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MEH > MEH 1.2 > Flashcards

MEH 1.2 Flashcards

1
Q

What is the general formula of carbohydrates?

A

(CH20)n

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2
Q

Which glycosidic bonds are present in glycogen?

A

Alpha 1,4 and 1,6

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3
Q

What enzyme is present in the saliva and begins carbohydrate breakdown?

A

amylase

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4
Q

What enzymes are involved in carbohydrate breakdown in the small intestine?

A 
Disaccharidases:
Lactase
Sucrase 
Pancreatic amylase
Isomaltase
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5
Q

What is primary lactase deficiency?

A

Absence of lactase

Only occurs in adults

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6
Q

What symptoms are associated with lactose intolerance?

A 
Diarrhoea
Bloating 
Vomiting 
Flatulence
Rumbling stomach
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7
Q

What is secondary lactase deficiency and how does it differ from primary lactase deficiency?

A

Caused by injury to small intestine - gastroenteritis, coeliac disease, crohn’s disease, ulcerative colitis

  • occurs in both infants and adults
  • generally reversible
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8
Q

How are monosaccharides taken up into the intestinal epithelial cells?

A

Active transport by sodium-dependent glucose transporter (SGLT1)

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9
Q

How are monosaccharides transported into the blood from the epithelial cells?

A

Facilitated transported using GLUT2 transporter

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10
Q

Where is GLUT2 expressed?

A

Kidney, liver, pancreatic beta cells, small intestine

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11
Q

Where is GLUT4 expressed, why is this transported particularly important?

A

Adipose tissue
Striated muscle
Insulin regulated

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12
Q

Which cells have an absolute requirement for glucose?

A 
Erythrocytes - no mitochondria 
Neutrophils
Innermost cells of kidney medulla 
Lens of the eye 
CNS prefers glucose
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13
Q

Give an example for the clinical application of glycolysis.

A

The rate is increased in cancer.
This can be measured by using a radioactive modified hexokinase substrate (FDG) and imagine with position emission tomography.

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14
Q

Which enzyme is the main, key regulator of glycolysis?

A

Phosphofructokinase

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15
Q

How is PFK allosterically regulated?

A

ATP inhibits

AMP stimulates

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16
Q

How is PFK hormonally regulated?

A

Insulin stimulates

Glucagon inhibits

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17
Q

What is the difference between hyperlactaemia and lactic acidosis?

A

Hyperlactaemia - 2-5mM, no change in blood pH (buffered)

Lactic acidosis - >5mM, blood pH lowered

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18
Q

Deficiency of which 3 enzymes will result in galactosaemia?

A
  • Galactokinase
  • Uridyl transferase
  • UDP- galactose epimerise
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19
Q

Which enzyme is absent in essential fructosuria, is there any clinical significance?

A

Fructokinase

No clinical signs, fructose in urine

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20
Q

Which enzyme is absent in fructose intolerance, what is the clinical significance?

A

Aldolase
Fructose-1-P accumulates in the liver, causing damage
Treatment - remove fructose from diet

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21
Q

What is the starting substrate of the pentose-phosphate pathway?

A

Glucose-6-phosphate

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22
Q

Which enzyme is responsible for the first step in the pentose phosphate pathway?

A

G6PDH

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23
Q

Pentose phosphate pathway is an important source of NADH. What is this required for?

A
  • reducing power for biosynthesis of steroids and fatty acids
  • maintenance of GSH levels
  • detoxification reactions
24
Q

Other than NADPH, what else does the pentose phosphate pathway produce?

A

C5- sugar ribose

25
Q

What is ribose needed for?

A

Synthesis of nucleotides, DNA and RNA

26
Q

What is the rate-limiting enzyme of the pentose-phosphate pathway?

A

Glucose 6-phosphate deyhydrogenase

27
Q

Where do both glycolysis and the pentose phosphate pathway occur?

A

Cytosol

28
Q

What dietary component does the enzyme salivary amylase hydrolyse?

A

Starch.

Amylase in both saliva and pancreas break down starch and glycogen to dextrins and monosaccharides.

29
Q

What is congenital lactase deficiency?

A

Autosomal recessive defect in lactase gene - extremely rare

Cannot digest breast milk

30
Q

Which enzyme converts DHAP to glycerol phosphate?

A

Glycerol 3-phosohate deyhydrogenase

31
Q

Which tissues produce glycerol phosphate?

A

Adipose & Liver

32
Q

What is glycerol phosphate used for?

A

Combined with fatty acids to form TAG in liver and adipose tissue.

33
Q

Which enzyme coverts 1,3 bpg to 2,3 bpg?

A

Bisphosphoglycerate mutase

34
Q

Which cells produce 2,3-BPG, what does it do?

A

Red blood cells, promotes release of oxygen

35
Q

Which enzyme is used to regenerate NAD+ from NADH in anaerobic conditions or cells lacking electron chain?

A

Lactate dehydrogenase:

NADH+ + pyruvate -> lactate + NAD+

36
Q

What is the normal plasma lactate concentration?

A

<1 mM

37
Q

What lactate conc is considered hyperlactaemia?

A

2-5 mM

38
Q

What are the consequences of hyperlactaemia?

A

Still below renal threshold, no change in blood pH as buffered

39
Q

What lactate conc is considered lactic acidosis?

A

> 5mM

40
Q

Why is lactic acidosis an important clinical marker?

A

Suggests acutely unwell patient. Lactate levels above renal threshold and pH of blood becomes lowered.

41
Q

Deficiency of which 3 enzymes can cause galactosaemia?

A

UDP- galactose epimerase
Uridyl transferase
Galactokinase

42
Q

What occurs in essential fructosuria?

A

Fructokinase deficiency.
No conversion of fructose to fructose-1-P, fructose excreted in urine.
No clinical signs

43
Q

What occurs in fructose intolerance?

A

Aldolase enzyme deficiency.

Accumulation of Fructose 1-P in the liver, causing liver damage.

44
Q

What substate goes the pentose-phosphate pathway start from?

A

Glucose 6P

45
Q

What enzyme is the rate limiting enzyme in the pentose-phosphate pathway?

A

Glucose-6P- dehydrogenase

46
Q

What does the pentose-phosphate pathway produce?

A 
NADPH
Ribose sugar (5C)
47
Q

What is NADPH needed for?

A

Reducing power for biosynthesis
Maintenance of GSH levels
Steroid biosynthesis
Detoxification reactions

48
Q

What is ribose sugar needed for?

A

Synthesis of RNA, DNA, co-enzymes and nucleotides

49
Q

Does the pentose-phosphate pathway produce ATP?

A

No

50
Q

Explain the clinical consequences of severe protein deficiency in children.

A

Reduced rate of protein synthesis as lack of amino acids:
Growth failure.
Tiredness, weakness, poor exercise tolerance
 Impaired mental development
 Negative nitrogen balance due to Nin < Nout
 Oedema
 Increased risk of infection- reduced immunoglobulin
 Anaemia- reduced haemoglobin synthesis.
 Fatty liver- reduced lipoprotein synthesis.

51
Q

What reaction is catalysed by creatine kinase?

A

Creatine phosphate + ADP ->  ATP + creatine

52
Q

What conditions may lead to increased plasma lactate?

A

Decreased utilisation: liver disease, thiamine deficiency and during alcohol metabolism.
Increased production: strenuous exercise, hearty eating, shock and congestive heart disease

53
Q

Compare and contrast the functions of glycolysis in adipose tissue, skeletal muscle and red blood cells.

A

Red blood cells -only way to produce ATP, 2,3 -BPG intermediate
Skeletal muscle - ATP during anaerobic conditions
Adipose - minor ATP source, glycerol phosphate production

54
Q

Which is the most common form and more severe form of galactosaemia?

A

Galactose -1P uridyl transferase deficicency

55
Q

Which form of galactosaemia is less severe and less common?

A

Galactokinase deficiency

56
Q

Why is Uridyl transferase deficiency more severe than a galactokinase deficiency?

A

Both galactose and Galactose 1P accumulate in tissues

57
Q

What cofactor is needed for glutathione peroxidase?

A

Selenium

MEH (19 decks)

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