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Biochemistry MBBS > Lipids > Flashcards

Lipids Flashcards

1
Q

Eg of derived lipids

A

Fatty acids, glycerol, fat soluble vitamins,ketone bodies,…

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2
Q

Short chain fatty acids

A

C2- C6

Seen in vinegar and butter

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3
Q

Medium chain Fatty acids

A

C8 - C14
Lauric acid C12
Myristic acid C14

Present in coconut milk, oil

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4
Q

Very long chain fatty acids- part of long chain fatty acids

A

> C 20-22

Animal fat

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5
Q

Unsaturated MUFA

A

Palmitoleic acid C16
Oleic acid C18
Elaidic acid C18

Mustard oil/ rapeseed oil

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6
Q

PUFA

A

Linoleic acid 18C and 2=
Alpha linolenic acid 18 C 3=
Gamma Linolenic acid (GLA) 18 C 3=
Arachidonic acid 20C 4=
Timnodonic acid (Eicosa Pentanenoic acid) 20C 5=
Cervonic acid (Docosa Hexaenoic acid DHA) 22C 6=

Safflower oil (sunflower oil)
Least in coconut oil
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7
Q

List of various PUFA present in ___ oil

A

Linoleic acid - safflower oil
Alpha linolenic acid - flax seed oil
Gamma linoleic acid - oil of primrose/Borage oil
Arachidonic acid - animal fat
Timnodonic acid and cervonic acid - fish oil, breast milk

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8
Q

EFA and semi essential FA

A

Linoleic acids
Alpha linolenic acid

Semi essential FA
Arachidonic acid
Gamma linolenic acid

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9
Q

Delta numbering and omega numbering

A

In delta numbering the 1st carbon is the carboxylic carbon

In omega numbering the first carbon is at the end

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10
Q

Omega 3 FA

A

ATC
Alpha linolenic acid
Timnodonic acid
Cervonic acid

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11
Q

Omega 6 FA

A
  1. GLA
  2. Linoleic acid
  3. Arachidonic acid
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12
Q

Omega 3 and 6

A

Linoleic acid (indirectly) and Arachidonic acid (omega-6) leads to PGs and leukotrienes.
Thus omega 6 increases inflammation and thrombosis.
Omega 3 decreases inflammation, CV risk, ADHD, Rheumatoid arthritis, Azheilmers disease and cancers

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13
Q

Cervonic acid or DHA

A

Omega 3
Needed for infant and foetal brain development and retina development.
Decreased HA leads to Retinitis pigmentosa
It can pass transplacentally.

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14
Q

Cis form of FA

A

Increases the fluidity of the membrane and decreases the melting temperature

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15
Q

Sources of trans fatty acids

A
  1. Hardening of fat / partial hydrogenation to vanaspathi

2. Reheating of food

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16
Q

Ill efects of trans fatty acids

A

Increases:

  1. LDL
  2. Triglycerides
  3. Atherosclerosis
  4. Rigidity of membrane, becoming insensitive to receptors like insulin receptor
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17
Q

Maximum level of trans fatty acid that can be consumed

A

2-7 gm/day

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18
Q

Classification of phospholipids

A

Glycerolphospholipids and sphingophospholipids
Glycerophospholipids are classified into :
1. nitrogen containing (lecithin, cephalin, phosphatidyl serine)
2. non nitrogen containing (phosphatidyl glycerol, cardiolipin, phosphatidyl inositol)
3. unclassified (phosphatidic acid, ether lipids).

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19
Q

Phosphatidic acid

A

Diacyl glycerol + phosphate (no base)

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20
Q

Lecithin

A

Phosphatidyl choline (DPPC - DiPalmitoyl …)

  1. Most abundant phospholipid in cell membrane, lung surfactant.
  2. Store house of choline
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21
Q

Cephalin

A

Phospatidyl ethanolamine

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22
Q

Phosphatidyl serine

A

Phosphatidic acid + serine
Mediator of apoptosis
Usually present in the inner surface of plasma membrane but during apoptosis it is present in the outer surface for phagocytosis

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23
Q

Phosphatidyl inositol

A

Phosphatidic acid + inositol
Present in cell membrane
Mediator/ source of secondary messengers (as PIP2 Phosphatidyl inositol 4,5 bisphosphate)

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24
Q

Cardiolipin

A

Diphosphatidyl glycerol
No base
1. Isolated first from cardiac muscle
2. Only antigenic phospholipid (cross react with antibodies formed against Treponema pallidum)
Hence false +ve in the test for syphillis
3. Present in inner mitochondrial membrane
a)Cardio skeletal myopathy (Barth syndrome)
b)Aging, hypothyroidism, heart failure,…

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25
Q

Ether lipids

A

Eg plasmalogen, PAF

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26
Q

Plasmalogen

A

Glycerol + ( unsaturated alkyl , acyl, phosphate-ethanolamine)

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27
Q

PAF

A

Glycerol + (saturated alkyl, acetyl, phosphate-ethanolamine)

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28
Q

Sphingosine

A 
3 carbons
1. -OH
2. -NH2
3. -Fatty acid
Amino alcohol
Derived from serine+palmitic acid
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29
Q

The one sphingolipid

A

Sphingomyelin
(Sphingosine + an FA attaching to the -NH2) = ceramide
Ceramide + -PO4-nitrogenous base(choline) = sphingomyelin

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30
Q

Significance of sphingomyelin

A
  1. Cell membrane
  2. Specialised structure like lipid rafts
  3. Myelin sheath, white matter
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31
Q

Glycolipids

A

Also called glycosphingolipids

Non phosphorylated sphingophospholipids

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32
Q

Cerebroside

A

Ceremide (sphingosine+FA) + monosaccharide = cerebroside or glycolipid

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33
Q

Glucocerebroside

A

Non neural tissues

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34
Q

Galactocerebroside

A

Neural tissue

FA of the ceramide in it is cerebronic acid (24C)

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35
Q

Globoside

A

Ceramide (sphingosine+FA) + oligosaccharide = globoside
Eg lactosyl ceramide
Globotriocyl ceramide

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36
Q

Ganglioside

A

Ceramide (sphingosine+FA) +oligosaccharide containing NANA

N Acetyl Neuraminic Acid is a sialic acid residue i.e, a monosaccharide with 9C

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37
Q

Nomenclature of gangliosides

A

GMn
G-ganglioside
M-monosialo containing
n-number assigned based on chromatography

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38
Q

GM1

A

Ganglioside that acts as a receptor for cholera toxin in human intestine

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39
Q

GM3

A

Simplest ganglioside

Ceramide + Gal-Glu-NANA

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40
Q

Sphingolipidosis

A

Defect in degradation of sphingosin containing compounds like sphingophospholipids and glycolipids.
Accumulation of lipid substrates containing Ceramide in lysosome

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41
Q

GM1 Gangliosidoses

A

GM1 ganglioside is converted to GM2 ganglioside by beta galactosidase

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42
Q

Skeletal deformities of GM1 gangliosidosis

A

Low set ears
Long philtrum
Depressed nasal bridge
Frontal bossing

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43
Q

Clinical features of GM1 gangliosidosis

A
  1. Hepatosplenomegaly
  2. Angiokeratoma
  3. Developmental delay
  4. Blindness
  5. Deafness
  6. Cherry red spot in the macula
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44
Q

GM2 gangliosidosis

A

GM2 is converted to GM3 by beta hexosaminidase

Tay Sachs disease or Sandhoffs disease

45
Q

Tay Sachs disease

Sandhoffs disease

A

Beta hexosaminidase A (ab) Or defect in alpha subunit

Both beta hexosaminidase A and B (bb)
Or defect in beta subunit

46
Q

Tay Sachs disease

A
  1. Developmental delay
  2. Neurological defect
  3. Hyperacusis (increased startle reflex)
  4. Cherry red spot
47
Q

Sandhoffs disease clinical features in addition to Tay Sachs disease

A
  1. Hepatosplenomegaly

2. Cardiac abnormalities

48
Q

Krabbes disease

A

Galactocerebroside is converted to ceramide by beta galactocerebroside/ beta galactosidase (same name as GM1 gangliosidosis)

Increased galactocerebroside

49
Q

Clinical features of Globoid cell leukodystrophy

A

Krabbe’s disease

Severe neurological deficits
No hepatosplenomegaly
Cherry red spot variable

50
Q

Gauchers disease

Biochemical defect

A

Most common lysosomal storage disorder

Glucocerebroside is converted to ceramide by beta glucosidase / glucocerebrosidase

51
Q

Clinical features of Gaucher’s disease

A

No mental retardation (in the common type 1 and most other types)
Visceromegaly
Hepatosplenomegaly
No cherry red spot (present in the rare type 2)

52
Q

Accumulation of glucocerebrosides in Gaucher’s disease causes

A
  1. Pancytopenia
  2. Decreased thrombocytes leads to bleeding manifestations
  3. Pain and pathological fractures of long bones
53
Q

Treatment of Gaucher’s disease

A 
1. ERT - Acid beta glucosidase, 
Other ERT
a)velaglucerase alpha
b) Taleglucerase alpha
2. Substrate Reduction therapy
Miglustat inhibits glucosyl ceramide synthase
3. Bone marrow transplantation
54
Q

Diagnosis of Gaucher’s disease

A
  1. X ray of femur shows Erlenmeyer Flask deformity

2. Bone marrow biopsy- Gaucher’s cell is present having a crumpled tissue paper appearance

55
Q

Niemann Pick disease

A

Sphingomyelinase which converts sphingomyelin to ceramide
Cherry red spot
Zebra body inclusions

56
Q

Farbers disease

A

Ceramidase which converts ceramide to sphingosine + fatty acid

Resembles rheumatoid arthritis (pain,swelling,nodules in the joints)

57
Q

Fabrys disease

A

X linked recessive
Alpha galactosidase
Increased globotriocyl ceramide

58
Q

Clinical features of Fabrys disease

A
  1. Angiokeratoma in bathing trunk areas
  2. Hypohydrosis (decreased sweating)
  3. Fabry’s crisis-agonising pain,swelling because of inflammation of proximal joints
  4. Urinary sediments (lipid inclusions excreted in urine have the shape of Mattese cross)
  5. Corneal and lenticular opacities with whirled appearance in the lens
59
Q

Treatment of Fabry’s disease

A
  1. ERT-recombinant alpha galactosidase (agalzidase beta or Fabrazyme)
  2. Agalzidase alpha
60
Q

Wolman’s disease/cholesterol ester storage disease (CESD)

A

Acid lipase is defective
Increased TAG and cholesterol ester in histiocytic foam cell
Lysosomal storage disorder

61
Q

Wolmann’s disease clinical features

A
  1. Watery green diarrhoea
  2. Relentless vomiting
  3. Hepatosplenomegaly
  4. Calcification of adrenal
62
Q

Metachromatic leukodystrophy

A

Acrylic sulfatase A deficiency

63
Q

General characteristics of sphingolipidosis

A
  1. All are autosomal recessive except Fabry’s disease
  2. Cherry red spot (except Fabry’s and Gaucher’s disease)
  3. Mental retardation (except Gaucher’s and Fabry’s disease)
  4. Hepatosplenomegaly (except Fabry’s ,…)
64
Q

Sphingolipidosis with no hepatosplenomegaly

A

Fabry’s disease
Metachromatic leukodystrophy
Krabbe’s disease

65
Q

Corneal clouding seen in sphingolipidosis like

A

Fabry’s disease

GM1 gangliosidosis

66
Q

Sites of beta oxidation occurs

A

Mitochondria

Liver, adipose tissue, muscle

67
Q

Steps of beta oxidation

A
  1. Activation of FA
  2. Transport of activated FA to mitochondria
  3. Beta oxidation
68
Q

Activation of FA

A

By acyl CoA synthetase
FA to Acyl CoA
1ATP to 1AMP (2 high energy PO4)

Energy requiring step of beta oxidation
Outer mitochondrial membrane (cytoplasm)

69
Q

Enzymes involved in transport of activated FA to mitochondria

A

Via carnitine

  1. CAT-1 (CPT-1) Carnitine Acyl Transferase
  2. CAT-2 (CPT-2) inner membrane
  3. Carnitine Acyl Carnitine translocase
70
Q

Carnitine

A

Beta OH gamma trimethyl NH4+ butyrate
Synthesised and stored in muscle from lysine and methionine (SAM)
Not required by FA with less than C<14

71
Q

Product formed in the inter mitochondrial space during beta oxidation

A

Acyl carnitine and CoA by CAT-1

72
Q

Substrate of carnitine Acyl carnitine translocase

A

Acyl carnitine is transported as it is both directions

73
Q

Does carnitine enter the cystosol during beta oxidation

A

No. It does not cross the outermitochondrial membrane.

74
Q

Gateway of beta oxidation

A

CAT-1 (CPT-1)

75
Q

First step of beta oxidation in mitochondria

A

Acyl CoA is converted to Enoyl CoA by Acyl CoA dehydrogenase with the help of FAD.

76
Q

Second step of beta oxidation in mitochondria

A

Enoyl CoA is converted to Hydroxy Acyl CoA by Hydratase.

77
Q

Third step of beta oxidation in mitochondria

A

Hydroxy Acyl CoA is converted to Keto Acyl CoA by Hydroxy Acyl CoA dehydrogenase with the help of NAD

78
Q

Last step of beta oxidation

A

Keto Acyl CoA is converted to a new Acyl CoA + Acetyl CoA by Thiolase

79
Q

Regulation of beta oxidation

A

Malonyl CoA is an allosteric inhibitor of CAT-1

80
Q

Jamaican vomiting sickness biochemical defect

A

Asked fruit contains a toxin called hypoglycin.
Inhibits Acyl CoA dehydrogenase (first step of beta oxidation)
1. Decreased ATP and Acetyl CoA leads to decreased gluconeogenesis. Leads to fasting hypoglycaemia (non ketotic).
2. Decreased ketone body synthesis.

81
Q

Clinical features of Jamaican vomiting sickness

A
  1. Sudden onset of vomiting (leads to fasting)

2. Non-ketotic Fasting hypoglycaemia leads to coma,convulsions,death.

82
Q

Medium chain Acyl CoA dehydrogenase deficiency

A

Most common disorder associated with FA
Decreased MCAD (first step of beta oxidation)
Decreased gluconeogenesis and ketone body synthesis.
Fasting hypoglycaemia
Increased omega oxidation leading to formation of decarboxylic acid (double headed FA).

83
Q

Clinical features and treatment of MCAD deficiency

A

Coma,seizures,death due to fasting non-ketotic hypoglycaemia.

Frequent meals with low fat, high carb diet.

84
Q

VLCFA oxidation/

A

In peroxisome / glyoxysome
Modified beta oxidation
Releases Acetyl CoA and H2O2 which is detoxified by catalase
Occurs upto octanoyl CoA (8C) rest in mitochondria (beta oxidation)

85
Q

Zellweger syndrome

A

Cerebrohepatorenal syndrome
Peroxisomal protein targeting disorder (due to defective peroxin protein)
Peroxisomal Targeting Sequence-1 (PTS-1) is defective

86
Q

Clinical features of Zellweger syndrome

A
  1. Mongoloid facies
  2. Hypertelorism
  3. High forehead
  4. Unslanting palpebral fissure
  5. Epicanthal folds.
  6. Brushfield spots in iris
  7. Severe neurological symptoms

Resembles Down’s syndrome

87
Q

Diagnosis of Zellweger syndrome

A
  1. Decreased no. of peroxisomes
  2. Peroxisomal ghosts (empty)
  3. Increased VLCFA in plasma (eg, pipecolic acid)
  4. Increased phytanic acid in plasma (alpha oxidation)
88
Q

Unsaturated FA oxidation

A

Modified beta oxidation in mitochondria
Normal beta oxidation occurs ,except for every double bond in even position ,first step is skipped (Acyl CoA dehydrogenase)

1.5 ATP less for every double bond in even position

89
Q

Odd chain fatty acids oxidation

A

Beta oxidation occurs in mitochondria as usual with products Acetyl CoA and propionyl CoA (glycogenic)

90
Q

Propionyl CoA metabolism

A
  1. It is carboxylated to D Methyl Malonyl CoA by Propionyl CoA carboxylase (biotin) and ATP
  2. It is then isomerised to L form by D Methyl Malonyl CoA Racemase
  3. It is then converted to succinyl CoA by Methyl Malonyl CoA mutase
  4. Then to TCA to OAA
91
Q

Alpha oxidation

A

Peroxisome and ER
No ATP is produced

Happens when decreased beta oxidation or to those FA with a branch in the beta carbon like phytanic acid

92
Q

Sources of phytanic acid

A
  1. Dairy products

2. Green leafy vegetables

93
Q

Classic Refsum’s disease

A

Defect in alpha oxidation
Phytanoyl CoA hydroxylase/oxidase
Peroxisomal targeting disorder

94
Q

Clinical features of Refsum’s disease are

A
  1. Icthyosis
  2. Retinitis pigmentosa
  3. Decreased vision
  4. Ataxia
  5. Peripheral neuropathy
  6. Increased phytanic acid in plasma
95
Q

Omega oxidation

A

Occurs when beta oxidation does not occur
No ATP produced
Occurs in Microsomes (SER)

Omega carbon, i.e, last carbon is oxidised leading to double headed FA or dicarboxylic acid

96
Q

Parameters checked in plasma lipid profile

A
  1. Serum total cholesterol
  2. Serum triglycerides
  3. LDL Cholesterol
  4. HDL cholesterol
97
Q

Serum cholesterol levels according to Adult Treatment plan 4 (ATP-4)

A

Desirable level < 200 mg/dl

Borderline high 200-239 mg/dl

High > 240 mg/dl

Non-fasting level can be used in addition to fasting cholesterol level

98
Q

Serum triglyceride level according to ATP-4

A

Normal level < 150 mg/dl

Borderline high 150-199
High 200-499

Very high > 500 mg/dl

Fasting sample should be used

99
Q

LDL cholesterol level according to ATP-4

A 
Optimum <100 mg/dl
Near or above optimum 100-129
Borderline high 130-159
High 160-189
Very high >190 mg/dl
100
Q

HDL cholesterol level according to ATP-4

A

Low level <= 40 mg/dl

High level >= 60 mg/dl

101
Q

New parameters for plasma lipid profile

A
  1. Apo B/apo A1 ratio
  2. hsCRP (high sensitive C reactive protein)
  3. Lp(a)
  4. Total cholesterol/HDL-C ratio
  5. Non HDL cholesterol
102
Q

Apo B/Apo A1 ratio

A

Ideal value is 0.7-0.9

Can be tested without fasting

103
Q

Ideal level of Lp(a)

104
Q

Ideal level of total cholesterol/HDL ratio

105
Q

Ideal level of non HDL cholesterol

A

<130 mg/dl

106
Q

Exception for VLDL = TAG/5

A

TAG >400 mg/dl

107
Q

Deficiency of essential FA E results in

A

Scaly Dermatitis
Hair loss
Poor wound healing

As it is essential for maintaining skin integrity and cell membrane

108
Q

FFA are transported by

Biochemistry MBBS (10 decks)

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