Unit 2 Flashcards
(375 cards)
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.
2
Q
Sensitivity equation?
A
100 x (TP / TP + FN)
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.
4
Q
Specificity equation?
A
100 x (TN / TN + FP)
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)
6
Q
What is the positive predictive value?
A
The percent of animals that test positive that are actually diseased.
7
Q
Positive predictive value equation?
A
100 x (TP / TP + FP)
8
Q
What is the negative predictive value?
A
The percent of animals that test negative that are actually diseased.
9
Q
Negative predictive value equation?
A
100 x (TN / TN + FN)
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)
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.
12
Q
What is test accuracy?
A
How close a result is to a “true” value.
13
Q
What is test precision?
A
How repeatable a test value is.
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.
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.
16
Q
What are isoenzymes?
A
Enzymes with different structures that catalyze the same reactions.
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.
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)
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
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
21
Q
What are the three most common causes of increases in induction enzymes?
A
Corticosteroids
Hyperplasia of cells
Neoplasia
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)
23
Q
What pathologies can cause muscle damage (5)?
A
Trauma (surgery, injections) Infectious or non-infectious myositis Ischemia Nutrient deficiencies Hypo/hyperthermia
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
25
Name an example of a non-infectious myositis in horses that causes muscle damage
Exertional Equine Rhabdomyolysis
26
Name an example of a nutrient deficiency in cats that causes muscle damage
Deficits in essential amino acids
27
Name an example of a pathology that causes muscle ischemia in cats.
Saddle thrombus
28
What sample property will interfere with CK values?
Hemolysis - no true increase in CK but Hgb interferes with CK assay.
29
How long after injury will CK return to normal?
1-3 days
30
Name two secondary enzymes that can be used to measure muscle injury. Why are they less specific?
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.
31
What does an isolated elevated CK value mean?
Very acute muscle injury (when paired with appropriate clinical signs!)
32
What does an elevated CK with elevated AST mean?
Recent muscle injury (when paired with appropriate clinical signs!)
33
What does an isolated elevated AST mean?
Muscle injury two or more days in the past (when paired with appropriate clinical signs!)
34
Name the major non-enzymatic test that will be performed to look for muscle damage.
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.
35
Name three serum chemistry (non-enzymatic) abnormalities that may be seen with muscle damage.
Hyperkalemia (release of intracellular K+)
Hyperphosphatemia
Hypocalcemia (due to dystrophic mineralization of damaged muscle)
36
What are the three major functions of the liver?
Synthesis
Metabolism
Detoxification
37
Name some synthetic functions of the liver
```
Albumin
Globulin
Fibrinogen
Clotting factors
Gluconeogenesis
```
38
Name some metabolic functions of the liver
Storage - fat, glycogen
Fat mobilization/redistribution (formation of lipoproteins and triglycerides)
Protein catabolism
Bile acid uptake and excretion (to help absorb fats)
39
Name some detoxification functions of the liver
Bile acid uptake and excretion (to eliminate toxins in bile)
Exogenous toxins
Endogenous toxins
40
How much of the liver must be damaged before clinical signs are evident?
80%
41
How much of the liver can be regenerated?
70%
42
What are the two main types of liver tests?
Serum hepatic enzyme tests (leakage or induced)
| Functional tests
43
Name four commonly tested liver leakage enzymes
AST
ALT
SDH
GLDH
44
Name two commonly tested liver induction enzymes
ALP
| GGT
45
Name three common liver function tests and how they are run.
Bile acids (send out)
Bilirubin (normal chem panel)
Ammonia (send out)
46
What can the magnitude of hepatic leakage enzymes tell us about the liver lesion? What can't it tell us?
Magnitude is roughly proportional to amount of cells injured.
Tells us nothing about cause or reversibility of injury.
47
What type of animal is AST measured in and why?
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.
48
What three major pathological states are seen with AST elevations?
Hepatocellular damage
Skeletal muscle damage
Severe hemolysis
49
What is the function of AST in normal hepatocytes?
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
50
What is the half-life of AST in cats, dogs, and horses?
Cats: 1.3 hours
Dogs: 12 hours
Horses: 50 hours
51
What is the half-life of ALT in cats, dogs, and horses?
Cats: 3.5 hours
Dogs: 2-3 days
Horses: Test not significant
52
What does AST stand for?
Aspartate aminotransferase
53
What does ALT stand for?
Alanine aminotransferase
54
What is the function of ALT in normal hepatocytes?
Catabolism of amino acids to create pyruvate for gluconeogenesis.
Alanine + a-ketoglutarate >ALT> pyruvate + glutamate
55
When will you see ALT elevation after liver injury (in a dog)?
Approximately 12 hours
56
When will ALT be normal after resolution of liver injury (in a dot)
A few weeks
57
What type of drugs can increase ALT?
Corticosteroids (slightly)
58
What feline disorder is strongly associated with a chronically elevated ALT?
Hyperthyroidism, due to hyper metabolism of the liver.
59
What does SDH stand for?
Sorbitol dehydrogenase
60
What is another name for SDH?
ID (iditol dehydrogenase)
61
When is SDH used?
Test of choice for hepatocellular damage in LA
| Can be used in SA but generally is not because ALT is better measure for SA.
62
What is the function of SDH in normal hepatocytes?
Conversion of fructose to sorbitol using NAD
| Fructose + NAD >SDH> Sorbitol + NADH
63
What are some disadvantages of using SDH?
Unstable enzyme
Must test in 8-12 hours (5 best) if room temp
Must test in 48 hours if frozen
64
What are some advantages of using SDH?
Highly sensitive (cytosolic) and specific (liver only)
65
When do you expect to see peak SDH levels after liver injury?
Less than 12 hours
66
When do you expect to see SDH levels return to normal after the resolution of acute liver injury?
3-5 days.
67
What does GLDH stand for?
Glutamate dehydrogenase
68
When might GLDH be used?
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.
69
What are some disadvantages of GLDH?
Not specific - also see increases with parturition.
| Most US labs do not offer this test.
70
What is another liver enzyme used in humans but not in vetmed?
Lactate dehydrogenase.
71
Name three primary causes of increased liver induction enzymes
Drugs
Cholestasis
Biliary hyperplasia
72
What does GGT stand for?
Gamma glutamyltransferase
73
Name the 5 bodily tissues with the highest concentrations of GGT
```
Pancreas
Kidney
Intestines
Liver
Mammary glands
```
74
Why are neonatal cows tested for GGT?
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
75
Why can GGT be used for liver if it isn't very specific?
SERUM GGT is primarily from liver
76
When does serum GGT normalize in neonatal dogs, calves, and lambs?
Dogs: 10 days
Calves: 6-13 wks
Lambs: 1 month
77
Which type of animals is GGT primarily used in and why?
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.
78
How can GGT be used to test for renal dysfunction?
An increased GGT:CRE ratio in the URINE is indicative of renal tubular damage.
79
What does ALP/AP stand for?
Alkaline phosphatase.
80
Which tissues have highest ALP activity?
Kidney and intestines, then liver and placenta.
81
Why isn't ALP used to measure kidney or intestine function?
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.
82
What is special about ALP in the cat?
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.
83
What are the three recognized serum ALP isoenzymes?
LALP - liver (mc)
BALP - bone
CALP - corticosteroid (dog only)
84
What are the common reasons for increased LALP?
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)
85
What is the relationship between ALP and icterus in dogs and horses?
Increased ALP precedes icterus.
86
Which cells are responsible for increased LALP due to cholestasis?
Bile caniliculi cells
87
What are the common reasons for increased BALP?
Bone growth or proliferation
88
Why might elevated BALP be normal in young animals or abnormal in old animals?
```
Young = growing bone
Older = bone disease or primary/secondary neoplasms
```
89
What liver panel is run for a small animal?
ALT, ALP, GGT
90
What liver panel is run for a large animal?
SDH, AST, GGT
91
What general problems will cause abnormal liver function tests?
Decreased number of functional hepatocytes
| Dysfunction of hepatocytes
92
What is the primary source of bilirubin in the body?
Hemoglobin breakdown
93
How does bilirubin normally get to the liver?
Red blood cells lysed and Hgb broken down by macrophages in the spleen.
Unconjugated bilirubin carried by plasma protein (generally albumin) to the liver.
94
What is another name for unconjugated bilirubin?
Indirect bilirubin
95
What is another name for conjugated bilirubin?
Direct bilirubin
96
How does bilirubin get into hepatocytes
Requires a different carrier protein, which can be saturated (such as in severe cases of hemolytic anemia)
97
What is delta bilirubin?
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.
98
What is bilirubin conjugated to?
Glucuronide in most species
| Glucose in the horse
99
Why is jaundice less diagnostically useful in cows than other species?
Cows have a lower threshold for bilirubin than other species, and can have bilirubinemia with anorexia or rumen stasis as well as hepatic disease.
100
What type of bilirubinemia does fasting cause in horses?
Unconjugated bilirubinemia - fasting decreases bilirubin uptake by the hepatocytes.
101
What is the average plasma threshold for bilirubin before icterus occurs?
1.5 mg/dl
102
What is the average tissue threshold for bilirubin before icterus occurs?
2-3 mg/dl
103
When is bilirubinuria diagnostic?
Can be normal in small amounts in dog
| Any level abnormal in the cat.
104
Why is herbivore serum normally slightly yellow?
Carotenoid pigments
105
What is the normal process of bile acid recycling called?
Enterohepatic circulation
106
To see normal enterohepatic circulation you must have:
Good portal circulation
Functional hepatocytes with normal blood flow
Unimpaired bile flow
107
Two general mechanisms by which BAs may be elevated are:
Decreased BA clearance from portal blood (shunt or decrease in hepatocyte function)
Decreased biliary excretion of BAs (cholestasis)
108
When should a BA be run?
In a non-icteric patient when liver disease is suspected (BA more sensitive than bilirubin)
If a shunt or hemolysis is suspected
109
How is a bile acid test run in a dog?
Tested twice - 12 hours fasted and 2 hours post-prandially
110
How is a bile acid test run in a horse?
Tested once after fasting - horses have no gall bladders
111
What is it indicative of if pre-meal bile acids are higher than post-meal bile acids?
Not clinically relevant - probably just from a spontaneous gall bladder contraction before testing
112
What is it indicative of if pre-meal bile acids are higher than post-meal bile acids?
Not clinically relevant - probably just from a spontaneous gall bladder contraction before testing
113
Why shouldn't a bile acid test be run in an icteric patient
Except in cases of hemolysis, you can assume that BA will be high in icteric animals already
114
What will decrease serum bile acids? (Rare)
Delayed gastric emptying/intestinal transit time
| Diseased ileum
115
How is blood ammonia produced?
Endogenous protein catabolism or bacterial production of ammonia
116
How is blood ammonia measured?
```
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
```
117
Why measure blood ammonia?
Generally used to confirm hepatic encephalopathy.
| For most other hepatic diseases, less sensitive than BA.
118
Name the two most common causes of hyperammonemia
Shunts (defective liver blood supply)
| Significantly decreased hepatocellular mass (diffuse liver disease)
119
Name less common causes of hyperammonemia (4)
Post prandial increase
Rare genetic mutations of urea cycle
Urea toxicosis (ingestion by cattle)
Increased bacterial production (esp in horses)
120
What are three less other tests (non-enzymatic, non-functional) that can be used to evaluate the liver?
Evaluation of compounds synthesized by the liver (Chem/clotting factors)
Hematology
Urinalysis
121
What compounds synthesized by the liver (5) can be tested and what results will be seen with dysfunction?
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)
122
What hematological changes can be seen with liver disease?
Anemia
Poikilocytosis - target cells and acanthocytes (change in phospholipid to cholesterol ratio of lipid membranes)
Microcytosis with portosystemic shunts
123
What may lead to hyposthenuria or isothenuria seen with liver disease?
PU/PD
Decreased urea production = medullary washout
Bilirubinemia or hyperammonemia leading to renal tubule damage.
124
What crystals may be seen during the urinalysis of a patient with liver disease?
```
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).
```
125
What do you see with hepatic enzymes in an end-stage liver?
They will be normal or decreased
126
If you decide to do a liver biopsy...
Always run a coag panel first!
127
What are the main enzymes secreted from the exocrine pancreas? (6)
```
Lipase (fats)
Amylase (carbohydrates)
Trypsin
Chymotrypsin
Carboxypeptidase
Elastase
```
128
What are the 4 basic stimuli for pancreatic stimulations?
Cholecystokinin
Secretin
Gastrin
Neural input
129
What changes might be seen on the CBC of an animal with pancreatitis?
Inflammatory (neutrophilia with left shift) or stress (just neutrophilia) leukogram
+/- toxic neutrophils
Relative erythrocytosis from dehydration
+/- Anemia with hemorrhage or hemolysis
130
What changes might be seen on the biochemistry of an animal with pancreatitis?
```
Hyperlipemia
Hyperglycemia
Azotemia
Hypocalcemia
Abnormal liver enzymes/hyperbilirubinemia
Electrolyte abnormalities
```
131
Why do we see hyperlipemia with pancreatitis?
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)
132
Why do we see hyperglycemia with pancreatitis?
Either stress, endogenous corticosteroids, or if chronic could see from diabetes mellitus.
133
Why do we see azotemia with pancreatitis?
Pre renal - due to dehydration
134
Why do we see hypocalcemia with pancreatitis?
From saponification (dystrophic mineralization) of the fats of the mesentery.
135
Why do we see abnormal liver enzymes +/- hyperbilirubinemia with pancreatitis?
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.
136
Why do we see electrolyte abnormalities with pancreatitis?
Dehydration and vomiting.
137
What other serious condition may rarely be seen with pancreatitis?
DIC due to trypsin activation of clotting factors, fibrinolytic factors, or elastase.
138
What is the normal role of amylase in the body?
Catalyzes hydrolysis of complex carbs (starch, glycogen) to form maltose and glucose.
139
What is the normal role of lipase in the body?
Catalyzes hydrolysis of triglycerides to fatty acids and glycerol.
140
What might cause elevated amylase or lipase?
```
Pancreatic injury (inflammation, necrosis, neoplasia)
Obstruction of pancreatic duct
Renal insufficiency (deceased GFR)
GI disease, obstruction, or perforation
Hepatobiliary disease or neoplasia
Glucocorticoids
```
141
When might elevated amylase or lipase be suggestive of pancreatitis?
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.
142
Where are amylase and lipase inactivated normally?
The kidney tubular cells - filtered and then inactivated as they are resorbed.
143
Where is amylase found in the body?
```
Liver
Small intestines
Kidney
Uterus
Pancreas
```
144
Where is lipase found in the body?
Pancreas
| Gastric mucosa
145
What is the diagnostic of choice for pancreatitis?
PLI
146
What is a quantitative PLI test?
SPEC
147
What is a qualitative PLI test?
SNAP
148
What is a TAP analyte?
TAP = trypsinogen activation peptide.
| The product of the activation of trypsinogen to trypsin by enterokinase in the intestinal lumen
149
What is the diagnostic test of choice for EPI?
TLI
150
Why can't TLI be used for pancreatitis?
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.
151
When might false negatives for EPI occur?
If animal has:
Concurrent renal disease (in SA)
Concurrent pancreatitis
Concurrent GI disease/obstruction (in horse)
152
When might TLI testing not detect EPI without concurrent disease?
```
Secondary EPI (blockage of pancreatic duct)
Congenital deficiency of enteropeptidase - zymogen still detected by test.
```
153
When should you perform laboratory tests for an animal with GI symptoms?
If disease is chronic (more than 2 weeks) or signs are severe.
154
What do you look for in a CBC/Chem/UA with GI disease?
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
When would a serum gastrin test be indicated and what would an abnormal result be indicative of?
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
When would serum folate and cobalamin tests be indicated?
Chronic weight loss and diarrhea of unknown of origin FOR WHICH EPI HAS BEEN EXCLUDED AS A CAUSE.
157
What is cobalamin's normal function?
Aka Vitamin B12
| Cofactor for multiple enzymes needed for DNA synthesis
158
How is cobalamin normally absorbed?
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
What happens to cobalamin after absorption?
It is either stored in the liver or excreted in the bile.
160
What could a decreased cobalamin level be indicative of?
```
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
What do you have to remember when collecting serum for cobalamin testing?
Cobalamin is sensitive to light. Wrap tube in vet wrap.
162
What is folate and what is it's normal role in the body?
The anionic form of folic acid that will be converted to THF by cobalamin and used in DNA synthesis.
163
What does serum folate measure? Why is this important?
The precursor for THF
| If cobalamin is low, serum folate may be normal but there may be a functional cellular deficiency of THF.
164
What could decreased serum folate be indicative of?
Small intestinal malabsorption
| Sulfonamide antibiotic usage
165
What could increased serum folate be indicative of?
SIBO (folate synthesized by bacteria)
Inappropriate supplementation
Hemolysis (erythrocytes contain folate)
166
Decreased folate and cobalamin is indicative of?
Severe, chronic disease of the entire small intestine
167
Decreased folate and normal cobalamin is indicative of?
Upper small intestine dysfunction (duodenum and jejunum absorbs folate)
168
Decreased cobalamin and normal folate is indicative of?
Lower small intestine dysfunction (ileum absorbs cobalamin)
| Can also see with rare genetic disorder that change the cobalamin/IF receptor.
169
Decreased cobalamin and increased folate is indicative of?
Small intestinal bacterial overgrowth (in DOGS specifically)
170
Name one other obscure way to test for SIBO
Duodenal juice culture
171
Name the two sugars used for carbohydrate absorption tests and their advantages/disadvantages.
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
What will a normal carbohydrate absorption curve look like?
2x baseline carb peak (max absorption) after about 2 hours.
173
What will a carbohydrate absorption curve look like with partial or full malabsorption?
```
Partial = 15 - 65% increase 2 hrs post admin
Full = <15% increase 2hrs post admin
```
174
What will a carbohydrate absorption curve look like with insulin resistance?
>2.5x increase in 2 hours and prolonged return to baseline values.
175
When are carbohydrate absorption tests generally run?
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
What elements besides malabsorption change the results of carbohydrate absorption tests?
```
Delayed gastric emptying
Vomiting
Gastric or enteric bacterial overgrowth
Rapid intestinal transit
Abnormalities with glucose metabolism/regulation (with glucose tests only)
```
177
When is a fecal occult blood test run?
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
What does a fecal occult blood test measure?
Pseudoperioxidase activity of hemoglobin
179
What can cause false positives on fecal occult blood tests?
Iron supplementation
| Diet rich in hemoglobin/myoglobin
180
How is a fecal a-1 protease inhibitor test run and what does it evaluate?
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
When is peritoneal effusion evaluated? How is it evaluated?
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
What three parameters are evaluated when looking at ruminal fluid?
pH = 6-7
Cl- concentration: <30mEq/L
Live protozoa/flora
183
What does ruminal acidosis suggest?
Carbohydrate overload
184
What does ruminal alkalosis suggest?
Either reduced microbial fermentation or excessive ammonia generation (abnormal flora)
185
Name the four major normal functions of the kidneys.
Homeostasis of water, electrolytes, and acid/base balance.
Production of urine
Excretion of wast products
Production of hormones
186
What are the four major parts of the nephron?
Glomerulus
Proximal tubule
Loop of Henle
Distal tubule and collection ducts
187
What is the major function of the glomerulus?
Filtration
188
What is the major function of the proximal tubules?
Reabsorption and Secretion
189
What is the major function of the LOH?
Creation of medullary concentration gradient
190
What is the major function of the distal tubules/collection ducts?
Concentration and dilation of urine.
191
What four things can affect GFR?
Blood volume
Cardiac output
Number of functional glomeruli
Constriction/dilation of the arterioles around the glomerulus
192
What affects the ability of a molecule to be filtered through the glomerulus?
Size (smaller is better)
| Charge (positive or neutral is better)
193
What three measurements taken together are indicators of glomerular function?
BUN and CRE (GFR)
| Proteinuria (filtration function)
194
Define a renal threshold
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
What are the three requirements necessary for the concentration of urine?
ADH is present
Tubular epithelium is able to respond to ADH
Medullary concentration gradient
196
What do BUN and CRE evaluate?
Indirect measurements of the glomerular filtration rate.
197
What does BUN stand for?
Blood urea nitrogen.
198
How is BUN produced?
Produced from ammonia (the byproduct of protein metabolism) in the liver.
199
What may cause increases in BUN?
High protein diet
Gastrointestinal hemorrhage
Decrease in GFR
200
What may cause decreases in BUN?
Low protein diet
| Liver failure
201
What does CRE stand for?
Creatinine
202
How is CRE produced?
A normal byproduct of muscle metabolism, produced at a rate that is relatively constant to the proportional muscle mass of the animal.
203
What causes increased CRE?
Specific to a decrease in GFR. Not changed much by muscle damage or any other pathology.
204
What are the three causes of azotemia?
Pre-renal: Change in perfusion of kidneys.
Renal: 75% of nephrons are non-functional
Post-renal: obstruction of or damage to urinary tract
205
What does SDMA stand for? What is an SDMA test?
Symmetric dimethylarginine. A new biomarker that can be tested for CRF.
206
What is the normal function of SDMA in the body?
It is a byproduct of protein methylation released into the bloodstream during protein degradation.
207
What are the advantages and disadvantages of SDMA?
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
What is Cyastatin C?
Low molecular weight protein used to evaluate renal function in a research setting.
209
Name three types of clearance tests.
Endogenous CRE clearance
Exogenous CRE, inulin, or iohexol clearance
Fractional clearance test.
210
How is a clearance test run?
Starting with an empty bladder, CRE or the administered/testable substance is measured in relation to urine volume over 24 hours.
211
When might a fractional clearance test be warranted?
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
What is USG and what does it measure?
```
Urine Specific Gravity
Measures density of urine compared to water - measure of:
Number of solutes
Size of solutes
Molecular weight of solutes
```
213
What is the USG of isosthenuric urine?
1.007 - 1.013
| Same as the SG of the ultra filtrate coming out of the glomerulus.
214
What is the USG of hypostenuric urine?
<1.007
215
What is the USG of hypersthenuric urine?
Dog: >1.030
Cat: >1.035
Horse, cow: >1.025
216
When does an animal become isosthenuric?
When 66-70% of functional nephrons are damaged.
217
What is the USG gray zone and if an animal tests in this ranges what should be done?
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
What lab values classify pre-renal azotemia?
Normal USG
219
What lab values classify renal azotemia?
Abnormal (isosthenuric) USG
220
What lab values classify post-renal azotemia?
Variable USG
221
Name one cause of extra-renal tubular insufficiency due to lack of ADH secretion.
Central (pituitary) diabetes insipidus
222
Name some causes of extra-renal tubular insufficiency due to lack of tubule response to ADH.
Hypocalcemia
Pyometra
Steroids
Hyperadrenocorticism
223
Name some causes of extra-renal tubular insufficiency due to loss of the medullary concentration gradient.
Diuresis (fluids, Pu/Pd)
Chronic hyponatremia (hypoadrenocorticism, diuretics)
Hepatic insufficiency
224
Name one cause of extra-renal tubular insufficiency due to increased blood flow to the kidneys.
Hyperthyroidism.
225
Name the advantages and disadvantages of a midstream catch urine collection.
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
Name the advantages and disadvantages of a manual expression urine collection.
A: At vets leisure
D: May be traumatic or force contaminated urine into the ureters, contamination with cells and bacteria of the LUT.
227
Name the advantages and disadvantages of a catheterization for urine collection.
A: At vets leisure, less contamination.
D: May iatrogenically introduce LUT bacteria into the bladder, possibly traumatic.
228
Name the advantages and disadvantages of a cystocentesis for urine collection.
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
What are the three most important elements of handling a urine sample?
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
What are the four components of a complete urinalysis?
USG
Gross observation
Urine chemistries
Sediment exam.
231
What four qualities should be assessed in gross observation of the urine?
Volume
Color
Turbidity/Transparency
Odor
232
What does red urine indicate?
Hemoglobinuria (serum will also be yellow)
Hematuria (will see a pellet)
Myoglobuinuria (serum will be normal in color)
233
Why is urine normally yellow?
Urochromes
234
What does brown urine indicate?
Can be indicative of bilirubinuria
235
What does cloudy urine indicate?
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
What does an ammonia smell to urine indicate?
Presence of bacteria (bacterial urease converting urea to ammonia)
237
What does a acetone smell to urine indicate?
Presence of ketones (ketosis)
238
What does urobilinogen in the urine indicate?
Generally not considered diagnostically relevant
| CAN be increased with hemolytic or hepatic disease due to the degradation of bilirubin in the intestines.
239
How does one test for urine protein?
Dipstick
Sulfosalicylic acid test (SSA)
Urine protein to creatinine ratio (UPC)
Urine microalbumin tests
240
What are the advantages and disadvantages of a dipstick?
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
What are the advantages and disadvantages of sulfosalicylic acid?
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
What are the advantages and disadvantages of a UPC?
A: Quantitative
D: NOT useful if inflammation is present (must have a quiet sediment)
243
What are the advantages and disadvantages of a urine micro albumin test?
A: Semi-quantitative and species specific, so most sensitive test for urine albumin.
D: no tests currently available.
244
What are the causes of proteinuria?
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
What is the clinical relevance of proteinuria?
It has a POOR PROGNOSIS - high morbidity/mortality associated with proteinuria.
246
What can be ruled out to localize proteinuria?
Extrarenal causes (test via cystocentesis)
Pre renal causes (look at CBC/Chem)
Post glomerular causes (look at urine sediment)
247
What can be ruled in when localizing proteinuria?
Pathologic interstitial renal disease: inflammatory sediment, clinical signs of nephritis, azotemia
Glomerular pathology: UPC >2.0
Functional glomerular pathology: Mild and transient proteinuria.
248
What are the three elements of proteinuria to assess clinically?
Localization
Persistence
Magnitude
249
What is nephrotic syndrome?
```
A syndrome defined SYMPTOMATICALLY as:
Proteinuria
Hypoalbuminemia
Hypercholesterolemia
Edema (generally of face or limbs)
+/- azotemia.
```
250
What are two physiologic causes of glomerular proteinuria?
Strenuous exercise
| Fever
251
What is the normal pH of the urine for cats, dogs, horses, and bovine?
Cats/dogs: acidic, 5.5 - 7.5
Horses: neutral to alkaline, 7.0 - 8.5
Cows/small rums: alkaline, 7.5 - 9.0
252
What can cause aciduria?
The increased excretion of H+ due to:
Acidosis
Hypochloremic metabolic acidosis
Hypokalemia
253
What can cause alkalinuria
The decreased excretion of H+ due to;
Artifactual urea hydrolyse
Hydrolysis of urea due to urinary bacteria
Distal renal tubular acidosis
254
How does a dipstick measure blood in urine?
Changes color with the peroxidase reaction of heme.
255
How does a dipstick measure ketones in urine?
Acetoacetate and acetone form colored complexes with nitroprusside on dipstick.
256
How does a dipstick measure bilirubin in urine?
Color change when bilirubin couples with substance on test strip.
257
How does a dipstick measure glucose in urine?
Dipstick has glucose oxidase to create hydrogen peroxide on contact with glucose.
258
What might cause false positives on a dipstick when looking for hematuria?
Myoglobinemia or hemoglobinemia (all have a heme group and so have peroxidase activity).
Any other oxidizing compounds.
259
What might ketones in the urine be indicative of?
If ketonuria is present, ketonemia is present
Negative energy balance (increased fat metabolism)
Diabetes mellitus (decreased carb. metabolism)
260
What are the 3 types of ketones produced by the body?
Acetone
Acetoacetate
Beta-hydroxybutric acid
261
What might bilirubin in the urine be indicative of?
Anything that causes icterus
262
What might glucose in the urine be indicative of?
Blood glucose has exceeded the normal renal threshold for glucose
Renal tubules have been damaged, lowering the renal threshold for glucose
263
What might cause false negatives on the bilirubin dipstick?
Absorbic acid
| Exposing urine to UV light before urinalysis
264
What might cause false positives on the glucose dipstick?
Any other oxidizing agents
265
What may cause false negatives on the glucose dipstick?
Cold urine
Ketones
Absorbic acid.
266
What may cause false negatives on the glucose dipstick?
Cold urine
Ketones
Absorbic acid.
267
What is normal to see in a urinalysis?
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
Where are transitional cells located in the urinary tract?
Between the renal pelvis and the urethra.
269
Where are squamous cells located in the urinary tract?
In the urethra (distal / lower urinary tract)
270
What are casts in urine indicative of?
Acute renal tubular damage. These are formed either due to necrosed/sloughed epithelial cells or during healing of the tubules.
271
What types of casts might be seen (6)?
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
What types of crystals might be seen (7)?
```
Struvite (magnesium ammonium phosphate)
Calcium carbonate
Urates
Calcium oxalate
Cystine
Cholesterol
Bilirubin
```
273
What are struvite crystals indicative of? What do they look like?
Rectangular crystals.
Neutral or alkaline urine.
Normal except with evidence of calculi.
274
What are calcium carbonate crystals indicative of? What do they look like?
Round
Alkaline urine.
No clinical sig. in horses and rabbits.
275
What are urate crystals indicative of? What do they look like?
Amorphous in acidic urine.
Ammonium Biruate in alkaline urine.
Indicative of hepatic disease or PSS, may be seen in dalmatians.
276
What are calcium oxalate crystals indicative of? What do they look like?
Dihydrate or monohydrate (squares or rupees)
Variable urine.
Often seen with ethylene glycol toxicity.
277
What are cystine crystals indicative of? What do they look like?
Hexagonal.
Seen in acid urine.
Indicative of a cysteine resorption defect.
278
What are cholesterol crystals indicative of? What do they look like?
Sharp, angular, and rectangular or rhomboid.
| Unknown significance.
279
What are bilirubin crystals indicative of? What do they look like?
Sharp star like brown or yellow needle clusters.
| Suggests an abnormal bilirubin metabolism.
280
Why might you do a water deprivation test?
An animal is not azotemic, but is polyuric and isosthenruic. So which came first, the polyuria or the isosthenuria?
281
What are some counter indications for a water deprivation test?
```
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
When would you stop a water deprivation test?
Azotemia
Clinical dehydration
Urine concentrations
loss of 5% body weight
283
What does an abnormal water deprivation test indicate?
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
When is an ADH response test done and what does it indicate?
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
Why is a modified water deprivation test called modified?
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
What are urinary enzymes and how are they used?
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
Name some other laboratory abnormalities that may be seen with liver disease.
```
Non-regenerative anemia
Hyperphosphatemia (hypo in horses)
Hypo / hyper calcemia
Hypokalemia
Metabolic acidosis
Hypercholesterolemia
```
288
Why might non-regenerative anemia be seen with renal disease?
Only with chronic renal disease due to reduction in production of erythropoietin.
289
Why might hyperphosphatemia be seen with renal disease?
Decreased GFR - more time for reabsorption of phosphate.
290
Why might hypocalcemia be seen with renal disease?
Acute: decreased reabsorption of Ca2+
Chronic: reduced activation of Vitamin D. May also be secondary as compensation for increased phosphorus.
291
Why might hypercalcemia be seen with renal disease?
Common in horses because the kidneys excrete Ca2+ normally.
292
Why might hypokalemia be seen with renal disease?
Excess renal loss, decreased dietary intake, and with cattle also see loss in saliva.
293
Why might metabolic acidosis be seen with renal disease?
Chronic - limited ability of the kidney to excrete hydrogen ions.
294
Why might hypercholesterolemia be seen with renal disease?
Is associated with hypoalbuminemia from protein losing nephropathies.
295
What is the name of the staging system used for renal disease?
IRIS (international renal interest society)
296
What is uremia defined as?
Clinical symptoms associated with kidney disease.
297
What is chronic renal disease defined as?
A lesion (structural or functional) lasting longer than 2-3 months as demonstrated by multiple urine samples or multiple azotemic blood samples.
298
What are some typical clinical symptoms of acute renal disease?
Azotemia
Isosthenuria
Anuria/Oligouria
Hyperphosphatemia/hyperkalemia/acidosis
299
What are some of the early signs of ethylene glycol toxicity?
```
CNS signs
Tachypnea
Tachycardia
Decreased bicarbonate
Increased anion gap
Increased osmolal gap
Hypocalcemia
Calcium oxalate crystalluria
```
300
What are some of the later signs of ethylene glycol toxicity?
Azotemia
Isosthenuria
Hyperphosphatemia
Hyperkalemia
301
What is the pathogenesis of ethylene glycol toxicity?
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
What are the causes of primary polydipsia?
Psychogenic (neurologic or hepatic)
303
What are the causes of primary polyuria?
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
When do you need arterial blood for a blood gas?
When measuring pO2, though it can be used for any other values.
305
When can you use venous blood for a blood gas?
pH
pCO2
HCO3-
306
How should you collect a sample for a blood gas?
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
What should you note about the patient before collecting sample for a blood gas?
Temperature and {Hgb}.
308
What is TCO2?
Essentially an estimate of bicarbonate (96% of TCO2)
| This is stable in the blood and so can be reported on most general chemistries.
309
What is BE?
Base excess: the actual bicarb concentration - the normal bicarb concentration.
310
What are the arterial/venous classic normals for pH?
A: 7.4
V: 7.4
311
What are the arterial/venous classic normals for pCO2?
A: 40
V: 45
312
What are the arterial/venous classic normals for pO2?
A: 90-100
V: 40-60
313
What are the arterial/venous classic normals for HCO3-?
A: 24
V: 24
314
What are the arterial/venous classic normals for O2 sat?
A: 95-100
V: 40-70
315
What is BE used for clinically?
Primarily used to determine the amount of bicarbonate to give an acidotic animal.
316
What is the most important buffer system in the animal?
Bicarbonate/carbonic acid system.
317
What does the Henderson-Hasselbach equation describe?
The relationship between pH, pCO2 and HCO3- in the animal.
318
What controls pCO2?
Respiration
319
What controls HCO3-?
Renal excretion and reabsorption.
320
What other two main variables control pH of the body besides the bicarbonate/carbonic acid system?
Protein concentration and electrolytes.
321
Compensation equation for metabolic acidosis?
For each 1 mEq/L decrease in HCO3-
| pCO2 decreases by 0.7 mmHg
322
Compensation equation for metabolic alkalosis?
For each 1 mEq/L increase in HCO3-
| pCO2 increases by 0.7 mmHg
323
What are the compensation equations based on?
Based off a DOG, but can be used at least to approximate compensation in other animals.
324
What are the two types of metabolic acidosis and how do you tell them apart?
Secretional/hyperchloremic acidosis : normal anion gap
| Titrational acidosis: increased anion gap
325
What are the three main causes of secretional metabolic acidosis?
```
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
Why do you see hyperchloremia with secretional metabolic acidosis?
Chloride is resorbed in the kidney to maintain the electroneutrality of the body when bicarbonate is lost.
327
What are the three main causes of titrational metabolic acidosis?
Retention of acid
Generation of acid
Ingestion of acid
328
How is the anion gap calculated?
Positive charges - negative charges
| Na+K+UC (constant) - HCO3+Cl+UA (variable)
329
Give 4 common examples of titrational metabolic acidosis
Lactic acidosis
Uremic acidosis
Ketoacidosis
Exogenous acid ingestion
330
Give 4 common examples of titrational metabolic acidosis
Lactic acidosis
Uremic acidosis
Ketoacidosis
Exogenous acid ingestion
331
What generates lactic acidosis?
Hypoxia/ischemia or grain overload
332
What generates uremic acidosis?
Decreased renal excretion of H2SO4 and H2PO4
333
What generates ketoacidosis?
Diabetes mellitus or starvation
334
What are some common exogenous acids that an animal might ingest?
Ethylene glycol
| Methanol
335
What can mask an anion gap change due to titrational metabolic acidosis?
Hypoproteinemia - decreases the normal UA-
336
How is metabolic acidosis treated?
TREAT THE UNDERLYING DISEASE
| Bicarbonate in fluid replacement.
337
What is the most common cause of metabolic alkalosis?
Loss of HCl rich fluid, usually from the stomach or abomasum.
338
Why does a loss in HCl result in increase of HCO3-?
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
What is paradoxical aciduria and why does it occur?
Animal is alkalotic but secreting H+ to make the urine acidic.
Typically only occurs in hypokalemic animals.
340
Name three less common causes of metabolic alkalosis?
Overadminstration of bicarbonate containing fluids (LRS)
Overuse of loop diuretics leading to hypokalemia
Low chloride intake (rare)
341
When is paradoxical aciduria seen clinically?
Cows with DAs.
342
What type of metabolic compensation is seen with acute respiratory abnormalities?
Cellular responses: H+ is released or absorbed by intracellular phosphates and proteins
343
What type of metabolic compensation is seen with chronic respiratory abnormalities? What is considered chronic in this case?
```
Renal responses (2-3 days)
Changes the renal excretion of H+ and HCO3-
```
344
What are the two main causes of respiratory alkalosis? How can they be differentiated?
ALVEOLAR HYPERVENTILATION
Extrathoracic:
Intrathoracic:
345
What are the two main causes of respiratory alkalosis? How can they be differentiated?
ALVEOLAR HYPERVENTILATION
Extrathoracic: transient, normal pO2
Intrathoracic: chronic, decreased pO2
346
What are some extrathoracic causes of respiratory alkalosis?
Pain
Fever
Fear/apprehension
Anemia
347
What are some intrathoracic causes of respiratory alkalosis?
```
Pneumonia
Pulmonary edema
Thoracic masses
Congestive heart failure with right to left blood shunting
Pulmonary thromboembolism
Pleural effusion
```
348
What are the two main causes of respiratory acidosis?
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
What are some causes of hypoventilation?
```
Decreased movement of diaphragm
CNS depression
Drugs
Neuromuscular disorders
Severe bloat or abdominal masses
```
350
How are pO2 and respiratory acidosis related?
pO2 is low.
351
What is the name of the most common non-traditional approach to acid-base metabolism?
Stewart's quantitive approach.
352
What are the three basic parameters of Stewart's quantitive approach?
pCO2
SID - strong ion difference (Na, Cl, and UA-)
Atot - total contraction of weak acids including protein and phosphates.
353
How should samples be collected to measure electrolytes?
Collect serum and separate it from red blood cells as quickly as possible.
354
What may cause ARTIFACTUAL hypernatremia or hyperkalemia? Why?
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
What is unique about electrolyte reference intervals?
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
What three hormones control body sodium concentration?
Aldosterone
Atrial natriuretic factor (ANF)
Anti-diarrheal hormone (ADH)
357
What are the three main causes of hypernatremia?
```
Solute gain (salt poisoning)
Pure water deficit
Hypotonic loss
```
358
What causes hyponatremia?
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
What causes solute gain?
Access to rich salt diet but limited access to water
Hypertonic fluid administration
Hyperaldosteronism (rare)
360
What causes a pure water deficit?
Inadequate water access
Decreased drinking in sick animals
Defective thirst response (rare)
Loss of water (diabetes insidious, panting, hyperventilation, fever)
361
What causes hypertonic water loss?
Renal osmotic diuresis
Vomiting or diarrhea
3rd space loss due to burns or pancreatitis
362
What is the action of ADH?
Promotes renal water conservation
363
What is the relationship between serum potassium and body potassium?
Very weak relationship - the cells can shift K+ in or out to maintain narrow functional potassium window.
364
What is the relationship between serum potassium and body potassium?
Very weak relationship - the cells can shift K+ in or out to maintain narrow functional potassium window.
365
Name three causes of hyperkalemia.
Decreased GFR
Acidosis (H+ shifts intracellularly and K+ moves out)
Tissue necrosis/hemolysis
366
Name three causes of hypokalemia.
Excessive GI loss from vomiting or diarrhea
Excessive urinary loss (diabetes or renal disease in cats)
Alkalosis
367
Name three causes of hypokalemia.
Excessive GI loss from vomiting or diarrhea
Excessive urinary loss (diabetes or renal disease in cats)
Alkalosis
368
Why should chloride be corrected to look for abnormalities?
Usually, chloride changes with Na+ to maintain electroneutrality, so primary changes in chloride are rare. Corrected Cl is significant if outside normal window.
369
What causes primary chloride abnormalities?
Hypochloremia due to sequestration/loss with metabolic alkalosis
Hyperchloremia with secretional metabolic acidosis
Artifactual rise with potassium bromide therapy.
370
What are the four main causes of lactic acidosis? ?
Shock
Hypoxia/ischemia/poor perfusion
Grain overload
Sustained heavy exercise
371
Why is lactate useful clinically?
It is a prognostic indicator - increased lactate shows amount of poor perfusion.
372
What is osmolality?
Number of particles / solution weight
373
What are the main substances used to calculate estimated osmolality?
Sodium, potassium, glucose, BUN
374
What is used to measure osmolality?
Osmometer
375
What is the osmolal gap?
The actual - estimated osmolality.
