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Cardio II: Exam 2 > Lipid Biochemistry > Flashcards

Lipid Biochemistry Flashcards

1
Q

chylomicrhons

A

apoB-48, apoC-11, apoE

transports dietary triglycerides

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2
Q

VLDL

A

transports tiglyceride from liver to tissue

apoB100, apoC11, ApoE

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3
Q

IDL

A

VLDL remnants - picks up cholesterol from HDL to become LDL

picked up by liver

ApoE, APoB100

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4
Q

LDL

A

delivers cholesterol into cells

apoB100

uptake by liver and other tissues via LDL receptor (apoB-100 receptor)

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5
Q

HDL

A

picks up cholesterol accumulating in blood vessels

apoA-1

delivers cholesterol to liver via scavenger receptor, shuttles ApoCII and ApoE into the blood

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6
Q

LPL

A

lipoprotein lipase

hydrolyzes the fatty acids from triglycerides carried by chylomicrons and VLDL - is activated by apoC-II

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7
Q

ApoB48

A

found on chylomicrons - attached and reqd for release from epithelial cells into lymphatics

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8
Q

apoB100

A

is added in hepatocytes and mediates release into blood

VLDL, IDL, LDL

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9
Q

LCAT

A

lecithin-cholesterol acytransferase

activated by apoA-1 on HDL, adds fatty acid to cholesterol - allowing HDL to transport cholesterol from periphery to the liver

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10
Q

SRB1

A

scavenger receptors- a way for HDL picked up in periphery to enter cells

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11
Q

Type I hypertriglyceridemia

A

genetic absence of LPL

  • dz triglyceride in blood
  • see orange-red eruptive xanthomas over mucous membranes and skin

can also be caused by diabetes, alcoholism and G6PD deficiency

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12
Q

carnitine problems?

A
  • see greatly elevated amounts of triglycerides w/ primary long chain fatty acids (decreased LCFA metabolism due to lack of carnitine shuttle)
  • large number of lipids vacuoles in mm. biopsy
  • mm. rely on Fas as long term source of energy
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13
Q

sx of carnitine problems?

A

Symptoms: accumulation of LCFAs in tissues → cardiomyopathy, skeletal mm. myopathy, encephalopathy and impaired liver function, mm. cramping, severe weakness, death
• muscle, kidney and heart tissues are primarily effected
• muscle weakness during prolonged exercise
• mm. necrosis, myoglobulinuria, hypoglycemia, fatty liver

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14
Q

causes of carnitine deficiency/

A

Causes:
• Primary carnitine deficiency: due to inherited CTPI or CPT II deficiency (can be treated by avoiding fasting, dietary restrictions of LCFAs and carnitine supplement)
• liver disease → impaired endogenous synthesis of carnitine
• inadequate intake of carnitine
• carnitine loss due to diarrhea, diuresis, hemodialysis

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15
Q

ddx of carnitine deficiency?

A

Diagnosis:
• based upon pt. very low plasma and mm. carnitine levels
• fasting ketogenesis is impaired
• hypoglycemia, precipitated by fasting/strenuous exercise
• mm. biopsy shows significant lipid vacuoles

Treatment:
• oral carnitine, avoidance of fasting/strenuous exercise, supplementation of medium-chain triglycerides, high-carbohydrate low fat diet

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16
Q

systemic primary carnitine deficiency?

A

Systemic primary carnitine deficiency, (SPCD) also known as carnitine uptake defect, carnitine transporter deficiency (CTD) or systemic carnitine deficiency is an inborn error of fatty acid transport.

Symptoms such as chronic muscle weakness, cardiomyopathy, hypoglycemia and liver dysfunction.
• The first suspicion of SPCD in a patient with a non-specific presentation is an extremely low plasma carnitine level
• Treatment for SPCD involves high dose carnitine supplementation, which must be continued for life

17
Q

CAT-1 or CPT-I deficiency

A

a rare metabolic disorder that prevents the body from converting certain fats called long-chain fatty acids into energy, particularly during periods without food.
• Symptoms include low levels of ketones and low blood sugar (hypoglycemia).
• People with this disorder typically also have an enlarged liver (hepatomegaly), muscle weakness, and elevated levels of carnitine in the blood.- see liver dysfunction

18
Q

CAT-2 or CPT-II deficiency

A

a metabolic disorder characterized by an enzymatic defect that prevents long-chain fatty acids from being transported into the mitochondria for utilization as an energy source.
• It is the most common inherited disorder of lipid metabolism affecting the skeletal muscle of adults – mm. weakness and brown urine
• Treatment:High-carbohydrate (70%) and low-fat (<20%) diet to provide fuel for glycolysis; use of carnitine to convert potentially toxic long-chain acyl-CoAs to acylcarnitines

19
Q

xanthomas

A
  • xanthomas are lesions characterized by accumulation of lipid-laden macrophages
  • xanthomas develop in altered systemic lipid metabolism or as a results of local cell dysfunction
20
Q

type I hyperlipidemia

A

: lipoprotein lipase deficiency
• deficiency results in massive accumulation of chylomicrons in plasma
• elevation of triglycerides
• manifests in childhood w/ acute pancreatitis
• see eruptive xanthomas

21
Q

type 2 HL

A

defective apo-B100 protein
• see accumulation of LDL and VLDL and cholesterol levels variably
• see tendinous xanthomas, tuberous xanthomas, xanthelasmas

22
Q

Type 3 HL

A

apo-protein E deficiency
• accumulation of IDL, triglycerides and cholesterol levels
• see premature atherosclerosis, plane xanthomas

23
Q

type 4 HL

A

: hypertriglyceridemia due to overproduction of VLDL
• elevated VLDL, plasma cholesterol levels are normal
• eruptive xanthomas
• associated w/ coronary heart disease, DM type II, obesity, alcoholism

24
Q

type 5 HL

A

genetic defects in apo-lip C
• accumulations of chylomicrons and VLDL
• severe elevation of triglycerides in plasma
• presents in early childhood with acute pancreatitis, eruptive xanthomas

25
Q

secondary HL?

A
  • Decreased synthesis of HDL:
    • see increased LDL levels
    • presents w/ premature CAD, plane xanthomas
  • Hepatic lipase deficiency:
    • presents with CAD, xanthomas
26
Q

secondary hypertriglyceridmeia?

A
  • diabetes mellitus, pancreatitis, gout, type 1 glycogen storage disease, alcoholism, oral contraceptives
27
Q

combined hypercholesterol and hyper triglyceridemia?

A
  • nephrotic syndrome, chronic renal failure, steroid immune suppression
28
Q
  1. Xanthelasma palpebrarum
A
  • is the most common xanthomas
    - lesions are soft, velvety, yellow, flat,
    around the eyelids
    - associated with hyperlipidemia
    - secondary to cholestasis
29
Q

Tuberous xanthomas

A

firm, painless, red-yellow nodules
usually develops in pressure areas,
extensor surfaces of knees, elbows
- associated with hypercholesterolemia
and increased levels of LDL
- secondary to nephrotic syndrome,
hypothyroidism

30
Q

. Tendinous xanthomas

A
  • associated with severe hypercholesterolemia
    and elevated LDL levels.
    • lesions often related to trauma
    • nodules related to tendons or ligaments
    • secondary to cholestasis
31
Q

Eruptive xanthomas

A
  • erupt as crops of small, red-yellow
    papules, may spontaneously resolve
    over weeks
  • secondary to diabetes
32
Q

Plane xanthomas

A
  • associated with dysbetalipoproteinamia
  • can occur in any site
  • covers large areas of face, neck, thorax
  • secondary to cholestasis
33
Q

statins

A

• Statins (Lovastatin, atorvastatin, fluvastatin, pravastatin and simvastatin):
- efficacious in lowering plasma cholesterol
- act as competitive inhibitors of the enzyme HMG-CoA reductase (plays a role in production of cholersterol in liver)
- these molecules mimic the structure of the normal substrate of the
enzyme (HMG-CoA) and act as transition state analogues
- while statins are bound to the enzyme, HMG-CoA cannot be converted
to mevalonate, thus, inhibiting the whole cholesterol biosynthesis process

34
Q

Type IIa HL?

A

Accumulation of LDL

Familial LDL receptor deficiency and familial defective apo-B100

Plasma cholesterol levels are elevated

Plasma triglyceride levels are normal

Manifest severe atherosclerosis

May present with:

  • tendinous xanthomas, or
  • tuberous xanthomas, as well as,
  • xanthelasmas
35
Q

type IIb HL?

A
  • accum. of both LDL and VLDL
  • defective apo-B100 protein
  • variable elevations of cholesterol and triglycerides

may present with:
- tendinous xanthomas, tuberous xanthomas, xanthelasmas

Cardio II: Exam 2 (7 decks)

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