5 LIPIDS Flashcards

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1
Q

If a patient has high levels of triglycerides, which component of lipoproteins should be examined to understand their role in triglyceride transport?

A

Lipoproteins, specifically VLDL (very low-density lipoproteins), which transport triglycerides in the blood.

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2
Q

How would you explain the role of lipids in energy storage in a patient consuming a low-carbohydrate diet?

A

Lipids are used for long-term energy storage; when carbohydrates are low, lipids are metabolized to provide energy.

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3
Q

Why are lipids essential for vitamin absorption, and how does this relate to the absorption of fat-soluble vitamins?

A

Lipids help absorb fat-soluble vitamins (A, D, E, K) in the small intestine, as these vitamins dissolve in the presence of fats.

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4
Q

If a person’s cell membranes are not functioning properly, which lipid structure should be examined for its integrity and why?

A

The phospholipid bilayer, as it provides structural support and controls cell membrane fluidity and permeability.

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5
Q

What would happen to lipid transport if lipoproteins were absent in the blood?

A

Lipids would not circulate efficiently due to their water-insolubility; lipoproteins are essential for transporting lipids in the bloodstream.

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6
Q

A lab result shows elevated blood cholesterol levels. Which molecule acts as a precursor for steroid hormone synthesis that may be affected?

A

Cholesterol, as it is the precursor for steroid hormones like estrogen, progesterone, and testosterone.

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7
Q

Why can lipids dissolve in organic solvents but not in water, and how does this property influence their role in the body?

A

Lipids are non-polar and hydrophobic, making them insoluble in water. This influences their role in forming cell membranes and requiring transport mechanisms for blood circulation.

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8
Q

How would you describe the difference in structure between triglycerides and phospholipids if a student is comparing their functions?

A

Triglycerides have three fatty acids bound to glycerol, mainly for energy storage, while phospholipids have a phosphate group, making them ideal for forming cell membranes.

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9
Q

A sample of fatty acids contains both saturated and unsaturated types. How would you determine if the sample has a higher proportion of cis or trans unsaturated fatty acids?

A

By observing the melting point; cis unsaturated fatty acids tend to be liquid at room temperature, while trans fatty acids are more likely solid.

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10
Q

If you needed a fatty acid to remain solid at room temperature for stability in a product, which type would you select based on saturation?

A

Saturated fatty acids, as they have no double bonds, which increases stability and allows them to be solid at room temperature.

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11
Q

A patient with high triglyceride levels is advised to reduce dietary fats. Which specific structural feature of triglycerides contributes to their role as the primary storage lipid in adipose tissue?

A

Triglycerides contain three fatty acids attached to glycerol, making them an efficient storage form for energy in adipose tissue.

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12
Q

How would the presence of cis unsaturated fatty acids in a triglyceride influence its physical state at room temperature?

A

Triglycerides with cis unsaturated fatty acids are more likely to be liquid at room temperature, as cis bonds create kinks, preventing tight packing.

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13
Q

Why are phospholipids, rather than triglycerides, the primary component of cell membranes?

A

Phospholipids have a hydrophilic head and hydrophobic tail, allowing them to form a bilayer that controls the movement of substances in and out of cells.

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14
Q

How would you describe the functional significance of the phospholipid bilayer in cellular communication?

A

The bilayer allows selective permeability and supports embedded signaling molecules, aiding in cell-to-cell communication and intracellular signal transduction.

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15
Q

In assessing fetal lung maturity, why would a test for phospholipids, like lecithin, be relevant?

A

Lecithin levels indicate lung maturity; high levels suggest the fetus can produce enough surfactant for breathing upon delivery, reducing respiratory distress risk.

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16
Q

A patient has impaired nerve signal transmission. Which phospholipid component might you investigate and why?

A

Sphingomyelin, as it is essential for myelin in neurons, which speeds up signal transmission along axons.

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17
Q

Why is it beneficial for cephalin to be present on either side of the cell membrane, and how does this relate to cell signaling?

A

Cephalin can serve as a receptor and facilitate signal transduction, aiding in effective communication between the extracellular and intracellular environments.

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18
Q

If a cell’s membrane has reduced fluidity, what structural aspect of phospholipids would you investigate to restore balance?

A

The balance of saturated and unsaturated fatty acids in phospholipids, as unsaturated fatty acids increase membrane fluidity.

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19
Q

If a patient shows an accumulation of sphingomyelin in their liver and spleen, which disorder should you suspect?

A

Niemann-Pick disease, as it is characterized by the accumulation of sphingomyelin in these organs.

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20
Q

What structural difference distinguishes sphingomyelin from other phospholipids, and why is this significant in neural function?

A

Sphingomyelin has a sphingosine backbone instead of glycerol, making it essential for forming myelin in nerve sheaths, which is crucial for fast nerve signal transmission.

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21
Q

A patient with high cholesterol levels is concerned about their risk of vitamin D deficiency. How is cholesterol related to vitamin D synthesis?

A

Cholesterol acts as a precursor for vitamin D synthesis; with sunlight exposure, it can be converted to vitamin D3, important for bone health.

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22
Q

In evaluating a patient with hyperlipidemia, what role does cholesterol play, and how would you differentiate between esterified and free cholesterol in blood tests?

A

Cholesterol is part of blood lipids, with esterified cholesterol bound to fatty acids and free cholesterol unbound. Elevated levels of either form may indicate hyperlipidemia.

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23
Q

If a patient has a liver disorder, why might they also have issues with cholesterol esterification?

A

The liver synthesizes LCAT, which catalyzes cholesterol esterification. Liver dysfunction can lead to reduced LCAT production, affecting cholesterol metabolism.

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24
Q

How does HDL facilitate cholesterol transport in the body through LCAT activation?

A

HDL activates LCAT via Apo A-1, promoting cholesterol esterification, which allows HDL to carry cholesterol in esterified form for removal from the bloodstream.

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25
Q

Why is cholesterol essential beyond its role in lipid metabolism, especially in terms of hormone production?

A

Cholesterol serves as a precursor for steroid hormones (e.g., cortisol, aldosterone) and bile acids, and it can also convert to vitamin D, which is vital for various physiological functions.

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26
Q

If a patient has a vitamin D deficiency due to limited sunlight exposure, how would cholesterol contribute to resolving this deficiency?

A

Cholesterol can be converted to vitamin D3 with adequate sunlight, which helps in maintaining healthy bones and preventing conditions like rickets in children.

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27
Q

How does the process of saponification relate to cholesterol’s availability in the body, particularly in the conversion of esterified cholesterol?

A

Saponification breaks the ester bond in cholesterol esters, freeing cholesterol for conversion into other compounds like steroid hormones and bile acids.

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28
Q

In a patient with high cortisol levels, which precursor molecule should you assess to understand the origin of steroid hormones?

A

Cholesterol, as it is the precursor for glucocorticoids like cortisol, along with other steroid hormones.

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29
Q

A patient’s blood sample appears turbid after a meal. Which lipoprotein is likely responsible for this turbidity, and why?

A

Chylomicrons are likely responsible as they carry dietary triglycerides, creating turbidity in postprandial (after eating) plasma.

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30
Q

If a patient needs to reduce “bad cholesterol” levels, which lipoprotein should be targeted in treatment, and what is its primary function?

A

LDL (Low-Density Lipoprotein), as it transports cholesterol from the liver to peripheral cells, contributing to plaque buildup in arteries.

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31
Q

Why would removing apolipoproteins from a lipoprotein particle lead to its disintegration?

A

Apolipoproteins maintain structural integrity; without them, the lipoprotein particle cannot stay intact.

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32
Q

A patient with liver dysfunction shows signs of poor lipid transport. Which apolipoprotein is essential for cholesterol esterification and HDL function that may be affected?

A

Apo A-1, as it activates LCAT (lecithin-cholesterol acyltransferase), which is crucial for cholesterol esterification and HDL’s cholesterol transport.

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33
Q

How does HDL’s role as “good cholesterol” help in cholesterol management, and what is its pathway in the body?

A

HDL transports cholesterol from peripheral cells back to the liver for excretion, reducing the risk of arterial plaque buildup.

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34
Q

A patient’s lipid profile shows high VLDL levels. What type of triglycerides does VLDL primarily transport, and where do they originate?

A

VLDL primarily transports endogenous triglycerides, which originate within the liver.

35
Q

If a patient’s blood test reveals a creamy top layer after centrifugation, what does this indicate about their recent dietary intake?

A

It suggests high chylomicron levels, likely due to recent consumption of dietary fats, as chylomicrons carry exogenous triglycerides from the intestine.

36
Q

Why are chylomicrons primarily produced in the intestine, and what is their main function?

A

Chylomicrons are produced in the intestine to transport dietary lipids, such as triglycerides, to the liver and peripheral cells.

37
Q

Explain the role of Lipoprotein Lipase (LPL) in lipid metabolism and how it affects triglycerides in chylomicrons.

A

LPL catalyzes the breakdown of triglycerides in lipoproteins, particularly in chylomicrons and VLDL, releasing fatty acids for cellular energy use or storage.

38
Q

If a patient has a genetic defect in LPL, what might you expect in terms of lipid levels and postprandial plasma appearance?

A

Elevated triglyceride levels and turbidity in postprandial plasma, as LPL is necessary for triglyceride breakdown in chylomicrons.

39
Q

A patient has a high VLDL level in their blood test. What does this indicate about their triglyceride transport and potential health risks?

A

High VLDL indicates elevated endogenous triglyceride transport from the liver to peripheral tissues, which may lead to increased turbidity in plasma and contribute to hyperlipidemia.

40
Q

During a lipid panel, how can one differentiate between chylomicrons and VLDL based on plasma appearance?

A

Chylomicrons create a creamy top layer in postprandial plasma, while VLDL causes turbidity without a creamy layer when fasting.

41
Q

Why is LDL often referred to as “bad cholesterol,” and what are its implications in cardiovascular health?

A

LDL is termed “bad cholesterol” because it can infiltrate vessel walls, leading to the formation of foam cells and atherosclerosis, increasing the risk of heart disease

42
Q

If a patient presents with foam cells in their arterial walls, what role did LDL play in this condition?

A

LDL contributed by depositing cholesterol in the extracellular space, where macrophages engulf the excess cholesterol, transforming into foam cells and contributing to plaque formation

43
Q

In terms of cardiovascular protection, how do HDL levels influence a patient’s health outcomes?

A

Higher HDL levels are protective as they transport cholesterol away from peripheral tissues to the liver for excretion, reducing the risk of atherosclerosis and heart disease

44
Q

What are the differences between HDL2 and HDL3 regarding their size and lipid content?

A

HDL2 is larger and richer in lipid than HDL3, reflecting differences in their composition and potential impact on cardiovascular health.

45
Q

Why might a clinician measure Lipoprotein (A) levels, and what are the associated risks?

A

Measuring Lipoprotein (A) is important because elevated levels indicate an increased risk of premature coronary heart disease and stroke, often linked to thrombosis or plaque formation.

46
Q

How does the structure of Lipoprotein (A) contribute to its risk factors in cardiovascular disease?

A

Lipoprotein (A) resembles plasminogen, and its elevated levels may interfere with fibrinolysis, increasing the risk of clot formation and associated cardiovascular events.

47
Q

How does IDL relate to VLDL and LDL in terms of lipid metabolism?

A

IDL is formed from the lipolysis of VLDL and can be converted into LDL, serving as an intermediary in the transition from triglyceride-rich to cholesterol-rich lipoproteins

48
Q

A patient is diagnosed with obstructive jaundice. What abnormal lipoprotein might be present in their plasma, and what is its significance?

A

Lipoprotein X (LpX) may be present, indicating a disruption in lipid metabolism due to bile duct obstruction, resulting in an accumulation of free cholesterol and phospholipids.

49
Q

In a case of type 3 hyperlipoproteinemia, what abnormal lipoprotein would you expect to find, and what does it signify about the patient’s lipid profile?

A

Beta-VLDL would be expected, indicating an accumulation of lipoproteins with properties similar to LDL, associated with altered triglyceride and cholesterol metabolism.

50
Q

Why is serum collected in a serum separator tube (SST) preferred for lipid profile analysis?

A

Serum is preferred because it does not contain fibrinogen, which can interfere with electrophoretic patterns and spectrophotometric measurements

51
Q

What impact does the presence of fibrinogen have on lipid profile measurements using spectrophotometry

A

Fibrinogen can cause turbidity, leading to falsely increased results in lipid profile measurements due to interference with light transmission

52
Q

What is the significance of a 12-14 hour fasting period before lipid profile testing

A

Fasting allows for the clearance of chylomicrons, which can cause turbidity and interfere with spectrophotometric methods, ensuring accurate results

53
Q

How does patient posture affect lipid measurement results?

A

Recumbent posture can decrease concentrations of total cholesterol (TC) and LDL-C by up to 10%, necessitating a 5-minute seated period before sampling to prevent hemoconcentration.

54
Q

What are the recommended storage temperatures for serum or plasma samples, and how do they differ for short-term and long-term storage

A

Samples should be stored at -70°C or lower for long-term storage and at -20°C for short-term storage (up to one to two months).

55
Q

What is the principle behind the Liebermann-Burchardt reaction for cholesterol measurement?

A

This chemical method detects a color reaction from the dehydration and oxidation of cholesterol, forming a green compound when combined with Cholestadienyl Monosulfonic Acid.

56
Q

How does the CDC reference method for cholesterol measurement utilize Gas Chromatography Mass Spectrometry (GC-MS)?

A

GC-MS provides precise identification and quantification of cholesterol in samples through separation and mass analysis of the cholesterol molecules.

57
Q

Describe the steps involved in the CDC reference method for triglyceride measurement

A

The method involves saponification with alcoholic KOH, extraction with chloroform, treatment with silicic acid to remove phospholipids, and results in a pink chromophore as the end product.

58
Q

What is the outcome of the Van Handel and Zilversmith method for triglyceride measurement?

A

This colorimetric method produces a blue color compound as a chromogen, indicating the presence of triglycerides.

59
Q

How does the Hantzsch condensation method differ from other methods for triglyceride measurement?

A

The Hantzsch condensation method is fluorometric, utilizing the fluorescent properties of the diacetyl lutidine compound, which can be detected using fluorescent microscopy, providing sensitivity in measurement.

60
Q

What are the two key enzymes involved in the glycerol kinase method for measuring glycerol?

A

Lipase and glycerol kinase are the two key enzymes used in this spectrophotometric method.

61
Q

How is ultracentrifugation used as a reference method for quantifying lipoproteins?

A

Ultracentrifugation quantifies lipoproteins based on their protein (CHON) and triglyceride (TAG) contents.

62
Q

Describe the migration pattern of lipoproteins during electrophoresis

A

HDL migrates with alpha1-globulins, LDL with beta-globulins, and VLDL with beta2-globulins towards the anode, with HDL stabilized in the alpha region and LDL in the beta region

63
Q

What staining dyes are commonly used to visualize lipoprotein electrophoretograms?

A

Common dyes include Oil Red O, Fat Red 7B, and Sudan Black B, with Oil Red O causing lipoproteins to appear red

64
Q

What HDL-C levels indicate a high risk for coronary heart disease (CHD)?

A

HDL-C levels below 35 mg/dL indicate a high risk for CHD, while levels above 60 mg/dL are considered protective.

65
Q

Explain the two-reagent procedure used in homogeneous assays for HDL-C measurement.

A

The first reagent forms a stable complex with non-HDL lipoproteins, while the second reagent releases HDL-C, allowing for its measurement.

66
Q

How does the Friedewald method calculate LDL-C?

A

The formula used is TC = HDL-C + (TAG/2.175) or 5, depending on the context.

67
Q

What is the significance of the De Long method in LDL-C measurement?

A

The De Long method is utilized when triglyceride (TGY) levels are 400 mg/dL or higher, using a modified formula to calculate TC

68
Q

Outline the steps involved in the beta quantification method for LDL-C calculation.

A

The steps include ultracentrifugation to remove VLDL and chylomicrons, measurement of total cholesterol (TC) in the bottom fraction, precipitation with heparin/manganese to isolate HDL-C, and calculation of LDL-C as TC - HDL-C

69
Q

What is a key advantage of the homogeneous direct LDL-C method?

A

This method directly measures LDL-C and is particularly useful when triglycerides are elevated, as it selectively removes non-LDL lipoproteins.

70
Q

What does a positive result in the standing plasma test indicate?

A

A positive result indicates a floating “creamy” layer, signifying the presence of chylomicrons, while a negative result indicates VLDL.

71
Q

What techniques are used for apolipoprotein analysis, and what do they measure?

A

Apolipoproteins are typically measured by immunoassay or immunophelometry, which assess turbidity caused by apolipoprotein-antibody complexes.

72
Q

What cardiovascular conditions are associated with atherosclerosis due to lipids and lipoproteins?

A

Myocardial infarction, cerebrovascular disease, and peripheral vascular disease are associated with atherosclerosis

73
Q

What is the difference between hyperlipidemia and hypolipidemia?

A

Hyperlipidemia refers to increased lipid concentrations, while hypolipidemia refers to decreased lipid concentrations

74
Q

What characterizes polygenic (nonfamilial) hypercholesterolemia?

A

It is multifactorial, not limited to family history, and accounts for approximately 85% of hypercholesterolemia cases in the population.

75
Q

What genetic defect causes familial hypercholesterolemia?

A

It is caused by a defective or deficient LDL-receptor gene on chromosome 19, resulting in high LDL levels in the circulation.

76
Q

What clinical findings are associated with the accumulation of beta-VLDL rich in cholesterol?

A

Patients may exhibit xanthomas and premature vascular diseases such as coronary artery disease (CAD) and peripheral artery disease (PAD).

77
Q

What is sitosterolemia, and what causes it?

A

Sitosterolemia is a rare autosomal recessive disorder characterized by the accumulation of phytosterols due to mutations in the ABCG8 or ABCG5 genes

78
Q

What are the key laboratory findings in abetalipoproteinemia

A

Patients lack VLDL, LDL, and chylomicrons in plasma, and acanthocytes (thorny-shaped RBCs) are present.

79
Q

What causes hypobetalipoproteinemia, and what are its laboratory findings?

A

It is caused by apo B deficiency resulting from a point mutation, leading to decreased LDL-C and total cholesterol levels

80
Q

What genetic mutation is associated with Tangier disease, and what are its key characteristics

A

Tangier disease is caused by a mutation in the ABCA1 gene, leading to very low levels of HDL and symptoms such as corneal opacities and renal failure.

81
Q

What syndrome is associated with lipoprotein lipase deficiency, and what are the laboratory findings?

A

LPL deficiency results in chylomicronemia syndrome with extremely high triglyceride levels (TAG = 10,000 mg/dL) and presents with abdominal pain and pancreatitis.

82
Q

What are the key features of chylomicron retention disease (Anderson’s disease)?

A

It is characterized by high levels of chylomicrons, hypocholesterolemia, chronic diarrhea, failure to thrive, and deficiency of fat-soluble vitamins.

83
Q

What are the conversion factors for cholesterol and triglycerides from mg/dL to mmol/L?

A

The conversion factor for cholesterol is 0.026, and for triglycerides, it is 0.0113