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Medical Biochemistry > Lipids > Flashcards

Lipids Flashcards

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USMLE® Step 1 flashcards
1
Q

Phosphatidic acid

A

Head group = H

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2
Q

Cardiolipin

A

Two phosphatidic acids esterified to an additional glycerol molecule, FOUND ONLY IN INNER MITOCHONDRIAL MEMBRANE

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3
Q

Plasmalogens

A

Glycerophospholipids w/ C1 fatty acid attached via an ether linkage rather than an ester linkage, almost 30% of glycerophospholipids in the brain are plamalogens, reduced levels assoc. w/ Alzheimer’s

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4
Q

Phosphatidalethanolamine

A

Plasmalogens with unsaturated ether linkage at C1 FA

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5
Q

Platelet-activating factor

A

Plasmalogens with saturated ether linkage at C1 FA and acetyl group at C2 FA

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6
Q

Glycerophospholipids with net charge = 0

A

PC, PE, SM, because alcohol = +1

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7
Q

Glycerophospholipids with net charge = -1

A

PI, PG, PS, because alcohol = 0

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8
Q

Saturated fatty acid is?

Unsaturated fatty acid is?

A

C1, C2

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9
Q

Ceramide

A

Sphingosine + acyl tail

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10
Q

How is phosphatidic acid formed?

A

2 acyl transferace rxns with activated acyl CoA substrate and glycerol 3 phosphate (from DHAP)

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11
Q

How are PC and PE formed?

A

1) both formed form dephos of phosphatidic acid (diacylglycerol), followed by condensation with CDP-choline/ethanolamine
2) PC can be made by methylating PE using SAMx3

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12
Q

How is PI formed?

A

Dephos of phosphatidic acid (diacylglycerol), followed activation of CDP-diacylglycerol and addition of inositol

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13
Q

How is PS formed?

A

Base exchange between serine and PE, which requires PLP

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14
Q

Formation of glycerol-3-P from glycerol occurs where?

A

Only in the liver

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15
Q

Formation of glycerol-3-P from DHAP occurs where?

A

Liver and adipose

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16
Q

How is sphinganine formed?

A

PalmitoylCoA + serine in NADPH rq rxn

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17
Q

Phospholipases

A

degrade glycerophospholipids by hydrolyzing

phosphodiester bonds

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18
Q

lysophosphoglyceride

A

remaining molecule after one acyl chain is removed by a phospholipase, PLA1(mammalian tissues) and PLA2(mammalian tissues and snake and bee venom) make these

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19
Q

PL-C

A

acts on PIP2 to make DAG (activates PKC) and IP3 (Ca++ release), found in bacteria

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20
Q

SMase

A

Removes phosphorylcholine from sphingomyelin to form ceramide (sphingasine + acyl tail)

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21
Q

Niemann-Pick disease

A

AR, defects in lysosomal acid SMase, type A (5%) type C and D is defect in transport proteins not SMase, cherry-red macula, hepatosplenomegaly

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22
Q

Neutral glycosphingolipids

A

glucocerebroside, glucocerebroside, globoside attached to ceramide through O-glycosidic bond

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23
Q

Acidic glycosphingolipids

A

negatively charged at physio pH because of NANA in gangliosides (some serve at receptors for bacterial toxins - cholera) or sulfate in sulfatides

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24
Q

Synthesis of glycosphingolipids

A

Made in Golgi by sequential attachment of UDP-sugars by glycosyl transferases, sulfate groups are attached to galactose by a sulfotransferase using PAPS as the sulfate donor

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25
Q

Degradation of glycosphingolipids

A

internalized by endocytosis into lysosomes, sugars are removed one at a time by lysosomal hydrolases producing ceramide, which can be degraded to sphingosine and FA

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26
Q

Tay-Sachs

A

accumulation of GM2 because lacking b-hexosaminidase A enzyme, fatal, cherry-red macula, blindness

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27
Q

Gaucher disease

A

accumulation of glucocerebrosides because lacking b-glucosidase/glucocerebrosidase, most common lysosomal storage disease, hepatosplenomegaly, osteoporosis of long bones

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28
Q

Fabry disease

A

accumulation of globosides because lacking a-galactosidase

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29
Q

Eicosanoids derived from?

A

20C, unstaturated n-6 FAs, usually arachidonic acid, that is released from membrane by PLA2

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30
Q

Synthesis of prostaglandins and thromboxanes

A

Arachidonic acid to PGH2 by PGH
synthase, an enzyme with two catalytic activities: COX (forms the intermediate PGG2) in an O2-requiring reaction, and a peroxidase, (converts PGG2 to PGH2) in a glutathione-requiring reaction

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31
Q

COX1 vs COX2

A

COX1 is constitutively-expressed in most tissues, COX2 is induced by cytokines during inflammation

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32
Q

NSAIDs

A

inhibit production of all prostaglandins and thromboxanes

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33
Q

Celecoxcib

A

selective COX2 inhibitor, increase in cardiovascular side effects because of decrease PGI2

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34
Q

PGH2 is converted to?

A

PGI2 in endothelial cells
TXA2 in platelets
PGF2 and PGE2 in other cells

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35
Q

TXA2

A

produced by platelets, promotes platelet aggregation, vasoconstriction, contracts SM

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36
Q

PGI2

A

produced by endothelial cells, promotes vasodilation, inhibits platelet aggregation, inhibited by COX2 inhibitors

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37
Q

PGF2a

A

produced in most tissues, promotes vasoconstriction, contraction SM, uterine contraction

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38
Q

PGE2

A

produced in most tissues, promotes vasodilation, relaxes SM, used to induce labor

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39
Q

Leukotriene synthesis

A

Arachidonic acid to LTA4 and HPETE intermediate by 5-LOX, LTA4 can then be converted in mast cells and eosinophils to LTC, LTD, LTE that contain cysteinyl leukotrienes that form slow-reacting substance of anaphylaxis (SRS-A), and in neutrophils and monocytes to LTB that induces activation and adhesion of leukocytes on endothelium and chemoattractant for neutrophils

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40
Q

Palmitic vs palmitoleic which is sat vs unsat?

A

Palmitic is sat

Palmitoleic is unsat

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41
Q

Sphingomyelin is major component of?

A

Myelin sheath

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42
Q

PL-A are inhibited by what?

A

glucocorticoids

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43
Q

Gangliosides come from what?

A

Globoside + CMP-NANA

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44
Q

Sulfatides come from what?

A

Galactocerebrosides + PAPS

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45
Q

Difference between Aspirin and other NSAIDs

A

Aspirin binds irreversibly to COX1 (platelets) vs other NSAIDS are competitive inhibitors that are not perminant

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46
Q

Structural difference between prostiglandins/thromboxanes and leukotrienes

A

prostiglandins/thromboxaines have cyclic portion leukotrienes do not, longer 1/2 life

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47
Q

LTB4 function

A

increased chemotaxis of leukocytes, adhesion of WBCs, release of lysosomal enzymes, allergic reactions

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48
Q

formation of LTC4, D4, E4

A

made from LTA4 + glutathione, contain cysteine LTC4 most important for asthma symptomes, mediate SRS-A Slow reacting substance of anaphylaxis

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49
Q

Where are prostiglandins/thromboxanes and leukotrienes catabolized?

A

ALL catabolized in peroxisomes

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50
Q

Drugs that prevent asthma?

A

5-LOX inhibitors and antagonsits of CysLT1 receptor

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51
Q

Hydroxyl group at C3 of ring A?

A

Sterol

52
Q

How much Cholesterol comes from diet vs synthesis

A

30% diet, 70% synthesis

53
Q

Where do C’s from cholesterol come from?

A

Acetyl coA

54
Q

Synthesis of cholesterol?

A

1) 2 acetyl CoA = acetoacetylCoA
2) acetoacetylCoA + acetylCoA = HMGCoA (HMGCoA synthase)
3) HMGCoA reduces to mevalonate 5C (HMGCoA reductase rqs NADPH - RL and Reg Step!!!!!!! inhibited by statins)
4) IPP 5C (costs 3ATP)
5) GPP 10C
6) FPP 15C***
7) Squalene 30C (18ATP
8) Lanosterol - ring closure step by ER-assocaited squalene monooxygenase
9) cholesterol

55
Q

Isoforms of HMGCoA

A

cytosolic - precursor to cholesterol

MT - used to make ketone bodies

56
Q

What can FPP funnel into?

A

ubiquinone (CoQ) for ETC, dolichol (N-linked glycosylation, prenylated proteins (adding lipid tail)

57
Q

Transcriptional control of HMGCoA

A

SREBP-2 binds SCAP which binds Insig in ER membrane if sterols are high
SCAP senses sterol levels
when sterols are low, SCAP doesnt assoc with Insig and SREBP-2 SCAP goes to golgi, where S1P and S2P cleave SREBP-2 to active amino-terminal domain TF

58
Q

Genes upregulated by SREBP-2

A

HMGCoA reductase, LDL-R and PCSK9

59
Q

SREBP-1?

A

regulates FA synthesis in a similar way to SREBP-2

60
Q

Proteosomal degredation of HMGCoA

A

HMGCoA binds Insig in ER, ubiquitination and proteosomal degr.

61
Q

HMGCoA phos/dephos

A

HMGCoA-P (inactive) with high levels of AMPK (AMP), HMGCoA activated by phosphatase

62
Q

Hormone regulation of HMGCoA

A

Insulin - active, via increased phosphatase
Glucagon - inactive, via increase AMPK
Thyroxine - increased synthesis
Glucorticoids - decrease synthesis

63
Q

Rate limiting step of bile acid production? What follows?

A

addition of -OH to B ring by cholesterol-7-a-hydroxylase (phase 1)

followed by phase 2 addition of glycine/taurine and secreted into ilium of intestines

64
Q

Almost all bile salts are?

A

Reabsorbed (95%)

65
Q

17-a-hydroxylase deficiency

A

no androgens or cortisol produced, increase mineral corticoids (aldos) increase Na retention/edema, pts have female genitalia

66
Q

21-a-hydroxylase deficiency

A

no mineral corticoids (aldos), get salt wasting and no cortisol, make more androgens, masculinization of external genitalia in females

67
Q

Testosterone to estradiol?

A

enzyme: Aromatase (CYP 19)

68
Q

Order of lipoproteins for density, % lipid, % TG, %protein, electrophoresis?

A 
Density: CM, VLDL, IDL, LDL, HDL
%PL: CM, VLDL, IDL, LDL, HDL
% TG: HDL, LDL, IDL, VLDL, CM
% Protein: CM, VLDL, IDL, LDL, HDL
Electrophor (-) to (+): CM, LDL, VLDL, HDL
69
Q

CM have what?

A

ApoB48 vs ApoB100 in VLDL and LDL

70
Q

Microsomal triacylglycerol transfer protein (MTP)

A

loads ApoB48 with lipid in ER for CM
necessary for loading TG to VLDL/CM
w/o MTP deficient in fat sol vit: ADEK because couldnt package them for distribution

71
Q

Abetalipoproteinemia

A

No MTP, cant make CM or VLDL

72
Q

Synthesis of CM

A

MTP loads ApoB48 with lipid in ER, moves to golgi, secreted to lymphatics then blood at nascent CM stage, in plasma gets ApoC-II and ApoE from HDL, ApoCII activates LPL on endothelia cells of caps (except liver), removal of TGs, ApoCII leaves to give CM remnant, ApoE stays and is the ligand receptor in liver, where remnant is degraded

73
Q

Lifetime of CM?

A

few hrs

74
Q

VLDL

A

carries TG to perifery, apoB100, produced in liver, need MTP, when TAGs are removed becomes IDL, when ApoC and ApoE level, becomes LDL

75
Q

CETP

A

TAGs transferred from VLDL to HDL for cholesteryl esters from HDL to VLDL

76
Q

LDL

A

carries CE/C to periphery and liver, want <100 LDL-R recognizes ApoB100 and not B48, and have higher affinity for ApoE on IDLs than ApoB100, receptor binding leads to endocytosis, drop in pH to separate receptor and keep LDL, return receptor to surface

77
Q

ACAT

A

esterfiest cholesterol with FA for better storage

78
Q

PCSK9

A

blocks LDL-R recycling to cell surface

79
Q

FH

A

AD, AA - 4-6x normal, Aa - 2-3x normal serum cholesterol

80
Q

Statins vs sequenstrins

A

Statins inhibit HMGCoA reductase, sequestrins makes you excrete bile acids, so you make more by increasing HMGCoA and LDL-R, should be given together!

81
Q

HDL

A

formed by lipids + ApoA1 (produced by liver and intestines), removes cholesterol from periphery to liver, want >60

82
Q

ABCA1

A

releases cholesterol that is taken up by HDL

83
Q

LCAT

A

activates ApoA1 on HDL, more discoidal shape, binds to SR-B1 in liver

84
Q

Friedewald equation

A

LDL = Total - HDL - TG/5 (VLDL)

85
Q

risk factors for atherosclerosis

A

Sex (male), family Hx of atherosclerosis, hypertension, hypothyroidism, obesity (abdominal), increasing age, smoking, low physical activity, and a diet high in cholesterol and saturated fats

86
Q

Type 3 hyperlipidemia (dysbetapiloproteinemia)

A

xanthomas at palmar crease, floating LDL on electropho, receptor defective apoE

87
Q

Type 1 Hyperlipidemia

A

increased CM, LPL/apoCII deficiency, Eruptive xanthomas (lipid deposits in skin b/c Macrophages phago CM, local to butt, knees and extensor surface of arms)

88
Q

disease associated with ApoE4

A

late onset form of Alzheimers disease

89
Q

Type 2a Hyperlipidemia

A

increased LDL, polygenic or familial, xanthomas on extensor tendons of hands and achilles tendons and ocular lipid deposits - corneal arcus

90
Q

Type 5 Hyperlipidemia

A

increased VLDL and CM, LPL/apoCII deficiency

91
Q

Where are VLDL made? and then where do they go?

A

RER on liver and post translationally modified by adding CHO, combine with products of lipid syn, pass through secretory pathway to golgi

92
Q

Low Lecitin/sphingomyelin

A

Need surgactant therapy as DPCC is lacking that is needed to reduce surface tension to prevent collapse of alveli (fetus doesnt have DPCC, risk of respiratory distress syndrome)

93
Q

Tay-Sachs

A

accumulate GM2 because lacking hexoseamindase

94
Q

Neimann Pick

A

deficiency of sphingomylinase, cant degrade sphingomyline to cermide

95
Q

All sphingolipidoses are?

A

lysosomal storage diseases, AR defect in lysosomal enzyme

96
Q

Gauchers common symtomes

A

hepatomegalyy, splenomegaly, bruising, low platelets, anemia, osteopina, Ashkenzi jewish prevalent

97
Q

PGI2 has how many double bonds?

A

double bonds - cox# = 2

98
Q

Enzymes that play a role in asthma?

A

LTC4

99
Q

Ductus arteriosus is due to?

A

PGE2

100
Q

Can sterol nucleus be catabolized?

A

not degraded or catabolized, must be secreted, cant be broken down for energy/down to Acetyl coA

101
Q

-OH is on what ring in cholesterol

A

C3 of A ring

102
Q

unsaturated ring in cholesterol?

A

B/2nd ring, C5-6

103
Q

Fatty Acid syn occurs where?

A

Liver

104
Q

B-ox occurs where?

A

MT

105
Q

Cholesterol syn occurs where?

A

cytosol, but HMGCoA Reductase in SER

106
Q

No HMGCoA Reduct, downstream issues?

A

No FPP thereofre GPI anchors, ETC and RAS will be messed up, and no Vit D from 7-dehydrocholestrol, issues with skin, also steroid hormones syn and bile acids syn

107
Q

Mutation in Ras proto-oncgo

A

gain of function, uncontrolled cell growth

108
Q

LDL receptor is degraded

A

FALSE- recycled

109
Q

Normal Cholesterol, LDL, HDL, TG

A

60, <150

110
Q

What do statins affect?

A

Everything downstream of HMGCoA reductase

111
Q

Gain of function vs loss of function mutation in PCSK9

A

gain - increased degradation of LDL-R, more blood LDL

loss - increase LDL-R, decrease blood LDL, lower blood LDL, and risk of CHD

112
Q

Use of statins and sequenstrins together does what?

A

Forces liver to make bile acids from blood cholesterol, lowering [ ]

113
Q

PAPS relation to steroid hormones

A

PAPS sulfates steroid hormones, making them more water sol, less tightly bound to binding proteins and can be filtered out of blood by kidney

114
Q

Metformin acting on VLDL and TG?

A

increases AMPK so insulin cant upreg. SREBP1 in liver for FA syn, so cant make FA, lowers TG levels, given to Type 2 DM, since you cant make FA, lower VLDL levels

115
Q

Niacin

A

in high doses, can raise HDL, by inhibit HSL, reducing FAs coming to liver to make VLDLs

116
Q

Location of ApoB48 vs B100

A

intestines vs liver

117
Q

Binding affinity of ApoB48 and ApoE on CM

A

ApoE has higher binding affinity in liver, so CM are rapidly taken up by liver (LDL still you E over B100 because of binding affinity)

118
Q

Different between B48 and B100

A

B48 lacks LDL-R domain

119
Q

HDL

A

highest phospholipid and protein, lowest TG (same as LDL)

120
Q

CM

A

lowest phospholipid, cholesterol ester and protein, highest TG

121
Q

LDL

A

highest C/CE, same TG as HDL

122
Q

LPL coactivator?

A

ApoCII, mutations in either results in high CM, VLDLs

123
Q

LACT coactivator?

A

ApoA-1

124
Q

ABCA1 transporter is for what?

A

cholesterol efflux from peripheral cells, mutation would lead to increase cholesterol in body tissues and decrease HDL

125
Q

Foam cells and HDL?

A

HDL takes cholesterol out of them, reduced sclerotic plaques

Medical Biochemistry (5 decks)

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