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Biochemistry MBBS > Carb 1 > Flashcards

Carb 1 Flashcards

1
Q

Well fed state

A

1-4 hrs after food

Increased protein synthesis

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2
Q

Fasting types

A

Early fasting 4 -16 glycogenolysis

Fasting 16-48 hrs gluconeogenesis (OAA decreases)

Prolonged fasting or starvation 2-5 days hydrolysis of TAG in adipose tissue to produce acetyl CoA(OAA has decreased) to ketone body synthesis

Prolonged starvation after 5 days muscle proteolysis/wasting

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3
Q

Role of beta oxidation in fasting

A

In gluconeogenesis , ATP is required
and
acetyl Co A is an activator of first step of it I.e pyruvate carboxylase

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4
Q

Ketone body important use

A

Prevent structural protein lysis

Prevents cachexia

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5
Q

Earliest effect of insulin

A

Increased GLUT4 in
1 skeletal muscle(very much)
2. Heart
3. Adipose

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6
Q

Insulin increases hexokinase or glucokinase?

A

Glucokinase

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7
Q

RBC glucose transport

A

GLUT 1

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8
Q

During starvation brain depends on

A

Glucose 80% GLUT
3( highest affinity)
Ketone body 20%

FA cannot cross blood brain barrier( bound to albumin)

No anabolic process so no storage of nutrition

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9
Q

Glucagon starts increasing at ___glucose level

Insulin starts at

A

50mg/dl

80mg/dl

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10
Q

cAMP dependent protein kinase A has in inactive state

A

2 regulatory and 2 catalytic subunit

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11
Q

Changes in beta cell in fed state following increased ATP production

A 
ATP sensitive K+ channels close 
Depolarisation 
Leads to opening Ca+2 channels
Ca+2 influx
Insulin vesicle exocytosed
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12
Q

Tyrosine and insulin

A

Insulin leads to Receptor Tyrosine Kinase phosphorylates tyrosine residues in the beta subunit of receptor

Leads to phosphorylation of IRS

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13
Q

Glycogen phosphorylase is active in __ state

A

Phosphorylated

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14
Q

Liver metabolic fuels

A

Fed glucose> FFA

Early fasting/fasting
FFA> glucose

Prolonged fasting, starvation
Amino Acids/FFA

NO ketone bodies

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15
Q

Heart metabolic fuels

A

fed/ early fasting/fasting
FFA>glucose

Prolonged fasting
Ketone bodies

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16
Q

Brain metabolic fuels

A

Fed /Early fasting/fasting
Glucose

Prolonged fasting
80% glucose
20% ketone bodies

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17
Q

Skeletal muscle metabolic fuel

A

Fed
Glucose> FFA

Early fasting/ fasting
FFA> glucose

Prolonged fasting
FFA,
(Slow twitch) ketone bodies

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18
Q

Adipocytes metabolic fuels

A

Fed
Glucose>FFA

Early fasting
FFA> Glucose

Starvation
FFA,ketone bodies

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19
Q

Fate of acetyl Co A in DM increased due to beta oxidation of increased FA (HS Lipase)

A

No OAA so no TCA cycle
No insulin so no FA synthesis
Increased ketone body synthesis

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20
Q

Lactulose

A

Galactose + fructose
Synthetic
Osmotic laxative

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21
Q

Glycogen occurs in liver and muscle as

A

Beta particle having 60000 glucose molecules

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22
Q

Dextran

A

Homopolysaccharide of glucose

Plasma volume expander

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23
Q

Product of glucose oxidase method

A

Gluconic acid an aldonic acid

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24
Q

Mucic acid test

A

Galactose test

it is a sachcharic acid of galactose

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25
Q

Dulcitol/ galactitol

A

Cataract in Galactosemia

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26
Q

Mannitol

A

Intracranial pressure reducer

Mannose alcohol

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27
Q

Fructose alcohol(s)

A

2 since an aldose

Sorbitol and mannose

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28
Q

Which carb function test is a liver function test

A

Galactose

Normally <3 gm appear in urine after 40gm galactose ingestion

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29
Q

The only GAG which is not formed by the Golgi apparatus

A

Hyaluronic acid at plasma membrane

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30
Q

Glycosaminoglycans or mucopolysaccharides are

A

Complex carbohydrates made of uronic acid and amino sugars

May be attached to proteoglycans ( which have bottle brush appearance)

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31
Q

Keratin sulphate 1 in

A

Cornea

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32
Q

Glycosaminoglycans are polysaccharides made of repeating

A

Disaccharide units of amino sugar and acidic sugar (glucuronic acid and iduronic acid)

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33
Q

Mucous secretions are slippery and resilient (compressibility) because

A

Glycosaminoglycans repel each other and absorb water due to negative charge

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34
Q

Chondroitin sulphate

A

Most abundant and most heterogenous GAG

Cartilage bones and CNS

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35
Q

Keratin sulphate

A

Two types I and II
It has galactose instead of uronic acid as the second unit

I cornea(transparent)
II cartilage , loose connective tissue
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36
Q

Heparan sulphate

A 
Glucosamine + glucuronic acid
Seen in plasma membrane receptors
Lipoprotein lipase is anchored by it
Basement membrane of renal glomeruli, it is present so charge selectiveness( albumin not allowed)
Present in synaptic and other vesicles
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37
Q

Heparin

A

Glucosamine+iduronic acid

Only intracellular GAG (Mast cells lungs)

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38
Q

Deramatan sulphate

A

Widely distributed GAG
Abundant in skin
It binds to LDL so atherogenic GAG

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39
Q

Hyaluronic acid

A

N acetyl glucosamine+ glucuronic acid (no sulphate)
Not covalently attached to proteins
Helps in cell migration( tumour metastasis, morphogenesis, wound repair)
Found in bacteria

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40
Q

Proteoglycan

A

Protein(5%)+ GAG( 95%)
GAG is attached by a stalk Gal- Gal- Xylulose to the protein frame
Thus a bottle brush appearance

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41
Q

Glycoprotein

A

Carb (5%) + protein (95%)

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42
Q

Synthesis of GA

degradation in

A

ER & Golgi apparatus

Lysosome

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43
Q

General clinical features of MPS

A

Coarse facial appearance
Frontal bossing
Depressed nasal bridge

Gingival hypertrophy
Large tongue 
   (noisy breathing, 
   ear infection( hearing loss) ,
   URTI( copious nasal discharge))

Mucopolysaccharides in urine

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44
Q

General skeletal features of MPS

A

Skeletal dysplasia
Dysostosis multiplex
Bullet shaped middle phalanx
Claw hand

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45
Q

Special manifestations of MPS I ,Hurler syndrome

A

Corneal clouding Visceromegaly
( protuberant abdomen and hernias)
Short stature
Mental retardation

Reilly body inclusions

46
Q

Visceral manifestations of MPS

A

Valvular heart diseases

Mitral and aortic regurgitations

47
Q

Scheie’s disease

A 
MPS I S
Normal intelligence 
Accumulation of dermatan sulphate
( rest as Hurler disease)
Alpha L idurorinidase (partial deficiency )
Gene IDA
48
Q

Hurlers disease biochemical effect

A

MPS I H
alpha L iduronidase
Heparan sulphate and dermatan sulphate in urine
Gene IDA

49
Q

Hunter’s disease

A

L iduronate
MPS II
Gene IDS

X linked
Males only affected

Clear vision
( like Sanfillippo syndrome)
Heparan sulphate & dermatan sulphate

50
Q

Difference between Hurler and hunter disease

A

Hunter is more common and has slower progression, hunters have clear vision and are males

51
Q

Most common MPS

A

Sanfillippo (MPS III) followed by Hunter

52
Q

MPS with no mental retardation

A

Scheie I S

Morquio MPS IV
(no visceromagaly and no leukocyte inclusion)

Maroteaux Lamy MPS VI

53
Q

I cell(inclusion cell) disease

A 
Protein targeting disorder to the lysosome
Resembles MPS( more severe)
Enzyme defect( N Acetyl Glucose Phospho transferase)
Mannose 6 P not formed
54
Q

Enzyme replacement therapy ( ERT) for MPS in

A 
MPS I (H &amp; S) Aldurazyme
MPS II (H) Elaprase
MPS VI (ML) Naglazyme
55
Q

GLUT 2 is found in

A
  1. Beta cells
  2. Sinusoidal cells of liver
  3. Basolateral side of intestine
    4 PCT

It can transport fructose also

56
Q

Fructose transporter

A

GLUT 5
(GLUT 2)
But it transports other sugars

57
Q

GLUT 6

A

Pseudogene in spleen and leukocyte

58
Q

GLUT 7

A

Liver ER

59
Q

Glycemic index of glucose and galactose( and hence lactose also)

A

100%
because all of it absorbed due to SGLT I
But not fructose and sucrose

60
Q

GLUT in blastocyst

A

GLUT 8

61
Q

Deficiency of glycolysis enzymes cause

A

Hemolysis
Eg pyruvate kinase ( 2nd most common enzyme deficiency )

PFK 1
Muscle fatigue and a glycogen storage disorder

62
Q

Inhibitor of glyceraldehyde 3 P dehydrogenase

A

Iodoacetate

63
Q

Inhibitor of 1,3 BP Glycerate kinase

A

Arsenate

64
Q

Gluconeogenesis occurs in

A

Liver , kidney
Their enzymes are seen in intestine

Cytoplasm and mitochondria

65
Q

Gluconeogenic substrate

A
  1. Glucogenic aa ( alanine - Cahill cycle)
  2. Lactate (Cori cycle)
  3. Glycerol
  4. Propionyl CoA
66
Q

In fasting state blood level of which aa increases

A

Alanine due to Cahill cycle

67
Q

Cori cycle involves which organs

A

Muscle (exercise)
RBC(always)
Lactate

68
Q

Which step of gluconeogenesis takes place in mitochondrion

A

Pyruvate carboxylase requiring ATP

The OAA then enter cytoplasm via malate aspartate shuttle

69
Q

PEPCK requires

A

GTP
OAA

CO2 and PEP are released
decarboxylation and phosphorylation

70
Q

Propionyl CoA enters gluconeogenesis via

A

Propionyl CoA carboxylase ( biotin) converts it into D methyl Malonyl CoA

Isomerised by racemase to L form

Then converted by methyl malonyl CoA mutase (B12) to Succinyl CoA

It enters TCA ,converged to OAA which enters gluconeogenesis

71
Q

Enzyme of gluconeogenesis requiring B12

A

Methyl malonyl CoA mutase converting l methyl malonyl CoA to succinyl CoA

72
Q

Explain glycogenin structure

A

A polypeptide

Has many tyrosine residues which are glycosylated

73
Q

Enzymes for production of UDP glucose

A

Hexokinase

Phosphoglucomutase (G-1-P formed)

UDP Glucose pyrophosphorylase

74
Q

RDE of glycogenesis

A

Glycogen synthase

75
Q

Branching enzyme

A

Alpha 1,4 1,6 glucan transferase

It transfers a hexasaccharide

76
Q

Why density of glycogen is more in liver

A

Roster of beta particles

77
Q

Storage organelles for glycogenolysis

A

Cytoplasm of muscle and liver
1-2% lysosome (pompe disease
Smooth endoplasmic reticulum involved

78
Q

Vitamin required for glycogen phosphorylase the RDS

A

Vitamin B6
Hence B6 is found mostly in muscle

It stops 4 glucose molecules from 1,6 linkage till which it removes mainly as G 6 P

79
Q

Name of debranching enzymes

A

Alpha 1,4 1,4 glucose transferase

Alpha 1,6 glucosidase ( removes as GLUCOSE)
This accounts for the small proportion of glucose among the glucose-6-P

80
Q

Enzyme common for glycogenesis and glycogenolysis

A

Phosphogluco mutase

81
Q

Enzyme absent in muscle but present in liver (in ___ organelle) and common to glycogenolysis and gluconeogenesis

A

Glucose 6 phosphatase
This enzyme is present in the smooth ER ( G-6-P is transported into SER by T1 protein and the glucose is transported to cytoplasm by GLUT7 )
Hence there is a delay in forming glucose

3 ATP from anaerobic glycolysis in muscle

82
Q

Glucagon acts in the

A

Liver
Not muscle
(Reference - glycogen metabolism )

83
Q

Mineral which is activated of glycogenolysis

A

Ca+2

84
Q

Regulation of muscle glycogenolysis (allosteric)

A

Activators are
Ca+2 (Calcium calmodulin dependent protein kinases) and AMP
Inhibitors are
ATP, G-6-P

Glucose is not an inhibitor for muscle glycogenolysis

85
Q

Regulators of liver glycogenolysis

A

Inhibitors are

ATP, Glucose, G-6-P

86
Q

Muscle in extreme anoxia

A

5’AMP acts as a allosteric activator without involvement of phosphorylation

87
Q

Liver glycogen storage disorder general features

A

Hypoglycaemia
Hepatomegaly(mostly)
Usually no exercise intolerance

88
Q

Muscle GSD features

A

No hypoglycaemia

Exercise intolerance

89
Q

Von gierke disease

Biochemical defect

A

Type 1 A GSD
Most common
Glucose 6 Phosphatase

Increased G-6-P
Increased glycogen

90
Q

Von gierke disease clinical features

A 
3-4 months
Doll like facies with thin extremities
Massive hepatomegaly but no splenomegaly
RENOMEGALY
Milky white plasma (triglyceridemia)
91
Q

Biochemical hallmarks of Von gierke disease

A 
Fasting Hypoglycaemia
Lactic acidosis
Hyperlidemia
Ketosis 
Hyperuricemia
92
Q

Ketosis and hyperlipidemia in Von gierke disease

A

As glycogenolysis is ineffective , gluconeogenesis takes place.
Thus OAA is depleted.
Beta oxidation of FA is increased.
Acetyl CoA cannot enter TCA as there is no OAA , thus ketosis and hyperlipidemias

93
Q

Type 1 B GSD

A

G6P transporter in liver ER is defective

Neutropenia and recurrent bacterial infection

94
Q

Forbes/ Chris disease / Limit dextrinosis

A

Type 3 GSD
Debranching enzyme
Abnormal glycogen
(limit dextrin with few outer branches)

IV corn starch syrup

95
Q

Clinical features of Forbes disease and Anderson’s disease

A 
Hypoglycaemia 
Hepatosplenomegaly
No renomegaly
Progressive liver cirrhosis
Myopathy

After puberty sometimes may be reversible or death in cori disease

But in Amylopectinosis , portal hypertension to death by about 5 years due to liver failure

96
Q

IV glucagon gives response in well fed state but no response after overnight fasting

A

Limit dextrinosis
No problem in absorption of glucose
But after overnight fast debranching enzyme is deficient so no response

97
Q

Anderson’s disease / amylopectinosis

A

Type 4 GSD
Branching enzyme
Abnormal glycogen insoluble in water and amylopectin-like

98
Q

Muscle glycogen disorder with hypertrophic cardiomyopathy

A

Pompe’s disease

Danon disease
Defect in LAMP 2 protein Lysosomal Associated Membrane Protein 2

99
Q

Muscle GSD without hypertrophic cardiomyopathy

A 
McArdle disease (type 5)
Tarui disease (type 7)
100
Q

Pompe’s disease

A

Type 2 GSD
Lysosomal storage disorder
Acid maltase/ acid alpha 1,4 glucosidase

101
Q

Clinical features of Pompe’s disease

A 
Hypotonia
Early onset 
Floppy infant
Failure to thrive
Macroglossia 
Cardiomegaly and progressive cardiac failure to death (2 years)
102
Q

Treatment for Pompe’s disease

A

ERT of

myozyme / aglucosidase alpha / recombinant acid alpha glucosidase

103
Q

Diagnosis of Pompe’s disease

A

Increased levels of serum :
Creatinine kinase
Lactate dehydrogenase
Acid phosphatase

104
Q

Enzymes elevated in type 3 and 4 GSD

A

Liver enzymes like aminotransferases especially ALT (AST)

105
Q

McArdle’s disease

A

Type 5 GSD
Muscle (glycogen) phosphorylase
Most common GSD in adolescents and adults

106
Q

Characteristics of McArdles disease

A

Normoglycemia
Exercise intolerance
Second wind phenomenon
(If they rest after the onset of first pain, they can resume the exercise with more ease.)
Rhabdomyolysis
(myoglobinuria - burgundy coloured urine)

107
Q

Tarui’ disease

A

Type 7 GSD
muscle and erythrocyte PFK

Exercise intolerance
No second wind phenomenon
Hemolysis

108
Q

Her’s disease

A

Type 6 GSD

Hepatic phosphorylase

109
Q

Fanconi Bickel syndrome

A

Affecting GLUT 2

recently added GSD

110
Q

Type 0 GSD

A

Glycogen synthase defect

111
Q

Tandem enzyme / bifunctional enzyme of glycolysis and gluconeogenesis

A

A single polypeptide having the activity of PFK-2 and F-2,6-BPase

PFK 2 produces F 2,6 BP from F-2-P
F-2,6-BPase

This takes part in reciprocal regulation

112
Q

PFK 2 role

A

The product of PFK-2 (F-2,6-BP) is an activator for PFK-1
i.e, PFK-2 activates glycolysis

F-2,6-BPase inhibits PFK-1 so activates gluconeogenesis

Biochemistry MBBS (10 decks)

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