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Biochemistry MBBS > Carb 2 > Flashcards

Carb 2 Flashcards

1
Q

HMP pathway terms, sites

A

Hexose monophosphate
Pentode phosphate pathway
Dicken Horecker pathway

Cytosol
Oxidative phase in fat,steroid,… synthesis and in lens, RBC,…

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2
Q

First step of HMP pathway

A

G-6-P to 6-PhosphoGluconate by G-6-PD

NADPH is produced
Irreversible
RDS

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3
Q

Production of Ribulose

A

6-PhosphoGluconate is decarboxylated by 6-PhosphoGluconate Dehydrogenase to Ribulose-5-P

NADPH is produced

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4
Q

Free radical scavenging by NADPH

A

H2O2 is converted to H2O by glutathione peroxidase

The oxidised glutathione is then converted back by glutathione reductase with NADPH and FAD

Required for transparency of lens ,Hb and RBC

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5
Q

Reactions of the non oxidative (reversible) part of HMP pathway

A

Ribose-5-P (from epimerase)
reacts with Xylulose-5-P
(from ketoisomerase)
5+5=3+7=4+6

Then 4+5=3+6 ( F-6-P)
The 2 F-6-P will form G-6-P
And the glyceraldehyde-3-P will form one half G-6-P
The remaining are 3 CO2

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6
Q

Reaction having trans ketolase and those having transaldolase

A

Transketolase 5+5=3+7
Then 4+5=3+7

Transaldolase
3+7=6+4

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7
Q

G-6-PD deficiency,the most common enzyme deficiency

A

NADPH decreases
Haemolytic anaemia and jaundice
Methemoglobinemia

Sulfa drugs, primaquine (anti-malarial), Fava beans (favism) aggravates this

Heinz bodies in RBC

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8
Q

G-6-PD deficiency is common in Africa because

A

The lifespan of RBC is too low for Plasmodium falciparum to complete its life cycle

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9
Q

Wernickes Korsakoff’s syndrome

A

Thiamine deficiency

Transketolase will be deficient

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10
Q

Enzymes involved in phosphorylation then UDP transfer of galactose

A

Galactokinase
Then galactose-1-P Uridyl transferase (GALT)
converts it into UDP galactose
(producing G-6-P as by product)

An epimerase can be used to convert UDP Galactose back to UDP Glucose

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11
Q

Classic galactosemia

A

GALT defect

Galactose 1 P increases, which is an inhibitor of glycogen phosphorylase
Leading to decreased glycogenolysis
Fasting hypoglycaemia (especially as the child vomits and has feeding difficulty)

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12
Q

Non classic galactosemia

A

Galactokinase or

Epimerase

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13
Q

Symptoms of classic galactosemia

A

Age of onset at 1-2 weeks (milk)

  1. Failure to thrive, vomiting, feeding difficulty
  2. seizures, coma, mental retardation
  3. Hepatomegaly, liver failure ,jaundice
  4. galactitol/ dulcitol (oil-drop cataract)
  5. Neonatal sepsis (E coli)
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14
Q

Diagnosis of classic galactosemia

A 
Benedictus test
Glucose oxidase test -ve
Galactose tolerance test (should not be done)
Music acid test
Enzyme/ genetic mutation studies
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15
Q

Treatment of classic galactosemia

A

No breast feeding
Lactose free diet up to 4-5 years ( as an enzyme Gal-1-P pyrophosphorylase which converts Gal-1-P to less toxic galactose)

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16
Q

Why does fructosemia does not exist

A

Because the renal threshold level for fructose is too low for it to be manifested
Instead only fructosuria occurs

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17
Q

Difference between fructokinase and hexokinase

A

Fructose is converted to fructose-1-P by fructokinase, bypassing PFK and then split by aldolase B to glyceraldehyde ( not 3 phosphate) and DHAP
Glyceraldehyde is later phosphorylated by kinase

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18
Q

Fructose and diabetes

A

Hyperlipidemia

Hyperuricemia (gout)

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19
Q

Essential fructosuria

A

Deficiency of fructokinase
No fructosemia
Benign
No manifestations

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20
Q

Hereditary fructose intolerance

A

Deficiency of aldolase B
Inhibits glycogen phosphorylase which inhibits glycogenolysis
Leads to fasting hypoglycaemia
(Convulsions, coma)

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21
Q

Clinical features of Hereditary fructose intolerance

A

Weaning leads to onset of the disease
Vomiting, feeding difficulties, failure to thrive

Liver failure,hepatomegaly, jaundice

No cataract, because no fructose accumulation

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22
Q

Diagnosis of hereditary fructose intolerance

A
  1. Benedicts test +ve, but glucose oxidase test -ve
  2. Rapid furfural test
    Seliwanoffs test
  3. Gene and enzyme studies
23
Q

Enzymes of first part of Krebs cycle (upto succinyl CoA)

A
  1. Citrate synthase
  2. Aconitase
  3. Isocitrate dehydrogenase ICDH (mitochondrial)
  4. Alpha keto glutarate dehydrogenase
24
Q

Special features of aconitase

A
  1. Contains Fe+2

2. Moonlighting enzyme , as it takes part in iron homeostasis

25
Q

NADH producing reactions in TCA

A
  1. ICDH
  2. Alpha ketoglutarate dehydrogenase
  3. Malate dehydrogenase
26
Q

Irreversible steps of TCA

A
  1. Citrate synthase

2. Alpha ketoglutarate dehydrogenase

27
Q

Enzymes of second half of TCA

A
  1. Succinate thiokinase
  2. Succinate dehydrogenase (not in matrix)
  3. Fumarase
  4. Malate dehydrogenase
28
Q

Succinate thiokinase produces succinate and

A

GTP where there is gluconeogenesis in which PEPCK requires GTP
otherwise ATP

29
Q

Inhibitor of aconitase

A

Fluoroacetate

Non competitive

30
Q

Inhibitor of alpha keto glutarate dehydrogenase

A

Arsenite

Non competitive

31
Q

Succinate dehydrogenase is inhibited by

A

Malonate

32
Q

Anaplerotic reactions of TCA

A

TCA cycle is a truly anaplerotic cycle
Filling up reactions / replenishment of depleted intermediates
1. Pyruvate to OAA (major)
2. Valine, Isoleucine,Methionine, threonine (VIMTee)
3.

33
Q

Regulatory enzymes of TCA

A
  1. Citrate synthase
  2. ICDH
  3. Alpha ketoglutaric acid dehydrogenase
  4. Pyruvate dehydrogenase (NOTE)
    • especially in the brain PDH is the major regulatory step
34
Q

TCA cycle and Calcium

A

All dehydrogenases are activated by Calium

Important in muscle

35
Q

Hormones and TCA cycle

A

no control over TCA as TCA cycle is essential

36
Q

Complex 1

A

NADH -Q oxidoreductase /NADH dehydrogenase

Components are:

  1. FMN
  2. Iron-sulphur complex

Pumps 4 H+

37
Q

Complex 2

A

Succinate dehydrogenase / succinate-Q oxidoreductase / succinate Q reductase

Components are

  1. FAD
  2. Iron-sulphur complex
38
Q

Complex 3

A

Q -cytochrome C oxidoreductase / cytochrome bc1 complex

Components :

  1. the cytochromes
  2. Reiske Fe-sulphur complex

Pumps 4H+

39
Q

Complex 4

A

Cytochrome C oxidase / irreversible complex

Components :

  1. Heme a a3/ cytochrome a a3
  2. CuA - CuB

Pumps 2 H+

40
Q

Complex 5 / ATP Synthase

A 
F0 - 10 C disc proteins
F1 (9 subunits) - 
a) 3 alpha
b) 3 beta (ATP synthesising)
c) gamma (bent axle and rotatory subunit)
d) epsilon
41
Q

ETC is in the ___ order of redox potential

A

Ascending

42
Q

Inhibitors of e- transfer

Complex 1

A

Rotenone (fish poison)
Amobarbital (barbiturate)
Piericidin (antibiotic)

43
Q

Complex 2 inhibitors

A

Malonate

Between FADH and CoQ
Carboxin
Trienoyl trifluoro acetate (TTFA) - iron chelating agent

44
Q

Inhibitors of complex 3

A

British Anti Lewisite (BAL)

Antimycin A

45
Q

Complex 4 inhibitors

A

Gases like CO
CN-
H2S
And Sodium azide

46
Q

Inhibitors of oxidative phosphorylation at level of Fo

A

Oligomycin

Venturicidin

47
Q

Inhibitor of F1

A

Aurovertin

48
Q

Inhibitors of ADP/ATP transport

A

Atractyloside

49
Q

Chemical uncouplers

A
  1. 2,4 DNP
  2. Dinitrocresol
  3. FCCP (Fluoro Carbonyl 4. Cyanide Phenyl hydrazine)
  4. Aspirin in high dose
50
Q

Physiological uncouplers

A
  1. Thermogenin ( uncoupling protein 1 UCP 1) of brown adipose tissue
  2. Thyroxine
  3. Long chain fatty acids
  4. (Unconjugated bilirubin )
51
Q

Ionophores

A 
Channel formers (therapeutic)
Dissipates electronic gradient
  1. Valinomycin
  2. Nigercin
  3. Gramicidin
52
Q

Non shivering thermogenesis

A

Thermogenin which prevents neonatal hypothermia

53
Q

High energy compounds

A 
Free energy > 7 kCal
PEP(highest energy)
Carbomoyl P
1,3 BPG
Creatine P
ATP ( to ADP and AMP)
54
Q

Creatine phosphate is present in

A

Skeletal muscle, heart, spermatozoa and brain

Biochemistry MBBS (10 decks)

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