Brainscape's Knowledge GenomeTM

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


See full index

820 > Dyslipidemia Patho > Flashcards

Dyslipidemia Patho Flashcards

1
Q

Dyslipidemia

A
  • Increase LDL-C, VLDL-C, Triglycerides

- Decrease in HDL-C

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

Dyslipidemia Primary Prevention

A

Prevention of atherosclerotic cardiovascular disease (ASCVD) in a person without a known history of disease

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

Dyslipidemia Secondary Prevention

A

Prevention of ASCVD in a person with a history of ASCVD

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

Modifiable CVD Risks

A
  • Physical inactivity
  • High blood pressure
  • Smoking
  • High cholesterol/lipids
  • Obesity
  • Diabetes mellitus
  • Metabolic syndrome

Risk factors are additive

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

Non-Modifiable CVD Risks

A
  • Age
  • Family history
  • Not being female

Risk factors are additive

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

Lipoproteins

A
  • High MW and water-soluble, responsible for cholesterol and TG transport
  • Chylomicrons, VLDL, IDL, LDL, HDL, and Lp(a)
  • Surface is made up of polar, hydrophilic constituents integrated between phospholipid monolayer
  • Inner core contains nonpolar hydrophobic lipids, CEs, and TGs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cholesterol

A
  • Necessary component of cell membranes, steroid hormones, and bile acid
  • Regulated by absorption (extrinsic) and hepatic production/hepatic and bile acid excretion (intrinsic)
  • Synthesis accounts for the majority of cholesterol in the body (greatest in liver and intestinal mucosal cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Major Plasma Lipids

A
  • Cholesterol
  • Triglycerides
  • Phospholipids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Phospholipids

A
  • Essential for cell function and lipid transport
  • Do not directly contribute to atherosclerosis
  • Lecithin is the major phospholipid
  • Amphophilic and essential in transport of hydrophobic cholesterol esters (CE) and TGs through the plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Triglycerides

A
  • Dietary TGs absorbed as monoglycerides and FFAs
  • TGs are formed in liver and transported to adipose tissue for storage
  • TG lipolysis releases FFAs allowing for utilization by tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Exogenous Pathway

A
  • Dietary fats are incorporated into chylomicrons from the intestine into circulation to move the fats to adipose tissue
  • CMs contain ApoCII that activates lipoprotein lipase which releases TG
  • TGs then form FFAs which deposit in muscle and adipose tissue for use
  • CM fragments are removed by the liver and recycled
  • Cholesterol bile acids promotes lipid emulsification and intestinal absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Endogenous Pathway (VLDL)

A
  • Liver transports TGs (from FAs via the liver or adipose) and some cholesterol
  • VLDLs contain ApoCII which performs the same function as in the exogenous pathway
  • IDL lose more TG and become LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

LDL

A
  • Major cholesterol carrier
  • Major lipoprotein: ApoB-100
  • CHD risk increases exponentially with increases total and LDL cholesterol
  • LDL enters cells by receptor-mediated endocytosis, their hydrolysis in lysosomes releases the free cholesterol
  • Number of LDL receptors adjusts cholesterol concentrations for cells (new, developing cells require more)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Formation of LDL

A
  • Liver produces VLDL
  • VLDL then interacts with lipoprotein lipase and becomes a VLDL remnant
  • VLDL remnant then interacts with hepatic lipase and becomes LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cholesterol Metabolism

A
  • LDLs are taken up by endocytosis
  • Lysosomes release free cholesterol
  • Cholesterol is then esterified by ACAT and stored
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HDL

A
  • Major lipoprotein: ApoA
  • HDL subclasses are based on size and lipid content (HDL 1-4)
  • HDL2 (larger, lipid-rich) and HDL3 (small, dense) are predominant in human plasma
  • Subclasses contribute differently to reverse cholesterol transport
17
Q

HDL Synthesis

A
  • ApoA becomes a pre-HDL that then interacts with macrophages to receive cholesterol efflux
  • Pre-HDLs then become HDLs
  • LDLs can also be converted to HDL
18
Q

Drugs that Induce Lipid Changes

A
  • Thiazide diuretics (increase total cholesterol and TGs)
  • Beta-blockers (increases TGs and decreases HDL)
  • Alpha-antagonist (decreases in total cholesterol and TGs and increases HDL)
19
Q

Artherosclerosis

A
  • INFLAMMATORY DISEASE
  • Initiating event = endothelial injury
  • Leads to endothelial activation and oxidation of LDLs
  • Foam cells form and muscle cells differentiate
  • Cells become hypoxic and the fibrous cap things, risking rupture
20
Q

Early Stages of Atheroma

A
  • Endothelial activation - increases permeability of cell wall (lets in more LDL), increases adherence, and loss of NO
  • Leukocyte recruitment/chemotaxis/adhesion occurs as well
21
Q

Middle Stages of Atheroma

A
  • Oxidation of LDL
  • Macrophage uptake of oxLDLand differentiates to Foam cells
  • Foam cells are pro-inflammatory and oxidative which creates a feed-forward chronic inflammation pathway
  • Smooth muscle differentiates from contractile to synthetic and growths
  • T cell/adaptive immunity mechanisms
22
Q

Late Stages of Atheroma

A
  • Lesion cells become hypoxic internally causes necrosis of internal cells and expression of VEGF and angiogenesis
  • Proteolytic degradation of the extracellular fibers of the fibrous cap occurs
  • Rupture can then occur which exposes procoagulant basement membrane proteins to the circulating factors
23
Q

Rupture Events

A
  • Macrophages and T-cells release proteolytic enzymes that degrade the fibrotic layer
  • Proteolysis in combination with mechanical stress can cause a rupture
  • The rupture then exposes tissue and other procoagulant factors and proteins into their circulation
  • Thrombus can form and completely occlude vessels
  • Can also heal over, but larger lesion leading to progression of occlusion can also occur
24
Q

Principle Interventions/Objective for Atherosclerosis

A

Interventions

  • Diet
  • Exercise
  • Pharmaceuticals

Objectives

  • Lower LDL
  • Lower TGs
  • Increase HDL

820 (19 decks)

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