Lipid Metabolism: Cholesterol/Eicosanoids Flashcards Preview

Medical Biochemistry > Lipid Metabolism: Cholesterol/Eicosanoids > Flashcards

Flashcards in Lipid Metabolism: Cholesterol/Eicosanoids Deck (33)
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1
Q

What structures can be made from cholesterol?

A
  • Cell membrane
  • Regulators of skin differentiation (Cholesterol 3-O-Sulfate)
  • Bile acid
  • Vitamin D3
  • Steroids precursor
2
Q

What cellular functions are cholesterol important for?

A
  • Intracellular transport
  • Cell signaling and Nerve conduction
  • Structure and functions of caveolae and clathrin coated pits w/ endocytosis
3
Q

What is the desirable level of cholesterol to be low risk HD?

A

<200Mg/dL or <5.2 mM/L

4
Q

Describe the general synthesis of mevalonate?

A

Three molecule Acetyl CoA Combine to form HMG CoA and then become reduced to form Mevalonate

5
Q

What is HMG reductase, and what is it’s clinical significance?

A
  • Enzyme which reduces HMG CoA to Mevalonate

- Statins block HMG Reductase

6
Q

What important products can be made from mevalonate?

A
  • Isoprenoids

- Cholesterol

7
Q

How many steps are required for cholesterol synthesis? Where is it made?

A
  • 37 Steps

- Mainly in liver; sometimes in intestine, reproductive tissue, and adrenal glands

8
Q

What are the biochemical controls cholesterol synthesis when levels are high?

A
  • High cholesterol inhibits HMG-CoA reductase
  • High Cholesterol Activates AMP Activates kinase which I Activates HMG CoA
  • High Cholesterol leads to proteosome degradation f HMG-CoA reductase
  • Hormonal regulation via insulin activating protein phosphatase —> inactivation of HMG- CoA reductase
9
Q

What are the genetic control for cholesterol synthesis when levels are low?

A
  • SREBP bonds SRE of HMG-CoA Reductase gene and LDL gene to stimulate transcription
10
Q

What are the genetic control fo cholesterol synthesis at high levels?

A
  • In high levels, SREBP is bound to SCAP and INSIG-1 not allowing transcription
11
Q

What are side effects of statins?

A
  • Muscle weakness and pain
  • Occasionally: myopathy
  • Peripheral neuropathy
  • Reduced cognition
12
Q

What are possible replacements for statins?

A
  • Co Q10
  • Ubiquinone - Mt can be damaged if not enough
  • Heme A - Prosthetc group for cytochrome C oxidase
  • Squalene synthase inhibitors
  • Zaragozic acid
13
Q

What is Smith-Leslie Optiz Syndrome?

A
  • Deficiency in DHCR7, an enzyme which converts 7-DHC to cholesterol
  • 15-27% reduced levels
  • Malformation and behavioral problems
14
Q

What is Arcus Senilis?

A
  • Results Form Cholesterol deposits in cornea

- indicates hypercholesterolemia

15
Q

What is xanthelasma?

A

Cholesterol deposit underneath the skin

16
Q

What are the most important chemicals in biles?

A
  • Phosphatadylcholine

- Bile salts

17
Q

What stimulates contraction of the gallbladder and release of bile?

A

CCK

18
Q

What are the end chain compounds of Bile salts?

A

Either glycine or Taurine

19
Q

How is bile conserved?

A
  • Bile acids are transported back from intestinal epithelium through portal vein to liver
  • Albumin in blood ties up bile acids and is picked up by liver
20
Q

What is cholelithiasis?

A
  • Less phospholipids and bile acids stored in gall bladder

- More cholesterol in bile causes precipitation of gallstones

21
Q

What biochemical function is Dolichol used in?

A

Synthesis of N-linked glycoproteins

22
Q

How many steps are involved in de novo synthesis of cholesterol?

A

37 Steps

23
Q

How are prostaglandins synthesized de novo?

A

Free Arachidonic acid (released by Phospholipasee A-2) —> PGG2 (COX) —> PGH2 (Peroxidase)

24
Q

What is the role of Cortisol signaled lipocortin?

A

Inhibits PLA-2

25
Q

How does aspirin regulate synthesis of prostaglandins?

A

Inhibits COX

26
Q

What is the role of prostacyclin (PGI2)?

A

Produced by vascular endothelial cells to inhibit platelet aggregation and stimulate vasodilation and block thrombogenesis

27
Q

What is PGF(alpha2) produced in?

A
  • Produced by most tissues
  • In corpus lute up
  • Contraction Of Smooth muscle
  • Stimulates uterine contraction
28
Q

What is the role of Thromboxane (TXA2)?

A

Thomboxanes A2 is produced in activated platelets. TX2 promotes adherence and aggregation of circulating platelets and contraction of vascular smooth muscle and promotes clot formation

29
Q

Describe de novo synthesis of leukotrienes.

A
  • Arachidonic acid is substate

AA —> (5-lipoxygenase) 5HPETE —> Leucotriene A4/B4/C4/D4

30
Q

Where is LTB4 produced and released?

A
  • Produced by polymorphonuclear leukocytes
  • Increases chemotaxis
  • release of lysosomal enzymes
  • Causes adhesion of WBC
31
Q

What are the effects of LTE4?

A
  • Bronchocontriction
  • Vasoconstriction
  • Increased vascular permeability
  • Contraction of smooth muscle
  • Components of slow-enacting substances of anaphylaxis
32
Q

What is the effect of Zyflo?

A

Inhibition of 5-lipoxygenase

33
Q

What is the actions f Accolate (Zafirlukast)?

A

Leukotrienes receptor inhibitor