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MCB 2 Block 2 > Phospholipids > Flashcards

Phospholipids Flashcards

1
Q

Classes of PL

A

Alcohol attached to phosphate attached to:
Diacylglycerol - based on phasphatidic acid
Sphingosine - no phosphatidic platform but with Pi (sphingomyelin w/o glycerol backbone)

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2
Q

Assembly of PL

A

Macro components already synth, ER they are put together to golgi to destination

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3
Q

Glycerol Spine

A

All PL based on phosphatidic acid posses glycerol spine
Tails (12-16 C) acyl at C2 unsat
Phosphatidic acid = simplest of all phosphoglycerides and precursor to large family

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4
Q

Origins of PT acid

A

With NADPH

DHAP (glycolysis is main supply), glycerol 3P, diacyl glycerol

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5
Q

Creating PLs - pos head groups

A

Draw pathway, CTP provides activating group w/ CMP leaving Pi behind

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6
Q

Synth of Phosphatidyl - choline, ethanolamine, serine

A

Draw pathway, Choline from diet, SAM donates methyl from methionine

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7
Q

Synth of Choline requires SAM

A

Donor of methyl groups

Condensation of methionine and adenosine releases Pi3 for hydrolysis - very costly

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8
Q

Choline and surfactant

A

Dipalmitoyl-phosphatidyl choline (DPPC) reduces alveolar surface tension

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9
Q

Surfactant Synth

A

ER of lung granular pneumocytes, activated by translocation from cytosol to ER via CTP-phosphocholine cytidyl transferase.

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10
Q

Surfactant insuff

A

Hyaline membrane disease (Resp distress syndrome)

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11
Q

Phosphatidic Acid to Cardiolipin and phosphatidyl inositol

A

Makes IM mito impermeable to H

Cardiolipin lends structural stability (2 PTs, 1 mid glycerol and 4 FA tails = strong acid and stable)

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12
Q

Plasmologens

A

Mammalian ether P-glycerolipids.
DHAP and FA CoA form ester leading to FA exchange for fatty alcohol = stable ether leading to C2 reduced and FA added for ester bond. Double bond forms between C1 and C2 of alkyl group at C1 forms stable plasmalogen: Choline-Pl or Ethanolamine PL. Made in peroxisome.

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13
Q

Peroxisomal synth

A

If PS def leads to zellwegers

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14
Q

Platelet Adhesion Factor

A

Is a plasmalogen
Ether glycero PL but with saturated FA at C1 and acetyl group at C2
Role = Defense, triggers thrombotic reactions

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15
Q

Sphingomyelin

A

Sole Pl with no glycerol - sphingosine is linked to FA via ceramide linkage
FA like tails = good conductor

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16
Q

Sphingomyelin pathway

A

draw

17
Q

Membrane PL’s and signaling

A

Continual resynth necessary

Phosphatidyl Inositol - Dominate PT acid (CDP activated DAG)

18
Q

PLC

A

Phospholipase C cleaves C1 leading to IP2 (gates Ca entry) and DAG

19
Q

Phosphatidyl Inositol

A

Also a GPI anchor
Special soluble water sugars create stable tether
Pi gorups also function in EC space

20
Q

PL signal pathway

A

On paper

21
Q

Degradation of PL

A

Phospholipases (PLs) - all tissues, panc juice etc

PLA2 - Functions in defense and inflammation, releases eiconosol FA (20C) and Arachidonic Acid. Inhib by glucocorticoids

Lysosomal Phosphodinase - Sphingomyelinase in lysosome

PLC - activated by PIP2 = 2nd msgrs

22
Q

Lysosomal Sphingomyeline

A
  1. Endocytosis and import
  2. Phosphatidyl Choline, leaves Ceramide (FA and sphingosine)
  3. Ceraminidase releases sphingosine and FA (Sphingosine inhibs PKC, ceramides involved in stress response)
23
Q

Niemann Pick

A

AR, resist to TB
Defect in sphingomyelin Degrade. Can’t remodel membrane. A (hepatosplenic accumulation; neurodegen leading to death) B(no neural; spleen, liver, marrow affected)

24
Q

Gm1 gangliosidosis

A

Defect in beta-galactosidase. Accumulation of GM1 and keraten sulfate. Neurodegen, hepatosplenomegaly, skl deform, cherry red macula

25
Q

Tay Sachs

A

Defect in beta-hexosominidase A. Accumulate GM2. Rapid neuro degen, blind, cherry red macula, muscle weakness, seizures

26
Q

Sadhoff’s disease

A

Defect in B-hexosaminidase A and B. Accum GM2 and globosides. Sym of Tay sachs but with visceral involvement

27
Q

Fabry Disease

A

Defect in alpha-galactosidase. Accum of globosides. Red purp rash, kid and heart fail, burning in lower extremities

28
Q

Gaucher Disease

A

Defect in Beta-glucosidase. Accum of glucocerobosides. Most common lysosomal storage disease, hepatosplenomegaly, osteoporosis.

29
Q

Farber Disease

A

Defect in Ceraminidase. Accum of Ceramide. Joint deform, hoarse cry, granulomas

MCB 2 Block 2 (10 decks)

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