Lipids And Lipoproteins

Front 1

Major lipids of the body

Back 1

Fatty acids, triglycerides, phospholipids, cholesterol, and lipoproteins.

Front 2

Lipoproteins

Back 2

Chylomicrons, VLDL, LDL, HDL.

Front 3

Apolipoproteins

Back 3

The "apos" are the protein fraction of plasma lipoproteins. They help keep the lipoproteins in solution while in circulation.

Front 4

Major apo of HDL

Back 4

Apo A.

Front 5

Major apo of LDL

Back 5

Apo B.

Front 6

Calories that supply calories to the body

Back 6

Fats, carbs, and proteins.

Front 7

How many calories per gram does fat add to diet?

Back 7

9. (more than twice the number provided by carbs and protein)

Front 8

Fatty acids in diet

Back 8

Provide fatty acids, which are not made by the body and must be obtained from food.

Front 9

Essential fatty acids and their function

Back 9

Linoleic and linolenic acid. Control inflammation, blood clotting, and brain development.

Front 10

What does fat serve as?

Back 10

The storage substance for the body's extra calories. It fills the fat cells (adipose tissue) that help insulate the body. Also an important energy source.

Front 11

When the body has used up calories from carbs, it depends on calories from?

Back 11

Fat. Calories from carbs are used up the first 20 minutes of exercise.

Front 12

What is maintained by fat?

Back 12

Skin and hair. Fat helps absorb and move vitamins A, D, E, and K through the bloodstream.

Front 13

Statins

Back 13

Cholesterol lowering meds.

Front 14

Where do free fatty acids circulate?

Back 14

In the plasma.

Front 15

Most fatty acids are components of:

Back 15

Phospholipids and triglycerides.

Front 16

Fatty acid chains

Back 16

1. Short Chain (4-6 atoms)

2. Medium Chain (8-12 atoms)

3. Long chain ( > 12 atoms)

Front 17

Saturated fatty acids

Back 17

Contains all C-C single bonds.

Front 18

Where are saturated fats found?

Back 18

Animal products such as butter, cheese, whole milk, ice cream, and fatty meats. Also in some vegetable oils like coconut, and palm kernel.

Front 19

Monosaturated fatty acids and examples

Back 19

Contains one double bond. Examples: olive and canola oils.

Front 20

Polyunsaturated fatty acids and examples

Back 20

Contains two or more double bonds. Examples: fish, sunflower, corn, and soybean oils.

Front 21

Trans fats

Back 21

Found in fried foods, commercial baked goods, processed foods, and margarine.

Front 22

Effect of trans fat on body

Back 22

Raises cholesterol. Raises bad LDL and lowers good HDL.

Front 23

What %of diet should be fats?

Back 23

Less than 25-35%.

Front 24

Limit saturated fat intake to less than___% of total daily calories.

Back 24

7

Front 25

Limit trans fat to less than ___% of total daily calories.

Back 25

1

Front 26

The remaining fat should come from:

Back 26

Sources of monsaturated and polysaturated fats such as nuts, seeds, fish, and vegetable oils.

Front 27

Limit cholesterol to less than ______mg per day.

Back 27

300. If you have coronary heart disease or your LDL level is 100mg/dL or greater, limit cholesterol to 200mg/day.

Front 28

Composition of

Triglycerides

Back 28

Three molecules of fatty acids and one molecule of glycerol. Both consumed and synthesized.

Front 29

What are triglycerides used for?

Back 29

Broken down and uses for energy source.

Front 30

Increase of triglycerides contributes to

Back 30

They are a type of fat in the bloodstream and fat tissue. Too much can contribute to narrowing of arteries. Increases risk of heart attack and stroke.

Front 31

Diseases associated with increased triglycerides

Back 31

Diabetes, obesity, kidney failure or alcoholism can cause high triglycerides. Often associated with high cholesterol.

Front 32

Phospholipids and composition

Back 32

Major component of cell membranes and outer shells of lipoproteins. Similar to triglycerides except they only have two fatty acids and instead of the third fatty acid, there is a phospholipid head group.

Front 33

Cholesterol and structure

Back 33

A large molecule. An unsaturated steroid alcohol consisting of four rings. This ring structure is common to all sterol compounds.

Front 34

Where does cholesterol originate from?

Back 34

Hepatic synthesis, steroid based hormones, diet, cell destruction, and intestinal secretions.

Front 35

What is cholesterol necessary for?

Back 35

Cell structure and synthesis of steroid based hormones of the body.

Front 36

What organ produces cholesterol?

Back 36

Liver.

Front 37

What happens once cholesterol is synthesized or absorbed? Why must all cholesterol be attached to lipoproteins?

Back 37

It is bound to lipoproteins. All lipids must be attached to lipopoteins for transport since lipids are water insoluble. Some processed cholesterol is excreted via the intestine.

Front 38

Cholesterol is the backbone for:

Back 38

Testosterone and estrogen.

Front 39

Food sources of cholesterol

Back 39

Meat, eggs (yolks), seafood, whole fat dairy products, and plant sterols.

Front 40

What happens once cholesterol is recycled by liver?

Back 40

Reused in formation of bile salts and bile.

Front 41

Plant sterols

Back 41

Although very chemically similar to cholesterol, plant sterols are poorly absorbed. When plant sterols ingestion increases, cholesterol absorption decreases.

Front 42

What is hepatic synthesis of cholesterol inhibited by?

Back 42

Dietary intake.

Front 43

Once synthesized, cholesterol is released into circulation for:

Back 43

Transport in lipoprotein complexes.

Front 44

What happens once cholesterol enters a cells?

Back 44

It is broken down by specific enzymes. Cholesterol reaching the liver is either secreted unchanged or metabolized into bile acids. Approximately 1/3 produced daily is changed into bile acids.

Front 45

What happens if the amount of cholesterol exceeds the capacity of solubilizing agents?

Back 45

A supersaturated state can occur. (Lithogenic bile)

Front 46

What are 80% of all gallstones composed of?

Back 46

Cholesterol.

Front 47

Function and composition of lipoproteins

Back 47

Carry lipids. Consist of a protein portion, phospholipids, and varying amounts of lipids.

Front 48

The transport mechanism of lipoproteins is necessary due to:

Back 48

Hydrophobic nature of lipids.

Front 49

Major lipoproteins are classified by:

Back 49

Density. The relative content of lipid and protein determines density.

Front 50

Chylomicrons

Back 50

Largest of lipoproteins. Arise from intestines and cause of milky layer. Enter circulation with their triglyceride and cholesteryl esters which are then hydrolyzed to lipases, then these particles are transported back to liver. Can be measured by electrophoresis. Absorbed into lacteals.

Front 51

VLDL

Back 51

Made in liver. Transports triglycerides synthesized in liver to adipose and muscle tissue. Calculated from other lipid values.

Front 52

LDL

Back 52

Bad cholesterol. Arise from VLDL. Transport cholesterol to liver for bile or tissue for structural components. Increased levels are associated with increased risk of developing atherosclerosis.

Front 53

HDL

Back 53

Higher in protein. Binds excess cholesterol and takes it to bile. Formed in liver and intestinal mucosa. Increased HDL is significant in reducing risk of heart disease.

Front 54

Lipid profile

Back 54

Consists of total cholesterol, triglycerides, HDL and LDL. A check for chylomicrons can be made by placing a fresh plasma specimen in fridge overnight. Then observed for milky layer which would indicate abnormal presence of chylomicrons.

Front 55

Instructions for lipid profile collection

Back 55

Patients should fast for at least 12 hours prior to testing. Ensures dietary lipids have had time to clear blood.

Front 56

Measurement of total cholesterol

Back 56

Enzymatic methods. First, ester linkages of the cholesterol ester must be hydrolyzed to free cholesterol. This is done using the enzyme cholesterol esterase. Free cholesterol is reacted by cholesterol oxidase which produces hydrogen peroxide. Hydrogen peroxide is the substrate from horseradish peroxidase to couple 2 colorless chemicals into a colored compound which can be read spectrophotometrically.

Front 57

Measurement of triglycerides

Back 57

Uses enzymes. Reaction begins by hydrolyzing the triglycerides into glycerol and fatty acids. It is acted upon by glycerol kinase to eventually produce a product that can be measured spectrophotometrically.

Front 58

Measurement of HDL and LDL

Back 58

Immunochemical methodologies are sensitive to the protein portion, Apo-A, and Apo-B of LDL.

Front 59

LDL measurement based on total cholesterol, HDL, and triglyceride formula

Back 59

LDL = TC - (HDL + Triglyceride/5)

Front 60

Disadvantage of calculation of LDL

Back 60

Triglyceride level can't be over 400.

Front 61

Cholesterol values

Back 61

Desirable 199 mg/dL or less

Borderline 200-239 mg/dL

Higher risk 240 mg/dL or higher

Front 62

Triglyceride levels

Back 62

Desirable 149 mg/dL or less

Borderline 150-199 mg/dL

Higher risk 200-499 mg/dL

Front 63

HDL values

Back 63

Desirable 40 mg/dL or greater

Higher risk 39 mg/dL or less

Front 64

LDL values

Back 64

Desirable 129 mg/dL or less 99 mg/dL or less if patient has CHD

Borderline 130-159 mg/dL

Higher risk 160 mg/dL or greater

Front 65

VLDL values

Back 65

Desirable 30 mg/dL or less

Front 66

Expanded lipid panels

Back 66

Consist of the same tests as the lipid panel with the exception of a direct measurement of LDL.

Front 67

Measurement of Apo A and Apo B

Back 67

Nephelometry.

Front 68

Apo E s mutations can be identified using:

Back 68

PCR/Fluorescence monitoring

Front 69

Non traditional risk markers

Back 69

hs-CRP

Apo A and B

Apo E

Lp(a)

Homocysteine

Kidney markers: serum creatinine, cystatin, and urine microalbumin.

Front 70

In most nations, what is the leading cause of arteriosclerosis?

Back 70

Arteriosclerosis due to artherosclerosis.

Front 71

Peripheral Vascular Disease (PVD)

Back 71

Plaque formation in the arteries of the arms and legs.

Front 72

Coronary Artery Disease (CAD)

Cerebrovascular Disease (CVD)

Back 72

Formation of plaque in heart.

Development of plaque in brain.

Front 73

Hereditary causes of of increased lipids (hyperlipoproteinemias) are often associated with:

Back 73

Lipid metabolism process and may include an enzyme deficiency, transport insufficiency, or the absence of inactivity at receptor sites.

Front 74

Increased total cholesterol may be found secondarily with:

Back 74

uncontrolled diabetes, nephrotic syndrome, bile duct blockage, and hypothyroidism.

Front 75

Increased triglycerides

Back 75

May be increased in some of the same conditions as cholesterol as well as acute pancreatitis and glycogen storage disease.

Front 76

Prevention if atherosclerosis

Back 76

Maintaining ideal weight, good nutrition, exercise.

Front 77

Other risk associated with CAD

Back 77

Increased BP, increased cholesterol, obesity, inactivity, and smoking.

Front 78

Other names for metabolic syndrome

Back 78

Dysmetabolic syndrome, hypertriglyceridemic waist, insulin resistance syndrome, obesity syndrome, and syndrome X.

Front 79

Number of people with metabolic syndrome and who is it most common in?

Back 79

47 million in U.S. 25%. Most common in African American women and Mexican American women. Affects white men and women equally.

Front 80

Metabolic syndrome

Back 80

Name of a group of risk factors linked to overweight and obesity. Risk factors increase chance of having heart disease and other health problems such as diabetes and stroke.

Front 81

Metabolic risk factors

Back 81

If you have 3 of the following:

1. Large waste line. Having an apple shape Aka abdominal obesity.

2. Higher than normal triglyceride levels.

3. Lower than normal HDL

4. High BP

5. High fasting blood sugar

Front 82

Waist measurement for metabolic risk factor

Back 82

Greater than 35 inches or more in women and 40 inches in men.

Front 83

Why is HDL good cholesterol?

Back 83

It helps remove cholesterol from your arteries.

Front 84

BMI

Back 84

Body mass index. Measure body fat based on height and weight that applies to both men and women.

Front 85

BMI categories

Back 85

Underweight = <18.5

Normal weight = 18.5-24.9

Overweight 25-29.9

Obesity = 30 or greater

Front 86

Largest internal organ and how much does it weigh?

Back 86

Liver. Weighs 1.5 kg.

Front 87

Structure of liver

Back 87

Divided into left and right parts by falciform ligament. A thin connective tissue covers the liver (Glisson's capsule).

Front 88

What carries blood from the capillary bed of the alimentary tract? What does this blood contain?

Back 88

Portal vein. Contains nutrients absorbed from the GI tract.

Front 89

Hepatic artery function

Back 89

Carries oxygenated blood to the liver.

Front 90

Functional units of liver

Back 90

Lobules. Each surrounded by connective tissue.

Front 91

What is in center of each lobule?

Back 91

Venule, bile duct, and hepatic arteriole.

Front 92

Parenchymal cells

Back 92

Radiate from the central vein. Functional cells of liver.

Front 93

What do sinusoids form?

Back 93

A vascular network that is directed toward the central vein.

Front 94

What is within the sinusoids?

Back 94

Kupffer cells (fixed macrophages). Accumulate ferritin and hemosiderin.

Front 95

Jaundice

Back 95

Icterus. Yellowish coloration of the sclerae, skin, and mucous membranes due to the buildup of bilirubin.

Front 96

Prehepatic jaundice

Back 96

Aka hemolytic jaundice. Due to an excessive production of bilirubin.

Front 97

Hepatic jaundice

Back 97

Aka medical. Occurs due to destruction of liver cells. Ex: cerrhosis from alcohol ingestion and hepatitis.

Front 98

Extrahepatic jaundice

Back 98

Aka surgical or obstructive jaundice. Due to interference either the removal of bile from the liver. Ex: gallstones, pancreatic cancer (close enough to liver to cause bile obstruction).

Front 99

Hypercarotenenia

Back 99

Caused by ingestion of large amounts of Vitamin A that leads to a yellowish discoloration of the skin that is similar to jaundice except that the sclerae do not discolor.

Front 100

Causes of jaundice

Back 100

Gallstones, cancer of the head of pancreas or intestinal cancer.

Front 101

Gilbert's Disease

Back 101

Common disorder passed down through families. Affects the way bilirubin is processed by the liver and causes jaundice.

Front 102

Symptoms of Gilbert's Disease

Back 102

Fatigue, yellowing of skin and whites of eyes. Jaundice typically appears during times of exertion, stress, not eating, and infection. No treatment necessary.

Front 103

Reye's syndrome

Back 103

Liver disorder of unknown etiology that can be sequela to viral diseases. Usually a disease of children although adults have sometimes been affected.

Front 104

Tumor of the _______ are somewhat uncommon. Most are:

Back 104

Liver. Metastatic tumors from other organs. Once cancer has invaded the liver, prognosis is poor.

Front 105

Lab results of Reye's syndrome

Back 105

Liver enzymes are elevated, but not bilirubin. Untreated, the patient may experience coma, seizures, and death.

Front 106

Amount of alcohol to cause cirrhosis of liver.

Back 106

Unknown. However, it is clear that increased use increases the chance of developing cirrhosis.

Front 107

What drug can lead to fatal hepatic necrosis?

Back 107

Acetaminophen.

Front 108

Measurement of serum bilirubin

Back 108

Jendrassik/Grof technique. Total bilirubin is measured by adding a caffeine reagent to the specimen followed by the addition of diazotized sulfanilic acid. Unconjugated and conjugated will react with the diazo reagent to produce azobilirubin.

Front 109

Measurement of conjugated bilirubin

Back 109

Serum is first acidified with dilute HCl and then mixed with diazotized sulfanilic acid to produce azobilirubin. Only the conjugated form reacts with the diazo reagent in the absence of the caffeine accelerator.

Front 110

Morning specimens are preferred to test for bilirubin:

Back 110

to avoid lipemia. Both forms of bilirubin are photo oxidized when exposed to white or UV light. Protect both specimens from artificial and sunlight as soon as they are drawn.

Front 111

Indirect bilirubin

Back 111

Total bilirubin - Direct = Indirect

Front 112

Reference ranges for adult bilirubin

Back 112

Conjugated: 0-0.2 mg/dL

Unconjugated: 0.2-0.8 mg/dL

Total: 0.2-1.0 mg/dL

Front 113

Newborn reference ranges for billirubin:

Back 113

24 hr: premature-1-6 full term-2-6

48hr: premature-6-8 full term- 6-7

3-5 days: premature-10-12 full term-4-6

Front 114

Kernicterus and reference range

Back 114

Term used to describe jaundice of the brain. This occurs in infants when bilirubin levels reach 15-20 mg/dL. CNS doesn't have well developed blood brain barrier.

Front 115

Another name for Kernicterus

Back 115

Nuclear jaundice.

Front 116

Reason babies get jaundice

Back 116

Physiologic jaundice. Don't have all enzymes. Premature babies have less. Destroy excess red cells.

Front 117

Causes of neonatal hyperbiliribinemia

Back 117

Low birth weight, breast feeding, Rh or ABO incompatibility, congenital defects in bilirubin metabolism or transport.

Front 118

Reference range of bilirubin in urine

Back 118

None.

Front 119

Dipsticks and reagents (Ictotest) are both based on:

Back 119

the diazo reaction.

Front 120

Reference range of urine urobilinogen

Back 120

0.2-1.0 mg/dL. 1 mg = 1 Ehrlich unit.

Front 121

Dipstick reagent for urobilinogen

Back 121

P-dimethylaminobenzaldehyde.

Front 122

Fecal urobilinogen (urobilin)

Back 122

Visual inspection sufficient. Decrease of fecal urobilin results in pale clay colored specimen. Colorless stool if urobilinogen isn't present.

Front 123

What is bilirubin the product of? What % comes from red cells and precursors?

Back 123

Heme catabolism. 85% from senescent (dying) RBCs. 15% is from RBC precursors destroyed in bone marrow (ineffective erythropoiesis) and from other heme containing proteins such as myoglobin, cytochromes, and peroxidases.

Front 124

First product formed in bilirubin metabolism

Back 124

Biliverdin. Green pigmented. It is then hydrogenated to bilirubin.

Front 125

What happens after production in peripheral tissues? (unconjugated Bilirubin)

Back 125

Transported to liver by albumin. Bilirubin is then taken up by hepatocytes. Inside the cells, bilirubin is conjugated (direct, esterified) with glucuronic acid to produce mono- and diglucuronide. Then excreted into bile.

Front 126

Bilirubin inside intestines

Back 126

Bilirubin glucorunides are not reabsorbed at any great extent. They are hydrolyzed to the unconjugated (nonesterified, indirect) pigment by the action of beta glucuronidase from the liver, intestinal epithelial cells, and intestinal bacteria.

Front 127

Conjugated

Back 127

= direct = esterified

Front 128

Unconjugated

Back 128

Nonesterified = indirect

Front 129

Unconjugated form in intestines

Back 129

Reduced by the anaerobic intestinal flora to form urobilinogen (a colorless conpound). Up to 20% reabsorbed from the intestines and enters the enterohepatic circulation.

Front 130

Most of this reabsorbed urobilinogen is taken up by:

Back 130

the liver and re-excreted in bile. Only about 2%-5% appears in circulation and urine.

Front 131

What gives stool their characteristic colors

Back 131

In the lower intestinal tract, urobilinogen is oxidized to urobilin which is orange brown in color and gives stool their characteristic colors.