Edwards Lectures Flashcards

1
Q

What is arachidonic acid synthesized from?

A

It is synthesized from fatty acids with lipases. It acts as a precusor for many signaling molecules (thromboxanes, prostaglandins)

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2
Q

What is cholesterol synthesized from, and what is it made into?

A

Made from Cholesterol esters (cholesterol esterase) and converted to steroid hormones (desmolase) and bile salts

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3
Q

What are the components fo bile salts

A

cholic acid & glycis

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4
Q

function of plasma lipoproteins (LPL)

A

transport lipids throughout the blood. Polar surface with proteins, and a very hydrophobic core, rich in TGs and CEs

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5
Q

What is the major compoenet of Chylomicons? VLDL? LDL? HDL?

A

Chylomicrons & VLDL= TGs; LDL: Cholesterol, HDL: low in bad stuff, protective

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6
Q

LDL & HDL relationship to CHD

A

LDL levels correlate strongly with CHD, HDL levels correlate inversely

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7
Q

Drug: Eztimibe

A

Blocks cholesterol absorption by enterocytes

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8
Q

Pancreatic lipase

A

TG to FA + Monoacyl glyceride

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9
Q

Cholesterol Esterase

A

Cholesterol ester to Cholesterol and FA

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10
Q

Trace the path of chylomicrons from the intesting

A

Chylomicrons: from small intestine to capillaries. LPL on adipose and muscle tissue, TG and FFA are delivered to these tissues–> Chylomicron remnants to the liver

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11
Q

LPL or ApoCII (Cofactor Deficency (mutation in eaither gene)

A

Causes Hyperchoomicronemia: xanthomata, pancreatitis, and death. Blood is very rich in CMs

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12
Q

How/why can type 1 diabetic exhibit hypertriglyceridemia/chylomicronemia?

A

LPL levels require insuline, thus LPL activity is reduced in the absence of insulin

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13
Q

What happens to fatty acids in muscle?

A

They undergo beta oxidation to generate ATP

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14
Q

What happens to FAs in adipose?

A

They are resynthesized into TGs for storage

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15
Q

Is the chylomicron remnant TG rich or TG poor

A

TG poor, LPL on muscle and fat, FFAs have been delivered to these tissues.

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16
Q

The liver takes up chylomicrons and converts them to this before sending them out…

A

VLDL, then VLDL is reabs or becomes LDL and is reabs.

17
Q

VLDL is very cholestrol rich. it is hydrolized by LPL and converted to LDL. LDL is…

A

very cholesterol ester rich, and it provides cholesterol to cells, which is necessary from growth. LDL is cleared, majority is endocytosed by the LDLR on hepatocytes.

18
Q

Statins: how do they work?

A

Partially inhibit HMG CoA reducatase, which converts acetate to cholesterol (inc acitivity when plasma glucose levels are high), thus there is a decrease intracelluar cholesterol, and this triggers increased transcription of the LDLR gene, so more LDL is cleared from the plasma and taken up int the liver

19
Q

SREBP2?

A

It is the transcription factor for HMG CoA reducatase. It is activated when plasma cholesterol levels are low and inhibited when they are high. Thus, statins causing lowered plasma cholesterol also increases the activity of the SREBP2 transcription factor and syntehsis of LDLR. s

20
Q

LDLR

A

Crucial in clearing LDL

21
Q

Familiar hypercholesterolemia

A

defective LDLR, thus there is high cholesterols in the blood, more LDL is depositied into tissued –> early MI

22
Q

High Cholesterol–> LDLR & HMGCR

A

High C–> low LDL R and HMGCA, Low C–> High LDLR, high HMGCR; thus regulated cholesterol levels.

23
Q

T/F Statins must be taken for life or cholesterol levels will return to normal

A

true

24
Q

Statins do not work for famliial hypercholesterolemia

A

because they do not have normally functionling LDLR, whcih is the main way that statins work, is by upregulating this transporter

25
Q

When statins increase clearance of LDL to the liver, where does the extra cholesterol go?

A

it is released as bnile.

26
Q

High Cholesterol–> LDLR & HMGCR

A

High C–> low LDL R and HMGCA, Low C–> High LDLR, high HMGCR; thus regulated cholesterol levels.

27
Q

T/F Statins must be taken for life or cholesterol levels will return to normal

A

true

28
Q

Statins do not work for famliial hypercholesterolemia

A

because they do not have normally functionling LDLR, whcih is the main way that statins work, is by upregulating this transporter

29
Q

When statins increase clearance of LDL to the liver, where does the extra cholesterol go?

A

it is released as bnile.

30
Q

What is arachidonic acid synthesized from?

A

It is synthesized from fatty acids with lipases. It acts as a precusor for many signaling molecules (thromboxanes, prostaglandins)

31
Q

What is arachidonic acid synthesized from?

A

It is synthesized from fatty acids with lipases. It acts as a precusor for many signaling molecules (thromboxanes, prostaglandins)