Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Exam 1 > Biochem > Flashcards

Biochem Flashcards

1
Q

Where are chylomicrons synthesized?

A

Intestinal epithelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Function of Lipoprotein Lipase (LPL).

A

Breaks up lipoproteins in the blood stream by liberating fatty acids from triglycerides. This enzyme is located on vascular endothelium in highest concentration around adipose tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Main structural protein of chylomicrons.

A

Apo B48

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Function of Apo CII and Apo E.

A

Apo CII: activates LPL
Apo E: binds receptors on hepatocytes (LRP) so chylomicron remnants and IDL (VLDL remnant) can be reabsorbed by the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where do chylomicrons obtain Apo CII and Apo E?

A

From interaction with HDL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Structural protein of VLDL.

A

Apo B100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where does VLDL obtain Apo CII and Apo E?

A

From HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why does the liver want to reabsorb chylomicron remnants and IDL?

A

Chylomicron remnant’s cholesterol is recycled for chylomicron production in the small intestines or bile salt production.

IDL can be used to synthesize LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which LDL protein binds the LDL receptor on endothelial cells to allow the LDL to migrate across the endothelium and deliver cholesterol to tissues?

A

Apo B100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is the LDL receptor involved in formation of atherosclerosis?

A

Both endothelial cells AND cells in tissues adjacent to the endothelial cells have LDL receptors. Once the cells in tissues have enough cholesterol they will down-regulate LDL receptors. The endothelial cells will NOT down-regulate the LDL receptors. The LDLs then get “stuck” inside the endothelial cells or in the interstitial space where they can accumulate and lead to plaque formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Main structural protein of HDL.

A

Apo A-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Location and function of LCAT.

A

Located in HDL

Enzyme that esterifies cholesterol within the HDL, making it more hydrophilic (so it can’t cross the HDL membrane and into the blood stream). This “traps” the cholesterol in the HDL molecule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Major way the body eliminates excess cholesterol.

A

Bile salt production and loss in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the Friedewald Equation? Why is it used?

A

Used to predict LDL levels in blood.

Total Cholesterol - HDL - 1/5(triglycerides) = LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the rate limiting step and major enzymes (2) for cholesterol synthesis?

A

Acetyl CoA —> mevalonate

HMG-CoA synthase
HMG-CoA reductase (target of statins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name and explain 3 ways cholesterol production is regulated by the body.

A
  1. Cholesterol binds a membrane protein SCAP which inhibits another membrane protein SREBP from releasing a transcription factor that goes to the nucleus to make the enzyme.
  2. Presence of sterols (steroid alcohols: cholesterol is a sterol) increases degradation of the HMG-CoA reductase enzyme
  3. Phosphorylation of HMG-CoA reductase inactivates it. Glucagon and AMP are low energy molecules that activate kinases which phosphorylate the enzyme. Insulin is a high energy molecule that activates phosphatases to re-activate the enzyme so more cholesterol can be made.
17
Q

What is the first step in atherogenesis?

A

Some kind of injury to the endothelial lining.

18
Q

After injury to the endothelium, describe the process of atherogenesis.

A
  1. Inflammatory mediators are released by injured endothelium. WBCs migrate to the area.
  2. LDL migrates into the injury and is modified (oxidized) by ROS released by WBCs.
  3. WBCs are then attracted to the mLDL molecules and will migrate into the injury to phagocytize the mLDL.
  4. The mass of foam cells weaken and break the elastic lamina separating the endothelium from the muscle cells allowing them the migrate inward.
  5. The inward migrating muscle cells have altered gene expression due to loss of uniformity and irregular location and start to calcify. This forms the plaque which may eventually rupture creating an embolus.
19
Q

Why is atherosclerosis very common in diabetics?

A

Just like the WBCs oxidize LDL to modify it, glucose can modify LDL by glycation.

20
Q

What 3 nutrient deficiencies are associated with atherogenesis?

A

Folate, B6 and B12

21
Q 
How do:
C-reactive protein (CRP)
Interleukin-6 (IL-6)
Serum amyloid A (SAA)
Lipoprotein-a (LP-a)

contribute to atherogenesis?

A

CRP: increases inflammatory response

IL-6: encourages hepatic production and release of CRP

SAA: recruits immune cells

LP-a: competes with plasminogen

22
Q

Describe the Frederickson Hyperlipidemia Classification: Class I

A

High chylomicrons and triglycerides due to defective or deficient LPL or Apo CII

23
Q

Describe the Frederickson Hyperlipidemia Classification: Class IIa

A

High LDL due to defect in the LDL receptor

24
Q

Describe the Frederickson Hyperlipidemia Classification: Class IIb

A

High LDL, VLDL, TGs due to defect in the internalization of the LDL receptor

25
Q

Describe the Frederickson Hyperlipidemia Classification: Class III

A

High IDL due to Apo E defect or decreased LDL production.

26
Q

Describe the Frederickson Hyperlipidemia Classification: Class IV

A

High VLDL and TGs due to multiple factors

27
Q

Describe the Frederickson Hyperlipidemia Classification: Class V

A

High VLDL, chylomicrons, and TGs due to multiple factors.

28
Q

Which Frederickson classes present with Xanthomas?

A

Class I and V. Due to accumulation of lipids under the skin.

29
Q

Name two mechanisms of statins to decreases cholesterol in the serum.

A
  1. Inhibits HMG-CoA reductase (major)

2. Increases LDL receptors on liver (minor)

30
Q

Function of Ezetimibe

A

Reduces absorption of cholesterol in the GI tract. Often combined with statins for therapy.

31
Q

Function of Bile Acid Sequestrants

A

Decrease bile acid reabsorption in the ileum. They bind to the bile salts and form a complex that the ileal receptors don’t recognize.

32
Q

Function of Niacin

A

Raises HDL levels

33
Q

Function of Fibrates.

A

Raises HDL levels

Cardio Exam 1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions