Brainscape's Knowledge GenomeTM

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


See full index

CPR > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

1
Q

What is precursor for isoprenoids (steroids), lipid soluble vitamins (isoprenoids),& ubiquinone’s?

A

IPP

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

Sources oAcetyl coa

A

Made in mitochondria: • oxidative decarboxylation of pyruvate Beta ox fatty acids • breakdown amino acids transported into cytoplasm via citrate shuttle

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

How many IPP units form sterne backbone ring?

A

6

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

What is alicyclic compound made of?

A

4 fused rings (sterane) W/ one hydroxyl group at c3

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

What’s most abundant steroid?

A

Cholesterol

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

T or F: Cells can degrade nucleus of cholesterol

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Biosynthesis of cholesterol is ____ to dietary intake

A

Inversely proportional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How many nadph ATP & Acetyl coa are used for making cholesterol

A

16 nadph 18ATP 18 AcetylCoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Rate limiting enzyme in cholesterol synthesis 2

A

HMG CoA reductase producing mevalonate & targeted statin, by

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Positive regulators of HMG CoA reductase?

A

Insulin & thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Negative regulators of HMG CoA reductase?

A

Glucagon, sterols, high amp, vitamin E, Statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of inhibition does a statin utilize?

A

Competitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the km for KMG CoA and ki for statins?

A

Km is 4 uM Ki is 5-45 nM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do statins lead to myotoxic side effects?

A

Statin mediated myopathy from deletion of muscle ubquirone (CoQ10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens with cholesterol In regards to CPR?

A

• Made into ACAT • packed into VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Active form of cholesterol ?

A

Dephosphorylated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does insulin activate HMG COA reductase

A

Dephosphorylates it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Transcriptional control of HMG CoA Reductase?

A

Binding of TF to promoter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does low cholesterol impact srebp?

A
  • Triggers translocation of SREBP-SCAP to Golgi
  • SREBP is cleaved & n-terminus released
  • SREBP tf dimer binds to SRE on HMGR promoter
20
Q

Inner core lipoproteins?

A

• Packed W TAGS, cholesterol, cholesterol esters

21
Q

Outer shell lipoproteins?

A

•mono-layer phosphiollpid, free cholesterol, & apolipoproteins

22
Q

Function of lipoproteins?

A
  • Transport & deliver TAGS
  • cholesterol homeostasis
  • Apolipoproteins act as cell targeting signals & ligand
  • lipid metabolism
23
Q

5 types of lipoproteins?

A
  • Chylomicrons (largest, but smallest density, Most TAGs, least protein)
  • VLDL
  • IDL
  • LDL
  • HDL (smallest, but highest density,least TAGs, most protein)
24
Q

Bad cholesterol?

A

LDL

25
Q

Where are chylomicrons formed?

A

Dietary fats in SI

26
Q

What does ApoB-48 & ApoE &ApoC-II do where are they found?

A
  • ApoB-48 facilitates transport
  • ApoE facilitates uptake to liver
  • ApoC-11 activates capillary lipoprotein lipase
  • chylomicron’s
27
Q

Where are VLDL made what are the proteins?

A

Liver

  • •ApoB-100: recognized by receptors in target cells
  • •Apoc-11: activates capilllary lipoprotein lipase
  • ApoE: promotes heaptic uptake
28
Q

HDL proteins?

A
  • • ApoA-1 activates enzyme to esterify cholesterol
  • ApoC-11: activates capilllary lipoprotein lipase
  • ApoE: promotes hepatic upatake
29
Q

IDL proteins?

A
  • ApoB-100
  • ApoE
30
Q

What apo proteins are found on a nascent chylomicron?

A
  • ApoB-48: promotes transport
31
Q

What apo proteins are found on the matrue chylomicrons?

A
  • ApoB-48
    • Transport
  • ApoC-II
    • activates capillary lipoprotein lipase
  • ApoE
    • deliver to liver
32
Q

Describe VLDL IDL and LDL processing.

A
  • Start with VLDL and capillary lipoprotein lipase hydrolyzes triacylglycerols to glycerol and free fatty acids. ApoCII is released and IDL remains
  • IDL gets internalized by liver via ApoE binding hepatocytes.
    • Hepatic lipoprotein lipase takes off more triacylglycerols and ApoE to become LDL
  • LDL deliver cholesterol to liver and tissues with binding of ApoB-100
33
Q

Role of LDL? significant Apo protein and core makeup?

A
  • Major carrier of cholesterol in blood to peripheral tissues and regulates de novo synthesis
  • Shell has ApoB-100 which is recognized by receptors in targt cells
  • Core is packed with 1500 cholesterol esters
34
Q

What causes familial hypercholesterolemia?

A
  • Receptors on LDL are unable to release LDL cargo
  • Cholesterol in LDL is not used
35
Q

What does LCAT do?

A
  • Gives rise to mature HDL
36
Q

Function of HDL?

A
  • Crucial for maturation of chylomicrons supplies apo C II and ApoE
  • Scavenges and removes LDL and transports it to liver for processing
  • “Reverse Cholesterol Transport” brings cholesterol from tissues to liver for excretion
37
Q

What happens when their is a mutation in ABCA1?

A
  • ABCA1 is a cholesterol transport protin in endothelial cells and macrophages
  • Loss of this results in Tangier disease characterized by HDL deficiency accumulation of cholesterol in macrophages and premature atherosclerosis
38
Q

What cholesterol molecule has antioxidant, anti-inflammatory, antithrombotic, and NO producing properites?

A

HDL

39
Q

How do you increase HDL-C levels?

A
  • Weight loss, exercise and smoking cessation
  • Antihypercholesterolemic drugs, fibrates, anti-diabetic thiazolidine drugs, estrogens and omega 3 FA
40
Q

What is type I Hyperlipoproteinemia, cause, sx and tx?

A
  • aka Hyperchylomicronemia
  • Inability to hydrolyze TAGs in chylomicrons and VLDL
  • Caused by a deficiency in Capillary lipoprotien lipase or ApoC-II
  • Sx: Abdominal pain, acute pancreatitis, cutaneous eruptive xanthomas
  • Tx: low fat diet

(Autosomal recessive)

41
Q

With type I hyperlipoproteinemia what are the two deficiencies that cause it?

A
  • ApoC-II deficiency, post adolescence
  • Primary LPL deficiency- manifiests in infancy
  • Plasma TAG levels are greater than 1000 mg/dL
42
Q

What is type II hyperlipoproteinemia, cause, genetics, sx, and tratement?

A
  • aka familial hypercholesterolemia
  • Caused by defects in LDL receptor resutling in defects in uptake of LDL via receptor mediated endocytosis
    • inability to recognize ApoB100 on LDL
  • Autosomal Dominant
  • Sx: Xanthomas, corneal eye deposits, angina
  • Tx:
    • heterozygous: responds to diet, statins and bile acid binding resins
    • homozygous: need LDL apheresis and liver transplant
43
Q

In Type II hyperlipoproteinemia (FH), what happens to excess LDL?

A
  • accumulates under endothelial cells lining blood vessesl and undergoes oxidation forming oxLDL
  • oxLDL initiates inflammatory response deading to development of atherosclerosis
44
Q

With type II FH, what happens with untreated homozygous patients?

A
  • Usually die of CAD Dbefore teenage yeaers
45
Q
A

CPR (18 decks)

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