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Clinical Pathology > Lipids & Glucose > Flashcards

Lipids & Glucose Flashcards

1
Q

What is hyperlipidemia? Hypolipidemia?

A

HYPER = increased circulating lipids, including cholesterol and/or triglycerides (NOT LIPEMIA)

HYPO = decreased circulating lipids, including cholesterol and/or triglycerides

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2
Q

What are the 5 major functions of lipids?

A
  1. physical: thermogenesis, thermal insulation, shock absorption
  2. energy source (triglycerides, fatty acids)
  3. structural components to cell membranes (phospholipids, cholesterol)
  4. substrates for hormones and other messengers
  5. precursors for synthesis of steroid hormones, vitamin D, and bile acids
  6. immunity
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3
Q

What happens to dietary lipids after they are ingested? What are the 5 major types found in the plasma?

A

digested by pancreatic lipas and emulsified by bile salts to monoglycerides and fatty acids

  1. cholesterol
  2. cholesterol esters
  3. triglycerides
  4. phospholipids
  5. non-esterified fatty acids (NEFAs)
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4
Q

What is the importance of triglycerides and cholesterol?

A

TRIGLYCERIDES - comprises stored fats and is metabolized for energy (most common and efficient form of energy storage in mammals)

CHOLESTEROL - make up cell membranes, are the building blocks for steroid hormones, and used to synthesize bile acids

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5
Q

What are the 2 major functions of non-esterified fatty acids (NEFAs)? What sources do they come from?

A
  1. energy source
  2. metabolic building blocks - incorporated into triglycerides

diet or mobilized from fat stores from triglycerides metabolism

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6
Q

What happens to non-esterified fatty acids (NEFAs) after the are ingested or mobilized from fat stores?

A
  • forms acetyl-CoA and enters the TCA cycle to produce ATP
  • converted into ketone bodies
  • reformed back into triglycerides in fat stores
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7
Q

How are lipids transported?

A

insoluble in water —> attach to apoproteins that stabilize and solubilize them in the aqueous phase of blood

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8
Q

What are lipoproteins?

A

proteins (apoprotein) + lipids

large spherical particles with a hydrophobic core containing TGs and cholesterol, and a hydrophilic surface composed of phospholipids, free cholesterol, and apoproteins

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9
Q

How is lipemia observed grossly? What does it indicate?

A

visibly hazy to white/opaque serum or plasma (larger particles = increased blocking of light transmission)

presence of chylomicrons or VLDLs

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10
Q

What is expected on biochemistry panels with lipemia?

A

increased triglycerides +/- increased cholesterol

(NOT increased cholesterol alone - serum/plasma with increased cholesterol alone appears normal)

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11
Q

What are 2 common artifacts caused by lipemia in vitro?

A
  1. falsely elevated Hgb, MCH, and MCHC due to its detergent effec on cell membranes, leading to RBC hemolysis
  2. falsely elevated plasma protein on refractometer byt causing the formation of and indistinct demarcation line
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12
Q

What chemistry panel artifacts are seen with lipemia

A
  • hyperglycemia
  • hypercalcemia
  • hyperphosphatemia
  • hyperbilirubinemia
  • hyponatremia
  • hypokalemia
  • hypoproteinemia
  • hypoalbuminemia

(depends on the methodology and analyzer)

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13
Q

What is a primary cause of hyperlipidemia?

A

hereditary alterations in lipoprotein metabolism or production

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14
Q

What are some secondary causes of hyperlipidemia?

A
  • postprandial
  • DM
  • acute necrotizing pancreatitis in dogs
  • equine hyperlipidemia in ponies, horses, and donkeys
  • hypothyroidism
  • hyperadrenocorticism
  • anorexia in horses
  • obstructive cholestasis in dogs and cats
  • nephrotic syndrome and protein-losing enteropathy
  • endotoxemia and inflammation

(secondary > primary)

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15
Q

How are lipid values affected by postprandial hyperlipidemia? In what animals is this most common?

A
  • triglycerides are mildly to markedly increased
  • mild increases in cholesterol possible

MONOGASTRICS - dogs and cats within 1-2 hr after a meal, peaks at 2-8 hr, and is cleared by 8-16 hours

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16
Q

Why is a 12-hour fast recommended before bloodwork?

A

increased lipid values typically clear within 8-16 hours after a meal

  • if still elevated after 12 hours = persistent hyperlipidemia
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17
Q

How are lipid values affected by diabetes mellitus? What causes the hyperlipidemia? In what animals is this common?

A
  • mild to marked hypertriglyceridemia
  • mild hypercholesterolemia

decreased insulin causes defective VLDL processing and LPL inhibition

cats, dogs, and horses with a complex pathogenesis, so lipid profile will be highyl variable

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18
Q

How are lipid values affected by acute pancreatitis? What causes this?

A
  • mild to moderate hypertriglyceridemia
  • mild hypercholesterolemia

decreased insulin production and the production of inflammatory cytokines inhibit lipoprotein lipase and LPL activity
(biliary excretion and increased hepatic production increases cholesterol)

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19
Q

How are lipid values affected by equine hyperlipidemia syndrome? In what animals is this most common?

A

marked hypertriglyceridemia

Shetland ponies, miniature horses, donkey mares

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20
Q

What is the mechanism of equine hyperlipidemia syndrome causing secondary hyperlipidemia? What are the 2 groups?

A

negative energy balance (decreased feed consumption, anorexia, pregnancy, lactation, obesity, renal failure, endotoexmia) causes the mobilization of fatty acid to the liver, which causes a marked increase in triglycerides and VLDL

  1. hyperlipidemia (mild disease): [TG] < 500 mg/dL
  2. hyperlipidemic syndrome (poor prognosis): [TG] > 500 mg/dL —> fatty liver with cholestasis and decreased liver function
21
Q

How does hypothyroidism cause secondary hyperlipidemia?

A

lack of thyroid hormones (T3, T4) decreases LPL and hepatic lipase activity

  • marked hypercholesterolemia
  • +/- concurrent hypertriglyceridemia
22
Q

How does hyperadrenocorticism cause secondary hyperlipidemia?

A

increased endogenous or exogenous steroids causes increased VLDL synthesis and insulin resistance

  • hypercholesterolemia +/- hypertriglyceridemia
23
Q

What is obstructive cholestasis most likely secondary to? How does it cause secondary hyperlipidemia? What is characteristic of lipid values?

A

decreased clearance of bile

obstruction causes an increased cholesterol content in hepatocytes and reduced cholesterol excretion

cholesterolemia without hypertriglyceridemia

24
Q

How do nephrotic syndrome and protein-losing enteropathy cause secondary hyperlipidemia? How are lipid values affected? What are the 4 most common signs?

A

increased VLDL production, defective lipolysis, and defective conversion of cholesterol to bile acids

hypercholesterolemia +/- hypertriglyceridemia

25
Q

What are the 4 most common signs of nephrotic syndrome and protein-losing enteropathy?

A
  1. hypercholesterolemia
  2. hypoalbuminemia
  3. proteinuria
  4. ascites
26
Q

How do endotoxemia and inflammation cause secondary hyperlipidemia?

A

pro-inflammatory cytokines lead to a reduced triglyceride clearance

27
Q

In what animal is hyperlipidemia commonly hereditary? How are lipid values affected?

A

Miniature Schnauzers*, Briards, Beagles, Brittany Spaniels, cats —> hereditary alterations in lipoprotein metabolism or production

hypertriglyeridemia +/- hypercholesterolemia

28
Q

Causes of hyperlipidemia:

A
29
Q

What are the 5 most common causes of hypocholesterolemia?

A
  1. decreased cholesterol production
  2. portosystemic shunts
  3. liver insufficiency/failure
  4. malabsorption/maldigestion (PLE)
  5. idiopathic: hypoadrenocorticism
30
Q

Is hypotriglyceridemia clinically significant? What is the suggested cause?

A

significance is uncertain

may be associated with severe malnutrition

31
Q

What is gluconeogenesis? Glycogenolysis?

A

formation of glucose in the liver from non-carb sources (amino acids and lactate)

biochemical pathway in which glycogen breaksdown into glucose-1-phosphate and glucose in the hepatocytes and myocytes

32
Q

What are the 3 major sources of blood glucose?

A
  1. intestinal absorption of carbohydrates
  2. hepatic production: gluconeogenesis, glycogenolysis
  3. kidney production
33
Q

What 3 factors does blood glucose levels depend on?

A
  1. time since last meal
  2. hormones
  3. utilization of glucose by peripheral tissues
34
Q

How do insulin and glucagon affect blood glucose?

A

INSULIN - decreased blood glucose by promoting tissue intake, inhibiting gluconeogenesis, and promoting glycogen synthesis

GLUCAGON - increased blood glucose by promoting gluconeogenesis and glycogenolysis and inhibiting glycogen synthesis

35
Q

How do glucocorticoids affect blood glucose?

A

increases blood glucose by antagonizing insulin, inducing insulin resistance, and promoting gluconeogenesis and glucagon release

36
Q

How do catecholamines affect blood glucose?

A

increase blood glucose by inhibiting insulin secretion and promoting glycogenolysis

37
Q

How do growth hormones affect blood glucose?

A

increase blood glucose by inhibiting insulin action nad promoting gluconeogenesis

38
Q

What are 6 causes of hyperglycemia?

A
  1. postprangial
  2. excitement/fright (epinephrine)
  3. DM
  4. endogenous or exogenous corticosteroids
  5. pancreatitis
  6. drugs/chemicals
39
Q

What are the postprandial effects on blood glucose? When is it common for glucose levels to remain longer than usual?

A

blood glucose increases for 2-4 hours after a meal and is cleared within 12 hours

elevated blood glucose may be prolonged in hepatic disorders due to reduced glycogenesis

40
Q

How does excitement/fright affect blood glucose? How is this reflected in the biochemistry profile?

A

elevates blood glucose due to increased epinephrine promoting glycogenolysis

mild hyperglycemia (dogs < 150 mg/dL)

41
Q

What are the 2 types of diabetes mellitus? In what animals are each common in?

A

1: decreased insulin production; juvenile (dogs)

2: insulin resistance (cats)

42
Q

How do corticosteroids affect blood glucose? What condition commonly causes this?

A

antagonize insulin —> decreased glucose uptake and utilization (decreased glycogenolysis) = HYPERGLYCEMIA

hyperadrenocorticism

43
Q

How does pancreatitis affect blood glucose?

A

causes decreased insulin production —> decreased glucose uptake and utilization = HYPERGLYCEMIA

44
Q

What 5 drugs/chemicals commonly cause hyperglycemia?

A
  1. ethylene glycol
  2. glucose-containing fluids (Dextrose)
  3. ketamine
  4. phenothiazine
  5. xylazine
45
Q

What are 5 common causes of hypoglycemia?

A
  1. excessive insulin administration
  2. excessive endogenous insulin, commonly caused by insulinomas
  3. hypoadrenocorticism
  4. hepatic disease
  5. excessive glucose utilization seen in sepsis, pregnancy, neoplasia, and extreme physical exertion
46
Q

What are 5 commo situations that result in decreased glucose intake or inadequate gluconeogenesis that results in hypoglycemia?

A
  1. neonates due to hepatic insufficiency
  2. severe malnutrition
  3. severe malabsorption
  4. starvation
  5. ketosis in cattle
47
Q

What is the most common cause of artifactual (pseudo) hypoglycemia? What is also commonly seen in this situation?

A

prolonged contact of serum with RBCs in vitro, causing the RBCs to utilize glucose for metabolism

in vitro hemolysis

48
Q

What 4 drugs/chemicals commonly cause hypoglycemia?

A
  1. xylitol toxicosis in DOGS
  2. ethanol
  3. mitotane
  4. salicylates

Clinical Pathology (33 decks)

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