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Med 2024-2028 > Metabolism 2.2 > Flashcards

Metabolism 2.2 Flashcards

1
Q

State intermediates of glycolysis

A
  1. DHAP
  2. 1,3 - BPG (1,3 - bisphosphoglycerate)
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2
Q

State uses of 1,3 - bisphosphoglycerare

A

Regulation of haemoglobin affinity for O2
(reduces affinity for oxygen promoting O2 release)

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2
Q

State uses of DHAP

A

DHAP converted to Glycerol 3 phosphate
Glycerol 3 phosphate used to synthesise TGs in adipose tissue + liver
Glycerol 3 phosphate used to synthesises phospholipids (cell membrane components)

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3
Q

State where 1,3 BPG is produced

A

RBCs (high conc here)

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4
Q

Describe regulation of glycolysis

A

Enzymes catalysing irrervsivbe steps (1,3,10) are sites of control

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5
Q

State which enzymes are involved in regulation of glycolysis and state their functions

A
  1. Hexokinase - alosterically inhibited bt G-6-P (product inhibition)
  2. Phosphofructokinase-1 - in muscle, allosterically inhibited by high ATP : AMP ratio (feedback inhibiton) - in liver, activated by high insulin:glucagon ratio through dephosphorylation
  3. Pyruvate kinase - activated by high insulin : glucagon ratio through dephoshorylation
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6
Q

Describe regenration of NAD+ in glycolysis

A

IMPORTANT

NAD+ re-oxidised in stage 4 aerobic catabolism (AEROBIC GLYCOLSIS) / stage 2 anaerobic catabolism (ANAEROBIC GLYCOLYSIS)

Most cells:
occurs in Stage 4 Catabolism - Oxidative Phosphorylation
NADH⁺ + H⁺ is re‐oxidised to NAD⁺

However, in some cells, NAD+ is regenerated in anaerobic glycolsyis. For examples,

RED BLOOD CELLS (no mitochondria)
Kidney medulla, lens, cornea (few mitochondria), this means that stages 3 and 4 of catabolism are insuficcient in these cells

Another example where NAD+ is regenrated using anaerobic respiration is during vigorous exercise of muscles, stage 4 catabolism is not efficient.

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7
Q

State monosaccharides which make up sucrose

A

FRUCTOSE
GLUCOSE

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8
Q

State where fructose is metabolised

A

Liver

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9
Q

Describe fructose catabolism

A
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10
Q

State the cause of essential fructosuria

A

Fructokinase deficiency
(in fructose catabolism, converts fructose to Fructose-1-Phosphate)
GENETIC

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11
Q

State a symptom of Fructosuria

A

Fructose in urine
(no other symptoms)

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12
Q

State the cause of fructose intolerance

A

Aldolase deficiency
(in fructose catabolism, aldolase cleaves fructose-1-phosphate into glyceraldehyde + DHAP)

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13
Q

How does fructose intolerance lead to liver damage and hypoglycaemia?

A

Fructose intolerance due to aldolase deficiency. Aldolase cleaves fructose-1-phosphate into glyceraldehyde and DHAP.
This does not happen without aldolase, fructose-1-phosphate accumulates in liver, leads to liver damage + hypoglycaemia

GENETIC CONDITION

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14
Q

State symptoms of fructose intolerance

A
  1. Vomiting
  2. Nausea
  3. Abdominal Pain
  4. Failure to thrive
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15
Q

State a treatment for a fructose intolerance patient

A

Elimenation of SUCROSE + FRUCTOSE from diet

16
Q

State which 2 monosaccharides produce lactose

A

Galactose + Glucose

17
Q

State where galactose is metabolised

A

Liver

18
Q

Diagram showing galactose metabolism

A

Important enzyme:

GALACTOKINASE
(Gactose phosphorylated to galactose-1-phosphate)

GALT
This coverts galactose-1-Phosphate to Glucose-1-Phosphate

PHOSPHOGLUCOMUTASE
Glucose-1-Phosphate isomerised (phosphoglucomutase)
Glucose-6-Phosphate

19
Q

State causes of Galactosaemia

A
  1. Galactokinase deficicency (non-classic galactosaemia)
    Galactose in blood (galactosaemia), galactose in urine (galactosuria)
    Galactose + GALACTTITOLaccumulates in lens (leads to CATARCT)
  2. GALT Deficiency (classic galactosaemia)
    galactoseamia, galctosuria, Galactose + GALACTITOL accumulates in lens (leads to CATARCT), BRAIN + LIVER DAMAGE
20
Q

State how accumulation Galacitol leads to cataract and liver damage

A

Deplets tissues of NADPH+ + H+

21
Q

Which enzyme is responsible for reducing galactose to galactitol

A

Aldolase reductase

22
Q

State symptoms of galactasaemia

A
  1. Vomiting
  2. Nausea
  3. Abdominal Pain
  4. Failure to thrive
  5. Diarrhoea
23
Q

State treatment options for a patient suffering with galactosaemia

A

Elimination of lactose and galactose from diet

24
Q

State the location of pentose phoshate pathway

A

Cytosol

25
Q

State where pentose phosphate pathway is most common

A

Liver
Adipose tissue
RBCs

26
Q

Overview of Pentose Phosphate Pathway

A
27
Q

State the oxidative reaction in the pentose phosphate pathway

A
28
Q

State the non-oxidative reaction

A

Rearrangement to glycolytic intermediates

29
Q

State functions of the pentose phosphate pathway

A
  1. Production of NADPH+ + H+
    this is reducing power, used in:
    -used in fatty acid synthesis in liver, adipose tissue, lactating mamary glands
    -maintains reduced state of GSH - glutathione - antioxidant
  2. Production of intermediates for glycolysis F-6-P, G-3-P)
  3. Production of 5 carbon carbs for nucleotides in nucleic acid synthesis
30
Q

State causes of glucose-6-phosphate dehydrogenase deficiency (G6PDH)

A

Genetic deficiency in Glucose-6-Phosphate Dehydrogenase

31
Q

State effects of G6PDH deficiency

A

Low levels of NADPH+ + H+
(inability to keep gluathione in reduced state, so oxidative damage to cells

Haemolysis of RBCs
(Haemoglobin + other proteins become cross linked by disulfide bridges
This forms insoluble aggregates (Heinz bodies) attaching to RBC membranes, leading to haemolysis (destruction of RBCs)

32
Q

Which cells are worst affected by G6PDH deficiency

A

RBCs
Pentose phosphate pathway is only way they generate NADPH+ + H+
also, undergo oxidative damage
(glutathione in oxidused state)

33
Q

State how we can diagnose G6PDH Deficienecy

A

Full Blood Cell Count
G6PDH activity

34
Q

State symptoms of G6PDH Deficicency

A
  1. Haemolytic anaemia
    (Pallor, fatigue, jaundice)
35
Q

State treatment options for patients suffering with G6PDH Deficiency

A
  1. Blood transfusion
  2. Folic acid
  3. Splenoctomy (removal of spleen)

Med 2024-2028 (56 decks)

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