Exam 2 Flashcards

1
Q

locations of pathology associated w/ GI symptoms

A

Primary GI

• Inflammatory +/- infectious
• Neoplasia

• Drug induced

Non-GI

• Metabolic (e.g. hyperthyroidism, DKA, Addison’s)
• Liver failure

• Kidney disease

Pancreatic

• Pancreatitis
• Exocrine pancreatic insufficiency

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2
Q

First Steps in Diagnosing dog or cat w/ GI symptoms

A
  • Minimum data base (CBC/Chem & urinalysis)
  • Fecal
  • Cats: T4 , FelV/FIV
  • Dogs: cortisol +- ACTH stim
  • Pancreatic Serum tests
  • GI serum tests
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3
Q

Anatomy of the pancreas & enzyme production

A
o Exocrine
•	Acinar cells
•	Secrete: trypsin (protien), pancreatic lipase (fat), pancreatic amylase (carb)
o Endocrine
•	Secretes insulin & glucagon
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4
Q

Stimuli for Pancreatic Secretion

A

o Acetylcholine from vagus N. stimulates digestive enzymes
o Cholecystokinin (CCK) from GI stimulates digestive enzymes
o Secretin from GI stimulates H2O & bicarb secretion

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5
Q

Diagnosing Pancreatitis

A

o Inflammatory leukogram: neutrophilia, +- toxic neutrophils,
o +- stress leukogram: lymphopenia
o Erythrocytosis due to dehydration
o Possible anemia due to hemorrhage
o Hyperlipidemia (fatty serum)
o Hyperglycemia
o Azotemia (high nitrogen due to dehydration)
o Increased hepatic enzymes & hyperbilirubinemia
o Electrolyte abnormalities
o May have DIC (increased PT/PTT, increased D dimer, increased FDPs)
o High PLI & TLI

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6
Q

Testing Amylase & Lipase

A

o Amylase: complex carbs -> maltose and glucose
o Lipase: triglycerides -> fatty acids and glycerol
o in other organs but highest conc. in pancreas & small intestine
o amylase decreased w/ corticosteroid use
o lipase increased w/ corticosteroid use
o inactivated by kidney -> renal disease can cause increased amy/lipase
o Limited diagnostic utility in dogs; suggestive if 3-4X high + no azotemia
o No diagnostic value for cats

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7
Q

Pancreatic Lipase Immunoreactivity (PLI)

A

o Measurement of serum lipase derived only from the exocrine pancreas
o High Sensitivity and specificity

o Result of tests not affectd by GFR, gastritis, or corticosteroid use
o Magnitude of elevation no correlated w/ prognosis
o Spec or SNAP

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8
Q

Spec PL Vs SNAP PL Vs TLI

A
  • all are biochemical tests that measure presence / conc. of macromolecules in a solution through the use of an antibody or immunoglobulin
  • Spec quantitative (numerical conc. of PL)
  • SNAP qualitative (normal or abnormal amount of PL)
  • TLI decreased w/ EPI, increased w/ acute pancreatitis
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9
Q

Be able to contrast sensitivity and specificity of enzymes detecting muscle injury and pattern of elevation.

A
  • Specificity: increases due specifically to muscle injury

- Sensitivity: increases even if muscle damage is minor

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10
Q

Know what tests you should ask for to detect muscle injury.

A
  • CK

- AST

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11
Q

Know how to differentiate muscle injury from non-muscle disease processes.

A
  • sometimes secondary to other diseases

- Cardiomyopathy -> aortic thromboembolism 
-> hypoxia of hind limb muscles 
-> Muscle necrosis -> high CK & AST

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12
Q

Be familiar with other chemistry changes that can be seen with muscle injury.

A
  • Myoglobinuria (urine only tells you blood present; look at other bloodwork to identify hemoglobin, myoglobin, or intact RBCs)
  • Hyperkalemia
  • Hyperphosphatemia
  • Hypocalcemia
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13
Q

Explain the four basic mechanisms that lead to increased serum enzyme activity

A

Release from damaged cells

  • Concentration of enzyme within the cell and/or intracellular distribution,
  • enzyme half-life,
  • number of cells damaged, severity 


Increased production

- Inducers (drugs), neoplasia, hyperplasia, young patient

Decreased removal

- enzymes that are excreted by the kidneys will see increased levels with renal disease 


Ingestion or absorption

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14
Q

Correctly select and interpret the enzyme changes used for detection of muscle damage 


A

CK

  • Mostly muscle 

  • Specific, sensitive 

  • Short half-life 


ALT

  • Mostly liver
  • Not very sensitive for muscle

AST

  • Liver or muscle
  • Longer half life than CK (rises more slowly than CK)
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15
Q

Understand diagnostic sensitivity and specificity and explain how they influence our interpretation of assay results. Know your equations!

A

Sensitivity:

  • will always detect positives but may falsely identify negatives as positive
  • (true pos/(true pos+false neg)) X100

Specificity:

  • Will always correctly identify negatives but will sometime incorrectly identify positives as negative
  • (true neg/(true neg+false pos)) X100
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16
Q

Understand positive and negative predictive values and prevalence and explain how they influence our interpretation of assay results. Know your equations!

A

Positive:

  • Tells you what % of animals with a positive (abnormal) test result will actually have the disease
  • (true pos/(true pos+false pos)) X100

Negative

  • Tells you what % of animals with a negative (normal) test actually don’t have the disease
  • (true neg/(true neg+false neg)) X100
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17
Q

What are 3 phases of laboratory testing needed to ensure proper quality assurance?

A
  • Pre-analytical: Sampling, transport/sample handling
  • Analytical (Instrument measurement)
  • Post-analytical: recording & interpreting data
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18
Q

List 5 things that should be included in a quality control program

A
  • Systematic monitoring of equipment operation 

  • System for monitoring reagent inventory 

  • Use of controls for external QC on some instruments-results can be plotted in a Levey- Jennings plot 

  • Written/computerized logs and documentation 

  • Proper training of ALL instrument users 

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19
Q

Identify and be able to discuss hepatic enzyme tests and know which are preferred for small versus large animals.

A

Small Animals


  • ALT – hepatocellular injury

  • ALP – cholestasis, isoenzymes
  • GGT - cholestasis

Large Animals


  • SDH – hepatocellular injury

  • AST – hepatocellular injury and muscle injury
  • GGT – cholestasis, colostrum
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20
Q

Explain the similarities and differences between hepatocellular disease, biliary disease, and hepatic insufficiency. Identify laboratory data that indicate or suggest the presence of each.

A

Hepatocellular Dz

  • enzymes in organelles/cytoplasm
  • enzymes leak out through disruption of membrane
  • enzymes in serum increase

Biliary Dz

  • enzymes on membrane
  • enzymes leak out due to disruption of bile flow
  • elevated serum enzymes

Hepatic Insufficiency

  • enzymes in organelles/cytoplasm
  • too few functional hepatocytes to raise serum enzyme levels
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21
Q

Know the 3 different processes in dogs that produce increased ALP

A
  • Liver ALP:
    cholestasis, drugs (dogs)
  • Bone ALP: bone growth
  • Corticosteroids ALP (dogs only)
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22
Q

Understand the explained hepatic function tests and know what test you would want to run in cases with suspected liver disease.

A

if no icterus, bile acids most important

Total Serum Bilirubin

  • Hyperbilirubinemia: rate of bilirubin production exceeds liver’s ability to deal w/ it
  • Any bilirubinuria in cats is SIGNIFICANT

Bile Acids

  • More sensitive indicator of liver function than bilirubin
  • Increase = decreased clearance from portal blood or cholstasis

Blood Ammonia

  • Less sensitive than bile acids
  • may perform if suspected hepatic encephalopathy
  • Increase – portosystemic shunt, significantly decreased liver function, urea toxicosis (cows), ammonia producing bacteria (horses)
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23
Q

Describe hematology or urinalysis abnormalities that may be associated with liver disease.

A

Hematology

  • Mild-moderate anemia
  • Target cells, ancanthocytes, microcytosis

Urinalysis

  • Bilirubinuria / crystals
  • Ammonium biurate crystals
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24
Q

Understand how liver disease can cause increased hepatic enzymes, hypocholesterolemia or hypercholesterolemia, hypoglycemia, decreased BUN, hypoproteinemia with hypoalbuminemia, prolonged coagulation times, and ascites.

A

Hepatic enzymes:
- shows liver damage because lysis of hepatocytes releases enzymes

Hypoglycemia:
- liver isn’t performing gluconeogenesis

Hypoprotinemia, hypoalbumenia, Hypo/hypercholesterolemia, Decreased BUN
- decreased production by liver due to non functioning hepatocytes

Prolonged coag time:
- decreased production of clotting factors by liver due to non functioning hepatocytes

ascites
- due to portal hypertension

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25
Q

Basics of Liver Failure

A
  • Liver Can’t clear toxins or process ammonia and bilirubin 

  • Inability to produce proteins, lipids, carbohydrates 

  • Serum enzymes may not be elevated in end stage 

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26
Q

Exocrine Pancreatic Insufficiency (EPI) Basics & Causes

A

o failure of the acinar cells to produce pancreatic enzymes and HCO3-
o primary or secondary

Causes
o	destruction of acini, 
o Deficiency of CCK and secretin, 
o Deficiency of enterokinase, 
o Excessive secretion of HCl
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27
Q

Exocrine Pancreatic Insufficiency (EPI) Clinical Signs, Breed Disposition, Diagnosis

A
o	Clinical Signs
•	Weight loss
•	Polyphagia
•	Vomiting
•	Greasy Ds

o Breeds
• Shepherds
• Collies

o Diagnosis
• Unremarkable CBC/Chem
• TLI is test of choice (TLI is decreased)
• Often occurs w/ SIBO

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28
Q

Tests for GI Disease

A
o cobalamin
o folate
o gastrin
o carb absorption (horses)
o fecal occult blood
o Alpha-1 Protease Inhibitor
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29
Q

Serum Cobalamin (B12)

A
  • Requires intrinsic factor to be absorbed in ilium
  • Decreased due to Distal small intestinal mucosal disease, EPI, Bacterial overgrowth
  • Increased due to B12 supplement
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30
Q

Serum Folate (B9)

A
  • Absorbed in proximal small intestine
  • Decreased concentration: Mucosal disease in proximal small intestine
  • Increased: SIBO, EPI, B9 supplement
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31
Q

When to evaluate Cobalamin & Folate

A
  • Patients with suspected small intestinal disease (Once EPI & parasites excluded)
  • intestinal malabsorptive abnormalities
  • bacterial overgrowth
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32
Q

Gastrin Test

A
  • Gastrin stimulates release of HCl in stomach
  • Elevated gastrin = vomiting
  • elevated due to: Neoplasia, ulcer, obstruction, renal failure, drugs, hepatobiliary dz
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33
Q

Carb Absorption test

A
  • evaluate small intestinal function 

  • Oral D-xylose and D-glucose absorption test 

  • Sugar conc. measured at different time intervals
•	Decreased absorption 
= 
o Delayed gastric emptying
o Vomiting

o bacterial overgrowth
o Rapid intestinal transit

o small intestinal dz
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34
Q

Fecal Occult Blood Test

A
  • Identification of small intestinal bleeding
by detecting pseukoperoxidase activity of hemoglobin
  • very sensitive
  • False positives due to Diet, Iron supplementation, Contamination
  • A repeatable negative result rules out bleeding into the GI tract
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35
Q

Alpha-1 Protease Inhibitor Test

A
  • Test looks for pathologic protein loss in feces 

  • Shows protein loss in intestine or blood loss in intestine
  • Take 3 fecal samples over 3 days
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36
Q

Bovine GI Content Analysis

A

o Rumen
• pH > 7 = ruminal alkalosis = decreased microbial fermentation
• pH < 5.5 = ruminal acidosis = carb overload & lactic acid accumulation

o Abomasum
• should have pH ~2-3
• pH can rise due to displacement or parasitisim

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37
Q

Clinical assessment of renal function

A

o Evaluate creatinine and BUN on serum chemistry (estimation of GFR)
o Evaluate urine specific gravity
o Urinalysis: evaluate proteinuria and sediment changes

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38
Q

How to investigate glomerular function

A

o urea blood/serum nitrogen (BUN or SUN)
o creatinine
o SDMA
o clearance test

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39
Q

Urea Blood/Serum Nitrogen (BUN)

A
  • Produced in liver from protein metabolism
  • Expressed in terms of nitrogen content (BUN)
  • More accurate term is serum urea nitrogen (SUN)
  • Freely filtered through glomerulus with some tubular resorption

increase in BUN
• decreased GFR
• increased production due to GI bleeding or high protein meals

decreased BUN
• decreased production due to liver dysfunction
• increased excretion due to diuresis

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40
Q

Creatinine

A
  • Freely filtered through glomeruli and not reabsorbed
  • better estimate of GFR than BUN
  • product of muscle metabolism
  • Heavily muscled animals = mildly increased creatinine levels
  • Will not significantly increase with muscle damage
  • Increases in serum creatinine = Decreased GFR
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41
Q

Azotemia

A

Increase in Creatinine and/or BUN = decreased GFR, but not specific
• Prerenal Azotemia
• Renal Azotemia
• Post renal Azotemia

  • If azotemia due to kidney disease = loss of 75% of kidney function
  • Urine Specific Gravity is necessary to evaluate an azotemic animal!!
42
Q

Pre-renal Vs Renal Vs Post-renal azotemia

A

Pre Renal Azotemia
• Most common
• Decreased renal perfusion
• Dehydration, cardiac dz, shock

Renal Azotemia
• Renal dz w/ at least 75% loss of function
• Due to infectious, toxins, renal amyloidosis, neoplasia, etc

Post Renal Azotemia
• Rupture bladder or ureters
• Causes obstruction -> no peeing -> resorption of creatinine or BUN

43
Q

Symmetric dimethylarginine Test (SDMA)

A
  • Product of protein methylation & released into circulation
  • Excreted exclusively by kidneys
  • Good estimate of GFR
  • Increases earlier than creatinine (40% loss of kidney function)
44
Q

Clearance Test

A
  • Measures GFR or clearance of analytes thru kidneys
  • Endogenous creatinine clearance
  • Exogenous creatinine clearance
  • Fractional excretion of electrolytes
  • Not easily performed = rare in clinic
45
Q

Urine Specific Gravity (USG)

A

o Measure conc. of solutes in urine using refractometer
o Affected by amount & size of molecules in urine
o Wide range of normal
o Compare USG to specific gravity of plasma conc. entering renal tubules (1.007-1.013)

46
Q

Isothenuric Vs Hypersthenuric Vs Hyposthenuric Vs Gray range

A

Measure of Urine Conc.
Isosthenuric
• 1.007-1.013 = same as plasma ultrafiltrate

Hypersthenuric
• >1.025 (horse, cow)
• >1.030 (dog)
• >1.035 (cat)

Hyposthenuric
• <1.007

Gray range
• 1.014 to hypersthenuric

47
Q

What does different combinations of azotemia and USG mean?

A
  • Azotemia + hypersthenuria = poor renal perfusion = pre-renal azotemia
  • Azotemia + isosthenuria = renal failure = renal azotemia
  • Azotemia & variable USG = rupture or urinary tract obstruction = post renal azotemia
  • Azotemia + hyposthenuria = functioning renal tubules but poor renal perfusion = pre-renal azotemia
48
Q

Meaning of USG without azotemia

A

Hypersthenuria
• tubules functioning & urine concentrated

Isosthenuria
• normal in well hydrated animal OR
• indicate renal insufficiency
• USG will decrease before azotemia develops in most species with renal disease.

Hyposthenuria
• function of tubules because they are actively diluting.
• Can see w/ ADH abnormalities.

Grey Zone
• may be normal OR
• could indicate beginning renal insufficiency.

49
Q

Kidney requirements for concentration of urine

A

o Sufficient nephrons
o ADH present
o Ability of tubules to respond to ADH
o High osmolarity of renal interstitial fluid

50
Q

Extra-renal causes of abnormal USG

A

Lack of ADH secretion
• Pituitary (central) diabetes insipidus

Lack of response of the tubules to ADH
• Hypercalcemia, Pyometra, etc

Loss of medullary concentration gradient
• Prolonged hyponatremia due to Diuretics or Hypoadrenocorticism
• Diuresis (e.g.fluids, Diabetes Mellitus..)
• Hepatic insufficiency
• Hyperthyroidism

51
Q

Ways to collect urine

A

Midstream catch
• Easy but contamination occur

Manual
• Not easy
• Can traumatize bladder

Catheterization
• Decreased contamination
• Can cause trauma

Cystocentesis
• Preferred method in small animals
• Decreased contamination but may have RBCs

52
Q

Urobilinogen

A
  • formed from bilirubin
  • May see increase w/ increased bilirubin = Hemolytic disease or liver disease
  • usually not diagnostically helpful
53
Q

Tests for protein in urine

A
  • SSA Test
  • protein creatinine ratio (UPC)
  • Microalbumin test
54
Q

SSA Test

A
o	Use to confirm (+) protein on dipstick
o	Performed on supernatant
o	Picks up proteins other than albumin
o	No false + in alkaline urine
o	If positive & urine sediment normal, a quantitative test is recommended
55
Q

Protein Creatinine Ration (UPC)

A

o Quantitatively evaluates proteinuria
o Used on urine w/ no cystitis or overt blood
o Disregards urine dilution
o Urine microprotein / urine creatinine = UPC
o Normal = <0.5

56
Q

Microalbumin Test

A

o Most sensitive test for urine albumin
o P.O.C. and ELISA tests available
o Detects urinary albumin >1 mg/dL - <30 mg/dL
o Used on urine w/ no cystitis or overt blood

57
Q

Proteinuria

A

o If persistent associated w/ increased morbidity/ mortality
o Pre-glomerular/Renal
o glomerular / renal
o Post glomerular/renal

58
Q

Proteinuria: Pre-glomerular/Renal
Vs glomerular / renal
Vs Post glomerular/renal

A

o Pre-glomerular/Renal
• Abnormal plasma content of protein (Bence Jones proteins- multiple myeloma, hemoglobin, myoglobin)
o Glomerular/Renal
• Abnormal renal handling of normal proteins
o Post glomerular/renal
• Most common!
• Entry of protein into urine after urine enters renal pelvis
• Due to inflammation or hematuria

59
Q

3 elements to assess w/ proteinuria

A

Localize

• Exclude extra-renal, pre-renal, and post renal causes
• Rule in other causes of proteinuria with clinical signs

Persistence
• Evaluate over multiple days

Magnitude

• Need to look for persistance
• need a quantitative test!

60
Q

Nephrotic Syndrome

A

• Severe proteinuria -> nephrotic syndrome

Characterized by
•	Proteinuria
•	Hypoalbuminemia
•	Hypercholesterolemia
•	Edema
•	lose anti-thrombin & start to throw clots = death
•	+/- azotemia
61
Q

Define balottement

A

fluid wave in abdomen

62
Q

Blood on dipstick

A
  • Should be negative
  • If (+) = RBCs, hemoglobin, or myoglobin
  • Look at sediment exam, hematology/chem, serum color, ammonium sulfate, & history to figure out (+)
  • IMHA dog will have red urine & plasma
63
Q

Ketones on dipstick

A
  • Should be (-)

* If (+) consider: negative energy balance or diabetes

64
Q

Bilirubin on dipstick

A
  • Should be (-) (except dogs in small amounts)
  • If (+) consider: cholestasis, hemolysis
  • Use ictotest (more sensitive) to confirm (+)
65
Q

Glucose on dipstick

A
  • Should be (-)

* If (+) consider: hyperglycemia (renal threshold) or renal tubule dysfunction

66
Q

Urine Sediment Exam

A
  • 10x objective (LPF)
  • 40x objective (HPF) – used to look at cells
  • RBCs & WBCs should be <5
  • can see casts
  • can see crystals
67
Q

Urinary Casts

A
  • Formed in tubules by sloughing of cells
  • Can be normal in small numbers
  • When excessive = tubular necrosis
  • Granular (concern)
  • Fatty (rare)
  • Hyaline (horses & insignificant)
68
Q

7 Types of Crystals

A
  • Magnesium ammonium phosphate (struvite)
  • calcium carbonate
  • urate
  • calcium oxalate
  • cystine
  • cholesterol
  • bilirubin
69
Q

Magnesium ammonium phosphate crystals (struvite)

A

o rectangular
o May be normal
o Associated w/ neutral or alkaline urine
o Can form calculi

70
Q

Calcium Carbonate Crystals

A

o round
o Normal in horse
o Associated w/ alkaline urine
o No clinical significance

71
Q

Urate Crystals

A

o Thorny round shape

Ammonium biurate
• Associated w/ slight acidic, neutral or alkaline urine
• Yellow/brown

Amorphus urates
•	Associated w/ acidic urine
•	Yellow/brown
•	Common in dalmations
•	Associated hepatic dz
72
Q

Calcium oxalate crystals

A

Dehydrate:
o square

monohydrate:
o flat & oblong
o ethylene glycol poisoning

73
Q

Cystine Crystals

A

o Hexagonal
o Amino acid problem
o Formed in acidic urine

74
Q

Bilirubin Crystals

A

o Reddish-orange needles
o Normal in concentrated dog urine
o High numbers = abnormal bilirubin metabolism

75
Q

Why use Modified Water deprivation test & what should you test first?

A

Use when no azotemia, no dehydration, PU/PD & USG <1.020

Test these first:
• CBC/Chem & U/A to rule out underlying metabolic abnormality, cystitis, etc 

• Bile acids to exclude hepatic insufficiency 

• Urine culture +/- ACTH stimulation test to rule out 
Hyperadrenocorticism

76
Q

Method for Modified Water deprivation test

A
  • Slowly limit water intake over a few days (modified) ->
  • Take USG, body weight, hydration status, BUN/Creatinine ->
  • remove water and re-evaluate parameters every 1-2 hours 


Stop if:

o Urine concentrates (>1.030)
o Animal becomes dehydrated or azotemic
o Body weight decreases 5% 


Results:
o If animal concentrates - primary polydipsia problem
o If animal doesn’t concentrate 
-> Give ADH.
• Response to exogenous ADH = pituitary diabetes insipidus
• No response to ADH = Nephrogenic cause

77
Q

Renal Dz

A
  • refers to any lesion of the kidney

* Can progress to renal failure

78
Q

Acute Kidney Injury (AKI)

A
  • sudden renal injury ranging from mild nephron loss to acute renal failure.
  • IRIS* staging system used to denote severity
79
Q

AKI Grading Criteria

A
  • Grade I: non-azotemic; other evidence of kidney injury
  • Grade II: mild AKI
  • Grade III-V: moderate to severe AKI leading to renal failure
80
Q

Late Stage AKI / Renal Failure

A
  • Not seen as commonly as chronic kidney disease
  • Sudden onset

  • Oliguria or anuria

  • Usually looking for toxic or infectious cause (ethylene glycol)
81
Q

Stages of Ethylene Glycol Toxicity

A

Stage 1
• 30 min to 12 hours post ingestion
• CNS signs, PU/PD, vomiting

Stage 2
• 12-24 hours
• Tachypnea and tachycardia from developing metabolic acidosis

Stage 3
•	24-72 hours (dogs)
•	12-24 hours (cats)
•	Acute renal failure
•	vomiting, oliguria, anuria
82
Q

Symptoms of Ethylene Glycol Toxicity

A
Early Abnormalities (1-6 hours)
•	Decreased bicarbonate (TCO2)
•	Increased anion gap

•	Increased osmolal gap 
•	Possible hypocalcemia

•	Crystalluria (calcium oxalate monohydrate) 
Late Abnormalities (24-72 hours)

•	Azotemia (seen as early as 12 hours in cats) 
•	Isosthenuria
•	Hyperphosphatemia

•	Hyperkalemia
83
Q

Chronic Renal Failure (CKD)

A
  • Common
  • structural or functional abnormalities of kidneys present for 3 months or longer w/ late stage leading to renal failure.
  • IRIS staging system used to denote severity
  • Impaired urine conc. & increased SDMA before azotemia
  • PU/PD
  • isosthenuria, azotemia, anemia, (hypercalcemia in horses)
84
Q

PU/PD

A

Primary polydipsia
o psychogenic, hepatic or neurologic disease

Primary polyuria
o Osmotic
o Lack of ADH 

o Primary nephrogenic diabetes insipidus
o Secondary nephrogenic diabetes insipidus
o Medullary washout 


85
Q

Renal Failure

A
  • functional renal tissue is inadequate to maintain health.
  • IRIS staging can be used to indicate severity.
  • Generally both azotemia and inappropriate renal concentration (check USG) are noted.
86
Q

Uremia

A

• clinical signs associated with severe renal disease (eg, vomiting)

87
Q

Proper Sample Collection for Acid-Base Evaluation

A

Heparinized syringe

Arterial better than venous sample

Avoid air exposure
• increases pH

Record temperature
• CO2 drops 2mmHg & O2 drops mmHg every 1C below 37C

Evaluate ASAP!

88
Q

Organs involved in acid base balance

A

Lungs
• remove H+ & CO2 (acids)

kidneys
• add HCO3 (base)
• remove H+ (acid)

89
Q

Systemic Approach for Evaluating Acid-Base Disorders

A

o Acidemia or alkalemia?
o Respiratory or metabolic?
o Compensatory response?

Subclassify
• Is metabolic acidosis titrational or secretional?
• Is it a mixed acid-base disturbance?

90
Q

Secretional V Titrational Metabolic Acidosis & relation to anion gap

A

Secretional
• HCO3 loss -> decreased HCO3, normal anion gap, increased Cl-
• Diarrhea, Renal loss, Excess salivation

Titrational
• Acid accumulation -> decreased HCO3, increased anion gap
• Lactic acidosis, ketoacidosis, uremic acids, toxins

91
Q

Basics to remember for inflammatory & stress leukograms

A

o inflammatory: neutrophelia +/- L shift & tox change

o stress: lymphopenia

92
Q

Start w/ pH and figure out respiratory or metabolic acidosis or alkalosis

A

o low pH = acidemia ->
o high pCO2 -> resp acidosis
o low HCO3 -> met acidosis

o high pH = alkalemia ->
o low pCO2 -> resp alkalosis
o high HCO3 -> met alkalosis

93
Q

paradoxical aciduria

A

cows can have metabolic alkalosis w/ acidic urine

Must have
o hypovolemia
o hypochloremia
o hypokalemia

94
Q

Calculate Anion Gap

A

anion gap = (Na) – (Cl + HCO3)

TCO2 = (HCO3 + CO2)

95
Q

Causes of respiratory alkalosis

A
Extrathoracic
• PO2 is normal 
• Fear
• Pain
• Anxiety

Intrathoracic:
• PO2 decreased
• Pulmonary disease
• Airway obstruction/mal function

96
Q

Causes of respiratory acidosis

A
• Severe pulmonary disease
• CNS disease that decreases
respiratory rate
• Airway obstruction
• Pleural effusion/masses 
• Neuromuscular disorders
97
Q

Hypernatremia

A

Hypotonic fluid losses
• GI: vomiting, diarrhea
• Renal: Diabetes insipidus
• polyuria

Pure water deficits
• Primary hypodipsia
• Water unavailable or unable to drink

Gain of solute
• Salt poisoning (ruminants)
• Iatrogenic causes

98
Q

Hyponatremia

A
  • Hypoadrenocorticism
  • Diarrhea
  • Renal disease
  • Dietary salt deficiency
  • Diabetes mellitus
  • 3rd space loss
  • False decrease with lipemia or hyperproteinemia
99
Q

Hyperkalemia

A
  • decreased urinary excretion
  • marked exercise or metabolic acidosis
  • pseudo due to thrombocytosis or hemolysis
100
Q

Hypokalemia

A
  • anorexia
  • insulin or metabolic alkalosis
  • GI or renal loss
  • sweating or burns
101
Q

Hypochloremia

A
  • chronic vomiting

* aggressive diuretic therapy

102
Q

Hyperchloremia

A
  • fluid therapy

* small bowel Ds