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Clin Path > Proteins, lipids, carbs Ch 6 D&P > Flashcards

Proteins, lipids, carbs Ch 6 D&P Flashcards

1
Q

Compare serum to plasma proteins.

A

Plasma has everything, Serum is missing fibrinogen, factor V and factor VIII. (think serum separator)

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2
Q

What accounts for the majority of colloid osmotic pressure of plasma and why?

A

Albumin. Due to abundance and small size.

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3
Q

What influence does albumin have on coagulation? So what may happen with low albumin?

A

It dampens platelet aggregation and augments AT III and so low albumin > prothrombotic implications.

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4
Q

What are the types of globulins and where do they come from?

A
  • Alpha and Beta (lipoproteins, acute phase proteins and some globulins like IgM and IgA) ( Made in the Liver.)
  • Gamma (B lymphocytes and plasma cells)
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5
Q

What are the different ways to measure TOTAL protein and how sensitive are they in the different types of fluids (3)?

A
  • Biuret method (colorimetric, spectrophotometric) > accuracy for plasma or serum, accurate from 1-10g/dl.
  • Precipitation and Dye binding assays > for small amounts, accurate from 10-200mg/dl, for CSF or urine proteins.
  • REfractometry for plasma, serum and body cavities (read in g/dL); high conc of glucose, urea, sodium, chloride, lipemia, hemolysis, any turbidity may falsely elevate readings. Icterus doesn’t affect the reading as long as the sample is clear.
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6
Q

How is albumin measured individually most often? What is an alternative way to measure it?

A

Bromcresol green dye binding method (this is different from total protein measurement).
False high test results occur when levels are very low cause it can bind to other proteins.
Serum protein electrophoresis is an alternative way to quantitate albumin.

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7
Q

How is globulin concentration determined?

A

Usually calculated by subtracting albumin from total protein in a serum sample.

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8
Q

What Serum IgG concentrations tell you there is failure of passive transfer in a foal or calf?

A

Below 200mg/dL at 24-48 hrs.
200-400 mg/dL = partial failure
> 800mg/dL = good to go

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9
Q

What are the IgG screening tests for failure of passive transfer? (4)

A 
Zinc sulfate turbidity 
Latex agglutination
Glutaraldehyde coagulation
ELISA
(remember "LEGZ")
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10
Q

When would you have a decrease or increase in A:G ratio?

A

Decrease > Renal proteinuria and/or Ig production following following Ag stimulation.
Increase > lack of IgG production in adults or lack of colostrum in foals or calves.
NOTE: THE BODY DOESN’T OVERPRODUCE ALBUMIN.

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11
Q

How is fibrinogen concentration determined?

A
  • Indirectly by refractometry using two centrifuged hct tubes and measuring fibrinogen and then heating the other and measuring it (fibrinogen is precipitated by heat denaturation) and subtracting them and you get fibrinogen in mg/dL.
    The method is crude and can be used for hyperfibrinogenemia but not really for hypofibrinogenemia.
  • its more accurate to determine thrombin clotting time, or use direct automated measurement.
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12
Q

What does hyperalbuminemia tell you?

A

Dehydration, an absolute increase in albumin doesn’t really happen. (Globulins would also be increased so A:G would be normal unless something else is going on).

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13
Q

What does hyperfibrinogenemia tell you?

A

Inflammatory or neoplastic dz, its an acute phase protein, and also in dehydration. Early inflammation in large animals. Not on serum biochemical profiles cause its only in plasma.

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14
Q

Hyperglobulinemia may occur under what conditions?

A

Infection or inflammation
Near term pregnancy
Birds prior to egg laying
Acute phase response cause mild increase (alpha globulins mostly, some beta)

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15
Q

Besides inflammation, or tissue injury, what else results in production of acute phase proteins?

A

Estradiol
Physical stress
Steroid administration
(extra-hepatic production may also occur)

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16
Q

What stimulates production of acute phase proteins?

A

IL-1, IL-6, TNF, from macrophages at site of injury and maybe other cells too.

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17
Q

In terms of identifying an inflammatory response, which values are most useful?

A
  • Acute phase proteins (more sensitive than WBC count, can be used in early detection and monitoring response to treatment).
  • WBC count
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18
Q

Which tumors often have an elevation of acute phase proteins?

A

Lymphomas or tumors with significant inflammation.

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19
Q

What are examples of early responding acute phase proteins (within 24 hours) and later responding ones (w/in 48 hours and later)?

A

Rapid > Amyloid A, C reactive protein
Later > Haptoglobin, fibrinogen, LPS binding protein
(note amyloid a is better than fibrinogen cause it occurs faster and is higher)

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20
Q

Which acute phase protein has the greatest cross-species utility?
Which is best for dogs?
Dogs and cats?
Ruminants and horses?

A

Cross spp > Serum amyloid A
Dogs > C reactive protein
Dogs and cats > alpha 1 acid glycoprotein
Ruminants and horses > Haptoglobin

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21
Q

If you don’t have blood what may be used to test for acute phase protein?

A

Saliva

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22
Q

Which coagulation proteins are considered acute phase proteins?

A

Factors V, VIII and fibrinogen.

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23
Q

Which acute phase protein may be good for monitoring pancreatitis in dogs versus cats?

A

C reactive protein in dogs.

Serum amyloid A in cats.

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24
Q

What is haptoglobin?

A

Acute phase protein considered more sensitive than fibrinogen. It binds free hemoglobin and decreases in intravascular hemolysis..
Increases occur in Cushings or steroid admin.

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25
Q

What is Ceruloplasmin?

A

Copper transport protein. Acute phase protein.

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26
Q

Another important acute phase protein set involving the immune system>

A

Complement proteins, especially C3.

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27
Q

What is alpha1 acid glycoprotein?

A

Acute phase protein.
Often elevated in lymphoma, produced by lymphocytes too. (other tumors too)
Increased in FIP and useful to support the dx.

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28
Q

Name three other important acute phase proteins not previously mentioned?

A

TNF alpha
LPS binding protein
Hepcidin (controls iron availability)

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29
Q

What are 5 important negative acute phase proteins?

A 
Albumin
Transferrin (iron txport protein; think cattle and pigs)
alpha 2 macroglobulin in cattle
Cortisol binding protein
Alpha 1 apolipoprotein
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30
Q

What happens with gloulins during nephrotic syndrome?

A

Increased LDL, beta-lipoprotein, VLDL and alpha 2 macroglobulin result in increased alpha 2 globulins on the serum electrophoretogram. LDL and others increase to to albumin loss nad hypoproteinemia with edema and protein uria.

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31
Q

Which acute phase protein are considered beta globulins?

A

Transferrin, IgM, hemopexin and/or complement C3 (may also increase in acute liver dz)

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32
Q

Whats indicated by increase in the beta and gamma globulin regions of the serum electrophoretogram?

A

Ig elevations and these are chronic phase proteins

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33
Q

Bridging of the beta and alpha regions in the serum electrophoretrogram is highly suggestive of what condtion?

A

Chronic active hepatitis.

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34
Q

Polyclonal gammopathy is associated with what THREE groups of conditions?

A

Inflammatory
Immune mediated
Liver dz

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35
Q

Monoclonal gammopathy is caused by what and where is the peak on the serum electrophoretogram?

A
  • Also referred to as paraproteinemia
  • Produced by a single clone of B lymphocytes or plasma cells.
  • Can be located in the ALPHA, BETA or Gamma regions.
  • Due to lymphoid neoplasia (plasma cell myeloma, lymphoma, chronic lymphocytic leukemia, macroglobulinemia.
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36
Q

Which non neoplastic conditions may result in Monoclonal gammopathy?

A 
Canine amyloidosis
Canine ehrlichiosis
Canine visceral leishmaniasis
FIP
Plasmacytic gastroenteritis
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37
Q

What other important clin path abnormality is seen with monoclonal gammopathy?

A

Bence Jones proteinuria due to overproduction of IG light chains. Can detect in urine on electrophoresis.

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38
Q

What are some common causes of hypoalbuminemia?

A
  • decreased production due to liver dz, pregnancy, lactation, intestinal malabsorbtion, cachexia, EPI etc.
  • Loss of albumin via hemorrhage, proteinuria of renal dz, PLE, exudative skin lesion, burns, intestinal parasitism, high protein effusions
  • Nephrotic syndrome (proteinuria, hypoalbuminemia, hypercholesterolemia, azotemia)
  • The mild decrease in albumin associated with inflammation as a negative acute phase protein is offset by the increase in alpha and beta globulins so you won’t see hypoproteinemia.
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39
Q

What are the causes of hypoglobulinemia? (3)

A

Failure of passive transfer
SCID
Agammaglobulinemia; selective IgM, IgA, IgG deficiencies;

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40
Q

What is the main cause of hypofibrinogenemia and how is it detected?

A

DIC

Thrombin time is best to detect it, heat precipitation is not sensitive enough.

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41
Q

What is the major contributor to COP / colloid osmotic pressure? How is it evaluated?

A

Plasma proteins, mostly albumin.

Evaluated using colloid osmometer (even works in patients tx’d with synthetic colloids.)

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42
Q

What are troponins?

A

Intracellular myofibrillar proteins involved in calcium ion regulated striated muscle contraction.

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43
Q

What are the isoforms of troponin used to assess cardiac muscle?

A

Troponins I and T (cTnI, cTnT).

  • cTnI is more sensitive (note the “I” also present in sensitive) and magnitude correlates with severity of injury. (ie in cats with hyperthyroidism, horses on endurance rides and dogs with GDV).(also used to diff cardiac versus non cardiac dyspnea in cats.)
  • cTnT increases associated with more severe injury.
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44
Q

What are natruiuretic peptides, endothelin and beta type natriuretic peptides?

A
  • They are indicators of sympathetic nervous system cardio responses and early responders in cardiac injury and are followed by
  • endothelin, which indicates alterations in the vasculature.
  • Beta type natriuretic peptides show greater utility in diff’ing cardiac from non-cardiac causes of dyspnea than cTnI or atrial natriuretic peptides.
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45
Q

What are the 5 types of lipid in plasma?

A 
Cholesterol
Cholestorol esters
Triglycerides (triacylglycerols)
Phospholipids
Nonesterified fatty acids (long chain fatty acids)
46
Q

What does most dietary lipid consist of and whats it turned in to?

A

Long chain triglycerides (and fewer cholesterol, cholesterol esters, phospholipids, etc).
Digested > monoglycerides and FFAs by pancreatic lipase and bile acids. > next is micelle formation.

47
Q

What are micelles and how do the jejunal enterocytes absorb and digest fats and how do they get into plasma?

A

Micelles = monoglycerides and FFAs, cholesterol, bile salts, fat soluble vitamins > absrobed into jejunal enterocytes > degrade micelles into FA, monoglycerides, and cholesterol > Triglycerides are formed > chylomicra (fat plus txport protein) are synthesized from triglycerides, cholesterol, phospholipids, apolipoproteins > chylomicra excreted into intestinal lymph of the lacteals > enter plasma via thoracic duct.

48
Q

How do chylomicra get broken down so the fats can be used in the body?

A

Hydrolysis by lipoprotein lipase (in plasma) > fatty acids and glycerol are absorbed especially by adipocytes and hepatocytes > stored as tryglycerides or oxidized fro energy.

49
Q

How are endogenous lipids transported in the body?

A

Attached to apolipoproteins (lipid peptide complexes with tryglyceride, cholesterol, phopholipid); called lipoproteins

50
Q

Where are lipoproteins synthesized?

A

Liver and SI and secreted into plasma. (these are txport proteins for fat in the blood)

51
Q

How are fats removed from the blood?

A

Lipoprotein lipase and the presence of appropriate cell receptors.

52
Q

*How are lipoprotiens characterized?

A

Via their density which depends on ratio of protein to lipid. The ones with the highest density have the greatest proportion of protein.

53
Q

What are the five classes of lipoproteins in order from least to most dense?

A
  1. Chylomicra (lease dense, made by enterocytes from dietary triglycerides txported in blood).
  2. VLDL (made in liver, txport hepatic triglyceride and cholesterol to muscle, adipose tissue).
  3. Intermediate density lipoproteins (formed in vasculature following lipase hydrolysis of VLDLs).
  4. LDLs, rich in protein with small amounts of cholesterol and triglyceride (formed in vasculature when lipase removes lipids from IDLs.)
  5. HDLs, cholesterol protein and phospholipid with very little triglyceride; txport cholesterol to liver.
54
Q

How does the majority of cholesterol circulate in domestic spp?

A

as HDLs
Dogs and cats have the highest percentage of HDLs and are very resistant to atherosclerosis due to low concentrations of LDLs in these species.

55
Q

What are nonesterified fatty acids?

A

FREE FATTy ACIDS, Another type of endogenous lipids, they are long chain fatty acids. They are released from adipose tissue when you are fasting. In contrast to dietary fats, aka Triglycerides, they are nonesterified.
Made in liver , adipose and mammary tissue.
Regulated by glucogon which decreases synthesis and insulin which increases synthesis.
Increases with high carb low fat diets and decreases with fasting, diabetes mellitus and high fat low carb diets. (THIS IS ESSENTIALLY BODY FAT)

56
Q

When are nonesterified fatty acids increased?

A

During negative energy balance and increased lipolysis > released into plasma and processed in liver > triglucerides and Acetyl-CoA > TCA cycle > energy or ketones.

57
Q

In what conditions do you see increased fatty acids?

A 
Hyperlipidemia w/ increased lipase activity:
diabetes mellitus
equine fasting hyperlipidemia
postexercise ketosis
hepatic lipidosis
equine cushings
bovine ketosis
seems like conditions where the body is short of glucose to the tissues
58
Q

Where do ketones come from?

A

organic anions produced by fatty acid breakdown

59
Q

What is the lipemia refrigeration test?

A

Flocculant layer on top with clearing below = chylomicra.
Persistent turbidity = triglyceride rich lipoproteins
(note you can have both turbidity and the layer on top if both is present).

60
Q

What increases with serum cholesterol, what breed is this seen in dogs, and what condition is this associated with in dogs?

A

Increased serum cholesterol concentration reflects increased cholesterol rich lipoproteins like LDL, HDL.
Miniature schnauzer have abnormal primary cholesterol metabolism.
Serum cholesterol conc is inversely related to thyroid hormone activity.

61
Q

Where does serum triglyceride come from, what cuases it to be high and what are elevations associated with?

A

Analyze fasting sample b/c it elevates post prandial and high fat diets may also increase it due to tryglyceride rich chylomicra.
Hypertriglyceridemia = chylomicronemia and/or increased VLDL; postprandial OR endocrine, pancreatic, hepatic or renal dz.

62
Q

How are triglyceride rich lipoproteins cleared from the plasma? How is this enhanced?

A

Lipoprotein lipase.

This enzyme is enhanced by insulin, thyroid hormone.

63
Q

What precisely does hyperlipidemia mean? What about hyperlipoproteinemia?

A

Increase in plasma lipids. (triglyceride, cholesterol, phospholipid). Increases in Free/nonesterified fatty acids DOES NOT constitute hyperlipidemia (generally just means either hypertriglyceridemia or hypercholesterolemia).
Can be persistent in some dzs.
Hyperlipoproteinemia = hyperlipidemia (same thing cause both triglycerides and cholesterol are both complexed with lipoproteins.)

64
Q

In what breed is idiopathic primary hyperlipidemia seen?

A

Idiopathic hyperlipidemia in Miniature schnauzers, have hypertriglyceridemia, hypercholesterolemia (notice these two are often seen together) and hyperchylomicronemia. Also have excess VLDLs and also reported in other breeds.
Other conditions like hypertriglyceridemia and hyperchylomicronemia also reported by rare but may be associated with xanthomas, granulomas, lipemia retinalis, peripheral neuropathies etc.

65
Q

What do dogs with corneal lipodystrophy have?

A

Primary hypercholesterolemia.

66
Q

Three examples of Primary hyperlipidemia? (rare)

A

Hypercholesterolemia with corneal lipodystrophy.
Idiopathic hyperlipoproteinemia of Miniature Schnauzers.
Hypertriglyceridemia in Burmese cats.

67
Q

7 causes of secondary hyperlipidemia? (common)

A

Acute pancreatitis
Cholestasis
DM (low insulin = lack of lipoprotein lipase activity)
Equine hepatic lipidosis (decreased feed consump)
Liver dz
Endocrine dz, Hypothyroid /Cushings/ excess steroids
Nephrotic syndrome

68
Q

Why are lipids high in hypothyroidism?

A

Cholesterol use decreases while cholesterol synthesis increases. Decreased LDL receptor expression and lipoprotein lipase activity.

69
Q

Why is lipid elevated in diabetes mellitus?

A

Lack of insulin > reduced lipoprotein lipase activity. Increased lipolysis / FFA as fats are used as alternative energy source and VLDLs increase with marked hypertriglyceridemia.

70
Q

Is feline hepatic lipidosis associated with lipemia?

A

NO

71
Q

How does excess steroid administration cause hyperlipidemia?

A

INcreased lipolysis, insulin resistance, decreased lipoprotein lipase activity (common theme/mechanism here when there is elevated lipids).

72
Q

What does lipemia refer to?

A

Milky appearance of serum or plasma caused by increased concentration of triglyceride carrying lipoproteins (chylomicra and VLDL)
NOTE increased cholesterol does not cause lipemia.

73
Q

What affect does lipemia have on other serum values?

A

It enhances hemolysis.
Messes up measure of Glc, Ca, Phos, T Bili (falsely high);
Na and K, T. protein and Alb falsely low (except if measured by refractometry they may be falsely high).

74
Q

Chronic obesity in dogs and cats have increases in which values?

A

Dogs > increases in total cholesterol and triglyceride

Cats > Free Fatty Acids, Triglycerides, VLDL (lower HDL)

75
Q

What are adipokines are what are some examples?

A

Produced by adipocytes and macrophages and participate in a variety of fxns including fat metabolism, immune fxn, cardio dynamics, etc.
Leptin, Adiponectin, Resistin

76
Q

What is Leptin and whats it do?

A

GOOD, INCREASES WHEN FAT, CAN DEVELOP RESISTANCE.
Promotes energy burning, suppresses appetite, suppresses apoptosis, stimulates angiogenesis, increased in obese individuals who develop LEPTIN resistance. Levels correlate with body fat content.

77
Q

What is Adiponectin and whats it do?

A

GOOD, DECREASES WHEN FAT.
Antiinflammatory properties, vasodilation, increasing insulin sensitivity, lowering blood glucose and lowering tissue triglycerides. DECREASED in obesity.

78
Q

What is Resistin and whats it do?

A

BAD, INCREASES WHEN FAT.
Secreted by adipocytes or macrophages and increases with increasing body fat.
Pro inflammatory and contributes to insulin resistance.

79
Q

How are carbs absorbed in the diet?

A

Dietary carbs + pancreatic amylase > disaccharides + mucosal disaccharidases > monosaccharides (glucose, fructose, galactose) > Absorbed.

80
Q

How do ruminants absorb dietary carbohydrates?

A

They are fermented by microbes to volatile fatty acids (acetic, propionic and butyric acid) in the rumen.

81
Q

Three options for carbs / monosaccharides once absorbed?

A

In liver via portal blood > either metabolized for energy, stored as glycogen or converted to AA or fats.

82
Q

Two other sources of glucose in the body besides the diet?

A

Glycogenolysis > degradation of glycogen to free up glucose. (may be low glycogen in dz states or negative energy balance).
Gluconeogenesis > synthesis of glucose from AA and fats, muscle wasting etc is seen with this.

83
Q

Compare glycogenolysis in liver versus muscle.

A

Liver > Glycogen degraded to glucose and released into blood.
Muscle > Glyogenolysis produces lactate and pyruvate, txported to liver and converted to glucose.

84
Q

Three things that can promote glycogenolysis?

A
  • Catecholamines (epi) (in hepatocytes and myocytes)
  • Glucagon (response to hypoglycemia, promotes glycogenolysis, antagonizes insulin)
  • Certain drugs like glucocorticoids, thiazide diuretics, growth hormone, morphine.
85
Q

What is the relationship between glucocorticoids and glycogen and insulin?

A
  • Steroids cause hyperglycemia BUT also decrease glycogenolysis (so this is a paradox) and glycogen stores increase.
  • The hyperglycemia is via other mechanisms like gluconeogenesis, so they don’t get hypoglycemic from decreased glycogenolysis.
  • Steroids are antagonistic to insulin and decrease uptake and use of glucose by tissues.
    BLUF:STEROIDS CAUSE HYPERGLYCEMIA BUT NOT VIA GLYCOGEN BKDOWN. Think of steroids doing the same thing that glucagon does.
86
Q

Which factors promote gluconeogenesis?

A
  • Steroids (endogenous from stress or pain, or from Cushings).
  • Glucagon
  • Growth hormone
  • Certain drugs
87
Q

What are the two fates of blood glucose?

A

Glycogenesis

Tissue utilization

88
Q

What stimulates cellular uptake of glucose and in which tissues?

A

INsulin and muscle, liver and fat are the major tissues.

89
Q

*In which tissues is insulin NOT necessary for glucose uptake (3)?

A

RBCs, Neurons, Renal tubule epithelial cells.

90
Q

In which conditions may you see increased tissue use of glucose and hypoglycemia (6)?

A
  • Excess insulin (Beta cell tumor, iatrogenic etc.)
  • Decreased hormones as in Addison’s disease (decreased glucocorticoids)
  • Decreased hepatic storage of glycogen (liver dz, bacterial sepsis, glycogen storage dz’s)
  • Excess glucose use (sepsis, extreme exertion, pregnancy, neoplasia etc).
  • Reduced glucose intake or inadequate gluconeogenesis (neonate, malabsorption, maldigestion, starvation).
  • Pseudohyperglycemia in serum due to prolonged contact with RBCs.
91
Q

In which conditions may you see decreased tissue use of glucose and subsequent hyperglycemia?

A 
- Insulin antagonists like:
Steroids (endogenous or exogenous)
Glucogon
Growth hormone
Diabetes (type 1 w/ decreased insulin or Type 2 w/ delayed or inadequate response to insulin).
92
Q

What glucose value is suggestive of hypoglycemia?

A

Blood glucose concentration below 40mg/dL after a 24 hour fast. If above 50 its less suggestive of hypoglycemia.

93
Q

Does glucosuria increase urine specific gravity?

A

Yes.
Also note, the resorptive capacity of the proximal renal tubule for glucose is different in different spp, and so glucosuria occurs at different blood glucose levels in different domestic spp.

94
Q

What are the different glycated proteins and how are they used? (3)

A 
Fructosamine (glycated proteins include albumin and others and tells you glc over previous 2-3 wks; need serial measurements in cats d/t variability)
Hemoglobin A1c (reflects glc over 2-3 mos)
Glycoalbumin (alternative to fructosamine in dogs and cats)
95
Q

What do decreased fructosamine levels mean (2)?

A
  • Hypoproteinemia (cats) and/or hypoalbuminemia

- Hyperinsulinism (Insulinoma may present with normal fasting glucose and low fructosamine).

96
Q

Some common causes of persistent hyperglycemia.

A 
Acromegaly / Excess GF
DM
Cushings
Hyperglucagonemia
Pheochromoctoma
Hyperthyroidism
97
Q

Some common causes of Transient hyperglycemia.

A 
Acute pancreatitis
Acute severe colic
Bovine displaced abomasum
Bovine milk fever
Fear/excitemetn, catecholamine release
Stress, endogenous steroids
Ovine enterotoxemia and listeriosis
98
Q

What are the ketone bodies?

A

These are anions of buffered ketoacids and include: (acetoacetate, Beta-hydroxybutyrate and acetone);
NOTE the first two are biproducts of lipid metabolism and the last is a waste product.

99
Q

Three main categories that result in hypoglycemia?

A
  1. Increased use (sepsis, leukocytosis, preg tox, polycythemia)
  2. Decreased production or intake (stavation, neonatal, ketosis in cattle - preg tox I think)
  3. Messed up controls (includes admin or secretion of insulin & insulin analogs like in TUMORS; decreased hormones that maintain glc homeostasis; reduction in glycogen storage in liver; various drugs).
100
Q

What are the hormones that help maintain glucose homeostasis (and so their decrease may cause hypoglycemia)?

A

Hypoadrenocorticism/cortisol
Hypopituitarism/ growth hormone
Hypothyroidism/ thyroid hormone

101
Q

Which tumors may produce insulin or an insulin analog and cause hypoglycemia?

A 
Beta cell tumor producing insulin in the pancreas.
Extrapancreatic neoplasms: 
HSA
Hepatocellular carcinoma
Leiomyoma/leiomyosarcoma
melanoma
renal carcinoma
salivary adenocarcinoma
102
Q

When does ketone production increase?

A

When carbohydrate depletion and increased gluconeogenesis occur.
There is oxaloacetate depletion in the Krebs cycle and suppressed lipogenesis, which leads to acetoacetyl coenzyme A production, which is the precursor to ketogenesis.

103
Q

Are ketones detected first in the blood or urine?

A

Urine. The renal threshold for ketones is low and they are detected via dipstick analysis via nitroprusside reaction.

104
Q

How are ketones generally detected in serum? (ie what do they result in?)

A

Biochemical profiles don’t detect them; their presence is suggested indirectly by titrational acidosis with decreased bicarb/TCO2 and an increase in Anion Gap.

105
Q

What is the purpose of ketones and what do high levels generally result in?

A

Alternate energy source to numerous tissues.
Survival mechanism.
But acetoacetate and beta hydroxybuterate are very acidic and often result in ketoacidosis.

106
Q

When should ketonemia be suspected and which one of the ketones is it primarily due to in DKA?

A

When the anion gap is increased.
DKA is primarily due to beta hydroxybuterate (but does not react with the dipstick nitroprusside test so negative serum ketone test doesn’t exclude ketonemia causing the increased AG.)

107
Q

What are some common causes of ketonemia and ketonuria?

A
  • Anorexia, starvation,
  • DM, bovine ketoacidosis, displaced abomasum, ovine pregnancy toxemia,
  • equine hyperadrenocorticism,
  • high fat diet, bovine hepatic lipidosis syndrome.
108
Q

How do you diff ketonemia of DM from ketonemia of other causes?

A
  • Ketonemia of DM > hyperglycemia

- Ketonemia of other causes > normo or hypoglycemia

109
Q

What is lactate and where does it come from? Whats it do in the body?

A

Organic anion of buffered lactic acid.

  • Produced in excess during anaerobic metabolism AND
  • Enteric organisms produce it during carbohydrate overload or diarrhea
  • In both cases when absorbed or when enters ECF it dissociates into lactate and H+
110
Q

How is it measured or when is it suspected?

A

Most methods detect L-lactate using L lactate dehydrogenase (I think thats the endogenous one), not D-lactate (the one from bacteria).
- Should be suspected when there is an increased anion gap and clinical circumstances are appropriate.

111
Q

Causes of hyperlactermia?

A

Shock, grain overload, sustained heavy exercise, DKA, colic in horses with torsion or strangulation.

Clin Path (14 decks)

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