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Clinical Pathology > Lecture 26 - Lipids and Glucose > Flashcards

Lecture 26 - Lipids and Glucose Flashcards

1
Q
  • Hyperlipidemia = increase in _________ _______
  • NOT synonymous with _______ –> refers to turbidity of sample due to lack of fasting before obtaining blood.
  • Includes increased _________ ____/__ _______
A
  • Hyperlipidemia = increase in circulating lipids
  • NOT synonymous with lipemia –> refers to turbidity of sample due to lack of fasting before obtaining blood.
  • Includes increased cholesterol and/or triglycerides
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2
Q
  • Hypolipidemia = __________ in circulating lipids
  • Includes decreased ___________ _____/____ _______
A
  • Hypolipidemia = decrease in circulating lipids
  • Includes decreased cholesterol and/or triglycerides
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3
Q
  • Cholesterol → ?
A

hyper-/hypo- cholesterolemia

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4
Q
  • Triglycerides →
A

hyper-/hypo- triglyceridemia

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5
Q

Lipid Functions
* Physical — - Fat is very important for _________, ________ insulation, _____ absorption. Some animals may have to accumulate more fat than others, depending on where they _____.
* Energy Source — _________ and ______ _____ are the most important.
* Structural components to cell membranes — _________, __________
* Substrates for ________ and other messengers
* Precursors for synthesis of ______ hormones, Vitamin _____, and ______ acids
* Immunity

A

Lipid Functions
* Physical — - Fat is very important for thermogenesis, thermal insulation, shock absorption. Some animals may have to accumulate more fat than others, depending on where they live.
* Energy Source — triglycerides and fatty acids
* Structural components to cell membranes — phospholipids, cholesterol
* Substrates for hormones and other messengers
* Precursors for synthesis of steroid hormones, Vitamin D, and bile acids
* Immunity

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6
Q
  • Ingested dietary lipids are digested by pancreatic lipase and
    emulsified by bile salts to monoglycerides and fatty acids
A
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7
Q

What are the 5 major types of lipids in plasma?

A
  • Cholesterol <– important
  • Cholesterol esters
  • Triglycerides <– important
  • Phospholipids
  • Non-esterified fatty acids (NEFAs)
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8
Q

Triglycerides
* Comprises stored _____; metabolized for _______
* Most common and efficient form of energy storage in _________
* Comes from ______ or synthesized in the _____

A

Triglycerides
* Comprises stored fat; metabolized for energy
* Most common and efficient form of energy storage in mammals
* Comes from diet or synthesized in the liver

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9
Q

Cholesterol (free and esterified)
* Component of cell _________
Building blocks for _______ hormones
Used in synthesis of ?
Comes from ______ or synthesized in the _____

A

Cholesterol (free and esterified)
* Component of cell membranes
Building blocks for steroid hormones Used in synthesis of bile acids
Comes from diet or synthesized in the liver

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10
Q

Lipids of Importance: Non-Esterified Fatty
Acids (NEFAs)
Source of _______; metabolic _______ _______
A. Come from the ____ or mobilized from ___ stores
* Breakdown product of ____
B. Form ______ _____
* Enters the _____ cycle for ____ production or Converted into ? or Reformed into _____
C. Incorporated into ________

A

Lipids of Importance: Non-Esterified Fatty
Acids (NEFAs)
Source of energy; metabolic building blocks
* Come from the diet or mobilized from fat stores
* Breakdown product of TGs
* Form acetyl CoA
* Enters the TCA cycle for ATP production
* or Converted into ketone bodies
* or Reformed into TGs
* Incorporated into triglycerides

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11
Q

Lipids are ________ in water, so they travel attached to ________ that stabilize and solubilize them in the _______ phase of blood

A

Lipids are insoluble in water, so they travel attached to apoproteins that stabilize and solubilize them in the aqueous phase of blood

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12
Q

Proteins (________) + _______ = Lipoproteins

A

Proteins (apoproteins) + Lipids = Lipoproteins

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13
Q

Lipoproteins
* Large in size spherical in shape particles
* Hydrophobic core containing TGs and Chol
* Hydrophilic surface composed of phospholipids, free
Chol, apoproteins

A

Lipoproteins
* Large in size spherical in shape particles
* Hydrophobic core containing TGs and Chol
* Hydrophilic surface composed of phospholipids, free
Chol, apoproteins

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14
Q
A
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15
Q
A
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16
Q
A

Normal = clear
Milky appearance = lipemia
- presence of chylomicrons or VLDLs present aka animal has not been fasted enough. It does NOT tell us other changes

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17
Q

Lipemia
* Visibly hazy to white/opaque serum or plasma
* Lipemia indicates either chylomicrons or VLDLs
are present
- The feature of visible lipemia is related to particle size
(large lipoproteins block light transmission)
* Expect to see ↑ TGs +/- ↑ Chol on a chemistry
(both CM and VLDLs contain some cholesterol)
* Serum plasma with ↑Chol w/o ↑TGs will appear
normal (aka. not lipemic)

NOT caused by hypercholesterolemia alone

A
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18
Q

Lipemia effects in vitro
* CBC artifacts due to lipemia, which mostly occurs in vitro, the lipemia can be acting as a detergent on cell membranes –> RBC hemolysis
Results:
* Falsely elevated Hgb, MCH, MCHC
* Can also have falsely elevated plasma protein (using refractometer method)
* Indistinct demarcation line on refractometer scale may be interpreted as an increased value

A
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19
Q

Lipemia Interferes with
refractometer total protein reading

A
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20
Q

What are the lipemia effects in vitro?
[Marked as important]

When you have a lipemic sample?

A

Chemistry panel artifacts
* Hyperglycemia
* Hypercalcemia
* Hyperphosphatemia
* Hyperbilirubinemia
* Hyponatremia
* Hypokalemia
* Hypoproteinemia
- Hypoalbuminemia

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21
Q

What are the primary causes of Hyperlipidemia?

A

Hyperlipidemia: Either the increase of TG AND/OR Cholesterol

Primary causes
* Hereditary alterations in lipoprotein metabolism or production

22
Q

What are the secondary causes of Hyperlipidemia?

A

Secondary causes
* Postprandial
* Diabetes Mellitus
* Acute necrotizing pancreatitis (dogs)
* Equine hyperlipidemia of ponies,
horses, and donkeys
* Hypothyroidism
* Hyperadrenocorticism
* Anorexia (horses)
* Obstructive cholestasis in dogs and cats
* Nephrotic syndrome and protein-losing
enteropathy
* Endotoxemia and inflammation

these causes are more common

23
Q

Postprandial (after animal has eaten a meal)
A. Triglycerides are ______ to ________ _________
B. May seen mild ________ in _________
C. Dogs and Cats –_________-
* Occurs ___-___ hours after eating a _____ meal
* Transient and peaks at ___-___ hours
* Blood samples may appear _____ to ______
* Cleared by ___-____ h
D. Persistent hyperlipidemia: presence of ______ lipids in blood after a ____-hour fast

A

Postprandial (after animal has eaten a meal)
A. Triglycerides are mildly to markedly increased
B. May seen mild increases in cholesterol
C. Dogs and Cats –monogastrics-
* Occurs 1-2 hours after eating a meal
* Transient and peaks at 2-8 hours
* Blood samples may appear hazy to lipemic
* Cleared by 8-16 h
D. Persistent hyperlipidemia: presence of excess lipids in blood after a 12-hour fast

24
Q

Diabetes mellitus
* Hyperlipidemia will be caused by a mild to moderate increase in TG or mild increase in cholesterol
* Lack of insulin release induced a defective VLDL processing the LPL (LPL inhibition)
* Hypertriglyceridemia is mildly to moderately
* Hypercholesterolemia is mild
* Seen in monogastric animals Cat, dogs, horses
* Complex pathogenesis, lipid profile can be highly variable.

A
25
Q

Acute pancreatitis
* Hypertriglyceridemia is mild to moderate
* +/-Hypercholesterolemia –if does, tend to be Mild-
* Seen in Cat, dogs
* The mechanism might possibly be due to
↓ insulin production → ↓ LPL activity … and then inflammatory cytokines are also likely involved
* Cholesterol increases due to decreased biliary excretion (patient will have cholestasis), and increased hepatic production.

A
26
Q

Equine hyperlipidemia Syndrome
* Mainly have Hypertriglyceridemia can be Marked!
* Seen in Shetland ponies, miniature horses, donkey mares
* Causes: Mainly caused by a decrease in feed consumption or negative energy balance; anorexia, obesity, pregnancy, lactation, renal failure, endotoxemia

Mechanism: negative energy balanceàmobilization of Fatty acids –> ↑ fatty acids to liver–> ↑ synthesis of TG in hepatocytes –> ↑VLDL (thus ↑ [TG])

Division of 2 groups = FYI info

Will have FATTY liver with cholestasis & decreased liver function

A
27
Q

Hypothyroidism
* Lack of thyroid hormones (T3, T4) → induces a ↓LPL activity and also a ↓hepatic lipase activity
- These patients will have a ↑TGs, ↑-↑↑↑ Chol
- This is due to an Increase in cholesterol synthesis –> hypercholesterolemia
* +/- concurrent hypertriglyceridemia

A
28
Q

Hyperadrenocorticism
* Causes by endogenous or exogenous steroids
* Usually will have hypercholesterolemia, but +/- hypertriglyceridemia
* Increased VLDL synthesis, and insulin resistance

A
29
Q

Obstructive cholestasis
* Seen in dogs and cats
* Hypercholesterolemia without hypertriglyceridemia
* Increased cholesterol content of hepatocytes
- Reduced biliary cholesterol excretion

A
30
Q

Nephrotic syndrome and PLN
* Hypercholesterolemia
* Hypoalbuminemia
* Proteinuria
* Ascites
* Hypercholesterolemia +/- hypertriglyceridemia
* Increased VLDL production, defective lipolysis, defective conversion of cholesterol to bile acids

A
31
Q

In cases of Endotoxemia and inflammation
* Hyperlipidemia occurs due to reduced TG’s clearance from actions of Pro-inflammatory cytokines

A
32
Q

Primary hyperlipidemia
Hereditary
* Hereditary alterations in lipoprotein metabolism or production
* Hyperlipidemia of Miniature Schnauzers
* Hypertriglyceridemia +/- hypercholesterolemia
* Also rarely seen in Briards, Beagles, Brittany Spaniels, and cats
* Mechanism unknown

A
33
Q
A
34
Q

Hypocholesterolemia
* Decreased cholesterol production
* Portosystemic shunts (dogs and cats)
* Liver insufficiency/failure
* Malabsorption/maldigestion: PLE
* Unknown / Multiple Mechanisms
* Hypoadrenocorticism (Addison’s)

A
35
Q

Hypotriglyceridemia
* Significance is uncertain
* Maybe associated with severe malnutrition

A
36
Q
A
37
Q
A
38
Q

Glucose metabolism
* Sources of blood glucose
* Main source: Intestinal absorption of carbohydrates
* Other source: Hepatic production (hepatocytes and myocytes) via
- Gluconeogenesis = formation of lyocen from non-carb soures, such as AA and lactate
- Glycogenolysis = glycogen braks down into glucose.
* Kidney production (minor)

A
39
Q
  • Blood glucose levels are dependent upon:
  • Time since last meal
  • Hormonal influences
  • Utilization of glucose by peripheral tissues
A
40
Q

–> Hormonal regulation: [Important]
A. Insulin – decreases BG by:
* Promoting tissue glucose uptake
* inhibiting gluconeogenesis
* Promoting glycogen synthesis
B. Glucagon – increases BG by:
* Promoting gluconeogenesis
* Promoting glycogenolysis
* Inhibiting glycogen synthesis

A
41
Q

A. Glucocorticoids – increase BG by:
* Antagonizing insulin – inducing “insulin resistance”
* Promoting gluconeogenesis and glucagon release
B. Catecholamines – increase BG by:
* Inhibiting insulin secretion
* Promoting glycogenolysis
C. Growth hormone – increases BG by:
* Inhibiting insulin action
* Promoting gluconeogenesis

A
42
Q

What are the causes of hyperglycemia?

A

CAUSES OF HYPERGLYCEMIA
1. Postprandial
2. Excitement/fright (epinephrine)
3. Diabetes mellitus
4. Endogenous or exogenous corticosteroids
5. Pancreatitis
6. Drugs/chemicals

43
Q
  1. Postprandial
    * Blood glucose increases for 2-4 hours after a meal in monogastrics
    * Cleared by 12 hours
    * May be prolonged in hepatic disorders (reduced glycogenesis)
A
44
Q
  1. Excitement/fright (epinephrine)
    * Promotes glycogenolysis
    * Typically mild hyperglycemia
    * Dogs: glucose usually < 150 mg/dL
A
45
Q
  1. Diabetes mellitus
    * Type 1: decreased insulin production (dogs)
    * Type 2: insulin resistance (cats)
A
46
Q
  1. Endogenous or exogenous corticosteroids
    * Hyperadrenocorticism
    * Corticosteroids antagonize insulin –> decreased glucose uptake and utilization (decreased glycogenolysis)
A
47
Q
  1. Pancreatitis
    * Decreased insulin production –> decreased glucose uptake and utilization
A
48
Q
  1. Drugs/chemicals
    * Ethylene glycol
    * Glucose-containing fluids (e.g. Dextrose)
    * Ketamine
    * Phenothiazine
    * Xylazine
A
49
Q

What are the causes of Hypoglycemia?

A

CAUSES OF HYPOGLYCEMIA
* Excessive insulin administration (exogenous)
* Excessive endogenous insulin
- Insulinoma [Marked as important = exam question]
* Hypoadrenocorticism
* Hepatic disease
* Excessive glucose utilization
- Sepsis
- Pregnancy
- Neoplasia
- Extreme physical exertion

50
Q
  • Reduced glucose intake or inadequate gluconeogenesis can also lead to Hypoglycemia.
  • Neonates (hepatic immaturity)
  • Severe malnutrition
  • Severe malabsorption
  • Starvation
  • Ketosis in cattle
A
51
Q
  • Artifactual hypoglycemia (pseudohypoglycemia) caused by manipulation of samples. If we do not run our serum in a timely manner, we can see this.
  • Prolonged contact of serum with erythrocytes in vitro
  • RBCs utilize glucose in the serum for metabolism
  • May see concurrent in vitro hemolysis
A
52
Q

What drugs/chemicals can cause hypoglycemia?

A
  • Drugs/chemicals
  • Xylitol toxicosis –> severe hepatic insuffiency; mechanism is still unknown
  • Ethanol
  • Mitotane
  • Salicylates

Clinical Pathology (31 decks)

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