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Clinical Pathology > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

What is test sensitivity? What would a test with high sensitivity do?

A

The ability of a test to identify diseased (positive) animals. A high sensitivity test would ID all of the diseased animals in a population but may include some false positives.

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2
Q

Sensitivity equation?

A

100 x (TP / TP + FN)

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3
Q

What is test specificity? What would a test with high specificity do?

A

The ability of a test to identify normal (negative) animals. A high specificity test would ID all the normal animals in population but may include some false negatives.

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4
Q

Specificity equation?

A

100 x (TN / TN + FP)

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5
Q

What is a predictive value?

A

A predictive value that takes prevalence of disease in a group of animals into account (gives you the likelihood of disease in animals tested)

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6
Q

What is the positive predictive value?

A

The percent of animals that test positive that are actually diseased.

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7
Q

Positive predictive value equation?

A

100 x (TP / TP + FP)

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8
Q

What is the negative predictive value?

A

The percent of animals that test negative that are actually diseased.

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9
Q

Negative predictive value equation?

A

100 x (TN / TN + FN)

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10
Q

What are the three main things a quality assurance program assesses?

A 
Pre-analytical factors (sample acquisition/storage)
Analytical factors (machine) 
Post-analytical factors (data reporting/interpretation)
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11
Q

Name some important elements of a quality assurance plan in the hospital

A

Quality Assurance Plan
Well trained staff
Logs for periodic system monitoring/maintenance
Proper sampling and storage
Periodic review of machine data for abnormal trends
Blood smear review of ALL CBCs.

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12
Q

What is test accuracy?

A

How close a result is to a “true” value.

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13
Q

What is test precision?

A

How repeatable a test value is.

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14
Q

What is a Levey-Jennings control chart and how can it be used?

A

Values plotted against a mean to graph test accuracy and test precision. Any value outside of 3SDs typically implies service is needed.

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15
Q

What is POC proficiency testing?

A

Reference lab sends in a sample with known values to be tested on hospital POC machines, then compares the hospital’s results.

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16
Q

What are isoenzymes?

A

Enzymes with different structures that catalyze the same reactions.

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17
Q

What are blood enzymes usually measured in?

A

Units - a measure of ENZYME ACTIVITY that represents the amount of enzyme catalyzing the conversion of one micromole of substance.

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18
Q

Where are enzymes localized in the cells and what does this is tell us about why they may be elevated in the blood?

A

Cell membranes (typically inducible enzymes)
Dissolved in cytoplasm (leakage enzymes that can be seen without severe damage)
Mitochondria (leakage enzymes seen only with necrosis)

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19
Q

What does the amount of increase of a leakage enzyme depend on? (6)

A 
Enzyme concentration in cell 
Intracellular distribution of enzyme
Severity of cell damage
Number of cells damaged
Enzyme half life in serum
Enzyme access to plasma
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20
Q

What are then four major mechanisms of enzyme elevation in the serum?

A

Release from damage cells (leakage)
Increased production (induction)
Decreased removal
Ingestion/absorption

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21
Q

What are the three most common causes of increases in induction enzymes?

A

Corticosteroids
Hyperplasia of cells
Neoplasia

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22
Q

What do decreased serum enzymes indicate?

A

No diagnostic significance - enzymes do not detect atrophy. Often low enzymes are an artifact of:
Poor sample handling
Inappropriate reference ranges
Interference from another serum element (bilirubin, lipids, hemoglobin)

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23
Q

What pathologies can cause muscle damage (5)?

A 
Trauma (surgery, injections)
Infectious or non-infectious myositis 
Ischemia
Nutrient deficiencies 
Hypo/hyperthermia
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24
Q

What enzyme is most useful to evaluate muscle damage? What kind of enzyme is it and what are it’s key properties (What, where, normal function, half-life)?

A

Creatinine kinase (CK)
Leakage enzyme of skeletal, smooth, and cardiac
Cytoplasmic (increase with less severe damage)
Normally works in ATP production
Short half life in serum

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25
Q

Name an example of a non-infectious myositis in horses that causes muscle damage

A

Exertional Equine Rhabdomyolysis

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26
Q

Name an example of a nutrient deficiency in cats that causes muscle damage

A

Deficits in essential amino acids

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27
Q

Name an example of a pathology that causes muscle ischemia in cats.

A

Saddle thrombus

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28
Q

What sample property will interfere with CK values?

A

Hemolysis - no true increase in CK but Hgb interferes with CK assay.

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29
Q

How long after injury will CK return to normal?

A

1-3 days

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30
Q

Name two secondary enzymes that can be used to measure muscle injury. Why are they less specific?

A

AST (aspartate aminotransferase)
Leakage of skeletal muscle from cytosol and mitochondria
Can also be seen with liver damage
Longer serum half-life than CK.

ALT (alanine aminotransferase)
Leakage of cardiac/skeletal - but generally a hepatic enzyme so always assume hepatic first unless clinical signs indicate otherwise.

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31
Q

What does an isolated elevated CK value mean?

A

Very acute muscle injury (when paired with appropriate clinical signs!)

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32
Q

What does an elevated CK with elevated AST mean?

A

Recent muscle injury (when paired with appropriate clinical signs!)

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33
Q

What does an isolated elevated AST mean?

A

Muscle injury two or more days in the past (when paired with appropriate clinical signs!)

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34
Q

Name the major non-enzymatic test that will be performed to look for muscle damage.

A

Urinalysis to look for myoglobinuria
Myoglobin is normally an oxygen reservoir in muscle and is released with severe damage/necrosis. Gathers in urine but NOT serum, and can cause damage to renal tubular cells in high concentrations.

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35
Q

Name three serum chemistry (non-enzymatic) abnormalities that may be seen with muscle damage.

A

Hyperkalemia (release of intracellular K+)
Hyperphosphatemia
Hypocalcemia (due to dystrophic mineralization of damaged muscle)

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36
Q

What are the three major functions of the liver?

A

Synthesis
Metabolism
Detoxification

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37
Q

Name some synthetic functions of the liver

A 
Albumin
Globulin
Fibrinogen
Clotting factors
Gluconeogenesis
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38
Q

Name some metabolic functions of the liver

A

Storage - fat, glycogen
Fat mobilization/redistribution (formation of lipoproteins and triglycerides)
Protein catabolism
Bile acid uptake and excretion (to help absorb fats)

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39
Q

Name some detoxification functions of the liver

A

Bile acid uptake and excretion (to eliminate toxins in bile)
Exogenous toxins
Endogenous toxins

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40
Q

How much of the liver must be damaged before clinical signs are evident?

A

80%

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41
Q

How much of the liver can be regenerated?

A

70%

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42
Q

What are the two main types of liver tests?

A

Serum hepatic enzyme tests (leakage or induced)

Functional tests

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43
Q

Name four commonly tested liver leakage enzymes

A

AST
ALT
SDH
GLDH

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44
Q

Name two commonly tested liver induction enzymes

A

ALP

GGT

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45
Q

Name three common liver function tests and how they are run.

A

Bile acids (send out)
Bilirubin (normal chem panel)
Ammonia (send out)

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46
Q

What can the magnitude of hepatic leakage enzymes tell us about the liver lesion? What can’t it tell us?

A

Magnitude is roughly proportional to amount of cells injured.
Tells us nothing about cause or reversibility of injury.

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47
Q

What type of animal is AST measured in and why?

A

Mainly large animals

ALT is not significant in LA. AST can be used in SA, but ALT is more specific so it tends to be the test of choice.

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48
Q

What three major pathological states are seen with AST elevations?

A

Hepatocellular damage
Skeletal muscle damage
Severe hemolysis

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49
Q

What is the function of AST in normal hepatocytes?

A

Assists in the catabolism of amino acids to create oxaloacetate, which can be used for the TCA cycle or gluconeogenesis.
Aspartate + a-ketoglutarate >AST> OAA + glutamate

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50
Q

What is the half-life of AST in cats, dogs, and horses?

A

Cats: 1.3 hours
Dogs: 12 hours
Horses: 50 hours

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51
Q

What is the half-life of ALT in cats, dogs, and horses?

A

Cats: 3.5 hours
Dogs: 2-3 days
Horses: Test not significant

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52
Q

What does AST stand for?

A

Aspartate aminotransferase

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53
Q

What does ALT stand for?

A

Alanine aminotransferase

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54
Q

What is the function of ALT in normal hepatocytes?

A

Catabolism of amino acids to create pyruvate for gluconeogenesis.
Alanine + a-ketoglutarate >ALT> pyruvate + glutamate

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55
Q

When will you see ALT elevation after liver injury (in a dog)?

A

Approximately 12 hours

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56
Q

When will ALT be normal after resolution of liver injury (in a dot)

A

A few weeks

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57
Q

What type of drugs can increase ALT?

A

Corticosteroids (slightly)

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58
Q

What feline disorder is strongly associated with a chronically elevated ALT?

A

Hyperthyroidism, due to hyper metabolism of the liver.

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59
Q

What does SDH stand for?

A

Sorbitol dehydrogenase

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60
Q

What is another name for SDH?

A

ID (iditol dehydrogenase)

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61
Q

When is SDH used?

A

Test of choice for hepatocellular damage in LA

Can be used in SA but generally is not because ALT is better measure for SA.

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62
Q

What is the function of SDH in normal hepatocytes?

A

Conversion of fructose to sorbitol using NAD

Fructose + NAD >SDH> Sorbitol + NADH

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63
Q

What are some disadvantages of using SDH?

A

Unstable enzyme
Must test in 8-12 hours (5 best) if room temp
Must test in 48 hours if frozen

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64
Q

What are some advantages of using SDH?

A

Highly sensitive (cytosolic) and specific (liver only)

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65
Q

When do you expect to see peak SDH levels after liver injury?

A

Less than 12 hours

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66
Q

When do you expect to see SDH levels return to normal after the resolution of acute liver injury?

A

3-5 days.

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67
Q

What does GLDH stand for?

A

Glutamate dehydrogenase

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68
Q

When might GLDH be used?

A

More stable, so may be a better indicator of hepatocellular damage (esp necrosis and biliary obstruction) in LA if the sample needs to be shipped.

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69
Q

What are some disadvantages of GLDH?

A

Not specific - also see increases with parturition.

Most US labs do not offer this test.

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70
Q

What is another liver enzyme used in humans but not in vetmed?

A

Lactate dehydrogenase.

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71
Q

Name three primary causes of increased liver induction enzymes

A

Drugs
Cholestasis
Biliary hyperplasia

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72
Q

What does GGT stand for?

A

Gamma glutamyltransferase

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73
Q

Name the 5 bodily tissues with the highest concentrations of GGT

A 
Pancreas
Kidney
Intestines
Liver
Mammary glands
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74
Q

Why are neonatal cows tested for GGT?

A

GGT is high in colostrum, and measuring GGT in the calves can be indicative of adequacy/inadequacy of passive transfer (<50 U/L = inadequate)
Up to 200x level in neonatal calves as adults

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75
Q

Why can GGT be used for liver if it isn’t very specific?

A

SERUM GGT is primarily from liver

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76
Q

When does serum GGT normalize in neonatal dogs, calves, and lambs?

A

Dogs: 10 days
Calves: 6-13 wks
Lambs: 1 month

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77
Q

Which type of animals is GGT primarily used in and why?

A

Mostly in LA because it has a narrower reference range than ALP
Can be used in SA - lower sensitivity but higher specificity for liver issues in dogs, so an elevation in SA is concerning for serious liver disease.

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78
Q

How can GGT be used to test for renal dysfunction?

A

An increased GGT:CRE ratio in the URINE is indicative of renal tubular damage.

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79
Q

What does ALP/AP stand for?

A

Alkaline phosphatase.

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80
Q

Which tissues have highest ALP activity?

A

Kidney and intestines, then liver and placenta.

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81
Q

Why isn’t ALP used to measure kidney or intestine function?

A

Half lives of kidney and intestine isoenzymes are VERY short in the serum. Most serum ALP that persists in the serum is of hepatic origin.

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82
Q

What is special about ALP in the cat?

A

It has a very short half live in the cat, and so may not be very sensitive. So, if you see any elevation in the cat this is SIGNIFICANT even with smaller magnitude than in dog.

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83
Q

What are the three recognized serum ALP isoenzymes?

A

LALP - liver (mc)
BALP - bone
CALP - corticosteroid (dog only)

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84
Q

What are the common reasons for increased LALP?

A

Cholestasis (intra or extra hepatic)
May also see with corticosteroids or anti-convulsants (can be normal in DOGS only, or else indicative of hepatopathy from these drugs in other species)

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85
Q

What is the relationship between ALP and icterus in dogs and horses?

A

Increased ALP precedes icterus.

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86
Q

Which cells are responsible for increased LALP due to cholestasis?

A

Bile caniliculi cells

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87
Q

What are the common reasons for increased BALP?

A

Bone growth or proliferation

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88
Q

Why might elevated BALP be normal in young animals or abnormal in old animals?

A 
Young = growing bone
Older = bone disease or primary/secondary neoplasms
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89
Q

What liver panel is run for a small animal?

A

ALT, ALP, GGT

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90
Q

What liver panel is run for a large animal?

A

SDH, AST, GGT

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91
Q

What general problems will cause abnormal liver function tests?

A

Decreased number of functional hepatocytes

Dysfunction of hepatocytes

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92
Q

What is the primary source of bilirubin in the body?

A

Hemoglobin breakdown

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93
Q

How does bilirubin normally get to the liver?

A

Red blood cells lysed and Hgb broken down by macrophages in the spleen.
Unconjugated bilirubin carried by plasma protein (generally albumin) to the liver.

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94
Q

What is another name for unconjugated bilirubin?

A

Indirect bilirubin

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95
Q

What is another name for conjugated bilirubin?

A

Direct bilirubin

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96
Q

How does bilirubin get into hepatocytes

A

Requires a different carrier protein, which can be saturated (such as in severe cases of hemolytic anemia)

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97
Q

What is delta bilirubin?

A

The small amount of conjugated bilirubin that moves into the plasma instead of the biliary tract and then binds to plasma proteins (rather than being excreted by the kidney), giving it a longer half-life.

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98
Q

What is bilirubin conjugated to?

A

Glucuronide in most species

Glucose in the horse

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99
Q

Why is jaundice less diagnostically useful in cows than other species?

A

Cows have a lower threshold for bilirubin than other species, and can have bilirubinemia with anorexia or rumen stasis as well as hepatic disease.

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100
Q

What type of bilirubinemia does fasting cause in horses?

A

Unconjugated bilirubinemia - fasting decreases bilirubin uptake by the hepatocytes.

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101
Q

What is the average plasma threshold for bilirubin before icterus occurs?

A

1.5 mg/dl

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102
Q

What is the average tissue threshold for bilirubin before icterus occurs?

A

2-3 mg/dl

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103
Q

When is bilirubinuria diagnostic?

A

Can be normal in small amounts in dog

Any level abnormal in the cat.

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104
Q

Why is herbivore serum normally slightly yellow?

A

Carotenoid pigments

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105
Q

What is the normal process of bile acid recycling called?

A

Enterohepatic circulation

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106
Q

To see normal enterohepatic circulation you must have:

A

Good portal circulation
Functional hepatocytes with normal blood flow
Unimpaired bile flow

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107
Q

Two general mechanisms by which BAs may be elevated are:

A

Decreased BA clearance from portal blood (shunt or decrease in hepatocyte function)
Decreased biliary excretion of BAs (cholestasis)

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108
Q

When should a BA be run?

A

In a non-icteric patient when liver disease is suspected (BA more sensitive than bilirubin)
If a shunt or hemolysis is suspected

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109
Q

How is a bile acid test run in a dog?

A

Tested twice - 12 hours fasted and 2 hours post-prandially

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110
Q

How is a bile acid test run in a horse?

A

Tested once after fasting - horses have no gall bladders

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111
Q

What is it indicative of if pre-meal bile acids are higher than post-meal bile acids?

A

Not clinically relevant - probably just from a spontaneous gall bladder contraction before testing

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112
Q

What is it indicative of if pre-meal bile acids are higher than post-meal bile acids?

A

Not clinically relevant - probably just from a spontaneous gall bladder contraction before testing

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113
Q

Why shouldn’t a bile acid test be run in an icteric patient

A

Except in cases of hemolysis, you can assume that BA will be high in icteric animals already

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114
Q

What will decrease serum bile acids? (Rare)

A

Delayed gastric emptying/intestinal transit time

Diseased ileum

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115
Q

How is blood ammonia produced?

A

Endogenous protein catabolism or bacterial production of ammonia

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116
Q

How is blood ammonia measured?

A 
Highly unstable, so hard to do. 
Fast patient
Collect in heparinized tube
Separate erythrocytes within 30 min
Keep on crushed ice
Minimal exposure to air
Test or freeze within 60 min
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117
Q

Why measure blood ammonia?

A

Generally used to confirm hepatic encephalopathy.

For most other hepatic diseases, less sensitive than BA.

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118
Q

Name the two most common causes of hyperammonemia

A

Shunts (defective liver blood supply)

Significantly decreased hepatocellular mass (diffuse liver disease)

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119
Q

Name less common causes of hyperammonemia (4)

A

Post prandial increase
Rare genetic mutations of urea cycle
Urea toxicosis (ingestion by cattle)
Increased bacterial production (esp in horses)

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120
Q

What are three less other tests (non-enzymatic, non-functional) that can be used to evaluate the liver?

A

Evaluation of compounds synthesized by the liver (Chem/clotting factors)
Hematology
Urinalysis

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121
Q

What compounds synthesized by the liver (5) can be tested and what results will be seen with dysfunction?

A

Cholesterol (hypocholesterolemia with liver failure, hypercholesterolemia with obstructive liver disease)
Albumin (hypoalbuminemia with liver failure)
Urea (decreased BUN with liver failure)
Glucose (wild fluctuations or hypoglycemia with liver failure)
Coagulation factors (decreased number with liver failure - may also see coagulation deficiencies due to decreased vitamin K if fat is not being absorbed)

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122
Q

What hematological changes can be seen with liver disease?

A

Anemia
Poikilocytosis - target cells and acanthocytes (change in phospholipid to cholesterol ratio of lipid membranes)
Microcytosis with portosystemic shunts

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123
Q

What may lead to hyposthenuria or isothenuria seen with liver disease?

A

PU/PD
Decreased urea production = medullary washout
Bilirubinemia or hyperammonemia leading to renal tubule damage.

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124
Q

What crystals may be seen during the urinalysis of a patient with liver disease?

A 
Bilirubin crystals (with bilirubinuria)
Urate or ammonium biurate crystals (often due to decreased metabolism of uric acid that might be seen with a portosystemic shunt).
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125
Q

What do you see with hepatic enzymes in an end-stage liver?

A

They will be normal or decreased

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126
Q

If you decide to do a liver biopsy…

A

Always run a coag panel first!

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127
Q

What are the main enzymes secreted from the exocrine pancreas? (6)

A 
Lipase (fats)
Amylase (carbohydrates) 
Trypsin
Chymotrypsin
Carboxypeptidase
Elastase
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128
Q

What are the 4 basic stimuli for pancreatic stimulations?

A

Cholecystokinin
Secretin
Gastrin
Neural input

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129
Q

What changes might be seen on the CBC of an animal with pancreatitis?

A

Inflammatory (neutrophilia with left shift) or stress (just neutrophilia) leukogram
+/- toxic neutrophils
Relative erythrocytosis from dehydration
+/- Anemia with hemorrhage or hemolysis

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130
Q

What changes might be seen on the biochemistry of an animal with pancreatitis?

A 
Hyperlipemia 
Hyperglycemia
Azotemia
Hypocalcemia
Abnormal liver enzymes/hyperbilirubinemia
Electrolyte abnormalities
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131
Q

Why do we see hyperlipemia with pancreatitis?

A

Unknown mechanism - could be a predisposing factor for pancreatitis or due to a combination of inactivation of lipoprotein lipase (decreased triglyceride clearance) and cholestasis (decreased cholesterol clearance)

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132
Q

Why do we see hyperglycemia with pancreatitis?

A

Either stress, endogenous corticosteroids, or if chronic could see from diabetes mellitus.

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133
Q

Why do we see azotemia with pancreatitis?

A

Pre renal - due to dehydration

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134
Q

Why do we see hypocalcemia with pancreatitis?

A

From saponification (dystrophic mineralization) of the fats of the mesentery.

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135
Q

Why do we see abnormal liver enzymes +/- hyperbilirubinemia with pancreatitis?

A

One of many mechanisms - liver ischemia, digestion by pancreatic enzymes, local inflammation around the bile duct. May also see due to hepatic lipidosis in the cat.

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136
Q

Why do we see electrolyte abnormalities with pancreatitis?

A

Dehydration and vomiting.

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137
Q

What other serious condition may rarely be seen with pancreatitis?

A

DIC due to trypsin activation of clotting factors, fibrinolytic factors, or elastase.

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138
Q

What is the normal role of amylase in the body?

A

Catalyzes hydrolysis of complex carbs (starch, glycogen) to form maltose and glucose.

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139
Q

What is the normal role of lipase in the body?

A

Catalyzes hydrolysis of triglycerides to fatty acids and glycerol.

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140
Q

What might cause elevated amylase or lipase?

A 
Pancreatic injury (inflammation, necrosis, neoplasia)
Obstruction of pancreatic duct
Renal insufficiency (deceased GFR)
GI disease, obstruction, or perforation
Hepatobiliary disease or neoplasia 
Glucocorticoids
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141
Q

When might elevated amylase or lipase be suggestive of pancreatitis?

A

If they are elevated 3-4 times without azotemia, USG abnormalities, or history of steroids. Only in the dog - not diagnostic in the horse or the cat.

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142
Q

Where are amylase and lipase inactivated normally?

A

The kidney tubular cells - filtered and then inactivated as they are resorbed.

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143
Q

Where is amylase found in the body?

A 
Liver
Small intestines
Kidney 
Uterus
Pancreas
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144
Q

Where is lipase found in the body?

A

Pancreas

Gastric mucosa

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145
Q

What is the diagnostic of choice for pancreatitis?

A

PLI

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146
Q

What is a quantitative PLI test?

A

SPEC

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147
Q

What is a qualitative PLI test?

A

SNAP

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148
Q

What is a TAP analyte?

A

TAP = trypsinogen activation peptide.

The product of the activation of trypsinogen to trypsin by enterokinase in the intestinal lumen

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149
Q

What is the diagnostic test of choice for EPI?

A

TLI

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150
Q

Why can’t TLI be used for pancreatitis?

A

TLI may be raised very acutely but at such a short half-life that it may not be detected. So, TLI has a low sensitivity for pancreatitis.

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151
Q

When might false negatives for EPI occur?

A

If animal has:
Concurrent renal disease (in SA)
Concurrent pancreatitis
Concurrent GI disease/obstruction (in horse)

152
Q

When might TLI testing not detect EPI without concurrent disease?

A 
Secondary EPI (blockage of pancreatic duct) 
Congenital deficiency of enteropeptidase - zymogen still detected by test.
153
Q

When should you perform laboratory tests for an animal with GI symptoms?

A

If disease is chronic (more than 2 weeks) or signs are severe.

154
Q

What do you look for in a CBC/Chem/UA with GI disease?

A

Generally, looking for normal basic lab work to rule out diseases of other organs. May see slight changes in leukogram, electrolytes, serum protein, or amylase/lipase, but not anything super specific.

155
Q

When would a serum gastrin test be indicated and what would an abnormal result be indicative of?

A

In cases of chronic, unexplained vomiting (as gastrin can cause vomiting) and a result 3-10x normal could be indicative of a gastric adenocarcinoma.

156
Q

When would serum folate and cobalamin tests be indicated?

A

Chronic weight loss and diarrhea of unknown of origin FOR WHICH EPI HAS BEEN EXCLUDED AS A CAUSE.

157
Q

What is cobalamin’s normal function?

A

Aka Vitamin B12

Cofactor for multiple enzymes needed for DNA synthesis

158
Q

How is cobalamin normally absorbed?

A

In stomach: binds to R factor secreted by gastric mucosa under acidic conditions.
In duodenum: binds to intrinsic factor produced by the pancreas under alkaline conditions.
In ileum: C-IF complex binds to receptor and is absorbed by enterocytes.

159
Q

What happens to cobalamin after absorption?

A

It is either stored in the liver or excreted in the bile.

160
Q

What could a decreased cobalamin level be indicative of?

A 
EPI (decreased bicarb and IF production)
SIBO (cobalamin binds to intestinal bacteria)
Ileal disease (cannot absorb)
Deficiency (rare in small animals unless on a stupid diet, more common with cobalt deficiencies in cattle).
161
Q

What do you have to remember when collecting serum for cobalamin testing?

A

Cobalamin is sensitive to light. Wrap tube in vet wrap.

162
Q

What is folate and what is it’s normal role in the body?

A

The anionic form of folic acid that will be converted to THF by cobalamin and used in DNA synthesis.

163
Q

What does serum folate measure? Why is this important?

A

The precursor for THF

If cobalamin is low, serum folate may be normal but there may be a functional cellular deficiency of THF.

164
Q

What could decreased serum folate be indicative of?

A

Small intestinal malabsorption

Sulfonamide antibiotic usage

165
Q

What could increased serum folate be indicative of?

A

SIBO (folate synthesized by bacteria)
Inappropriate supplementation
Hemolysis (erythrocytes contain folate)

166
Q

Decreased folate and cobalamin is indicative of?

A

Severe, chronic disease of the entire small intestine

167
Q

Decreased folate and normal cobalamin is indicative of?

A

Upper small intestine dysfunction (duodenum and jejunum absorbs folate)

168
Q

Decreased cobalamin and normal folate is indicative of?

A

Lower small intestine dysfunction (ileum absorbs cobalamin)

Can also see with rare genetic disorder that change the cobalamin/IF receptor.

169
Q

Decreased cobalamin and increased folate is indicative of?

A

Small intestinal bacterial overgrowth (in DOGS specifically)

170
Q

Name one other obscure way to test for SIBO

A

Duodenal juice culture

171
Q

Name the two sugars used for carbohydrate absorption tests and their advantages/disadvantages.

A

D-xylose: Not normally found in serum so more specific but is expensive and very few assays for this are available.
D-glucose: Easy to find/assay but have to fast animal and can see changes in curve due to abnormalities in glucose metabolism.

172
Q

What will a normal carbohydrate absorption curve look like?

A

2x baseline carb peak (max absorption) after about 2 hours.

173
Q

What will a carbohydrate absorption curve look like with partial or full malabsorption?

A 
Partial = 15 - 65% increase 2 hrs post admin
Full = <15% increase 2hrs post admin
174
Q

What will a carbohydrate absorption curve look like with insulin resistance?

A

> 2.5x increase in 2 hours and prolonged return to baseline values.

175
Q

When are carbohydrate absorption tests generally run?

A

In horses: with chronic weight loss and malformed feces.
In dogs: less common, but may be used with weight loss/diarrhea issues if pancreatic abnormalities have been ruled out.
Not run in cats, pretty useless.

176
Q

What elements besides malabsorption change the results of carbohydrate absorption tests?

A 
Delayed gastric emptying
Vomiting 
Gastric or enteric bacterial overgrowth
Rapid intestinal transit
Abnormalities with glucose metabolism/regulation (with glucose tests only)
177
Q

When is a fecal occult blood test run?

A

With unexplained diarrhea or microcytosis that may be due to a upper GI bleed that is not visible in feces, or in patients where a GI bleed is probable (GI tumors, NSAIDs, etc)

178
Q

What does a fecal occult blood test measure?

A

Pseudoperioxidase activity of hemoglobin

179
Q

What can cause false positives on fecal occult blood tests?

A

Iron supplementation

Diet rich in hemoglobin/myoglobin

180
Q

How is a fecal a-1 protease inhibitor test run and what does it evaluate?

A

Run on 3 separate fecal sample only at Texas A&M, looking for protease inhibitor generally found only in lymph and plasma.
If found in feces, indicative of PLE, especially as this protein is similar in size to albumin.

181
Q

When is peritoneal effusion evaluated? How is it evaluated?

A

Predominantly on horses with colic.
Look for bacteria/protozoa (within phagocytes, not just extracellularly), food material.
Normal peritoneal effusion will have lots of neutrophils or lymphocytes, so inflammation can be hard to evaluate.

182
Q

What three parameters are evaluated when looking at ruminal fluid?

A

pH = 6-7
Cl- concentration: <30mEq/L
Live protozoa/flora

183
Q

What does ruminal acidosis suggest?

A

Carbohydrate overload

184
Q

What does ruminal alkalosis suggest?

A

Either reduced microbial fermentation or excessive ammonia generation (abnormal flora)

185
Q

Name the four major normal functions of the kidneys.

A

Homeostasis of water, electrolytes, and acid/base balance.
Production of urine
Excretion of wast products
Production of hormones

186
Q

What are the four major parts of the nephron?

A

Glomerulus
Proximal tubule
Loop of Henle
Distal tubule and collection ducts

187
Q

What is the major function of the glomerulus?

A

Filtration

188
Q

What is the major function of the proximal tubules?

A

Reabsorption and Secretion

189
Q

What is the major function of the LOH?

A

Creation of medullary concentration gradient

190
Q

What is the major function of the distal tubules/collection ducts?

A

Concentration and dilation of urine.

191
Q

What four things can affect GFR?

A

Blood volume
Cardiac output
Number of functional glomeruli
Constriction/dilation of the arterioles around the glomerulus

192
Q

What affects the ability of a molecule to be filtered through the glomerulus?

A

Size (smaller is better)

Charge (positive or neutral is better)

193
Q

What three measurements taken together are indicators of glomerular function?

A

BUN and CRE (GFR)

Proteinuria (filtration function)

194
Q

Define a renal threshold

A

The plasma concentration of a filtered substance (such as glucose) that can be reabsorbed by the proximal tubules. This is a function of filtration rate and the ability of transporters in the tubule.

195
Q

What are the three requirements necessary for the concentration of urine?

A

ADH is present
Tubular epithelium is able to respond to ADH
Medullary concentration gradient

196
Q

What do BUN and CRE evaluate?

A

Indirect measurements of the glomerular filtration rate.

197
Q

What does BUN stand for?

A

Blood urea nitrogen.

198
Q

How is BUN produced?

A

Produced from ammonia (the byproduct of protein metabolism) in the liver.

199
Q

What may cause increases in BUN?

A

High protein diet
Gastrointestinal hemorrhage
Decrease in GFR

200
Q

What may cause decreases in BUN?

A

Low protein diet

Liver failure

201
Q

What does CRE stand for?

A

Creatinine

202
Q

How is CRE produced?

A

A normal byproduct of muscle metabolism, produced at a rate that is relatively constant to the proportional muscle mass of the animal.

203
Q

What causes increased CRE?

A

Specific to a decrease in GFR. Not changed much by muscle damage or any other pathology.

204
Q

What are the three causes of azotemia?

A

Pre-renal: Change in perfusion of kidneys.
Renal: 75% of nephrons are non-functional
Post-renal: obstruction of or damage to urinary tract

205
Q

What does SDMA stand for? What is an SDMA test?

A

Symmetric dimethylarginine. A new biomarker that can be tested for CRF.

206
Q

What is the normal function of SDMA in the body?

A

It is a byproduct of protein methylation released into the bloodstream during protein degradation.

207
Q

What are the advantages and disadvantages of SDMA?

A

It is highly sensitive and specific and may detect CRF with only a 40% loss of functional nephrons - up to 9-14 months earlier than other tests.
It is currently only run through IDEXX.

208
Q

What is Cyastatin C?

A

Low molecular weight protein used to evaluate renal function in a research setting.

209
Q

Name three types of clearance tests.

A

Endogenous CRE clearance
Exogenous CRE, inulin, or iohexol clearance
Fractional clearance test.

210
Q

How is a clearance test run?

A

Starting with an empty bladder, CRE or the administered/testable substance is measured in relation to urine volume over 24 hours.

211
Q

When might a fractional clearance test be warranted?

A

If renal loss may be contributing to blood electrolyte abnormalities. In this case, electrolytes in urine are compared to CRE in the urine, as both will be affected by urine concentration. Increase in electrolytes compared to CRE in the urine may be a sign of tubular insufficiency.

212
Q

What is USG and what does it measure?

A 
Urine Specific Gravity 
Measures density of urine compared to water - measure of: 
Number of solutes
Size of solutes
Molecular weight of solutes
213
Q

What is the USG of isosthenuric urine?

A

1.007 - 1.013

Same as the SG of the ultra filtrate coming out of the glomerulus.

214
Q

What is the USG of hypostenuric urine?

A

<1.007

215
Q

What is the USG of hypersthenuric urine?

A

Dog: >1.030
Cat: >1.035
Horse, cow: >1.025

216
Q

When does an animal become isosthenuric?

A

When 66-70% of functional nephrons are damaged.

217
Q

What is the USG gray zone and if an animal tests in this ranges what should be done?

A

Gray zone = values between isosthenuria and hypersthenuria. May be normal if the animal is well hydrated but especially if the animal is azotemic then it is an indication that the animal’s urine should be retested.

218
Q

What lab values classify pre-renal azotemia?

A

Normal USG

219
Q

What lab values classify renal azotemia?

A

Abnormal (isosthenuric) USG

220
Q

What lab values classify post-renal azotemia?

A

Variable USG

221
Q

Name one cause of extra-renal tubular insufficiency due to lack of ADH secretion.

A

Central (pituitary) diabetes insipidus

222
Q

Name some causes of extra-renal tubular insufficiency due to lack of tubule response to ADH.

A

Hypocalcemia
Pyometra
Steroids
Hyperadrenocorticism

223
Q

Name some causes of extra-renal tubular insufficiency due to loss of the medullary concentration gradient.

A

Diuresis (fluids, Pu/Pd)
Chronic hyponatremia (hypoadrenocorticism, diuretics)
Hepatic insufficiency

224
Q

Name one cause of extra-renal tubular insufficiency due to increased blood flow to the kidneys.

A

Hyperthyroidism.

225
Q

Name the advantages and disadvantages of a midstream catch urine collection.

A

A: NO trauma to the bladder (no artifactual blood). Easy.
D: At the patients leisure, contamination with the cells and bacteria of the LUT.

226
Q

Name the advantages and disadvantages of a manual expression urine collection.

A

A: At vets leisure
D: May be traumatic or force contaminated urine into the ureters, contamination with cells and bacteria of the LUT.

227
Q

Name the advantages and disadvantages of a catheterization for urine collection.

A

A: At vets leisure, less contamination.
D: May iatrogenically introduce LUT bacteria into the bladder, possibly traumatic.

228
Q

Name the advantages and disadvantages of a cystocentesis for urine collection.

A

A: At vets leisure, little risk of contamination, tolerated well, aids in problem localization.
D: Needs a large bladder, may introduce blood, hard to do in large animals.

229
Q

What are the three most important elements of handling a urine sample?

A

Perform the U/A in 30 minutes or refrigerate
Never run a U/A on cold urine
Never allow urine to sit in the sun (oxidizes the urine bilirubin).

230
Q

What are the four components of a complete urinalysis?

A

USG
Gross observation
Urine chemistries
Sediment exam.

231
Q

What four qualities should be assessed in gross observation of the urine?

A

Volume
Color
Turbidity/Transparency
Odor

232
Q

What does red urine indicate?

A

Hemoglobinuria (serum will also be yellow)
Hematuria (will see a pellet)
Myoglobuinuria (serum will be normal in color)

233
Q

Why is urine normally yellow?

A

Urochromes

234
Q

What does brown urine indicate?

A

Can be indicative of bilirubinuria

235
Q

What does cloudy urine indicate?

A

There are a lot of formed elements in the urine.

Abnormal in most species except the horse that has normal mucus in the urine.

236
Q

What does an ammonia smell to urine indicate?

A

Presence of bacteria (bacterial urease converting urea to ammonia)

237
Q

What does a acetone smell to urine indicate?

A

Presence of ketones (ketosis)

238
Q

What does urobilinogen in the urine indicate?

A

Generally not considered diagnostically relevant

CAN be increased with hemolytic or hepatic disease due to the degradation of bilirubin in the intestines.

239
Q

How does one test for urine protein?

A

Dipstick
Sulfosalicylic acid test (SSA)
Urine protein to creatinine ratio (UPC)
Urine microalbumin tests

240
Q

What are the advantages and disadvantages of a dipstick?

A

A: semi-quantitative
D: Mostly sensitive for albumin but does not detect globulins, hemoglobulins, mucoproteins, or bence-jones proteins well. Can see a false positive with very alkaline or very concentrated urine.

241
Q

What are the advantages and disadvantages of sulfosalicylic acid?

A

A: semi-quantitative, better at reacting to both albumins and more abnormal proteins. No false positives seen with alkaline urine.
D: Still read as trace -> 4+ and may have errors in reading.

242
Q

What are the advantages and disadvantages of a UPC?

A

A: Quantitative
D: NOT useful if inflammation is present (must have a quiet sediment)

243
Q

What are the advantages and disadvantages of a urine micro albumin test?

A

A: Semi-quantitative and species specific, so most sensitive test for urine albumin.
D: no tests currently available.

244
Q

What are the causes of proteinuria?

A

Prerenal/preglomerular: either abnormal protein concentration or abnormal proteins in the plasma.
Renal/glomerular: physiologic and transient or chronic and due to altered glomerular permeability.
Post-Renal/post-glomerular: Protein enters the urine after the renal pelvis (UTI, inflammation, etc)

245
Q

What is the clinical relevance of proteinuria?

A

It has a POOR PROGNOSIS - high morbidity/mortality associated with proteinuria.

246
Q

What can be ruled out to localize proteinuria?

A

Extrarenal causes (test via cystocentesis)
Pre renal causes (look at CBC/Chem)
Post glomerular causes (look at urine sediment)

247
Q

What can be ruled in when localizing proteinuria?

A

Pathologic interstitial renal disease: inflammatory sediment, clinical signs of nephritis, azotemia
Glomerular pathology: UPC >2.0
Functional glomerular pathology: Mild and transient proteinuria.

248
Q

What are the three elements of proteinuria to assess clinically?

A

Localization
Persistence
Magnitude

249
Q

What is nephrotic syndrome?

A 
A syndrome defined SYMPTOMATICALLY as: 
Proteinuria
Hypoalbuminemia
Hypercholesterolemia
Edema (generally of face or limbs) 
\+/- azotemia.
250
Q

What are two physiologic causes of glomerular proteinuria?

A

Strenuous exercise

Fever

251
Q

What is the normal pH of the urine for cats, dogs, horses, and bovine?

A

Cats/dogs: acidic, 5.5 - 7.5
Horses: neutral to alkaline, 7.0 - 8.5
Cows/small rums: alkaline, 7.5 - 9.0

252
Q

What can cause aciduria?

A

The increased excretion of H+ due to:
Acidosis
Hypochloremic metabolic acidosis
Hypokalemia

253
Q

What can cause alkalinuria

A

The decreased excretion of H+ due to;
Artifactual urea hydrolyse
Hydrolysis of urea due to urinary bacteria
Distal renal tubular acidosis

254
Q

How does a dipstick measure blood in urine?

A

Changes color with the peroxidase reaction of heme.

255
Q

How does a dipstick measure ketones in urine?

A

Acetoacetate and acetone form colored complexes with nitroprusside on dipstick.

256
Q

How does a dipstick measure bilirubin in urine?

A

Color change when bilirubin couples with substance on test strip.

257
Q

How does a dipstick measure glucose in urine?

A

Dipstick has glucose oxidase to create hydrogen peroxide on contact with glucose.

258
Q

What might cause false positives on a dipstick when looking for hematuria?

A

Myoglobinemia or hemoglobinemia (all have a heme group and so have peroxidase activity).
Any other oxidizing compounds.

259
Q

What might ketones in the urine be indicative of?

A

If ketonuria is present, ketonemia is present
Negative energy balance (increased fat metabolism)
Diabetes mellitus (decreased carb. metabolism)

260
Q

What are the 3 types of ketones produced by the body?

A

Acetone
Acetoacetate
Beta-hydroxybutric acid

261
Q

What might bilirubin in the urine be indicative of?

A

Anything that causes icterus

262
Q

What might glucose in the urine be indicative of?

A

Blood glucose has exceeded the normal renal threshold for glucose
Renal tubules have been damaged, lowering the renal threshold for glucose

263
Q

What might cause false negatives on the bilirubin dipstick?

A

Absorbic acid

Exposing urine to UV light before urinalysis

264
Q

What might cause false positives on the glucose dipstick?

A

Any other oxidizing agents

265
Q

What may cause false negatives on the glucose dipstick?

A

Cold urine
Ketones
Absorbic acid.

266
Q

What may cause false negatives on the glucose dipstick?

A

Cold urine
Ketones
Absorbic acid.

267
Q

What is normal to see in a urinalysis?

A

Up to 5 RBC/WBC per HPF
Epithelial (transitional or squamous) cells
1-2 granular or hyaline casts per LPF in concentrated urine
Artifactual crystals (generally struvite)
Fat droplets

268
Q

Where are transitional cells located in the urinary tract?

A

Between the renal pelvis and the urethra.

269
Q

Where are squamous cells located in the urinary tract?

A

In the urethra (distal / lower urinary tract)

270
Q

What are casts in urine indicative of?

A

Acute renal tubular damage. These are formed either due to necrosed/sloughed epithelial cells or during healing of the tubules.

271
Q

What types of casts might be seen (6)?

A

Renal epithelial cell casts - epithelial degeneration
Erythrocyte casts - hemorrhage/inflammation of kidney
Leukocyte casts - inflammation of kidney
Granular casts - cell and protein debris due to degeneration
Waxy casts - advanced stage of granular casts
Hyaline casts - mucoprotein casts.

272
Q

What types of crystals might be seen (7)?

A 
Struvite (magnesium ammonium phosphate) 
Calcium carbonate
Urates 
Calcium oxalate
Cystine
Cholesterol 
Bilirubin
273
Q

What are struvite crystals indicative of? What do they look like?

A

Rectangular crystals.
Neutral or alkaline urine.
Normal except with evidence of calculi.

274
Q

What are calcium carbonate crystals indicative of? What do they look like?

A

Round
Alkaline urine.
No clinical sig. in horses and rabbits.

275
Q

What are urate crystals indicative of? What do they look like?

A

Amorphous in acidic urine.
Ammonium Biruate in alkaline urine.
Indicative of hepatic disease or PSS, may be seen in dalmatians.

276
Q

What are calcium oxalate crystals indicative of? What do they look like?

A

Dihydrate or monohydrate (squares or rupees)
Variable urine.
Often seen with ethylene glycol toxicity.

277
Q

What are cystine crystals indicative of? What do they look like?

A

Hexagonal.
Seen in acid urine.
Indicative of a cysteine resorption defect.

278
Q

What are cholesterol crystals indicative of? What do they look like?

A

Sharp, angular, and rectangular or rhomboid.

Unknown significance.

279
Q

What are bilirubin crystals indicative of? What do they look like?

A

Sharp star like brown or yellow needle clusters.

Suggests an abnormal bilirubin metabolism.

280
Q

Why might you do a water deprivation test?

A

An animal is not azotemic, but is polyuric and isosthenruic. So which came first, the polyuria or the isosthenuria?

281
Q

What are some counter indications for a water deprivation test?

A 
Dehydrated or dehabilitated animal
Metabolic abnormalities (Chem) 
UTI (UA and urine culture) 
Hepatic insufficiency (bile acids) 
Hyperadrenocorticism (ACTH or low dose dexamethasone test) 
Previous renal disease
282
Q

When would you stop a water deprivation test?

A

Azotemia
Clinical dehydration
Urine concentrations
loss of 5% body weight

283
Q

What does an abnormal water deprivation test indicate?

A

Failure of the pituitary to release ADH
Failure of the tubules to respond to ADH
Osmotic diuresis (renal disease)
Medullary washout (renal tubular insufficiency)

284
Q

When is an ADH response test done and what does it indicate?

A

Exogenous ADH is given if the animal fails to concentrate urine during water deprivation test. If urine then concentrates, this confirms central diabetes insipidus. If not, then any of the other causes is possible.

285
Q

Why is a modified water deprivation test called modified?

A

Animal’s water is slowly reduced over a few days to regenerate medullary concentration gradient that would have dissipated with PU before water is completely removed.

286
Q

What are urinary enzymes and how are they used?

A

GGT, NAG, ALP
Released INTO the urine with tubular damage and most often used to monitor renal health while a patient is on nephrotoxic drugs.
Measured as a ratio in the urine to creatinine.

287
Q

Name some other laboratory abnormalities that may be seen with liver disease.

A 
Non-regenerative anemia
Hyperphosphatemia (hypo in horses) 
Hypo / hyper calcemia
Hypokalemia
Metabolic acidosis
Hypercholesterolemia
288
Q

Why might non-regenerative anemia be seen with renal disease?

A

Only with chronic renal disease due to reduction in production of erythropoietin.

289
Q

Why might hyperphosphatemia be seen with renal disease?

A

Decreased GFR - more time for reabsorption of phosphate.

290
Q

Why might hypocalcemia be seen with renal disease?

A

Acute: decreased reabsorption of Ca2+
Chronic: reduced activation of Vitamin D. May also be secondary as compensation for increased phosphorus.

291
Q

Why might hypercalcemia be seen with renal disease?

A

Common in horses because the kidneys excrete Ca2+ normally.

292
Q

Why might hypokalemia be seen with renal disease?

A

Excess renal loss, decreased dietary intake, and with cattle also see loss in saliva.

293
Q

Why might metabolic acidosis be seen with renal disease?

A

Chronic - limited ability of the kidney to excrete hydrogen ions.

294
Q

Why might hypercholesterolemia be seen with renal disease?

A

Is associated with hypoalbuminemia from protein losing nephropathies.

295
Q

What is the name of the staging system used for renal disease?

A

IRIS (international renal interest society)

296
Q

What is uremia defined as?

A

Clinical symptoms associated with kidney disease.

297
Q

What is chronic renal disease defined as?

A

A lesion (structural or functional) lasting longer than 2-3 months as demonstrated by multiple urine samples or multiple azotemic blood samples.

298
Q

What are some typical clinical symptoms of acute renal disease?

A

Azotemia
Isosthenuria
Anuria/Oligouria
Hyperphosphatemia/hyperkalemia/acidosis

299
Q

What are some of the early signs of ethylene glycol toxicity?

A 
CNS signs 
Tachypnea
Tachycardia
Decreased bicarbonate
Increased anion gap
Increased osmolal gap
Hypocalcemia
Calcium oxalate crystalluria
300
Q

What are some of the later signs of ethylene glycol toxicity?

A

Azotemia
Isosthenuria
Hyperphosphatemia
Hyperkalemia

301
Q

What is the pathogenesis of ethylene glycol toxicity?

A

Ethylene glycol converted by alcohol dehydrogenase in the liver
Glycoaldehyde
Glycol acid
Glyoxylic acid (CNS/nephrotoxic)
Oxalic acid (CNS/nephrotoxic)
Calcium oxalate (crystalluria and renal tubule obstruction leading to acute renal failure).

302
Q

What are the causes of primary polydipsia?

A

Psychogenic (neurologic or hepatic)

303
Q

What are the causes of primary polyuria?

A

Osmotic (diabetes mellitus, CRF, etc)
Lack of ADH (central diabetes insipidus)
Primary nephrogenic d. insipidus (rare, congenital)
Secondary nephrogenic d. insipidus (acquired)
Medullary washout.

304
Q

When do you need arterial blood for a blood gas?

A

When measuring pO2, though it can be used for any other values.

305
Q

When can you use venous blood for a blood gas?

A

pH
pCO2
HCO3-

306
Q

How should you collect a sample for a blood gas?

A

Quickly in a heparinized syringe which is then capped and run quickly or put on ice.
Make sure this is what the machine calls for.
Make sure that you collect amount of blood that the syringe calls for to maintain appropriate heparin/blood ratio.

307
Q

What should you note about the patient before collecting sample for a blood gas?

A

Temperature and {Hgb}.

308
Q

What is TCO2?

A

Essentially an estimate of bicarbonate (96% of TCO2)

This is stable in the blood and so can be reported on most general chemistries.

309
Q

What is BE?

A

Base excess: the actual bicarb concentration - the normal bicarb concentration.

310
Q

What are the arterial/venous classic normals for pH?

A

A: 7.4
V: 7.4

311
Q

What are the arterial/venous classic normals for pCO2?

A

A: 40
V: 45

312
Q

What are the arterial/venous classic normals for pO2?

A

A: 90-100
V: 40-60

313
Q

What are the arterial/venous classic normals for HCO3-?

A

A: 24
V: 24

314
Q

What are the arterial/venous classic normals for O2 sat?

A

A: 95-100
V: 40-70

315
Q

What is BE used for clinically?

A

Primarily used to determine the amount of bicarbonate to give an acidotic animal.

316
Q

What is the most important buffer system in the animal?

A

Bicarbonate/carbonic acid system.

317
Q

What does the Henderson-Hasselbach equation describe?

A

The relationship between pH, pCO2 and HCO3- in the animal.

318
Q

What controls pCO2?

A

Respiration

319
Q

What controls HCO3-?

A

Renal excretion and reabsorption.

320
Q

What other two main variables control pH of the body besides the bicarbonate/carbonic acid system?

A

Protein concentration and electrolytes.

321
Q

Compensation equation for metabolic acidosis?

A

For each 1 mEq/L decrease in HCO3-

pCO2 decreases by 0.7 mmHg

322
Q

Compensation equation for metabolic alkalosis?

A

For each 1 mEq/L increase in HCO3-

pCO2 increases by 0.7 mmHg

323
Q

What are the compensation equations based on?

A

Based off a DOG, but can be used at least to approximate compensation in other animals.

324
Q

What are the two types of metabolic acidosis and how do you tell them apart?

A

Secretional/hyperchloremic acidosis : normal anion gap

Titrational acidosis: increased anion gap

325
Q

What are the three main causes of secretional metabolic acidosis?

A 
All = loss of bicarb rich fluid
Intestinal fluid loss (diarrhea or GI entrapment)
Saliva loss (esp in ruminants that can't swallow)
Urine loss (kidney tubules unable to resorb bicarb)
326
Q

Why do you see hyperchloremia with secretional metabolic acidosis?

A

Chloride is resorbed in the kidney to maintain the electroneutrality of the body when bicarbonate is lost.

327
Q

What are the three main causes of titrational metabolic acidosis?

A

Retention of acid
Generation of acid
Ingestion of acid

328
Q

How is the anion gap calculated?

A

Positive charges - negative charges

Na+K+UC (constant) - HCO3+Cl+UA (variable)

329
Q

Give 4 common examples of titrational metabolic acidosis

A

Lactic acidosis
Uremic acidosis
Ketoacidosis
Exogenous acid ingestion

330
Q

Give 4 common examples of titrational metabolic acidosis

A

Lactic acidosis
Uremic acidosis
Ketoacidosis
Exogenous acid ingestion

331
Q

What generates lactic acidosis?

A

Hypoxia/ischemia or grain overload

332
Q

What generates uremic acidosis?

A

Decreased renal excretion of H2SO4 and H2PO4

333
Q

What generates ketoacidosis?

A

Diabetes mellitus or starvation

334
Q

What are some common exogenous acids that an animal might ingest?

A

Ethylene glycol

Methanol

335
Q

What can mask an anion gap change due to titrational metabolic acidosis?

A

Hypoproteinemia - decreases the normal UA-

336
Q

How is metabolic acidosis treated?

A

TREAT THE UNDERLYING DISEASE

Bicarbonate in fluid replacement.

337
Q

What is the most common cause of metabolic alkalosis?

A

Loss of HCl rich fluid, usually from the stomach or abomasum.

338
Q

Why does a loss in HCl result in increase of HCO3-?

A

Animals are hypovolemic from fluid loss.
Na retained by the kidneys to replace fluid
An anion must also be retained by the kidneys to maintain electroneutrality. This would normally be chloride, but in a hypochloremic animal bicarbonate is used instead.
Animal could also secrete H+ to maintain electroneutrality but this would also make the animal alkalotic.

339
Q

What is paradoxical aciduria and why does it occur?

A

Animal is alkalotic but secreting H+ to make the urine acidic.
Typically only occurs in hypokalemic animals.

340
Q

Name three less common causes of metabolic alkalosis?

A

Overadminstration of bicarbonate containing fluids (LRS)
Overuse of loop diuretics leading to hypokalemia
Low chloride intake (rare)

341
Q

When is paradoxical aciduria seen clinically?

A

Cows with DAs.

342
Q

What type of metabolic compensation is seen with acute respiratory abnormalities?

A

Cellular responses: H+ is released or absorbed by intracellular phosphates and proteins

343
Q

What type of metabolic compensation is seen with chronic respiratory abnormalities? What is considered chronic in this case?

A 
Renal responses (2-3 days) 
Changes the renal excretion of H+ and HCO3-
344
Q

What are the two main causes of respiratory alkalosis? How can they be differentiated?

A

ALVEOLAR HYPERVENTILATION
Extrathoracic:
Intrathoracic:

345
Q

What are the two main causes of respiratory alkalosis? How can they be differentiated?

A

ALVEOLAR HYPERVENTILATION
Extrathoracic: transient, normal pO2
Intrathoracic: chronic, decreased pO2

346
Q

What are some extrathoracic causes of respiratory alkalosis?

A

Pain
Fever
Fear/apprehension
Anemia

347
Q

What are some intrathoracic causes of respiratory alkalosis?

A 
Pneumonia
Pulmonary edema
Thoracic masses
Congestive heart failure with right to left blood shunting
Pulmonary thromboembolism
Pleural effusion
348
Q

What are the two main causes of respiratory acidosis?

A

Can be caused by any intrathoracic cause of respiratory alkalosis that becomes severe enough to prevent the diffusion of CO2 over the alveoli
Hypoventilation

349
Q

What are some causes of hypoventilation?

A 
Decreased movement of diaphragm
CNS depression
Drugs
Neuromuscular disorders
Severe bloat or abdominal masses
350
Q

How are pO2 and respiratory acidosis related?

A

pO2 is low.

351
Q

What is the name of the most common non-traditional approach to acid-base metabolism?

A

Stewart’s quantitive approach.

352
Q

What are the three basic parameters of Stewart’s quantitive approach?

A

pCO2
SID - strong ion difference (Na, Cl, and UA-)
Atot - total contraction of weak acids including protein and phosphates.

353
Q

How should samples be collected to measure electrolytes?

A

Collect serum and separate it from red blood cells as quickly as possible.

354
Q

What may cause ARTIFACTUAL hypernatremia or hyperkalemia? Why?

A

Hemolysis or lipemia.
These increase the NON-aqueous phase of the electrolytes which will then be measured by flame photometers or ion-specific electrodes.

355
Q

What is unique about electrolyte reference intervals?

A

They can vary widely depending on how the electrolytes are measured - make sure to use the RIs for your lab/machine and not others.

356
Q

What three hormones control body sodium concentration?

A

Aldosterone
Atrial natriuretic factor (ANF)
Anti-diarrheal hormone (ADH)

357
Q

What are the three main causes of hypernatremia?

A 
Solute gain (salt poisoning) 
Pure water deficit
Hypotonic loss
358
Q

What causes hyponatremia?

A

A loss in sodium rich fluids.
Examples:
Hypoadrenocorticism, diarrhea, renal disease, dietary salt deficiency, treatment with low sodium fluids, diabetes mellitus, or third space loss.

359
Q

What causes solute gain?

A

Access to rich salt diet but limited access to water
Hypertonic fluid administration
Hyperaldosteronism (rare)

360
Q

What causes a pure water deficit?

A

Inadequate water access
Decreased drinking in sick animals
Defective thirst response (rare)
Loss of water (diabetes insidious, panting, hyperventilation, fever)

361
Q

What causes hypertonic water loss?

A

Renal osmotic diuresis
Vomiting or diarrhea
3rd space loss due to burns or pancreatitis

362
Q

What is the action of ADH?

A

Promotes renal water conservation

363
Q

What is the relationship between serum potassium and body potassium?

A

Very weak relationship - the cells can shift K+ in or out to maintain narrow functional potassium window.

364
Q

What is the relationship between serum potassium and body potassium?

A

Very weak relationship - the cells can shift K+ in or out to maintain narrow functional potassium window.

365
Q

Name three causes of hyperkalemia.

A

Decreased GFR
Acidosis (H+ shifts intracellularly and K+ moves out)
Tissue necrosis/hemolysis

366
Q

Name three causes of hypokalemia.

A

Excessive GI loss from vomiting or diarrhea
Excessive urinary loss (diabetes or renal disease in cats)
Alkalosis

367
Q

Name three causes of hypokalemia.

A

Excessive GI loss from vomiting or diarrhea
Excessive urinary loss (diabetes or renal disease in cats)
Alkalosis

368
Q

Why should chloride be corrected to look for abnormalities?

A

Usually, chloride changes with Na+ to maintain electroneutrality, so primary changes in chloride are rare. Corrected Cl is significant if outside normal window.

369
Q

What causes primary chloride abnormalities?

A

Hypochloremia due to sequestration/loss with metabolic alkalosis
Hyperchloremia with secretional metabolic acidosis
Artifactual rise with potassium bromide therapy.

370
Q

What are the four main causes of lactic acidosis? ?

A

Shock
Hypoxia/ischemia/poor perfusion
Grain overload
Sustained heavy exercise

371
Q

Why is lactate useful clinically?

A

It is a prognostic indicator - increased lactate shows amount of poor perfusion.

372
Q

What is osmolality?

A

Number of particles / solution weight

373
Q

What are the main substances used to calculate estimated osmolality?

A

Sodium, potassium, glucose, BUN

374
Q

What is used to measure osmolality?

A

Osmometer

375
Q

What is the osmolal gap?

A

The actual - estimated osmolality.

Clinical Pathology (3 decks)

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