1
Q
What is the general feature of lipids?
A
Insolubility in water
2
Q
What are lipids mainly composed of?
A
Carbon-hydrogen bonds
3
Q
Main functions of lipids?
A
Energy, structural elements, electron carriers, enzyme cofactors
4
Q
Examples of lipids?
A
Triglycerides, cholesterol, phospholipids
5
Q
What is the structure of a fatty acid?
A
Linear chain of C-H bonds ending with a carboxyl group (-COOH)
6
Q
fatty acids In plasma, only a few amount exist as
free or unesterified form and most are
A
Bound to albumin
7
Q
Majority of fatty acids are part of?
A
Part of triglycerides and phospholipids
8
Q
what can fatty acids be used for?
A
gluconeogenesis
9
Q
triglycerides are the predominant form of
A
glyceryl esters found in plasma
10
Q
Other name for triglycerides?
A
Neutral fats
11
Q
Composition of triglycerides?
A
3 fatty acids + glycerol (ester bonds)
12
Q
Main storage lipid?
A
Triglycerides
13
Q
Percentage of tissue storage fat as triglycerides?
A
95%
14
Q
Hormones/enzymes involved in triglyceride breakdown?
A
Lipoprotein lipase (LPL), Epinephrine, Cortisol
15
Q
Advantages of triglycerides as energy?
A
- carbons atoms of fatty acids more reduced than sugar
- Hydrophobic → no water weight
16
Q
Required specimen for triglyceride test?
A
Serum or plasma
17
Q
Fasting requirement for triglyceride test
A
12–14 hours
18
Q
Normal triglyceride levels?
A
<150 mg/dL
19
Q
Borderline triglyceride levels?
A
150–199 mg/dL
20
Q
High triglyceride levels?
A
200–499 mg/dL
21
Q
Very high triglyceride levels?
A
> 500 mg/dL
22
Q
What are the triglycerides chemical methods
A
- Colorimetric method (Van Handel & Zilversmit)
- Fluorometric method (Hantzch Condensation)
23
Q
What is Folch’s reagent?
A
Chloroform-ethanol mixture used to extract serum lipids
24
Q
What is the principle of Van Handel & Zilversmit method?
A
- Extract lipids → Folch’s reagent (chloroform–ethanol).
- Remove phospholipids → adsorbent (zeolite/alumina/florisil).
- Hydrolyze TAG → alcoholic KOH → glycerol + fatty acids.
- Oxidize glycerol → periodic acid → formaldehyde.
- Color reaction → formaldehyde + chromotropic acid (H₂SO₄) → blue compound.
25
What is the principle of the fluorometric method (Hantzsch condensation)?
Formaldehyde + Diacetylacetone + Ammonium ions (NH₃) → 3,5-Diacetyl-1,4-dihydrolutidine
26
a yellow fluorescent compound with maximal absorbance at 412 nm
3,5-Diacetyl-1,4-dihydrolutidine
27
Old reference method for triglycerides? (chemical)
Modified Van Handel & Zilversmit
28
New reference method? (trigly chemical)
Gas chromatography / Mass spectrometry
29
Key enzyme in enzymatic triglyceride assays?
Glycerol kinase
30
Final detectable product in enzymatic triglyceride method?
Formazan (colored product)
31
Chemical classification of cholesterol?
Unsaturated steroid alcohol (sterol)
32
Structure of cholesterol?
4-rings + CH side chain + hydroxyl group at A-ring
33
Cholesterol is amphipathic. Why?
Contains both hydrophilic (-OH group) and hydrophobic regions (ring + side chain)
34
Clinical evaluation of cholesterol is important in?
Atherosclerosis, myocardial infarction, coronary artery occlusion
35
% of cholesterol esters in plasma?
60–70%
36
% of free cholesterol in plasma?
30–40%
37
Preferred specimen for cholesterol testing?
Plasma or serum
38
What is the reference method for cholesterol?
Abell, Levy, and Brodie method
39
What reagent is used for lipid extraction in Abell method?
Hexane (after alcoholic KOH hydrolysis)
40
What specimens should be avoided for cholesterol testing?
Hemolyzed, icteric, and watery samples
41
Enzymes used in enzymatic cholesterol assays?
1. Cholesteryl esterase → cholesterol + FA
2. Cholesterol oxidase → cholestenone + H₂O₂
3. Peroxidase → colored dye (read at 500 nm)
42
Does total cholesterol require fasting?
No, can be measured in non-fasting samples
43
What color reaction is used in the reference method? (chol. chemical method)
Liebermann-Burchard reaction
44
Principle of Liebermann-Burchard reaction?
Cholesterol + acetic anhydride + sulfuric acid → red → violet → blue-green color
45
Absorbance wavelength in Abell method?
620 nm
46
Advantage of enzymatic cholesterol method over chemical? & what does it utilize
- More accurate, no extraction needed
- utilizes cholesteryl ester hydrolase
47
phospholipids are derived from what compound?
Phosphatidic acid
48
Major role of phospholipids?
Structural elements of cell membranes
49
Chemical name of cholesterol?
3-hydroxy-5-6-cholestene
50
Are phospholipids routinely analyzed in clinical labs? Why/Why not
No, because:
1. Provide little extra info in dyslipoproteinemia
2. Levels not as altered as cholesterol/TG in disease
51
Structural difference between phospholipids and triglycerides?
Phospholipids have 2 esterified fatty acids + phosphate group, not 3 FAs
52
Composition of chylomicrons?
90% triglycerides, 1–2% protein
53
Origin of chylomicrons?
Intestines
54
What type of compound is cholesterol?
Unsaturated steroid alcohol (sterol)
55
Apoproteins present in chylomicrons
Apo B-48, Apo C, Apo E
56
General function of lipoproteins?
Transport triglycerides and cholesterol; keep lipids soluble
57
Composition of VLDL?
65% triglycerides, 16% cholesterol ester, 5–10% protein
58
Origin of VLDL?
Liver
59
Apoproteins present?
Apo B-100, Apo C, Apo E
60
Nicknames for HDL?
“Alpha-lipoprotein” or “Good cholesterol”
61
Composition of HDL?
45–50% protein, 20% cholesterol ester, 30% phospholipids, 2–7% TG
62
Size and density of HDL?
Smallest and most dense lipoprotein
63
Major apoproteins in HDL?
Apo A-I, Apo A-II, Apo C
64
Alternate name of VLDL? (Very-Low-Density Lipoprotein)
Pre-beta lipoprotein
65
Major function of chylomicrons
Transport exogenous (dietary) triglycerides
66
Structural features of cholesterol?
4-ring sterane system + single C-H side chain + hydroxyl group on A-ring (arranged in a tetracyclical sterane system)
67
Number of carbon atoms in cholesterol?
27
69
Composition of LDL?
50% cholesterol ester, 18% protein, 24–28% phospholipids, 6–8% cholesterol
70
Apoproteins in LDL?
Apo B-100, Apo E
71
How is LDL usually calculated?
Friedewald equation
72
Friedewald equation formula?
LDL-C = TC – [HDL-C + (TG/5)]
73
What tests are included in a standard lipid profile?
Triglycerides, total cholesterol, LDL, HDL (± VLDL)
74
Clinical purpose of lipid profile?
To assess lipid levels and cardiovascular disease risk
75
How are dietary lipids digested before absorption?
Lipase converts them into polar compounds
76
What structure helps lipids get absorbed by the intestine?
Micelles (lipids + bile salts)
77
What happens to lipids after absorption by enterocytes?
Re-esterified into triglycerides and cholesterol esters, packaged into chylomicrons with Apo B-48
78
How are short-chain fatty acids absorbed?
Directly into portal circulation, bound to albumin, transported to the liver
79
What lipoprotein carries dietary lipids in the exogenous pathway?
Chylomicrons
80
How do chylomicrons enter the bloodstream?
(lymphatic ducts) Through the thoracic duct → bloodstream
81
What enzyme hydrolyzes triglycerides from chylomicrons?
Lipoprotein lipase (LPL)
82
What happens to fatty acids released from chylomicrons?
Used for energy or stored as fat
83
What happens to chylomicrons after triglyceride removal?
Reduced to chylomicron remnants
84
What happens to chylomicron remnants?
Taken up by the liver → lysosomal enzymes release free cholesterol and fatty acids
85
What lipoprotein initiates the endogenous pathway?
VLDL (from the liver)
86
How is VLDL metabolized in circulation?
VLDL → VLDL remnants → IDL → LDL
87
What is the main role of LDL in this pathway?
Deliver cholesterol and triglycerides to peripheral tissues via LDL receptors
88
How are LDL-delivered triglycerides used?
Broken down into free fatty acids + glycerol → energy or storage
89
How is free cholesterol from LDL used in cells?
Incorporated into membranes or esterified by ACAT for storage
90
Where does LDL return after delivering lipids?
Back to the liver
91
What is the function of the reverse cholesterol pathway?
Removes excess cholesterol from peripheral cells → returns it to liver for excretion
92
Two mechanisms of reverse cholesterol transport?
1. Aqueous diffusion
2. ABCA1 and ABCG1 receptor-mediated transport
93
Which lipoprotein plays a central role in reverse cholesterol transport?
HDL
94
What happens to fatty acids with an odd number of carbons during β-oxidation?
They are oxidized like even-numbered ones until the last step.
95
Final products of odd-carbon fatty acid β-oxidation?
Acetyl-CoA + Propionyl-CoA
96
What is Propionyl-CoA converted into?
Succinyl-CoA (enters the citric acid cycle)
97
How can fatty acids be stored again as triglycerides?
Synthesized from fatty acids + excess carbohydrates
98
How is free cholesterol stored?
Esterified → cholesteryl esters
99
Role of triglycerides and cholesterol in membranes?
Used for membrane biosynthesis
100
Source of free fatty acids in biosynthesis?
From Acetyl-CoA
101
Hardening and narrowing of arteries caused by cholesterol plaque buildup
What is atherosclerosis?
102
Why is atherosclerosis dangerous?
Can lead to heart attack, stroke, and other cardiovascular diseases
103
What does plaque buildup cause?
Arteries narrow → reduced blood flow → possible clot formation
104
Early symptoms of mild atherosclerosis?
Usually none
105
Common symptoms once arteries are blocked?
Chest pain (angina), numbness/weakness, shortness of breath, fatigue
106
What happens during initiation phase?
Lipid deposition, pro-inflammatory conditions, endothelial dysfunction
107
What happens during progression phase?
Lipid accumulation → foam/engorged cells form
108
What happens during complication phase?
Plaques restrict blood flow → thrombus formation → clinical events (e.g., heart attack, stroke)
109
How does atherosclerosis progress?
By lipid accumulation and formation of lipid-engorged cells (foam cells).
110
What vascular change occurs during progression?
Migration of smooth muscle cells from media → intima.
111
Types of developing plaques?
Fibrous plaques (fibroatheroma) and fibrocalcific plaques.
112
How do atherosclerotic plaques cause clinical events
By limiting blood flow via thrombus formation.
113
What happens when coronary perfusion is impaired by plaque?
Ischemia
114
Most common cause of myocardial infarction (MI)?
Atherosclerotic plaque rupture.
115
What happens when plaque ruptures?
Thrombogenic core exposed → platelet aggregation + fibrin polymerization → thrombus.
116
What genetic/epigenetic factors can indicate risk for atherosclerotic CVD?
Genetic markers and epigenetic modifications related to platelet reactivity and thrombus formation.
117
What molecular tools can be used for risk profiling?
Transcriptional profiling and circulating microRNAs.
118
How can proteomics help in assessing complications?
Detects low concentrations of circulating proteins, allowing early MI detection.
119
Example of proteomic biomarker used clinically?
High-sensitivity troponins.
120
What is the role of metabolomics in cardiovascular disease?
Profiling circulating metabolites can detect myocardial injury and distinguish stable vs. unstable coronary artery disease (CAD).
121
What is an acute myocardial infarction?
Occurs when blood flow to part of the heart is blocked → insufficient oxygen → muscle damage.
122
Main cause of MI?
Atherosclerosis (plaque buildup in coronary arteries).
123
What are plaques composed of?
Cholesterol, fat, calcium, and other substances.
124
Most effective biomarker for MI?
Cardiac troponins (cTnI and cTnT)
125
Role of troponins in muscle?
Regulate muscle contraction
126
Why are troponins useful in MI?
Released into blood after heart muscle damage.
127
What is hs-cTn (high-sensitivity troponin)?
Improved troponin assay; detects very low troponin levels in healthy people and has superior prognostic performance in non-ST elevation ACS.
128
What cardiac biomarker is useful for heart failure diagnosis?
BNP (B-type natriuretic peptide) and NT-proBNP.
129
Source of BNP?
Synthesized and released by ventricular cells in response to volume/pressure overload.
130
Why is BNP important clinically?
Best single predictor of heart failure compared to history, physical exam, chest X-ray, and labs.
131
What is obesity?
A nutritional disorder with increased body fat mass caused by imbalance between energy intake and expenditure.
132
Why is childhood obesity important?
Obese children are more likely to become obese adults.
133
Major contributors to obesity?
Genetic and acquired alterations (lifestyle, environment).
134
Why is obesity a public health concern?
It has become one of the most pressing health issues of the 21st century.
138
Common method for HDL measurement?
Chemical precipitation (dextran sulfate or PEG)
CC LAB
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