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Jaspie - Biochemistry II > IV - Lipids > Flashcards

IV - Lipids Flashcards

1
Q

Lipids are hydro___, are soluble in _____ solvents and are compartmentalized to protect themselves for the _____ environment of cells.

A

hydrophobic, non-polar, watery cytoplasm

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2
Q

Functions of Lipids

A

major source of energy, provide hydrophobic barries, serve as coenzymes/regulators, hormones, mediators of inflammation

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3
Q

Phospholipids are _____ which enables formation of _____.

A

amphipathic, bilayers

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4
Q

Long chains of carboxylic acids

A

Fatty Acids

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5
Q

Fatty acids without double bonds

A

saturated

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6
Q

Fatty acids with one double bond

A

monounsaturated

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7
Q

Fatty acids with two or more double bonds

A

polyunsaturated

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8
Q

Fatty acids that increase risk for cardiovascular diseases

A

trans- and saturated FAs

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9
Q

Fatty acids that are protective against cardiovascular diseases

A

mono- and polyunsaturated FAs

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10
Q

Essential Fatty Acids

A

Linoleic Acid (Omega 6), Linolenic Acid (Omega 3)

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11
Q

Geometric isomer with the carbon moieties on the SAME side of the double bond

A

Cis fatty acid

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12
Q

Geometric isomer with the carbon moieties on the OPPOSITE side of the double bond

A

Trans fatty acid

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13
Q

Fluidity decreases with

A

increasing chain length (more C atoms, increasing saturation (less double bonds)

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14
Q

Becomes essential if linoleic acid is deficient

A

Arachidonic Acid

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15
Q

Decrease risk for cardiovascular disease by lowering thromboxane production reducing the tendency of platelts to aggregate

A

Omega Fatty Acids

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16
Q

FA Activation

A

FA + CoA + ATP → Fatty acyl-CoA + AMP + PPi

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17
Q

FA Activation: Enzyme

A

Fatty acyl-CoA synthetase

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18
Q

FA Activation: Cofactor

A

Panthotenic Acid - B5

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19
Q

FA Activation: Energy Use

A

2 ATP equivalents

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20
Q

Formation of palmitate (16:0)

A

Lipogenesis, FA Synthesis

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21
Q

Lipogenesis: Location

A

Cytosol, major: liver and lactating mammary glands, minor: adipose

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22
Q

Lipogenesis: Substrates

A

1 acetyl CoA, 7 malonyl CoA, 14 NADPH, ATP

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23
Q

Lipogenesis: Product

A

Palmitate

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24
Q

Lipogenesis: Rate-Limiting Step

A

acetyl CoA + ATP → malonyl CoA

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25
Q

Lipogenesis: Rate-Limiting Enzyme

A

Acetyl CoA carboxylase (ACC)

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26
Q

Acetyl CoA carboxylase (ACC) requires

A

Biotin

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27
Q

Important Steps in Lipogenesis

A

synthesis of cytoplasmic acetyl CoA, carboxylation of acetyl CoA to malonyl CoA, assembly of palmitate

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28
Q

Lipogenesis: Step 1

A

synthesis of cytoplasmic acetyl CoA - transfer of acetyl CoA from the mitochondria to the cytoplasm through a CITRATE shuttle in the well-fed state

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29
Q

Lipogenesis: Step 2

A

acetyl CoA + ATP → malonyl CoA (acetyl CoA carboxylase) - rate-limiting step

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30
Q

Acetyl CoA carboxylase cofactor

A

Biotin

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31
Q

Acetyl CoA carboxylase activators

A

insulin, citrate

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32
Q

Lipogenesis: Step 3

A

assembly of palmitate (fatty acid synthase)

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33
Q

A multienzyme complex that has an acyl carrier protein (ACP) with panthoenic acid as a cofactor

A

fatty acid synthase

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34
Q

Fatty acid synthase cofactor

A

Pantothenic Acid (B5)

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35
Q

Synthesizes palmitate from 1 acetyl CoA + 7 malonyl CoA, uses NADPH as a reducing agent

A

fatty acid synthase

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36
Q

Sequence of Palmitate Assembly

A

condensation → reduction → dehydration → reduction

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37
Q

Lipogenesis: Activators

A

citrate (allosteric), insulin (by dephosphorylation and induction of enzyme synthesis)

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38
Q

Lipogenesis: Inhibitors

A

fatty acyl-CoA (allosteric), glucagon and epinephrine (by phosphorylation and repression of enzyme synthesis)

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39
Q

FAs further elongate in _____ and _____.

A

SER, mitochondria

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40
Q

Lipogenesis is limited to

A

16C Palmitate

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41
Q

SER and mitochondria form 22C and 24C FAs for

A

Sphingolipids

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42
Q

FAs are desaturated in the ___ through mixed function oxidases (cytochrome _).

A

SER, cytochrome bs

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43
Q

The body can generate double bonds on FA’s but not beyond

A

Carbon 9

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44
Q

Short/Medium-chain FAs are bound to _____ until they are taken up by cells.

A

Albumin

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45
Q

Long-chain FAs (>12C) are transported in the bloodstream through _____.

A

Lipoproteins

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46
Q

FAs are converted to _____ before being stored as triacyglycerols

A

fatty acyl-CoA (active form)

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47
Q

Ester of trihydric glycerol and fatty acids, main storage form of FA, slightly soluble in water

A

Triacylglycerol

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48
Q

Coalesce within adipocytes to form oily droplets that are the major energy reserves of the body

A

Triacylglycerol

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49
Q

Triacylglycerol Synthesis

A

glycerol 3-P + 3FA → triglyceride

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50
Q

Triacylglycerol Synthesis: Location

A

liver, adipose

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51
Q

Source of glycerol 3-P in the liver & adipose

A

DHAP from glycolysis (glycerol 3-P dehydrogenase)

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52
Q

Source of glycerol 3-P in the liver only

A

phosphorylation of free glycerol (glycerol kinase)

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53
Q

Mobilization of Stored Fats

A

triglyceride → glycerol 3-P + 3FA (hormone-sensitive lipase + monoacylglycerol lipase)

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54
Q

Hydrolyzes TAGs yielding 2-monoacylglycerol + 2FA

A

Hormone-Sensitive Lipase

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55
Q

Hormone-Sensitive Lipase activators

A

glucagon, epinephrine, cortisol

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56
Q

Hormone-Sensitive Lipase inhibitor

A

insulin

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57
Q

Hormone-Sensitive Lipase can only release fatty acids from ___ and ___ of the TAG stored in fat

A

Carbon 1, Carbon 3

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58
Q

2-Monoacylglycerol → FA + Glycerol

A

Monoacylglycerol lipase

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59
Q

Removal of acetyl CoA fragments from the ends of FAs

A

Lipolysis, β-Oxidation of FAs

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60
Q

Lipolysis: Location

A

Mitochondria of all cells except neurons, RBCs, testis, kidney medulla

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61
Q

FA Activation: Location

A

Cytosol

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62
Q

Lipolysis: Substrates

A

palmitate, 7 NAD, 7 FAD, ATP

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63
Q

Lipolysis: Products

A

8 acetyl CoA, 7 FADH2, 7 NADH

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64
Q

Lipolysis: Rate-Limiting Step

A

fatty acyl CoA + carnitine → fatty acyl carnitine + CoA

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65
Q

Lipolysis: Rate-Limiting Enzyme

A

Carnitine acyltransferase I (carnitine palmitoyl transferase I)

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66
Q

Long-chain FAs have _ carbons and must be shuttles through the inner mitochondrial membrane via _____

A

> 12C, carnitine shuttle

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67
Q

Short-chain FAs have ___ carbons

A

2-4C

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68
Q

Medium-chain FAS have ___ carbons

A

6-12

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69
Q

fatty acyl carnitine + CoA → fatty acyl CoA + carnitine

A

Carnitine acyltransferase II - inside mitochondrial matrix

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70
Q

Catalyzed by carnitine acyltransferase II

A

fatty acyl carnitine + CoA → fatty acyl CoA + carnitine

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71
Q

Sequence of Lipolysis

A

oxidation → hydration → oxidation → thiolysis

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72
Q

FAs with an odd number of carbons will yield

A

acetyl CoA and propionyl CoA

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73
Q

Propionyl CoA is converted to _____.

A

succinyl CoA - a TCA Cycle intermediate

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74
Q

Catalyzed by propionyl CoA carboxylase

A

propionyl CoA + CO2 + ATP → methylmalonyl CoA + ADP + Pi

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75
Q

propionyl CoA + CO2 + ATP → methylmalonyl CoA + ADP + Pi

A

propionyl CoA carboxylase

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76
Q

Propionyl CoA carboxylase requires

A

Biotin

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77
Q

Catalyzed by methylmalonyl CoA mutase

A

methylmalonyl CoA → succinylt CoA

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78
Q

methylmalonyl CoA → succinylt CoA

A

methylmalonyl CoA mutase

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79
Q

Methylmalonyl CoA mutase requires

A

Vitamin B12

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80
Q

Oxidizes very long chain FAs (20C, 22C)

A

Peroxisomes

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81
Q

Oxidizes unsaturated FAs

A

3,2-enoyl CoA isomerase

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82
Q

Lipolysis yields __ ATP

A

129 ATP

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83
Q

Carnitine Palmitoyl Transferase I inhibitor

A

malonyl CoA

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84
Q

Indirectly inhibits lipolysis by activation acetyl CoA carboxylase and increasing malonyl CoA in the cytoplasm

A

Insulin

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85
Q

Alcohol leady to fat accumulation in the liver called _____ which ultimately leads to _____.

A

steatosis (fatty liver), cirrhosis

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86
Q

_____ eats up NAD to decrease _____ in the liver.

A

Alcohol dehydrogenase, lipolysis

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87
Q

Can occur in the newborn and manifest as hypoglcemia from impaired FA oxidation and muscle weakness from lipid accumulation

A

Carnitine Deficiency

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88
Q

Affects only the liver resulting in reduces FA oxidation and ketogenesis with hypoglycemia

A

Carnitine Palmitoyl Transferase I Deficiency

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89
Q

Affects skeletal muscle and, when severe, the liver

A

Carnitine Palmitoyl Transferase II Deficiency

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90
Q

Decreased FA oxidation, profound hypoglycemia during fasting due to lack of ATP for gluconeogenesis, can cause Sudden Infant Death Syndrome (SIDS)

A

Medium-Chain Fatty Acyl-CoA Dehydrogenase (MCAD) Deficiency

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91
Q

Medium-Chain Fatty Acyl-CoA Dehydrogenase (MCAD) Deficiency treatment and prevention

A

treatment: IV glucose, prevention: frequent feeding, high carbohydrate and low fat diet

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92
Q

Caused by eating unripe fruit of the akee tree which contains hypoglycin, a toxin that inactivates MCAD and SCAD leading to hypoglycemia

A

Jamaican Vomiting Sickness

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93
Q

Rare neurologic disorder due to a defect that causes accumulation of phytanic acid from plants which blocks lipolysis, causes neurologic symptoms due to improper myelinization

A

Refsum’s Disease

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94
Q

Cerebrohepatorenal syndrome from the absence of peroxisomes, liver dysfunction with jaundice, mental retardation, weakness, hypotonia, craniofacial dysmorphism

A

Zellweger’s Syndrome

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95
Q

Defect in the peroxisomal activation of VLCFA leads to accumulation of VLCFA leading to apathy, behavioral change, visual loss, spasticity, ataxia and death

A

X-linked Adrenoleukodystrophy

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96
Q

Converts acetyl CoA to ketone bodies

A

Ketogenesis

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97
Q

Ketogenesis: Location

A

liver mitochondria

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98
Q

Ketogenesis: Substrate

A

Acetyl CoA

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99
Q

Ketogenesis: Products

A

Ketone Bodies (polar): Acetoacetate & β-hydroxybutyrate (can be used as fuel), Acetone

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100
Q

Ketogenesis: Rate-Limiting Step

A

acetoacetyl CoA + acetyl CoA → HMG CoA

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101
Q

Ketogenesis: Rate-Limiting Enzyme

A

HMG CoA Synthase

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102
Q

Ketolysis

A

β-hydroxybutyrate → Acetoacetate → Acetyl CoA

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103
Q

β-hydroxybutyrate → Acetoacetate → Acetyl CoA

A

Ketolysis

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104
Q

Ketone bodies can serve as fuel for _____ tissues especially during fasting.

A

extrahepatic

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105
Q

Periheral tissues with mitochondria that can oxidize ketone bodies

A

skeletal muscle, renal cortex, brain (fasting > 2 weeks)

106
Q

The liver cannot convert acetoacetate to acetyl CoA since it lacks

A

succinyl CoA acetoacetyl CoA transferase (thiophorase)

107
Q

In prolonged starvation and _____, oxaloacetate is depleted for gluconeogenesis.

A

diabetic ketoacidosis

108
Q

In alcoholism, excess NADH shunts oxaloacetate to _____.

A

malate

109
Q

Seen in uncontrolled DM, starvation and chronic alcoholics

A

Ketoacidosis

110
Q

Dehydration, CNS depression, coma, potassium depletion, metabolic acidosis, sweet/fruity odor of breath

A

Ketoacidosis

111
Q

A very hydrophobic steroid alcohol with 27 carbons

A

Cholesterol

112
Q

Cholesterol is a precursor/raw material for

A

cell membranes, vitamin D, adrenal hormones, sex hormones, bile salts

113
Q

Cholesterol has _ fused hydrocarbon rings with an _-membered branched hydrocarbon chain attached to the _ ring.

A

4 fused hydrocarbon rings, 8-membered branched hydrocarbon chain, D ring

114
Q

Cholesterol has a single ___ group located at the carbon _ of the _ ring to which FA can be attached to form cholesterol esters.

A

single hydroxyl group, carbon 3, A ring

115
Q

Cholesterol Synthesis: Location

A

SER and cytosol, all cells (mainly in the liver and intestines)

116
Q

Cholesterol Synthesis: Substrates

A

acetyl CoA, NADPH, ATP

117
Q

Cholesterol Synthesis: Products

A

Lanosterol → Cholesterol

118
Q

Cholesterol Synthesis: Rate-Limiting Step

A

HMG CoA → Mevalonate

119
Q

Cholesterol Synthesis: Rate-Limiting Enzyme

A

HMG CoA Reductase

120
Q

Drugs used for the treatment of hypercholesterolemia to reduce the risk for cardiovascular disease, competitive inhibitors of HMG CoA reductase

A

Statins

121
Q

Important Steps in Cholesterol Synthesis

A

biosynthesis of mevalonate, formation of isoprenoid units (isopentenyl diphosphate), 6 isoprenoid units form isoprene, formation of lanosterol, formation of cholesterol

122
Q

Cholesterol synthesis intermediate used for synthesis of coenzyme Q for the ETC, synthesis of dolichol pyrophosphate (cofactor in N-linked glycosylation of proteins in the RER), prenylation of proteins that need to be held in the cell membrane by a lipid tail

A

Farnesyl pyrophosphate

123
Q

HMG CoA reductase inhibitors

A

glucagon, cortisol, epinephrine, phosphorylation, high cholesterol (limits the transcription factor SREBP - Sterol Regulatory Element-Binding Protein)

124
Q

Cholesterol rings _____ be metabolized in humans.

A

cannot

125
Q

Cholesterol is eliminated though _____ the secreted into the _____.

A

bile salts, bile

126
Q

_____ can reduce cholesterol to _____ and _____.

A

Intestinal bacteria, coprostanol, cholestanol,

127
Q

Synthesized in the liver from cholesterol

A

bile acids

128
Q

Bile Acid Synthesis: Rate-Limiting Step

A

cholesterol → cholic acid

129
Q

Bile Acid Synthesis: Rate-Limiting Enzyme

A

cholesterol-7-α-hydroxylase

130
Q

Cholesterol-7-α-hydroxylase activator

A

cholesterol

131
Q

Cholesterol-7-α-hydroxylase inhibitor

A

bile acids

132
Q

Primary Bile Acids

A

cholic acid, chenodeoxycholic acid

133
Q

Bile acids conjugated with either glycine or taurine

A

bile salts

134
Q

Emulsify lipids in the intestines, provide the only significant mechanism for cholesterol excretion, both as a metabolic product of cholesterol and as a solubilizer of cholesterol in bile

A

bile salts

135
Q

Secondary Bile Acids

A

deoxycholic acid, lithocholic acid

136
Q

95% of excreted bile is reabsorbed in the _____ through the _____.

A

terminal ileum, enterohepatic circulation (5% excreted in feces = amount liver must make)

137
Q

Mineralocorticoids

A

Zona Glomerulosa

138
Q

Glucocorticoids

A

Zona Fasciculata

139
Q

Sex Hormones

A

Zona Reticularis

140
Q

Zona Glomerulosa

A

Mineralocorticoids

141
Q

Zona Fasciculata

A

Glucocorticoids

142
Q

Zona Reticularis

A

Sex Hormones

143
Q

Steroid Hormone Synthesis: Location

A

SER of adrenal cortex, ovaries, testes, placenta

144
Q

Steroid Hormone Synthesis: Substrates

A

cholesterol, pregnenolone (mother enzyme)

145
Q

Steroid Hormone Synthesis: Rate-Limiting Step

A

cholesterol → pregnenolone

146
Q

Steroid Hormone Synthesis: Rate-Limiting Enzyme

A

desmolase

147
Q

Desmolase inhibitor

A

aminogluthetimide

148
Q

Lingual lipase and gastric lipase are both ___ labile hence they are destroyed in the _____. This is important in _____ who do not have very acidic stomachs.

A

acid labile, stomach, neonates

149
Q

In the gut, lipid components become enclosed in _____ then absorbed into _____.

A

micelles, enterocytes

150
Q

Mixed micelles contain the products of lipid digestion by _____ and _____.

A

lipase, cholesteryl esterase

151
Q

Secreted to lymphatics, reach the capillaries of skeletal muscle and adipose where TGs are broken into FA and glycerol via lipoprotein lipase

A

Chylomicrons

152
Q

Directly enter adjacent muscle cells or adipocytes or may be transported in blood bound to albumin

A

Free Fatty Acids

153
Q

Converted to DHAP then enters glycolysis or gluconeogenesis

A

Glycerol

154
Q

Pancreatic Lipase: Substrate

A

TAG from diet

155
Q

Pancreatic Lipase: Product

A

2-monoacylglycerol (MAG)

156
Q

Pancreatic Lipase: Activator

A

trypsin

157
Q

Lipoprotin Lipase: Substrate

A

TAG from chylomicrons and VLDL

158
Q

Lipoprotin Lipase: Product

A

free glycerol

159
Q

Lipoprotin Lipase: Activator

A

insulin

160
Q

Hormone-Sensitive Lipase: Substrate

A

TAG from adipose

161
Q

Hormone-Sensitive Lipase: Product

A

2-monoacylglycerol (MAG)

162
Q

Hormone-Sensitive Lipase: Activator

A

glucagon

163
Q

Manifests as steatorrhea (greasy stools), deficiency in fat-soluble vitamins and essential fatty acids

A

Lipid Malabsorption

164
Q

Lipid Malabsorption causes

A

liver disease (not enough bile), pancreatic disease (enzyme deficiencies), cholelithiasis (bile obstruction), shortened bowel (decreased absorption time), intestinal mucosal defects

165
Q

Spherical macromolecular complexes composed of neutral lipid core surrounded by a shell of amphipathic apolipoproteins, phospholiid and nonesterified cholesterol

A

Plasma Lipoproteins

166
Q

Keep their component lipids soluble as they transport them in plasma, provides an efficient mechanism for transporting their lipid contents to and from the tissues

A

Plasma Lipoproteins

167
Q

Plasma Lipoproteins: Highest in Protein

A

HDL (50%)

168
Q

Plasma Lipoproteins: Highest in TG

A

Chylomicrons (88%)

169
Q

Plasma Lipoproteins: Highest in Cholesterol

A

LDL (10%)

170
Q

Plasma Lipoproteins: Highest in Cholesterol Esters

A

LDL (48%)

171
Q

HIghest component of VLDL

A

TG (56%)

172
Q

HIghest component of IDL

A

Cholesterol Esters (34%)

173
Q

Transports dietary TG and cholesterol from the intestines to the tissues

A

Chylomicrons

174
Q

Chylomicron Apoproteins

A

Apo B-48 (secreted by epithellial cells), Apo C-11 (activates lipoprotein lipase), Apo E (uptake by the liver)

175
Q

Transports triglycerides from the liver to the tissues

A

VLDL

176
Q

VLDL Apoproteins

A

Apo B-100 (secreted by the liver), Apo C-11 (activates lipoprotein lipase), Apo E (uptake by the liver)

177
Q

Picks up cholesterol from HDL to become LDL

A

IDL

178
Q

IDL Apoprotein

A

Apo E (uptake by the liver)

179
Q

Delivers cholesterol into cells

A

Apo B-100 (uptake by the liver and other tissues via LDL receptor)

180
Q

Picks up cholesterol accumulation in blood vessels (reverse cholesterol transport)

A

HDL

181
Q

Delivers cholesterol to liver and steroidogenic tissues via scavenger receptor (SR-B1)

A

HDL

182
Q

Shuttles Apo C-11 and Apo E in blood

A

HDL

183
Q

HDL Apoprotein

A

Apo A-1 (activates lecithin cholesterol acyltransferase or LCAT to produce cholesterol esters)

184
Q

Activates LCAT

A

Apo A-1

185
Q

Binds to LDL and VLDL receptors

A

Apo B-100

186
Q

Cofactor for lipoprotein lipase, shuttled by HDLs

A

Apo C-11

187
Q

Chylomicron assembly and secretion

A

Apo B-48

188
Q

Mediates uptake of chylomicron remnant

A

Apo E

189
Q

Deposition of cholesterol and cholesteryl esters in the artery walls especially oxidized LDL, more sever in DM, lipid nephrosis and hypothyroidism

A

Atherosclerosis

190
Q

Oxidized LDLs can cause endothelial damage which predisposes to _____.

A

atherosclerosis

191
Q

Type I Familial Dyslipidemia

A

Hyperchylomicronemia

192
Q

Type II Familial Dyslipidemia

A

Hypercholesterolemia

193
Q

Type III Familial Dyslipidemia

A

Dysbetalipoproteinemia

194
Q

Type IV Familial Dyslipidemia

A

Hypertriglyceridemia

195
Q

Hyperchylomicronemia: Deficiency

A

Lipoprotein Lipase: high chylomicrons and VLDL, low LDL and HDL

196
Q

Xanthomas and pancreatitis without increased risk of coronary heart disease

A

Hyperchylomicronemia

197
Q

Hypercholesterolemia: Deficiency

A

LDL Receptors: high LDL

198
Q

Xanthomas and xanthelasmas with increased risk of atherosclerosis and coronary heart disease

A

Hypercholesterolemia

199
Q

Dysbetalipoproteinemia: Deficiency

A

Apo E: high remnants of chylomicrons and VLDL

200
Q

Increased risk of atherosclerosis and coronary heart disease without xanthomas

A

Dysbetalipoproteinemia

201
Q

Hypertriglyceridemia: Pathogenesis

A

increased VLDL productin

202
Q

Triad: coronary artery disease, T2DM, obesity

A

Hypertriglyceridemia

203
Q

Apo B-48 and Apo B-100 deficiency

A

Abetalipoproteinemia: no chylomicrons/VLDL/LDL

204
Q

Intestinal malabsorption with accumulation of lipids in the intestine and liver

A

Abetalipoproteinemia

205
Q

Apo A-1 deficiency

A

Familial α-Lipoprotein Deficiency (Tangier’s/Fisheye Disease): no HDL

206
Q

High triglycerides, premature atherosclerosis, neuropathy, enlarged yellow-orange tonsils

A

Familial α-Lipoprotein Deficiency (Tangier’s/Fisheye Disease)

207
Q

Increased HDL production

A

Familial Hyper-α-Lipoproteinemia: associated with benefits to health and longevity

208
Q

High Lipoprotein A

A

Familial Lipoprotein A Excess

209
Q

Early atherosclerosis and thrombosis

A

Familial Lipoprotein A Excess

210
Q

Phospholipids are _____ compounds composed of _____, _____ and _____.

A

amphipathic, alcohol, diacylglycerol or sphingosine backbone, phosphodiester bond

211
Q

Predominant lipids of cell membranes, degraded by phospholipases

A

Phospholipids

212
Q

Most abundant phispholipids

A

Phosphatidylcholine

213
Q

Large proportion of body’s store of choline, important in nervous transmission (acetylcholine), store of labile methyl groups

A

Phosphatidylcholine

214
Q

Plays a role in apoptosis, also found in cell membranes

A

Phosphatidylethanolamine (cephalin) and Phosphatidylserine

215
Q

Major component of lung surfactant, deficiency leads to RDS

A

Dipalmitoylphosphatidylcholine (DPPC) or Dipalmitoyllecithin

216
Q

Reservoir for arachidonic acid in membranes, source of 2nd messengers

A

Phosphatidylinositol

217
Q

2 molecules of phosphatidic acid esterified through their phosphate groups to an additional molecule of glycerol

A

Cardiolipin

218
Q

Found only in mitochondria and is essential for mitochondrial function

A

Cardiolipin

219
Q

Deficiency or defect can cause mitochondrial dysfunction in aging and in heart failure, hypothyroidism and Barth syndrome (cardioskeletal myopathy)

A

Cardiolipin

220
Q

_____ is antigenic. It reacts with antibodies produced against Treponema pallidum (syphilis). One of the non-treponemal tests for syphilis is an anti-_____ test.

A

Cardiolipin

221
Q

Part of the glycocalyx located on the outer layer of the cell membrane and functions in cell recognition and adhesion, found in high concentrations in nervous tissue

A

Glycolipids

222
Q

Ceramide

A

Sphingosine + Fatty Acid

223
Q

Cerebroside

A

Ceramide + Glucose or Galactose

224
Q

Globoside

A

Ceramide + Oligosaccharide

225
Q

Ganglioside

A

Ceramide + N-acetylneuramic Acid

226
Q

Sulfatides

A

Ceramide + Sulfatide Galactose

227
Q

Sphingosine + Fatty Acid

A

Ceramide

228
Q

Ceramide + Glucose or Galactose

A

Cerebroside

229
Q

Ceramide + Oligosaccharide

A

Globoside

230
Q

Ceramide + N-acetylneuramic Acid

A

Ganglioside

231
Q

Ceramide + Sulfatide Galactose

A

Sulfatides

232
Q

The only significant sphingophospholipid in humans, an important constituent of the myelin sheath in nerves

A

Sphingomyelin

233
Q

Deficiency in phospholipids and sphingolipids from white matter resulting in increased CSF phospholipids

A

Demyelinating Diseases

234
Q

Lipid storage diseases often manifested in childhood, lipid synthesis is normal, lipid degradation in lysosomes is abnormal

A

Sphingolipidoses

235
Q

Complex lipids accumulate in cells, neurodegeneration, enzyme deficiency is similar in all tissues

A

Sphingolipidoses

236
Q

Tay-Sach’s Disease: Deficiency

A

Hexosaminidase A

237
Q

Tay-Sach’s Disease: Accumulating Lipid

A

Ganglioside

238
Q

Tay-Sach’s Disease: Findings

A

cherry red macula, mental retardation, hypotonia

239
Q

Hexosaminidase A Deficiency

A

Tay-Sach’s Disease

240
Q

Fabry’s Disease: Deficiency

A

α-Galactosidase

241
Q

Fabry’s Disease: Accumulating Lipid

A

Globotriaosylceramide

242
Q

Fabry’s Disease: Findings

A

3 Rs: Recessive (X-linked), Rash, Renal failure

243
Q

α-Galactosidase Deficiency

A

Fabry’s Disease

244
Q

Gaucher’s Disease: Deficiency

A

β-Glucosidase

245
Q

Gaucher’s Disease: Accumulating Lipid

A

Glucosylceramide

246
Q

Gaucher’s Disease: Findings

A

hepatosplenomegaly, erosion of long bones, Gaucher cells: accumulation of fibrils in macrophage, crumpled tissue paper

247
Q

β-Glucosidase Deficiency

A

Gaucher’s Disease

248
Q

Niemann-Pick Disease: Deficiency

A

Sphingomyelinase

249
Q

Niemann-Pick Disease: Accumulating Lipid

A

Sphingomyelin

250
Q

Niemann-Pick Disease: Findings

A

hepatosplenomegaly, foam cells: small vacuoles, lipid-laden macrophages, sea-blue histiocytes

251
Q

Potents compunds that elicit a wide range of physiologic and pathologic responses

A

Eicosanoids

252
Q

3 Main Kinds of Eicosanoids

A

prostaglandin, thromboxane, leukotriene

253
Q

Eicosanoids: Dietary Precursor

A

Linoleic Acid

254
Q

Eicosanoids: Immediate Precursor

A

Arachidonic Acid

255
Q

Released from membrane lipids by phospholipase A2

A

Eicosanoids

256
Q

Synthesized by platelets, causes vasoconstriction and platelet aggregation

A

Thromboxane (TXA2)

257
Q

Produced by blood vessel walls, inhibitors of platelet aggregation

A

Prostacyclin (PGI2)

258
Q

mixture of leukotrienes C4, D4 and E4, potent bronchoconstrictors

A

Slow-Reacting Substances of Anaphylaxis (SRS-A)

259
Q

Slow-Reacting Substances of Anaphylaxis (SRS-A)

A

Leukotrienes C4, D4 and E4

260
Q

All sphingolipidoses are _____ recessive except _____.

A

autosomal recessive (sphingolipidoses), Fabry’s Disease (X-linked recessive)

Jaspie - Biochemistry II (15 decks)

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