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Cardio - Elam > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

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

A

*
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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2
Q

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

A

*
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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3
Q

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

A

*
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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4
Q

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

A

*
Source:
• Liver

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

Functional Role:
• VERY ATHERLOGENIC

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5
Q

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

A

*
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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6
Q

**Primary Chylomicronemia

  • Inheritance
  • Lipoprotein Abnormality
  • Pathophysiology
  • Clinical Characteristics
  • Complications
A

*
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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7
Q

**Familial Hypertriglyceridemia

  • Lipoprotein Abnormality
  • Pathophysiology
  • Clinical Characteristics
  • Complications
A

*
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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8
Q

**Familial Dysbetalipoproteinemia

  • Lipoprotein Abnormality
  • Pathophysiology
  • Clinical Characteristics
  • Complications
A

*
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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9
Q

**Familial Combined Hyperlipidemia (FCH)

  • Inheritance
  • Lipoprotein Abnormality
  • Pathophysiology
  • Clinical Characteristics
  • Complications
A

*
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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10
Q

**Familial Hypercholesterolemia (FH)

  • Inheritance
  • Lipoprotein Abnormality
  • Pathophysiology
  • Clinical Characteristics
  • Complications
A

*
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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11
Q

**Secondary Causes of Hyperlipoproteinemia

A 
*
• HypOthyroidism
• Kidney or Liver Disease 
• Medications
• Excess Calories and Simple Sugars 
• Genetic Factors
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12
Q

**What is the functional Role of:

• LDL-receptor

A

*

• LDL receptor binds ApoB-48 and pulls out Cholesterol

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13
Q

**What is the functional Role of:

• Apolipoproteins

A

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

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14
Q

**What is the functional Role of:

• CETP

A

*
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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15
Q

**What is the functional Role of:

• ApoCII

A

*
• Found on Chylomicrons, VLDL, and HDL

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

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16
Q

**What is the functional Role of:

• ApoCIII

A

*
• Found on Chylomicrons, VLDL, and HDL

• INHIBITS lipoprotein binding to receptors

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17
Q

**What is the functional Role of:

• ApoB

A

*
• 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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18
Q

**What is the functional Role of:

• PPAR-a

A

*

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

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19
Q

**What dietary Factors influence hyperlipidemia?

A

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

20
Q

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

A

*
Cholesterol:
• Reduce SATURATED and TRANS-FATS

TGs:
• Total Fat
• Alcohol
• Excess Calories

21
Q

What is the major carrier of cholesterol in the plasma?

A

LDL

22
Q

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

A

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

23
Q

What happens to chylomicron remnants?

• what are the risks of system overload with these?

A
  • Return to the liver to give TGs via the LDLR

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

24
Q

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

A

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

25
Q

What is the Friedwald Formula?

• what is it used for?

A

• Used to Calculate LDL-Cholesterol

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

26
Q

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

A

Source:
• Liver

Composition:

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

27
Q

When are patients at risk of developing pancreatitis?

A

• When TGs get above 1000

28
Q

Differentiate Primary Chylomicronemia and Familial Hypertriglyceridemia?

A

Chylomicronemia:
• involves mostly defective removal of chylomicrons

Familial Hypertriglyceridemia:
• Involves mostly defective removal of VLDL

29
Q

Functional Role of ApoE.

• what kind of particles is it associated with?

A

ApoE
• Ligand for binding to the LDL receptor

Particle association:
• Chylomicron Remnants, IDL, HDL

30
Q

How is familial Dysbetalipoproteinemia usually diagnosed?

• why is this the case?

A
  • 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.
31
Q

Which of the Primary Hyperlipoproteinemias is Autosomal Dominantly inherited?

A

• Familial Combined Hyperlipidemia (FCH)

32
Q

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

A

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

33
Q

What is the Optimal goal for LDL?

• what about in patients with atherosclerotic disease?

A

Optimal = 100 mg/dl

Atherosclerotic Disease = 70 mg/dl

34
Q

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

A
  • Nephrotic Syndrome

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

35
Q

What are some Liver Diseases that might cause hyperlipidemia?

A
  • Hepatitis - too many lipoproteins made

* Biliary Disease - bile goes back into the circulation

36
Q

What are some medication that can cause hyperlipidemia?

A
  • Estrogen
  • Beta Blockers
  • Thiazide Diuretics
37
Q

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

A
  • 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
38
Q

What is the job of the ABCG1 transporter?

A

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

39
Q

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

A
  • Achilles Tendon Xanthomas
  • Xanthomas on extensor tendons of hand

Xanthomas around the eyes are not as indicative

40
Q

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

A

Primary Chylomicronemia:
• Tons of chylomicrons would rise to the top and harden

Familal Hypercholesterolemia:
• Plasma would be cloudy from elevated VLDL

41
Q

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

A

• Mitigation of Inflammatory activity of Macrophages

42
Q

How are people with Hypertriglyceridemia typically treated?

A

TG depleting agents:
• Fibrate
• Niacin

43
Q

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

A

• DIETARY MAINLY

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

44
Q

What is the primary treatment for people with Familial Dysbetaliproteinemia?

A

HIGH TGs and Cholesterol

HIGH TGs:
• Niacin and Diet Treated

HIGH cholesterol:
• Statins

45
Q

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

A

Cholesterol:
• Saturated Fats
• Trans Fats

TGs:
• Total Fats
• EtOH
• Excess Calories

Eat Complex Carbs and Fiber

Cardio - Elam (4 decks)

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