be prepared.
   a) One smear is stained with Giemsa
   b) Second with Lugol-solution
   c) Third with Sudan III.-solution.
   Results:
   a) Giemsa: undigested striated muscle fibers (from meat)
   b) Lugol: undigested starch particles as bluish patches
   c) Sudan III: undigested lipid particles as red droplets.
   If EPI is suspected to be complicated with severe bacterial enteritis, Gram-staining of one faecal smear can help us choosing the right antibiotic before bacterial culture of the faeces is ready (it takes some days, but severe enteritis should be treated immediately).

Question 2

How can urine specific gravity be measured? When is the urine hypo-, normo- and hyperstenuric?

Answer 2

• Measured by:
  1. Urinometer: Most accurate, easy and cheap. Urine poured into glass cylinder, urinometer placed inside. Requires a lot of urine.
  2. Refractometer: Easy and one drop enough. Not reliable when urin is not transparent.
  3. Test strip: not very useful for SG meas. in animals.
  a) Hyposthenuria: <1,008.
• Physiol. if incr. water intake.
• Hyperadrenocorticism
• Decreased ADH-prod. (CDI)
• Resistance to ADH (PDI or NDI)
• Renal tubular damage and PP.
• Also hypoadrenocorticism, liver disease and prolonged fluid therapy - due to medullary washout.
  b) Isosthenuria: 1.008-1.012
• Physiol. if incr. water intake
• Severe tubular damage
• Medullary washout
• CDI, NDI or PP
  c) Hypersthenuria: >1.012 (normal urine)
• Decreased water intake
• Substantial water loss (vomiting, diarrhoea, excessive exercise: panting-dog, sweating-horse)
• Acute kidney failure (oliguria).
• May also be incr. in DM.

Question 3

What is ALT? Causes of increased activity?

Answer 3

Alanine-aminotranferase
-Liver cell (parenchymal) enzyme
-Location: liver cells, RBCs in cytoplasm
-Liver specific in Ca, not herbivores
-Determination: piruvic acid (converted from L-alanine by ALT) is converted to lactic acid by LDH in the reagent -> discoloration of a chromophor.
Causes of increased activity: 
-liver cell damage (esp Ca)
-chronic active hepatitis
-cholangiohepatitis
-virus hepatitis (human)
-hepatic lipidosis
-cirrhosis
-bile duct obstruction,
-liver neoplasm, 
-pancreatitis, 
-septicaemia, 
-some drugs
-copper storage disorder: Doberman pincher, West highland white and Bedlingtone terrier.

Question 4

Proximal and distal ileus

Answer 4

Distal ileus: (jejunum and more distal parts):
-Metabolic acidosis due to dehydration, anaerobic GL and LA form.
-Animals do not eat, stomach is empty
-Vomit contains small intestinal fluid (because of reflux - miserere) w. high pH
Proximal ileus (stomach, prox. duodenal part):
-Metabolic alkalosis in beginning, then metabolic acidosis
-Irritant (foreign body) is in/near the stomach, and there is obvious gas and fluid accum. in stomach -> tensor receptors in gastric wall are activated causing incr. HCl prod.
-Vomit contains HCl -> metabolic alkalosis.
-As the process becomes more severe, dehydration and anaerobic GL develops (lactic acid form) -> metabolic acidosis
-Clinical signs (severe vomiting, dehydration, anorexia, depression, etc.) are more prominent, and the general state of the animal is worsening more quickly.

Question 5

List and group the liver enzymes. What information is gained about the liver in case of enzyme deviations?

Answer 5

LIVER CELL (PARENCHYMAL) ENZYMES:
Incr. of cytoplasmic enzymes: mild liver cell damage
Incr. of mitoch. enzymes: more severe liver cell damage
- AST (Aspartate-aminotransferase) (mitochondria)
- ALT (Alanine-aminotranferase) (cytosol)
- GLDH (glutamate-dehydrogenase) (mitoch.)
BILE DUCT OBSTRUCTION ENZYMES:
- ALKP (AP-Alkaline-phosphatase) (every cell membr.)
- GGT (gamma glutamyl-transferase)
OTHER LIVER SPECIFIC ENZYMES:
(parenchymal enzymes)
Increase: liver cell damage
- OCT (ornityl-carbamyl-tranferase,
- Ar (arginase)
- SDH (sorbite dehydrogenase)

Question 6

What is AST, where is it found? When is it increased? In what species is it useful?

Answer 6

-AST (Aspartate-aminotransferase)
-Liver cell (parenchymal) enzyme
-Location: mitoch. of liver cells, muscles (incl. heart), RBCs
-Liver specific in herb.
Causes of increased activity:
-Muscle cells: intensive exercise, training, muscle necrosis, myositis, muscle injury (im. inj.), myocarditis, muscle neoplasm.
-Liver cells: ethanol consumption (Hu), hepatopathy (Herb.), severe parenchymal damage (Ca)
-from RBCs: haemolysis
Species it is useful: all (not routinely in dogs+cats)

Question 7

WHAT TO MEASURE of liver enzymes?

Answer 7

Dog: ALT, (AST, GLDH), ALKP, GGT
Cat: ALT, (AST, GLDH), GGT, (ALKP in acute processes)
Ruminants: AST, GLDH, (GGT)
Horse: AST, GGT, (Arg)
Swine: AST, GGT, ALKP, OCT, SDH

Question 8

What is GGT? Causes of increased activity?

Answer 8

GGT (gamma glutamyl-transferase)

• Bile duct obstruction enzyme
• Location: prod. by different organs (kidney, pancreas, intestines and liver)
• Endothelial cells of bile duct conc. it.
• GGT of liver origin appears in blood.
• Liver specific in horses (and cats).
• Increased: biliary stasis, cholangiohepatitis, cirrhosis, neoplasm (hepatic, pancreatic), hepatic lipidosis, barbiturates, ethanol (human)
• Measured in all animals (not routinely in Ru)

Question 9

Detecting protein from urine?

Answer 9

1. Test strip: brome-phenol-blue (semi-quant. in-house test). Most sensitive to albumin, not Bence-Jones proteins. Physiological result: negative. Not specific,
2. Sulphosalicylic acid test: (semi-quant. in-house test, by side of animal) coagulation: higher prot. cc. -> more opaque. Not specific.
3. Heller/Gmelin test: HNO3 (rough inhouse test). Show bile-pigment metabolites and proteins the urine. Semi-quantitative scale.
4. Spectrophotometric method: objective and quantitiative. Can measure TP content. Not specific.
5. Urine protein : creatinine ratio (UPC): gives info about the severity of proteinuria if there is no sign of inflam. or macrohaematuria.
6. Specific methods: Alb and/or glob can be evaluated using spectroscopy, (immune)electrophoresis, western-blot etc.
7. Determination of Bence-Jones proteins: (heat labile) heat urine to 40-60o -> the proteins are coag., but 80-100o -> dissolved (unlike other proteins). Precise and quantitative detection using urine electrophoresis or HPLC

Question 10

List the laboratory tests which allow us to evaluate the impairment of glomerulus-function.

Answer 10

1) Urea-colour test
NH3 in water forms NH4+. NH4+ forms green colour in alkalytic pH with Na-hypochloride and salycilic acid. Measured spectrophotometrically on 600 nm wave length.
(End point reaction, linear till 24.97 mmol/l urea cc.)
2) Enzymatic urea method: Change of NADH + H+ -> 2 NAD+ causing light emission change, measurable on 340 nm wave length. After 30 seconds of preincubation, the extinction change is measured within 1 min.
(Kinetic reaction, linear till 65 mmol/l urea cc.)
- Normal value: 8-10 mmol/l

Question 11

Causes of increased blood urea concentration?

Answer 11

1. ) Prerenal factors:
   - Increased Nitrogen (protein) intake
   - In ruminants: poor Energy status in the rumen.
   - Increased Intestinal protein catabolism
   - Intestinal or gastric bleeding
   - Haemolysis
   - Decreased blood perfusion of the kidneys
2. ) Renal factors:
   - Kidney function, decreased amount of functionally active nephrons, decreased tubular function
3. ) Postrenal factors:
   - Inhibition of urine flow through the lower urinary tract
   - Rupture of the kidneys, urether, urinary bladder, or urethra: “uroperitoneum”

Question 12

Causes of decreased blood urea concentration?

Answer 12

• Impaired liver function: decr. urea synthesis in liver cells from NH3, leading to incr. NH3 level.
• Haemodilution (hyperhydration)
• Decreased protein intake (starvation, anorexia)

Question 13

Causes of increased blood creatinine concentration?

Answer 13

(normal value : 50-200 µmol/l)

• inflam. of muscles (myocarditis, rhabdomyolysis)
• rhabdomyosarcoma
• muscle trauma
• increased meat intake

Question 14

Causes of decreased blood creatinine concentration?

Answer 14

(normal value : 50-200 µmol/l)

• cachexia
• chronic muscle atrophy

Question 15

What is proteinuria? General causes? Non renal causes?

Answer 15

-Presence of abnormal quantities of protein in the urine.
-Caused by glomerulonephropathy, tubular transport defect, inflammation, infection or marked haematuria within the urogenital tract.
Pre-renal (non-renal) causes of proteinuria:
(1) physiologic or benign: in neonates below 40 hours of age, after strenuous exercise/heat or cold exposure/stress.
(2) pathologic: incr. protein catabolism: in fever, seizures, incr. BP, dysproteinaemias, haemoglobinuria, severe intravascular haemolysis and severe muscle injury.

Question 16

What info is provided by the urine TP/creatinine ratio? Where can it be used?

Answer 16

-Provides valuable info about the severity of proteinuria if the evaluation of the sediment does not show evidence of inflammation or macrohaematuria. Calculation of UPC allows correction for variation in urine SG, due to the fact that creatinine excretion is relatively stable and after
excretion it is not reabsorbed in the tubules.
-Interpretation: normal: <0.5; grey zone, equivocal result: 0.5-1.0; proteinuria: >1.0; significant proteinuria: >2.0.
Proteinuria is indicative of glomerular disease (glomerulonephritis, PLN, amyloidosis).

Question 17

Water deprivation test - What is the goal of this test, its method and interpretation.

Answer 17

• Goal: to assess concentrating ability of tubules, to differentiate bw CDI, NDI and PP.
• Principle: artificial induction of 5% dehydration in controlled environment and repeated meas. of urine SG.
• Indications: persistent PU/PD, more than one
  urine SG meas. result in the range of hyposthenuria.
• Procedure:
  A) Partial water restriction for 2-3 days prior to test.
  B) Bladder emptied by catheterisation, urine SG and BW recorded. Water and food withheld.
  C) In 1-2 h. intervals BW monitored and bladder emptied (urine SG meas.) by catheterisation.
  D) Procedure continued until BW reache 5% decr. or urine SG>1.025 or animal becomes depressed/azotaemic.
  Interpretation:
  a) in case of PP urine SG will become > 1.025.
  b) In case of CDI or NDI urine SG will be ≤1.010
  c) Values bw. 1.010-1.020 are equivocal and may suggest suboptimal cc. ability in tubules.
  (differen. bw CDI and NDI: desmopressin response test)
• Contraindications: severe endocrine disturbance, dehydration, azotaemia, uraemia, liver dysfunction, pregnancy, lactation, growth and inflam. disease.

Question 18

What is the goal of Enzymuria Evaluation? How is it performed/tested?

Answer 18

Tubular cells contain enzymes (ALKP, GGT). Their release into the urine is incr. in case of acute/peracute tubular damage. The values must be referred to the creatinine levels in order to exclude the misdiagnosis caused by the high enzyme level in concentrated urine.
- Alkaline phosphatase (U/l) / Creatinine (µmol/l)
normal value: 0.02
- Gamma-glutamyl transferase (U/l) / Creatinine (µmol/l)
normal value: 0.01

Question 19

Causes of abnormal urine pH (increased, decreased).

Answer 19

Increased:
1. Feeding in Ca: transient postprandial alkalization of urine.
2. UTI caused by urease-prod. bacteria like Proteus spp. and Staphylococcus spp.
3. Metabolic and respiratory alkalosis
4. Alkalizing substances, overload of bicarbonate- or lactate containing infusion
5. Long storage time: causes urea decomposition
to ammonia - eg. urinary tract obstruction
Decreased:
1. Metabolic and respiratory acidosis
2. Vomiting (paradoxical aciduria)
3. Hypokalaemia
4. Treatment with acidifying drugs (e.g. ammonium chloride).
5. Distalis renalis tubularis acidosis
6. Abomasal displacement
7. Toxicosis with acidifying substances (ethylene glycol, metaldehyde)

Question 20

What is the goal of the electrolyte clearance, evaluation? How is it performed?

Answer 20

• Goal: Analysis of kidney tubular function (basic test)
• Generally in case of tubular damage, Na+ reabs. decr. (increased urinary sodium cc., and hyponatreamia), and usually K+ reabs. incr. (decr. urinary potassium cc., hyperkalaemia).
• Fractional electrolyte clearance %: (urinary Na+/plasma Na+) / (urinary creatinine/plasma creatinine) x 100

Question 21

What can be seen in the physiological urine sediment? List the pathological abnormalities in the urine sediment.

Answer 21

ORGANIC sediments:
-RBCs and WBCs. Normal: <5 /hpf. Abnor: haematuria.
- Cells from lower urogenital tract: urothelium cells,
renal tubular cells, prostatic acinar, ductal epithelial cells, squamous cells from penis or vagina, sperm cells, tumour cells. Normal: 0-2/hpf. Abnor: inflam. or infection of upper/lower urinary tract, genital tract inflam., neoplasm.
-Viral inclusion bodies
-Microbes: bacteria, parasites, fungi
-Mucin, fat droplets (normal in cats), starch and pollen grains - contaminants.
-Casts: Abnormal: incr. number of casts
INORGANIC sediments:
-Large number of crystals and persistent crystalluria may lead to stone formation.
-Mostly in alkaline urine: struvite, calcium-carbonate, amorphous phosphate, ammonium-ureate/biurate
Mostly in acidic urine: calcium oxalate, uric acid, cystine, tyrosine, leucine, bilirubin crystals, sulphonamides

Question 22

How can the presence of blood or haemoglobin be shown in the urine? How can the two be distinguished from each other?

Answer 22

-Benzidine test, urinary test-strip or microscopic evaluation
1. Benzidine test: Qualitative quick-test to show the presence of blood, haemoglobin or myoglobin. Use benzidine powder, H2O2 and acetic acid.
2. Urine test strip: (reagents of benzidine)
-Speckled appearance: haematuria
-Diffuse colour: haemoglobin- or myoglobinuria.
How to distinguish the two from each other:
1. Urine sediment analysis can diff. haematuria from haemoglobin- and myoglobinuria.
2. Centrifucation: Haematuria diff. from the other, since RBCs 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.

Question 23

How can the presence of pus be shown in the urine? What are the causes?

Answer 23

-Pus is the accumulation of neutrophil granulocytes, some tissue cells, and microbes.
-Can be shown by Donne-test, microscopic evaluation of the sediment or using urine test-strip.
Causes:
-Physiological in horses
-Kidney pelvis inflammation
-Cystitis (inflam. in the urine bladder)
-Inflam. in genital tract, e.g. balanitis (inflam. of the glans penis) or prostatitis in males or vaginitis/endometritis in females.

Question 24

What is TLI? Describe its usefulness in the diagnosis of EPI.

Answer 24

• Trypsine like immunoreactivity
• EPI if; TLI conc. is less than 2,5 µg/l
• Species specific parameter, which can be determined by RIA-method (radioimmunassay).
• Feature: antibodies are produced against one part of trypsinogen. ABs marked by radioisotopes are bound to trypsinogen of the sample. The marked AB-trypsinogen cause incr. radioactivity that can be measured by specific analyser.
• ELISA methods can also determine TLI.

Question 25

Describe the Gmelin-Test.

Answer 25

- Show bile-pigment metabolites and protein content of the urine. - Reagent used: cc. HNO3 - Bilirubin derivates, presence and the thickness of the opaque zone above biliverdin and below the clear urine. This opaque zone is formed by coagulation of proteins

Question 26

List the most important findings in the blood and urine for prehepatic icterus.

Answer 26

(haemolytic crisis) - Incr. Br 1 in serum (brownish colour) - Incr. stercobilin in stool (darker colour) - Incr. urinary UBG and quantity of metabolized bile pigments due to erythrocyte haemolysis.

Question 27

List the most important findings in the blood and urine for hepatic icterus.

Answer 27

- Incr. levels of Br 2 in serum - Lesser amount of Br 1 in serum, due to a decr. uptake of the pigment (still incr.) - Presence of Br 2 and incr. amounts of UBG in urine. - Hypocholic

Question 28

List the most important findings in the blood and urine for posthepatic icterus.

Answer 28

(bile in liver fails to reach intestines) - Incr. Br 2 in serum (regurgitation to the serum) - Biliprotein in serum (during cholestasis) - Incr. Br 2 in urine - No urinary UBG - No faecal stercobilin -> acholic

Question 29

What method is used in blood ammonia concentration measurement?

Answer 29

1. Simple measurements of NH3 cc.: a) Standard method: NH3 with alpha-ketoglutaric acid, NADH+H+, and GLDH produces glutamic acid and NAD+. Measured spectrophotometrically. Not widely used. b) Light-refraction based method: used more frequently (ammonia-checker). 2. Ammonia tolerance test: when there is no alteration of basal NH3-cc. values and there is strong suspect of portosystemic shunt. -24h starvation and pretreatment with neomycin -Take basal blood sample -Give NH4Cl in 5%-water solution -Blood samples taken 30/45min after treatment. -If liver function is normal: ammonia: <120 μmol/l in dogs, and <175 μmol/l in cats.

Question 30

In which diseases is blood ammonia concentration increased?

Answer 30

Causes of increased NH3 cc. in the blood, or positive ammonia tolerance test results: - Impaired liver function - decr. prod. of urea in case of peracute liver failure, liver cirrhosis, or neoplasia, portosystemic shunt, hepatic lipidosis, lipid mobilisation disease - Ruminal alkalosis or ammonia toxicosis - due to absolute or relative protein overload, or the intake of rotten feed. - Intestinal overgrowth of ammonia producing bacteria - in ruminants, horses, rabbits, swine or carnivores - Congenital enzymopathies - decreased activity of i.e. OCT.

Question 31

What are the causes of proteinuria vera and proteinuria spuria?

Answer 31

A) Proteinuria vera - Real proteinuria i.e. nephrogenic: (1) when intermediate molecular weight proteins appear in the urine: milder glomerular damage, specific tubulointerstitial lesions or infectious diseases. (2) non-selective proteinuria: high molecular weight proteins appear in the urine. Caused by glomerular dysfunction and in some cases severe tubular damage. B) Proteinuria spuria - Pseudo-proteinuria: originate from the lower urinary or genital tract. (1) physiological: after parturition in female animals, or in males due to high amount of sperm cells or mucous from praeputium. Normal in horses; urine contains highly viscous mucous (2) pathological: lower UTI, urolithiasis, prostatic or testicular inflam., hypertrophy or tumour of the prostate gland, vaginal tumour, etc.

Question 32

Rivalta test- goal, how to perform, interpretation

Answer 32

- GOAL: Determine body cavity fluid: exudate or transudate - METHOD: 1. Prepare 3% acetic-acid solution. 2. One-two drops of native (not centrifuged) samples must be dripped into the solution. - INTERPRETATION: - If coagulation = exudate: due to coag. of labile proteins, as weak acids can coag. these. - If no coagulation, but dissolved = transudate: due to that stabile proteins (eg. alb) does not coag. in weak acids. - Honey-like = much glob

Question 33

Causes of increased alpha-amylase activity?

Answer 33

- Acute and chronic kidney failure, especially acute - Duodenal perforation - Gall bladder rupture - Rupture of an abscess developed by pancreatitis. - Urine bladder rupture - Esophageal rupture

Question 34

EPI. What is it, how to test it? (Laboratory diagnosis of EPI)

Answer 34

-Exocrine pancreatic insufficienty -Developed due to chronic necrotic or atrophic damage to the pancreas, or sometimes it is an inherited disease. -Feauture: decr. prod. of digestive enzymes, or the enzymes do not get out from the organ into intestines -Faeces: very bad small, color can be very light grey. -vitamin deficiencies->skin and fur problems, incr. hair loss, unkempt hair coat, and sometimes mild anaemia -IDDM sometimes follows EPI How to test: -TLI-concentration: EPI if; TLI conc. is less than 2,5 µg/l -BT-PABA test -Dyed agar-gel digestion and Schwachmann-filmtest -Lipid absorption test -Faecal elastase test -Examining undigested particles in faecal sample

Question 35

Biochemical parameters for examination of free fluids.

Answer 35

1. Albumin/globulin ratio: -diag. imp. in cat: if more than 50% of TP are globulins - indicates FIP infection 2. Creatinine, urea cc.: -If values are higher in peritoneal fluid than in plasma, it indicates: rupture of urine bladder, kidney pelvis, or one of the urethers. 3. Alpha-amylase, lipase activity: -If values are higher in peritoneal fluid than plasma, it indicates: duodenal perforation, rupture of gall bladder or of an abscess developed by pancreatitis. -Elevation: in case of urine bladder rupture -If the sample is derived from pleural cavity and is highly inflammatory, and there is high alpha-amylase activity, it indicates: esophageal rupture. 4. LDH activity: -Increase in body cavity fluid, or higher in fluid than in plasma, it indicates: fluid of neoplastic origin. -In case of peritonitis, or pleuritis as neutrophils also contain LDH, so the activity can be high in the fluid 4. Triglycerol, cholesterol cc.: evaluate whether the fluid is lymphatic or not

Question 36

What is the lipid absorption test, and which disorders can it confirm or eliminate?

Answer 36

-Determines 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 cc. rises to twice as the normal value. -Method: Before testing, animals should starve for 24 hours: test starts with blood sampling (0 min.) for basal TG value, then 3ml/kg bw corn oil is given perorally. Blood sampling at 1st, 2nd, 3rd, 4th and 5th. -Result: Blood should be obviously lipaemic, and TG cc. should show a minimal 2 fold rise from normal (basal) value. If there is no such change: repeat test by giving predigested corn oil. Give same dose and check lipaemia in plasma every hour. -Final result: if incr. TG cc. and lipaemia, we can suspect that the original problem is EPI. If no change in TG cc. and no lipaemia, we can suspect intestinal absorption defect.

Question 37

Laboratory diagnosis of pancreatitis

Answer 37

- Clinical signs: anorexia, depression, severe abdominal pain, severe vomiting, exsiccosis signs of heart failure, vasculitis, kidney failure, liver failure, dyspnoe, paralytic ileus, septicaemia, DIC, multi organ failure, abscess formation in the pancreas and sometimes diarrhea / anaemia / icterus / peritonitis. - Lab. examinations: haematological, serum biochemical, cytological and microbiological analysis. - Haematological analysis: * polycythaemia * degradation of RBCs * anaemia (in chronic sever cases) * leukocytosis (or leukopenia in case of abscess) * neutrophilia (or -penia), left shift * leukemoid reaction - Serum (plasma) biochemistry: * incr. pancreatic enzymes * incr. glucose cc., as insulin prod. can be decr. by the organ damage, and DM can develop.

Question 38

What is ALKP? Causes of increased ALKP in the blood?

Answer 38

-ALKP (AP-Alkaline-phosphatase) -A bile duct obstruction enzyme -Location: every cell membrane, prod. by different organs (placenta, bones, liver, bile duct, intestines, kidney) - conversion in bile endothelial cells. -Only hepatic and bone ALKP appears in blood. -Not liver specific in cats. -Tubular cell damage causes incr. activity of ALKP in urine. -Has different isoenzymes (liver and bone origin) -Function: not active enzyme as it’s pH optim.=10. Phosphotransferases. Causes of increased activity: -bone origin: young dogs, pregnant animals, bone tumours, osteomyelitis, bone fractures, healing of fractures, -paraneoplastic proc. (lymphoid, lung, and hepatic tumours) -liver originated: liver cirrhosis!, cholestasis, bile acids, acute hepatic necrosis, intra- or extrahepatic biliary obstruction, cholangiohepatitis, hepatic lipidosis, barbiturates, salicilates -in connection with incr. SIAP synt.: hyperadrenocorticism, iatrogenous or endogenous (Cushing disease), chronic stress

Question 39

What is icterus? What can be the causes of increased plasma bilirubin concentration?

Answer 39

Jaundice. Yellowish/greenish pigmentation of the skin and whites of the eye, due to high Br levels. 3 types of jaundices/major causes of incr. plasma Br cc.: -Prehepatic: haemolysis -Hepatic: hepatocullular - liver cell damage and damage of the intrahepatic structure that leads to leakage bw. sinusoids and biliary vessels -Posthepatic: cholestasis, obstruction of bile vessels and/or bile ducts

Question 40

List the laboratory tests which allow us to evaluate the impairment of tubular-function (Tubular dysfunction test.)

Answer 40

1. Basic tests: - Specific gravity analysis of urine - Water deprivation test - Urine osmolality at 5% dehydration - Fractional electrolyte clearance % 2. Analysis of enzymuria: - Alkaline phosphatise (U/l) / Creatinine (μmol/l) - Gamma-glutamyl transferase (U/l) / Creatinine (μmol/l) 3. Urinary sediment analysis 4. Water deprivation test: - Tubular function test - Differentiate between: CDI, PDI, PP 5. Tubular clearance examinations: eg. para-amino-hyppuric acid, diodrast, phenolred clearance

Question 41

Bile acids. How to measure them, and what causes increased/decreased levels in the blood?

Answer 41

-Methods: HPLC, RIA or total bile acids (TBA) -spectrophotometric method. Causes of incr. levels in blood: - liver injury, hepatic cell damage - bile duct obstruction or bile endothelial cell damage - decr. liver function (therefore decr. uptake of them) - biliary stasis (cholangiohepatitis, cirrhosis, hepatic or pancreatic neoplasm, pancreatitis) - portosystemic shunt Causes of decreased levels in blood: - decr. abs. from intestines - intestinal wall damage - surgical removal of ileum - lymphangiectasia - severe liver cirrhosis (or other severe liver cell damage)

Question 42

Causes of development of transudates and cytological picture

Answer 42

Causes of the development: -Increased vessel permeability due to the underlining causes -increase of hydrostatic pressure of blood -decrease of plasma colloid oncotic pressure -impeded lymphatic flow -hormonal effects Cytology: -In case of low cellularity (esp. in liver failure), basic cell types are small lymphocytes. -In case of heart disease more blood cells (red and white) are entering into the cavities. -More macrophages and a few reactive mesothelial cells are seen. -Due to long term stasis secondary inflam. process develops that leads to incr. neutrophils and macrophages.

Question 43

Causes of development of exudates and cytological picture

Answer 43

Causes of the development: -Incr. permeability of vessels due to inflam. causes: bacterial, viral, parasitic, inflam. mediators -Incr. migration of phagocites -Incr. proliferation of mesothelial cells -Incr. production of inflammatory proteins Major causes of septic exudates: -Trauma of pleural, peritoneal, pericardial wall -Proliferation and overgrow of bacteria through walls of organs -Internal perforation of organs -Haematogenous or lymphatic spreading of bacteria Cytology: -Many neutrophils, macrophagses, and reactive mesothelial cells are seen. -Cells might show nuclear degeneration -Bacteria (rods and cocci) often visible generally IC phagocytosed form. -If bacteria appear out of the cells: indicator of the worsening (end stage) process. -If there are bacteria out of the cells only: indicator for bacterial contamination.

Question 44

How can the presence of bacteria be shown in urine?

Answer 44

- Increased nitrite cc. in the urine (nitrates are reduced to nitrites by bacteria) - urine test-strips (α-naphthylamine -Griess-Ilosvay's reagent). - Cytological evaluation of urine sediement analysis -> stained smear in microscope: organic sediment and inorganic (struvites: presence of urease + bact. in UTI)

Question 45

What causes elevated lipase cc. in blood?

Answer 45

(Normal value < 800 IU/l) - Chronic and acute kidney failure (esp. acute) - Gastric disorders (ulcer, inflam. process etc.) - Duodenal perforation or gall bladder rupture - Rupture of an abscess developed by pancreatitis. - Urine bladder rupture - Esophageal rupture

Question 46

Name some symptoms for kidney failures (Clinical signs)

Answer 46

``` In Acute kidney failure: -Oliguria -Anuria -Recumbence -Fatigueness In Chronic kidney failure: -Polyuria -Polydypsia -Weight loss -Dehydration -Vomiting -Anaemia ```

Question 47

Is urea a sensitive parameter?

Answer 47

Yes. (Normal value of urea is: 4-10 mmol/l. A deviation from the normal range will lead to drastic clinical signs. Such as in the case of Azotaemia and Ureamia.)

Question 48

What is GFR?

Answer 48

GFR = glomerular filtration rate. Both urea and creatinine are filtered by the glomeruli. But in the case of urea it is filtered through the glomeruli and then reabsorbed from the tubules. In cretinine it is filtered by the glomeruli and not reabsorbed and not secreted by tubules. Due to this character creatinine is a good indicator of glomerular function -> use creatine to calculate the GFR. C= U x V/P

Question 49

Name the changes in plasma urea and creatinine concentration of non-renal disease?

Answer 49

``` 1. High urea, low normal creatinine: High urea: -Increased protein intake -Gastrointestinal bleeding -Fever (increased protein catabolism) -Tetracycline, steroid treatment -Haemolysis -Necrotic processes -Hyperthyroidism (increased protein catabolism) -Catabolic drugs (amphetamine) Low, normal creatinine: -Cachexia -Chronic muscle atrophy 2. Low, normal urea, high creatinine Low, normal urea: -Liver failure, portosystemic shunt -Polyuria-polydypsia -Low protein intake -Anabolic steroids High creatine: -Inflammation of muscles (myocarditis, rhabdomyolysis) -Rhabdomyosarcoma -Muscle trauma -Increased meat intake ```

Question 50

Name the methods for the determination of creatinine

Answer 50

1. Jaffe method: - Commonly used - Colorimetric - Kinetic 2. Enzymatic method (Normal value: 50-200 μmol/l (40-160))

Question 51

Causes if increased Br 1 level in the serum

Answer 51

- Excess prod. of Br 1 due to incr. RBC destruction (hemolysis) - Decr. uptake of Br 1 from blood by liver cells (impaired hepatic function) - Decr. rate of conjugation of Br 1 by liver cells (impaired hepatic function)

Question 52

Organic components of urine, and one example why they would be found in the urine

Answer 52

- RBC and WBC: haematuria: renal or urinary tract disease - Cells from the lower urogenital tract: urothelium cells, renal tubular cells, prostatic acinar, ductal epithelial cells, squamous cells from the penis or vagina, sperm cells, tumour cells - inflam. or infection of upper and/or lower urinary tract -Viral inclusion bodies - distemper -Microbes: bacteria, parasites, fungi - feacal contamination or Candida spp. -Mucin, fat droplets - starch and pollen grains - contaminants. -Casts: acute tubular disease

Question 53

Inorganic components of urine, and one example why they would be found in the urine

Answer 53

Mostly in alkaline urine: - Struvite: presence of urease positive bacteria in UTI - Calcium-carbonate: hypercalcuria - Amorphous phosphate: meat and grain (high P) diet - Ammonium-ureate/biurate: severe impairment of hepatic function (e.g. PSS) Mostly in acidic urine: - Calcium oxalate: monohydrate: ethylene glycol poisoning - Uric acid: Dalmatians (congenital), or severe impairment of hepatic function (e.g. PSS) - Cystine, tyrosine, leucine: metabolic disease - Bilirubin crystals: in bilirubinuria e.g. prehepatic and hepatic jaundice - Sulphonamides: sulphonamide therapy

Question 54

What is GLDH? Causes of increased activity?

Answer 54

GLDH (glutamate-dehydrogenase) - Liver cell (parenchymal) enzyme - Location: liver specific, small amount in nerves and muscles, in mitochondria only - Liver specific in ruminants, horses and dogs. - Function: binds NH3 to form glutamic acid. - Causes of increased activity: severe liver cell necrosis that leads to mitochondrial membrane damage

Question 55

Urine test strip reagents

Answer 55

- Leukocytes: - Nitrites: α-naphthylamine (Griess-Ilosvay's reagent) - Br/UBG: Diazo-test - Proteins: Brome-phenol-blue - Ketones: Ross reagent - Glucose: GOD/POD - Blood (Hgb): Benzidine - pH: - SG:

Question 56

Effects/Consequences of EPI

Answer 56

- Maldigestion - Pancreatogenous dyspepsia - Loose weight, despite always very hungry, and eat remarkably more than normal. - Some animals overeat and vomit some of the food, then eat it again - Coprophagia, and/or allotriophagia (pica). - Intermittent chronic diarrhoea, bacterial enteritis and frequent flatulence.

Question 57

Examination methods for hepatic exocrine function

Answer 57

1. Brom-sulphalein (BSP) retention test 2. Measurement of BSP half life 3. Indocyane green (ICG) retention test

Question 58

Causes of increased BSP retention

Answer 58

(Brom-sulphalein) 1. Primary liver failure: - liver cirrhosis - liver tumour - hepatic lipidosis - "lipid mobilisation syndrome" 2. Decreased hepatic perfusion: - right sided heart failure - portosystemic shunt - arteriole-venous fistulas in liver - blockage in portal vessels 3. Other causes: - decreased UDP-glucuronyl transferase activity in liver cells (congenital disorder)

Question 59

Characteristics of exudates

Answer 59

1. Outlook: a) Color: generally opaque, bloody, greywhite, yellow-white, light brown b) Odor: often penetrating c) Consistency: often viscous 2. Rivalta test: +/++/+++ 3. Coagulation ability: + 4. Specific gravity: > 1,025 (g/ml) 5. pH: acidic 6. Nucleated cell count: > 50 (x109/l) 7. Total protein (TP): > 35 (g/l)

Question 60

Characteristics of transudates

Answer 60

1. Outlook: a) Color: bloody (heart failure, stasis of vessels), watery or yellowish (liver failure) b) Odor: no smell c) Consistency: watery 2. Rivalta test: - 3. Coagulation ability: - 4. Specific gravity: < 1,017 (g/ml) 5. pH: slightly alkaline or 7 6. Nucleated cell count: < 1-10 (x109/l) 7. Total protein (TP): < 25 (g/l)

Question 61

Characteristics of modified transudates

Answer 61

1. Outlook: a) Color: bloody, opaque, grey-white, reddish, yellowish, sometimes transparent b) Odor: sometimes c) Consistency: watery, sometime slightly viscous 2. Rivalta test: +/- 3. Coagulation ability: +/- 4. Specific gravity: 1,017-1,025 (g/ml) 5. pH: slightly alkaline, acidic, or 7 6. Nucleated cell count: 10-50 (x109/l) 7. Total protein (TP): 25-35 (g/l)

Question 62

Local and generalized ileus

Answer 62

- Intestinal spasm onto the irritant - Intestinal content decomposes -> bacteria overgrowth -> water influx into lumen. - Aboraly from foreign body intestines are empty, walls attached to each other. - Vessels of intestinal wall are compressed at site of ileus - Stasis behind block of venous flow, lack of blood after. - Local anaerobic GL and lactic acidosis -> local tissue necrosis and inflam. process. - Fluid accumulates in the intestine prox. from the block. - Some water filtrated through the vessels and can get into the abd. cavity, causing ascites, and if bacteria-> septic peritonitis. - Some water vomited due to antiperistalsis. - Accum. of int. content, bacterial overgrowth: int. wall damaged, endotoxaemia, shock, bacteraemia, sepsis, and peritonitis. - Dehydration. - Incr. gas accum. in the loops prox from ileus. - Int. damage->haemorrhage in lumen->blood loss. - Animal do not eat; abd. pain, stress and adrenalin effect. Adrenalin> intestinal atonia, no stimulus for gall bladder emptying -> can be enlarged. Endotoxaemia. - In some chronic cases pancreatitis and liver damage may develop. - Water loss due to profuse vomiting and water influx into int. lumen cause haemoconcentration and hypovolemia, poor tissue perfusion and general anaerobic GL and lactic acid prod., and sometimes hypovolemic shock. - As a consequence of dehydration GFR and renal function will be decr. - Hypokalaemia causes muscle weakness, also in resp.mm.: hypoxia, hyperkapnia, hypoxaemia, and even death! - Ventilartory disorder may cause resp. acidosis. - Due to dehydration, metabolic and resp. acidosis may develope, hypokalaemia, endotoxaemia and bacteraemia causes shock, and death.