Midterm 2 Flashcards
Describe Prox Ileus.
- Stomach + Prox duodenal parts
- Metabolic alkalosis in beginning + metabolic acidosis follows.
- Irritant ( foreign body) is in stomach or near stomach, gas + fluid accumulation in stomach so tensor R in gastric wall are activated causing increases HCL production.
- vomit contains HCL, animal looses acids so metabolic develops.
- Severe= dehydration, anaerobic glycolysis and metabolic acidosis.
- Anorexia, depression + general state of animal worsening more quickly.
Describe Dist Ileus.
- Jejunum + more dist parts.
- Metabolic acidosis.
- Animals not eat, stomach is empty, vomit contains small intestional fluid ( reflux) that has high pH; dehydration, anaerobic glycolysis, lactic acid formation.
- Prolonged time= miserere symptom.
- have reflux of intestinal contents back to stomach, so they vomit brown-greenish, malodorous intestinal contents ressembling faeces.
Differentiate prox + dist ileus with lab practicals.
X-ray, Ultrasound, Acid-base balance.
Pre Hepatic Icterus (PrHI).
(a)In blood.
- Br I + Br II + UBG + Free Hgb + Reticulocyte count increases.
- Haptoglob conc + Ht decreases.
- Coagulation parameters (PT, APTT, TT) increases or normal (DIC).
PrHI.
(b) In Urine.
UBG + Br + Hb increases.
PrHI.
(c) In Faeces.
Br- derivatives: Pleichromic, hyperchromic, hypercholic.
PrHI.
(d) Characteristics alterations in enzyme activities.
ALT + LDH increases.
PrHI.
(e) Characteristics alteration in substrate conc.
Urea increases.
Hepatic Icterus (HI). (a) In Blood.
- Br I + Br II + UBG increases.
- Free Hgb + Ht + Reticulocyte count decreases.
- Haptoglobin conc stays normal.
- Coagulation parameters increases and do not changes after Vit K administration.
HI.
(b) In Urine.
UBG + Br increases.
HI.
(c) In Faeces.
Hypocholic.
HI.
(d) Characteristics alterations in enzyme activities.
ALT + AST + GLDH increases.
HI.
(e) Characteristics alterations in substrate conc.
- NH3 + BA increases.
- Urea decreases.
Post Hepatic Icterus (PoHI).
(a) In Blood.
- Br II increases.
- Br I increases/ stays normal.
- Free Hgb + Haptoglobin conc + Ht + Reticulocyte count stays normal.
Coagulation parameters increases but changes after Vit K administration.
PoHI.
(b) In Urine.
- Br increases.
- UBG decreases or not present.
PoHI.
(c) In Faeces.
Acholic.
PoHI.
(d) Characteristics alterations in enzyme activities.
ALKP + GCT increases.
PoHI.
(e) Characteristics alterations in substrate conc.
BA increases.
Hepatocellular enzymes in dogs.
ALT ( Alanine- Aminotransferase).
GLDH ( Glu- Dehydrogenase).
Tubular Dysfunction Test.
- Specific Gravity analysis of urine, water deprivation test.
- Analysis of enzymuria, Urine sediment analysis, Tubular clearance examination.
Examination of glomerular function.
- Plasma/ Serum urea + creatinine level.
- Creatinine Clearance.
- Urinary TP and Creatinine ratio.
- Radioisotopic methods, C- inulin clearance.
- H-Tetraethyl- ammonium-CL clearance.
Urinary Sediment Analysis.
For postrenal Kidney function.
Acute Kidney Failure.
Urinalysis- Main tests.
Urine Specific Gravity.
Urine ph meter.
Urinary Sediment analysis.
Detecting protein from urine.
Urine test strip, SSA test, Heller probe, Ultrasensitive protein determination, Bence Jones proteins, Microalbuminuria.
How to detect pancreatitis?
Haematological, serum biochemical, cytological + microbiological analysis.
What is TLI? Describe it’s usefulness in the diagnosis of EPI.
- Trypsin like immunoreactivity.
- TLI level is normal/ high, EPI is caused by obstruction of pancreatic duct.
Describe the Gmelin Test.
- Conc HNO3 layered under urine in a test tube + width of differently coloured layers at the meeting of 2 fluid phases has to be evaluated.
BA. How to measure them and when is their conc elevated in serum/ blood?
- HPLC, RIA/TBA, Spectrophotometric.
- Liver injury, bile duct obstruction, decrease liver function, biliary stasis, portosystemic shunt.
When does alpha-amylase activity increase?
Acute pancreatitis, acute + subacute kidney failure, FIP, lymphoma, myeloma, DM, chronic enteritis.
EPI. What is it? How to test it?
- Developed due to chronic necrotic/ atrophic damage to pancreas.
- decrease production of digestive enzymes/ obstruction of pancreatic duct.
- TLI conc, BT-PABA test, lipid absortion test, Faecal elastase test.
What is the lipid absorption test, and which disorders can it confirm or eliminate?
- Determine there is lipid malabsorption, maldigestion.
- EPI.
What is icterus? What can be the causes of increased plasma Br?
- Haemolysis of RBC, increased Br I in serum, obstruction of bile duct.
- Prehepatic, Hepatic icterus.
What is ileus?
Local effects occur at intestines, general effects are changes of circulation, electrolyte + water balance, acid-base balance.
What faeces tests are useful for EPI determination/ diagnosis?
Faecal elastase test, Examining undigested particles in faecal sample.
What is ALT?
- Alanine- aminotransferase.
- Carnivores liver specific.
- Found in liver cells.
What is AST? Where is it found? Where can we see it’s elevation in the plasma? In what species is it useful?
- Aspartate- aminotransferase.
- Located in mitochondria of liver cells.
- Elevated in muscle + liver cells + RBC.
- Herbivores.
What is AP?
- ALKP ( AP alkaline phosphatase).
- Located in every cell membrane, produced by different organs.
What is GGT?
- Gamma glutamyl transferase.
- Locates in different organ, endothelial cells of bile duct concentrate it.
ALT- level in blood.
- Liver cell damage, bile duct obstruction, pancreatitis, liver neoplasm, septicaemia, liver lipidosis + cirrhosisl drugs, CH storage disorder.
Liver function tests.
- Measurements of NH3 conc, NH3 tolerance test.
- AST, ALT, GLDH.
Causes of increased of ALKP in blood.
- Paraneoplastic proc., Liver cholestasis, liver cirrhosis, hepatic lipidosis, barbiturates, iatrogenous, hyperadrenocorticism, chronic stress.
What are the causes of increased blood urea conc.?
- Prerenal factors: increased N intake, Ru poor E status in rumen, increased intestinal protein catabolism, intestinal/ gastric bleeding, Haemolysis, decreased blood perfusion of kidneys, hypotension, shock, dehydration, cardiac failure.
- Renal factors: Kidney function, decreased amt of functionally active nephrons, decreased tubular function.
- Postrenal factors: Inhibition of urine flow through lower urinary tract due to occlusion of pelvis, urether/ urethra; Rupture of kidneys, urether, urinary bladder or urethra.
What are the causes of increased blood creatinine conc.?
- M. content of diet.
- State of m: necrosis increased while cachexia decreased creatinine level.
- Kidney glomerulus function.
Water deprivation test - What is the goal of this test? Its method and
interpretation.
- Evaluate polyuria + polydypsia.
- At 1st total bladder emptying by catheter, then BW measurement + urine sampling every hr.
What is the goal of Enzymuria Evaluation? Goal and how is it performed/tested?
- Detection of paraacute/ acute tubular damage.
- ALKP + GGT increase release in urine, referred to creatinine levels.
Causes of low blood creatinine conc.
- Impaired liver function, haemodilution, decreased protein intake.
Urea conc in blood.
8- 10 mmol/L.
What can be seen in the physiological urine sediment? List the
pathological abnormalities in the urine sediment.
- Organic and anorganic sediment.
- Proteinuria, Pyuria, Hematuria, Hemoglobinuria, myoglobinuria, Br UBG.
Proteinuria, causes and types.
- Glomerular dysfunction.
- Albuminuria.
Why/how can the presence of bacteria be shown in urine?
- Because of pyuria.
- Donné probe, Microscopic evaluation of urinary sediment.
Urine and pH changes.
- pH <5.5: metabolic + respiratory acidosis, vomiting, hypokalaemia, treatment + toxicosis with acidifying drugs.
- pH > 7.5: UTI, metabolic + respiratory alkalosis, alkalizing substances, long storage.
How to differentiate hematuria from hemoglubinuria?
Centrifugation.
