Lab Exam 2 Flashcards

1
Q

Why is glucose important to the CNS?

A

Because the central nervous system as well as RBC’s require glucose for their energy needs and without it they die

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2
Q

What is a monosaccharide?

A

A single unit sugar

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3
Q

What is hexose?

A

Simple sugars whose molecules contain six carbon atoms

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4
Q

Why is the liver important in reference to glucose?

A

It synthesizes, stores, converts and releases glucose

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5
Q

What is the excess glucose stored as in the liver?

A

Glycogen

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6
Q

What organ releases insulin?

A

The pancreas

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7
Q

What hormones control the concentration of glucose?

A

Insulin and glucagon; insulin lowers BG levels while glucagon elevates it

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8
Q

How is glucose metabolized?

A

Via glycolysis followed by the TCA cycle (aka krebs cycle)

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9
Q

How many glucose atoms are produced as a result of glycolysis?

A

It produces 4 total, but 2 are eliminated, leaving a net gain of 2 glucose atoms

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10
Q

How many ATP atoms are produced at the conclusion of the TCA cycle?

A

36 ATP for every glucose molecule

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11
Q

What is required for the complete oxidation of glucose?

A

Because it is an aerobic response, it requires oxygen

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12
Q

What by-products are released by the oxidation of glucose?

A
  • CO2, H2O, ATP, and heat

- The heat produced helps maintain body temperature

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13
Q

What is fermentation of glucose?

A

Anaerobic metabolism that can produce ATP if the body is experiencing hypoxia

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14
Q

Is fermentation an effective way to produce ATP?

A

It is less effective than glycolysis because it only produces 4 ATP for every glucose molecule

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15
Q

Where is the highest concentration of glycogen stored?

A

In the liver, but because muscle tissue has a greater mass, there is more glycogen contained within it

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16
Q

What cells produce, monitor and control glucose?

A

Beta cells, which are created in the endocrine portion of the pancreas

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17
Q

What cells within the islets of langerhaans produce glucagon?

A

Alpha cells

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18
Q

What do the delta cells within the pancreatic islets produce?

A

Somatostatin, which regulates insulin and glucagon

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19
Q

What cell is the only cell in the body that does NOT require insulin to function?

A

Beta cells

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20
Q

At what concentration would a beta cell be triggered to release insulin?

A

When the blood glucose concentration exceeds 110 mg/dl

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21
Q

At what concentration is insulin synthesis and concentration inhibited?

A

When the blood glucose concentration falls between 60 mg/dl

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22
Q

What is euglycemia?

A

Normal concentration of glucose in the blood

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23
Q

How can euglycemia be maintained?

A

Exogenously, which is from outside the body, mainly through diet; or endogenously which is inside the body derived from the liver

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24
Q

What is gluconeogenesis?

A

The creation of more glucose

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25
Q

What hormone is the most dominant when lowering glucose?

A

Insulin

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26
Q

What hormones may elevate glucose?

A

Glucagon, epinephrine, growth hormone, and cortisol

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27
Q

What is Diabetes Mellitus?

A

Results from a decrease in insulin secretion from the beta cells and/or a decrease in insulin action

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28
Q

What is Type I Diabetes?

A
  • Insulin dependent diabetes mellitus

- There is a low amount of insulin in the body and it can’t produce enough to meet the need

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29
Q

What is the most common form of diabetes in dogs and cats?

A

Type I IDDM

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30
Q

What is the second most common form of diabetes in cats?

A

Type II NIDDM

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31
Q

What is Type II Diabetes?

A
  • Non-insulin dependent diabetes mellitus

- Spikes in BG levels usually after eating that require insulin which the body can produce

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32
Q

How is type I diabetes managed?

A

With insulin injections

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33
Q

How is type II diabetes managed?

A

With dietary therapy and oral hypoglycemic medications

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34
Q

What is Type III Diabetes?

A
  • Impaired glucose tolerance

- Can be caused by hormones or medications

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35
Q

Which type of diabetes can affect pregnant animals?

A

Type III

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36
Q

What long term medication use can result in type III diabetes?

A

Corticosteriods

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37
Q

What is thought to be the cause of canine diabetes?

A

It is considered to be immune mediated in which the body thinks beta cells are foreign and attacks them

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38
Q

What are some other causes of canine diabetes?

A

Genetic predisposition, chronic pancreatitis, and medication induced

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39
Q

At what percentage of destruction of pancreatic islets do diabetic clinical signs occur?

A

Progression is slow and 90% of islets are lost before diabetes mellitus occurs

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40
Q

What are the common causes of feline diabetes?

A

Obesity, pancreatitis, amyloidosis of pancreatic beta cells

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41
Q

What is amyloidosis?

A

Deposition of material around beta cells which prevents their measurement of glucose

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42
Q

What canine gender is typically afflicted with diabetes?

A

3x more likely to occur in females

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43
Q

At what age do canines typically become diagnosed with diabetes?

A

Peak incidence at 7-9 years

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44
Q

What breeds are genetically predisposed to diabetes?

A

Australian terriers, samoyed, mini and standard schnauzers, mini and toy poodles, pugs, fox terriers, keeshonds, bichon fries, finnish spitz, lhasa apso, cairn terriers

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45
Q

What feline gender is typically affected by diabetes?

A

Males generally greater than 6 years old

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46
Q

What feline breed is diabetes common in?

A

None, all can be affected equally

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47
Q

What are the clinical signs of diabetes?

A

Polyuria, polydipsia polyphagia, weight loss, cataracts in dogs, peripheral neuropathy in cats, plantigrade posture

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48
Q

How can diabetes be diagnosed?

A
  • CBC: red blood cells may be decreased
  • Chem panal: hyperglycemia; BG > 200 mg/dl
  • UA: glucosuria or ketonuria
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49
Q

What are some goals of diabetes treatment?

A
  • Elimination of clinical signs
  • Prevention or slowing or cataract formation and resulting blindness
  • Prevention of hypoglycemia or overtreatment
  • Prevention and/or treatment of concurrent diseases such as cushing’s, skin infections, or UTI’s
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50
Q

How is diabetes treated?

A

Dietary management, exercise, insulin injections, or oral hypoglycemic agents

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51
Q

What are some goals of dietary management?

A

Eliminate obesity and maintain consistency in the timing and caloric content of meals to minimize fluctuations by having slow release of carbohydrates in BG concentrations

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52
Q

What should a diabetic diet contain?

A

High fiber and low fat, cats should also be fed a high protein, low carb diet and semi moist foods should be avoided

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53
Q

What are some goals of exercise?

A

To promote fat loss and increase mobilization of insulin from its injection site, but avoid strenuous and sporadic exercise as it can cause severe hypoglycemia

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54
Q

What are the three types of insulin?

A
  • Short acting: emergency use of R insulin
  • Intermediate acting: canine use of NPH and Vetsulin
  • Long acting: feline use of Lantise and glargine
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55
Q

What are some problems with insulin therapy?

A
  • Rapid insulin metabolism
  • Insulin resistance if there is another disease present
  • Hypoglycemia aka insulin overdose
  • Somogyi phenomenon aka insulin induced hyperglycemia
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56
Q

How can hypoglycemia be treated at home?

A

If a diabetic animal is exhbiting signs of weakness, shaking, ataxia and seizures, they can be given karo syrup rubbed on the their gums

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57
Q

What is renal disease?

A

When something is physically wrong with the kidneys, but the function may not be affected

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58
Q

What is renal failure?

A

When something is functionally wrong with the kidney, at least 75% of total nephron population is non-functional

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59
Q

What happens to the kidneys in renal failure?

A

The kidneys are no longer able to maintain the regulatory, excretory and endocrine functions required

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60
Q

What happens to hormone production to kidneys in renal failure?

A

The kidney produces less erythropoietin hormone, which results in anemia especially in cats

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61
Q

What is the result of renal failure?

A

It results in retention of nitrogenous solutes and derangement of fluid, electrolyte, and acid balance

62
Q

What is azotemia?

A

A build up of waste in the blood due to failure of kidneys and an increased concentration of non-protein nitrogenous waste products in the blood

63
Q

What us pre-renal azotemia?

A

A problem occurring before the kidney involving impaired blood flow to the kidney

64
Q

What is pre-renal azotemia due to?

A

A decrease in glomerular filtration rate from circulatory disturbances causing decreased renal perfusion

65
Q

What is renal azotemia?

A

A primary failure of the kidney which results from decreased GFR, check functionality with a specific gravity

66
Q

What is post-renal azotemia?

A

When the urine does not leave the body and results from obstruction or rupture of urinary outflow tracts and hyperkalemia

67
Q

What is uremia?

A

A condition involving abnormally high levels of waste products in the blood from a critical loss of functioning nephrons

68
Q

What are the clinical signs of uremia?

A
  • PU/PD
  • Mild non-regenerative anemia
  • Vomiting
  • Weight loss
  • Depression
69
Q

What is ammonia?

A

Produced from dietary proteins and by catabolism of proteins and nitrogenous wastes in peripheral tissues

70
Q

What converts amino acids and urea into ammonia?

A

Gastrointestinal micro-organisms in the colon and cecum which are then absorbed into the portal circulation

71
Q

How much ammonia is shunted to the liver?

A

80-90% and then it is converted into urea via the urea cycle

72
Q

What peripheral tissues metabolize 10-20% of ammonia?

A

The kidneys, heart and brain

73
Q

How is ammonia measured?

A

With arterial blood collection and heparinized plasma samples

74
Q

What can result of increased ammonia?

A

Ammonia is toxic to the CNS and is one cause of hepatic encephalopathy (damage to the CNS due to the build up of ammonia)

75
Q

What could be a physiologic normal body function that would result in elevated ammonia?

A

A high protein diet, can also result in increase GFR and urea excretion

76
Q

What kind of artifact may result in a increased ammonia?

A

It may not be an accurate number

77
Q

What kind of disease may result in an increased ammonia level?

A

It can be a liver shunt, dehydration or a tumor

78
Q

How is urea formed?

A

2 NH3 molecules are combined with 1 molecule of CO2

79
Q

What is the chemical formula of urea?

A

CO(NH2)2

80
Q

What is urea?

A

The end product of protein and amino acid catabolism

81
Q

How is urea metabolized?

A

Synthesized in the liver using ammonia derived from amino acids

82
Q

How is urea excreted?

A

By the kidneys which is the most important route of urea excretion

83
Q

Where is urea filtered?

A

At the glomeruli and requires no metabolic work by the kidneys because glomerular filtration is driven by cardiac output

84
Q

How is urea concentration measured?

A

As blood urea nitrogen, and is a screen for decreased GFR

85
Q

What are the non-renal factors contributed to increased BUN?

A
  • High protein meal
  • Hemorrhage into gastrointestinal tract
  • Increased catabolism (breakdown of protein)
  • Drugs
86
Q

What are the renal factors contributing to increased BUN?

A
  • Pre-renal: shock, dehydration, congestive heart failure
  • Primary: kidney is not functioning properly
  • Post-renal: Urethral obstruction, ruptured bladder
87
Q

What are some reasons that could contribute to a decreased BUN?

A
  • Low protein diet
  • Severe liver disease of portosystemic shunting
  • Anabolic steroids due to building protein instead of breaking it down
88
Q

What is creatinine?

A

Spontaneous, non-enzymatic breakdown product of phosphocreatine in muscle and is released into the blood from muscle at a constant rate

89
Q

Which gender tends to have more creatinine?

A

Males due to higher muscle mass

90
Q

Where is creatinine excreted?

A

By glomerular filtration and the rate of excretion is relatively constant and a good estimate of GFR

91
Q

What is creatinine a measurement of?

A

It is a screen for decreased GFR?

92
Q

What might be some reasons for increased creatinine?

A
  • Non renal: massive muscle necrosis and prolonged strenuous exercise
  • Pre-renal: shock, dehydration, congestive heart failure
  • Post-renal: urethral obstruction, ruptured bladder
93
Q

What does an increased BUN:creatinine ratio suggest?

A

Non-renal azotemia, may be due to an increased protein diet

94
Q

What does a decreased BUN:creatinine ratio suggest?

A

Chronic liver failure

95
Q

What are plasma proteins?

A

Total proteins consist of albumins and globulins, also includes fibrinogen

96
Q

What could decreased plasma protein level indicate?

A
  • Glomerular disease
  • Liver disease
  • Starvation
  • Malabsorption
  • Hemorrhage
97
Q

What organ produces albumin?

A

The liver

98
Q

What could a increased plasma protein level indicate?

A
  • Severe dehydration

- Neoplasia (lymphoma and plasm- Infection

99
Q

What is albumin?

A

It contributes to plasma colloid oncotic pressure and synthesized in the liver and catabolized by all metabolically active tissues, serves as a carrier protein for many insoluble organize substances

100
Q

What can contribute for hypoalbuminemia?

A
  • Physiologic: low protein diet
  • Increased loss: kidney, liver, gut and bleeding
  • Catabolism
101
Q

Where are globulins produced?

A
  • Alpha and beta are synthesized by the liver, and gamma globulins are produced by b-lymphocytes and plasma cells
102
Q

What does a high total protein with a normal A:G ratio indicate?

A

Dehydration

103
Q

What does a high total protein with a low A:G ratio suggest?

A

Hyperglobulinemia

104
Q

What us hyperglobulinemia?

A

Decreased gamma globulins are seen when there is a deficiency of immunoglobulins

105
Q

What are the biochemical functions of the liver?

A
  • Detoxification of toxins
  • Synthesis of all coagulation factors
  • Synthesis of plasma proteins (mainly albumin)
  • Catabolism, degradation and storage of lipids
  • Formation and elimination of bile
106
Q

What tests can be used to diagnose liver disease?

A

Chem panel, CBC, bile acids, U/A, fecal, RADS, US, biopsy

107
Q

What are the clinical signs associated with liver disease?

A
  • Depression/lethargy
  • Anorexia, diarrhea, vomiting, weight loss
  • Fever, hemorrhage
  • Abdominal pain
  • CNS signs
  • Icterus/jaundice
  • PU/PD, dark brown urine, dark or light brown stool
108
Q

What is hematemesis?

A

Vomiting blood, which may occur in a patient with liver disease

109
Q

What is hemoptysis?

A

Coughing up blood, which may occur in a patient with liver disease

110
Q

What bleeding disorders may a liver patient suffer from?

A
  • Hematemesis
  • Hemoptysis
  • Hematochezia
  • Melena
  • Hematuria
  • Petecchia
  • Eccymoses
  • Pale MM
111
Q

Why would a patient with liver disease suffer from hepatic encephalopathy?

A

Due to the build up of ammonia not being converted to urea

112
Q

What kind of heart failure may a patient with liver disease suffer from?

A

Right sided heart failure, often associated with hepatomegaly

113
Q

What may hepatomegaly be due to?

A
  • Inflammation
  • Steatosis aka fatty liver
  • Neoplasia
  • Congestion or cholestasis (low bile flow)
114
Q

What is hepatodynia?

A

Liver pain

115
Q

Why would a patient with liver disease suffer from microhepatica aka small liver?

A

May be due to a congenital portosystemic shunt or cirrhosis

116
Q

What may ascites in the abdomen occur in a liver disease patient?

A

May be due to hypoalbuminemia or liver hemorrhage

117
Q

What is the only test that can determine the functionality of the liver?

A

Bile acids test

118
Q

What are the major enzymes found in the liver?

A
  • ALT
  • AST
  • ALKP
  • GGT
119
Q

Aside from the liver, where else may would you find ALT?

A

Mainly in the hepatocellular cytoplasm in the liver, but smaller amounts may be found in the kidney, heart, muscles and pancreas

120
Q

What would a increased ALT suggest?

A

Persistent hepatocellular disease

121
Q

When being treated, how often should ALT values decrease?

A

By 50% every 1-2 days, as the serum half life is <24 hours

122
Q

Where would you find AST?

A

As it is not liver specific, it may be found in RBC’s, heart, muscle tissue, pancreas and kidney in addition to the liver

123
Q

Which liver enzyme is a more sensitive indicator of hepatobillary (liver and gallbladder) disease in cats?

A

AST, in general it tends to parallel ALT with respect to liver damage

124
Q

What is ALKP?

A
  • A membrane bound enzyme present in many tissues
  • Dogs have 4 isoenzymes: bone, liver, corticosteroid, and intestines
  • Cats have 2 isoenzymes: bone and liver
125
Q

What would an elevated ALKP possibly indicate?

A
  • Osteoblast activity (2-3 times the normal range)
  • Feline hyperthyroidism
  • Canine glucocorticoids
  • Synthesis induced by other drugs aside from glucocorticoids
  • Primary or secondary hepatocellular disorders
  • Mammary neoplasia (will result in a milder increase)
126
Q

If a dog is on a prescription of prednisone, which liver enzyme may be elevated?

A

ALKP

127
Q

Where is most serum GGT activity in the dog and cat?

A

It is derived from the liver

128
Q

Where is the largest tissue GGT activity in the dog and cat?

A

In the kidney and pancreas

129
Q

What may an increased GGT level indicate?

A
  • Intrahepatic or extrahepatic cholestasis
  • Pancreatitis
  • Drug induction by corticosteriods or anticonvulsants
130
Q

What is intrahepatic cholestasis?

A

Cholestasis due to either a blockage, tumor, or tissue inflammation in the liver

131
Q

What is extrahepatic cholestasis?

A

Cholestasis due to either a gallstone or a tumor outside the liver

132
Q

Which liver enzyme is the most sensitive to diagnose liver disease than ALKP in cats?

A

GGT

133
Q

What diseases may have secondary effects on the liver?

A
  • Endotoxemia/septicemia
  • Diabetes
  • Hyper and hypothyroidism
  • Hyperthermia
  • Decreased hepatic perfusion with hepatocellular hypoxia due to shock, CHF, Hw disease, or anemia
134
Q

What is stercobilin?

A

It provides brown color to feces, if it lacks that it is referred to as acoholic or without bile

135
Q

What is bilirubin?

A

It is produced from the breakdown of RBC’s, when hemoglobin is converted to bilirubin

136
Q

Is bilirubin a normal finding in the urine of a cat?

A

Never

137
Q

When does jaundice in an animal develop?

A

When the bilirubin levels exceed 2.0 mg/dl to 3.0 mg/dl or 10x the normal amount

138
Q

How is jaundice classified?

A
  • Prehapatic: high RBC, typically seen in DIC
  • Hepatic: liver disease
  • Posthepatic: liver blockage
139
Q

What is the major plasma protein produced in the liver?

A

Albumin

140
Q

When would albumin decreased on a chem panel?

A

When greater than 70% of hepatobilary function has been compromised

141
Q

Where are alpha and beta globulins synthesized?

A

In the liver

142
Q

What are the primary bile acids synthesized in the liver?

A

Cholic acid and chenodeoxycholic acid come from cholesterol

143
Q

What is the secondary bile acids for cats?

A

Taurine

144
Q

Where are bile acids stored and concentrated?

A

In the gallbladder

145
Q

What stimulates the release of CCK into the small intestine?

A

The presence of hydrochloric acid, dietary fats and proteins after eating

146
Q

What does CCK do?

A

It stimulates the contraction of the gallbladder with the release of bile acids

147
Q

What does the small intestine do with bile acids?

A

It facilitates fat to emulsification, digestion and absorption, then most of the bile acids are reabsorbed in the ileum by active transport

148
Q

What is bile acids functionality based on?

A

The efficiency of the enterohepatic circulation

149
Q

What kind of food should you feed an animal with encephalopathic tendencies for a bile acids test?

A

High fat low protein, as it helps produce less ammonia

150
Q

What may happen to an animal with a liver shunt if fed a high protein meal?

A

They may develop seizures