Lipid Metabolism Flashcards by Barrett Thompson

**VLDL
• Source
• Composition (Apoprotein, TG:Chol)
• Functional Role

*
Source:
• Made by Liver (endogenous path)

Composition:
• ApoB-100, Apo CII, Apo CIII, Apo A-V
• Carries 5:1 ratio of Triglyceride to Cholesterol

Functional Role:
• Delivers TGs and Chol. to Adipose Tissue and Muscle

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**LDL
• Source
• Composition (Apoprotein, TG:Chol)
• Functional Role

*
Source:
• Breakdown Product of IDL

Composition:
• ApoB-100, Apo(a)
• LESS than 5% Triglyceride (almost solid cholesterol)

Functional Role:
• Returns Cholesterol to Liver or
• Puts more cholesterol in Peripheral Tissues (if overloaded)

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**Chylomicrons
• Source
• Composition (Apoprotein, TG:Chol)
• Functional Role

*
Source:
• made of TGs and Cholesterol that is absorbed in the Proximal Jejunum (exogenous path)

Composition:
• Apo-48, ApoC (II, III), ApoA (I, II, V), Apo E (on remnants)
• has 10:1 ratio of Triglyceride to Cholesterol

Functional Role:
• Secreted into the blood from intestines and Delivers Fat to Tissues via interactions with LPL receptors

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**Lp(a)
• Source
• Composition (Apoprotein, TG:Chol)
• Functional Role

*
Source:
• Liver

Composition:
• ApoB-100
• Apo(a) - Aberrent form of Thromboplastin

Functional Role:
• VERY ATHERLOGENIC

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**What are the desirable levels of:
• LDL-C
• HDL-C
• Triglyceride

*
LDL:
• Less than 130

HDL:
• Men = greater than 40
• Women = greater than 50

Triglycerides:
• Less than 120

**Typically want TOTAL CHOLESTEROL under 200

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**Primary Chylomicronemia

Inheritance
Lipoprotein Abnormality
Pathophysiology
Clinical Characteristics
Complications

*
Inheritance:
• Recessive

Lipoprotein Abnormality:
• ApoCII or LPL defect

Pathophysiology:
• ApoCII binds LPL to release TGs into tissues
• Disruption in this interaction means TGs build up in the blood

Clinical Characteristics:
• Usually found in Kids
• CHYLOMICRONS and VLDL elevated (in the 10,000 range)

Complications:
• PANCREATITIS
• Patients may get Xanthomas on chest and back

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**Familial Hypertriglyceridemia

Lipoprotein Abnormality
Pathophysiology
Clinical Characteristics
Complications

*
Lipoprotein Abnormality:
• none, this is a defect in LPL

Pathophysiology:
• LPL is needed to take TGs out of VLDL
• If its absent the VLDL and TGs inside it just build up

Clinical Characteristics:
• Adults with TGs in the 1000s
• AND have elevated VLDL

Clinical Complications:
• Pancreatitis
• Often seen in diabetics

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**Familial Dysbetalipoproteinemia

Lipoprotein Abnormality
Pathophysiology
Clinical Characteristics
Complications

*
Lipoprotein Abnormality:
• ApoE defect (E2/E2 alleles)

Pathophyiology:
• ApoE is used by Chylomicron remnants, IDL, and HDL to bind to the LDL receptor
• MOST IMPORTANTLY IDL never gets converted to LDL

Clinical Characteristics:
• VLDL and Chylomicron remnants High
• ELEVATED CHOLESTEROL AND TG in 1:1 ratio (~250-300)

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**Familial Combined Hyperlipidemia (FCH)

Inheritance
Lipoprotein Abnormality
Pathophysiology
Clinical Characteristics
Complications

*
Inheritance:
• Autosomal Dominant

Lipoprotein Abnormality:
• Overproduction of apoB

Pathophysiology:
• Overproduction of ApoB-100 leads to too many VLDL particles
• Ultimately this cause high cholesterol

Clinical Characteristics:
• STRONG FAMILY HISTORY of EARLY athlerosclerosis
• Variably high VLDL, LDL, or Both

Complications:
• Premature athlerosclerosis

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**Familial Hypercholesterolemia (FH)

Inheritance
Lipoprotein Abnormality
Pathophysiology
Clinical Characteristics
Complications

*
Inheritance:
• Autosomal Dominant

Lipoprotein Abnormality:
• LDL Receptor or ApoB defect

Pathophysiology:
• Decreased Receptor Mediated Removal of LDL from plasma

Clinical Characteristics:
• Young, skinny people with unusually high LDL
• LDL 400-600

Complications:
• Homozygotes = Artherlosclerosis by age 12

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**Secondary Causes of Hyperlipoproteinemia

*
• HypOthyroidism
• Kidney or Liver Disease 
• Medications
• Excess Calories and Simple Sugars 
• Genetic Factors

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**What is the functional Role of:

• LDL-receptor

• LDL receptor binds ApoB-48 and pulls out Cholesterol

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**What is the functional Role of:

• Apolipoproteins

*
• In general these mediate binding events with receptors that cause depletion of cholesterol or TG from Lipoproteins and Chylomicrons

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**What is the functional Role of:

• CETP

*
Cholesteryl ester transfer protein - transfers cholesterol and TGs between (V)LDL particles and HDL

• Makes HDL larger and more susceptible to uptake by the liver via SRB1 receptor

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**What is the functional Role of:

• ApoCII

*
• Found on Chylomicrons, VLDL, and HDL

• Co-factor for LPL - so it needed to drop TGs off in tissues

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**What is the functional Role of:

• ApoCIII

*
• Found on Chylomicrons, VLDL, and HDL

• INHIBITS lipoprotein binding to receptors

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**What is the functional Role of:

• ApoB

*
• Either ApoB-48 (chylomicrons) or Apo-100 (everything else) are the structural protein for all fat carrying particles

• LIGAND FOR BINDING LDL receptor

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**What is the functional Role of:

• PPAR-a

• Activates Genes such as Apo CII and deactivates genes such as Apo CIII allowing for REDUCTION IN SERUM TGs

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**What dietary Factors influence hyperlipidemia?

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*
• Alcohol intake
• Cholesterol and Saturated/Trans-Fat intake
• Simple Sugar Intake

**What are the principles of Dietary management of hyperlipidemia?

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*
Cholesterol:
• Reduce SATURATED and TRANS-FATS

TGs:
• Total Fat
• Alcohol
• Excess Calories

What is the major carrier of cholesterol in the plasma?

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LDL

T or F: Peripheral Tissues rely heavily on LDL to acquire appropriate amounts of Cholesterol.

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False, most tissues can synthesize the cholesterol they need by themselves

What happens to chylomicron remnants?

• what are the risks of system overload with these?

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Return to the liver to give TGs via the LDLR

* These are Athlerogenic particles so system overload can lead to CV disease

LDL and HDL are almost purely made of cholesterol, what makes LDL bad and HDL good?

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LDL:
• Bad because it just circulates and keeps dumping of cholesterol into tissues

HDL:
• Has Apoproteins that allow it pull cholesterol out of macrophages and return cholesterol to the liver

What is the Friedwald Formula? | • what is it used for?

• Used to Calculate LDL-Cholesterol Formula: • TC - (VLDL-C (TG/5) + HDL-C) = LDL

HDL • Source • Composition (Apoprotein, TG:Chol) • Functional Role

Source: • Liver Composition: Functional Role: • Retrieves Cholesterol from the Artery Wall and Inhibits the oxidation of atherogenic lipoproteins

When are patients at risk of developing pancreatitis?

• When TGs get above 1000

Differentiate Primary Chylomicronemia and Familial Hypertriglyceridemia?

Chylomicronemia: • involves mostly defective removal of chylomicrons Familial Hypertriglyceridemia: • Involves mostly defective removal of VLDL

Functional Role of ApoE. | • what kind of particles is it associated with?

ApoE • Ligand for binding to the LDL receptor Particle association: • Chylomicron Remnants, IDL, HDL

How is familial Dysbetalipoproteinemia usually diagnosed? | • why is this the case?

* People will have high TGs and cholesterol and Dr. will prescribe a statin * The statin ends up having only a minimal effect because the amount of LDL receptor being greater won't change the fact that ApoE can't bind to it.

Which of the Primary Hyperlipoproteinemias is Autosomal Dominantly inherited?

• Familial Combined Hyperlipidemia (FCH)

What similarities in pathophysiology exist between Primary Chylomicronemia and Familial Hypercholesterolemia?

**Both are defects of lipid actually getting into tissue for LPL primary issue is getting into peripheral tissues for LDL problems getting back to the liver are an issue** Primary Chylomicronemia • Defect between apoCII and LPL Familial Hypercholesterolemia • Defect between apoB and LDL receptor

What is the Optimal goal for LDL? | • what about in patients with atherosclerotic disease?

Optimal = 100 mg/dl Atherosclerotic Disease = 70 mg/dl

What are some kidney disorders that might be a secondary cause of hyperlipidemia?

* Nephrotic Syndrome | * Hypoalbuminemia - albumin naturally turns down levels of VLDL so if it gets turned down VLDL will go up

What are some Liver Diseases that might cause hyperlipidemia?

* Hepatitis - too many lipoproteins made | * Biliary Disease - bile goes back into the circulation

What are some medication that can cause hyperlipidemia?

* Estrogen * Beta Blockers * Thiazide Diuretics

If someone has high cholesterol that is asymptomatic, how should you treat them? • what if they are symptomatic?

* Asymptomatic - Modify their diet to get LDL-C below 100 mg/dl * CV disease then modify their diet to get LDL-C below 70 mg/dl

What is the job of the ABCG1 transporter?

• Moves Cholesterol from Macrophages into HDL particles so that Cholesterol can be returned to Liver

What are some physical finding that are pathopneumonic for Familial Hypercholesterolemia?

* Achilles Tendon Xanthomas * Xanthomas on extensor tendons of hand ***Xanthomas around the eyes are not as indicative***

What would refrigerated serum look like in a patient with: • Primary Chylomicronemia • Familial Hypercholesterolemia

Primary Chylomicronemia: • Tons of chylomicrons would rise to the top and harden Familal Hypercholesterolemia: • Plasma would be cloudy from elevated VLDL

What aspect of treating hyperlipidemia actually causes the reduction in risk for people who have had acute coronary events?

• Mitigation of Inflammatory activity of Macrophages

How are people with Hypertriglyceridemia typically treated?

TG depleting agents: • Fibrate • Niacin

What is the primary method of treatment for people with Hypertriglyceridemia?

• DIETARY MAINLY TG depleting agents: • omega-3 • Fibrate • Niacin

What is the primary treatment for people with Familial Dysbetaliproteinemia?

HIGH TGs and Cholesterol HIGH TGs: • Niacin and Diet Treated HIGH cholesterol: • Statins

What are some dietary changes that can be made to lower cholesterol? • Triglycerides?

Cholesterol: • Saturated Fats • Trans Fats TGs: • Total Fats • EtOH • Excess Calories ***Eat Complex Carbs and Fiber***

Lipid Metabolism Flashcards

(45 cards)