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Med 2024-2028 > Metabolism 2.1 > Flashcards

Metabolism 2.1 Flashcards

1
Q

State the 2 types of pathways involved in metabolism

A

Catabolic - breakdown
Anabolic - Synthetic

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2
Q

State the role of catabolism

A

Breakdown of chemicals to release

  1. Organic precurors e.g. pyruvate)
  2. Reducing power (NADH+ + H+)
  3. Energy (ATP)
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3
Q

Describe stage 1 catabolism

A
  1. Extracellular - GI tract
  2. Carbs, fats, proteins digested to monosaccharidesm fatty acids + glycerol, amino acids
  3. These fuel molecules absorbed from GI tract into circulation

NO ENERGY PRODUCED

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4
Q

Describe stage 2 catabolism

A
  1. Intracellular (cytosol + mitochondria)
  2. Fuel molecules transported to tissues and then converted into various metabolites
  3. This stage is oxidative - metabolites are all oxidised. This requires H+ carriers which are then reduced. Reducing power is released. Some energy produced as ATP
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5
Q

Describe stage 3 catabolism

A

TCA cycle / Krebs cycle / Citric acid cycle

  1. Intracellular (MITOCHONDRIA)
  2. Oxidative: Metabolites oxidised during this process:
    - Acetyl CoA oxidised to CO2
    - Requires H+ carriers: NAD+, FAD
    - So, reducing power is released
    - Some energy produced as GTP (GTP is energetcially equivalent to ATP)
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6
Q

Describe Stage 4 Catabolism

A

Electron transport + ATP synthesis (oxidative phosphorylation)

  1. Intracellular (Mitochondria)
  2. Oxygen is required
  3. This is because electrons from NADH+ and H+ and FADH2 are moved to oyxgen (so, oxygen is reduced to water and NADH+ and H+ and FADH2 are re-oxidised to NAD+ and FAD)
  4. This free energy from electron transport is used to synthesise large amounts of ATP
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7
Q

Body composition and Dietry Intake of Carbohydrates

A

15% intake, only 1% stored (mainly in liver or skeletal muscle) in male / female
This is because they are required for energy.
As soon as they have entereted our systems, they are catabolised.

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8
Q

State groups present in carbohydrates

A
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9
Q

Why are most carbohydrates hydorphillic?

A

Conatain many -OH groups

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10
Q

Why do most carbohydrates require active transport to pass through membranes?

A
  1. Many -OH groups
  2. Making them hydrophillic
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11
Q

Why do carbohydrates require less energy than fatty acids to complete oxidation?

A

Partially oxidised - high ratio of Oxygen to Carbon atoms

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12
Q

How do we characterise monosaccharides?

A

Single sugar units (3-9 C atoms)

  1. Triose - 3C (most common) e.g. glyceraldehyde
  2. Pentose - 5C (ribose)
  3. Hexose - 6C (glucose, fructose, galactose)
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13
Q

What are monoscaccharides which contain aldehyde groups most commonly called?

A

Aldoses - glucose, galactose

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14
Q

What are monoscaccharides which contain keto groups most commonly called?

A

Ketoses - fructose

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15
Q

Describe the 3D structure of trioses

A
  1. Asymmetric (chiral) carbon atom
  2. Exits as stereoisomers
  3. Mirror images of each other (enantiomers|)
  4. D-isomers: -OH on right
  5. L-isomers -OH on left
  6. Naturally occuring isomers are D-isomers
  7. Enzymes + receptors distinguish between D and L isomers
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16
Q

Describe the 3D structure of pentoses

A

Ring Structures

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17
Q

State the two structures of D-glucose

A

Alpha D glucose
Beta D glucose

The position of OH group on C1 determines whether D-glucose has alpha / beta structure
can be on bottom / top of carbon 1

2/3 of glucose = Beta-D glucose
1/3 of glucose = alpha D glucose
VERY SMALL AMOUNT: liner D-glucose

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18
Q

Polymers of monocaccharides

A
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19
Q

Describe formation of polymers of monosaccharides

A
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20
Q

State 2 types of glycosidic bonds

A
  1. alpha 1,4 glycosidic bonds: OH group below C1
  2. beta 1,4 glycosidic bond: OH group above C1
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21
Q

Polysaccharides table

A
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22
Q
A
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23
Q

Describe digestion of dietery carbohydrates

A
24
Q

Describe monosaccharide transport (talk about transport proteins involved)

A
  1. Glucose, galactose, fructose transported to enterocytes bt facilitated / active trabsport
  2. Enterocytes to blood via GLUT 2
  3. Enter target tissues via (GLUT 1-14)
  4. Tranport proteins include:
    - GLUT 2 (glucose transporter type 2)
    - SGLT 1 (Na+/glucose/galactose cotransporter)
    - GLUT 5 (fructose transporter type 5)
25
Q

Describe tissue distrobution of GLUTs

A

GLUT 1 - Eryhtocytes
GLUT 2 - liver, pancreatic beta cells, intestine, kidneys
GLUT 3 - Brain
GLUT 4 - fatty tissue, skeletal muscle, heart
GLUT 5 - jejunum, kidney

26
Q

Explain causes of lactose intolerance

A
  1. Loss / reductiomn of lactase activity
  2. Lactose not hydrolysed to glucose + galactose

GENETIC CAUSE
1. Lactase activity reduces after 5 years of age in most populations (especually African, Asian, most common)

NONGENETIC CAUSE
1. Injuty to small intestine (by: inflammatory bowel disease, surgery, infections, antibiotics)

27
Q

Describe consequences of lactose intolerance

A
  1. Undigested lactoe passed to large intestine
  2. Colonic bacteria ferment lactose and produce organic acids + gases
  3. Lactose + organic acids increase osmotic pressure + draw in water causing diarrhoea
  4. Gases cause abdominal cramps + bloating
28
Q

State symptoms of lactose intolerance

A
  1. Abdominal pain
  2. Bloating
  3. Diarrhoea
  4. Discomfort
  5. Nausea
    symptoms should appear 30 - 120 min following lactose consumption
29
Q

Describe the diagnosis of lactose intolerance

A
  1. Positive hydorgen breath test
  2. Positive stool acidity tesy
30
Q

Describe management of lactose intolerance

A
  1. Decrease / elimination of lactose in diet
  2. Consumptuon of lactase-treated foods / lactase supplements
31
Q

Describe glucose requirements of tissues

A
  1. 180g glucose needed per day in human body
  2. Optimum blood glucose level 5mM
    3.
32
Q

Describe the 2 phases of glycolysis

A

2 phases (10 steps)

  1. Phase 1 - Preperation - ATP consuming
    (REACTIONS 1-3)
    2 moles of ATP per mole of glucose are used
  2. Phase 2 - ATP generating
    (REACTIONS 4-10)
    4 moles of ATP per mole of glucose produced
33
Q

Describe phase 1 of glycolysis

A

REACTIONS 1-3

REACTION 1: Glucose phosphorylated to glucose-6-phosphate by hexokinase (glucokinase in liver)
This process prevents glucose going back through plasma membrane
This process also increases reactivity of glucose to permit subsequent steps

REACTION 2: Isomerisation of G-6-P to frtuctose-6-phosphate by phosphoglucose isomerase

REACTION 3:Phosphorylation of fructose-6-phosphate to fructose1,6 bis phosphate by phosphofructokinase-1
THIS IS A COMMITING STEP. The first step that commits glucose to glycolysis

34
Q

State regulatory points in glycolysis

A

Reaction 1
Reaction 3
Reaction 10

-ve delta G
Highly exergonic
Irreversible

35
Q

Describe phase 2 of glycolysis

A

REACTIONS 4-10

REACTION 4: Fructose-1,6-bis phosphate cleaved into 2x 3 carbon units by aldolase

3C unit 1: DHAP - Dihydroxyacetone phosphate
3C unit 2: Glyceraldehyde 3-phosphate (G-3-P)

REACTION 5: DHAP rapidly converted to G-3-P by triose phosphate isomerase
therefore, 2 molecules of G3P enter rest of glycolysis

REACTION 6: (redox reaction)
oxidation of aldehyde egroup in G3P- to a carboxyl group
Then, addition of inorganic phosphate forming 1,3-bis phosphoglycerate (1,3 - BPG). This reaction is catalysed by G-3-P Dehydrogenase
Reduction of NAD+ to NADH+ + H+
(reversible)

REACTION 7: substrate level of phosphorylation
Transfer of phosphoryl group from 1,3- bisphosphoglycerate to ADP to give ATP and 3 - phosphoglycerate by phosphoglycerate kinase

REACTION 8: 3-phosphoglycerate to 2-phosphoglycerate by phosphoglyceromutase

REACTION 9: dehydration of 2-phosphoglycerate to form phosphoenylpyruvate (PEP) by enolaase

REACTION 10: substrate level phosphorylation
Transfer of phosphoryl group from PEP to ADP to form pyurvate and ATP by pyruvate kinase
(large -ve delta g + irrerversible)

36
Q

Diagram showing reactions 7-10 of glycolysis

A
37
Q

Describe the causes, effects, diagnosis and management of PKD (Pyruvate Kinase Deficiency)

A

CAUSE:
- inherited deficicency in pyruvate kinase affecting RBCs
- Reduced ATP level in RBCs leads to defective metabolism
(reduced ATP level in RBC affects RBC shape, they become defective, broken down by body by haemolysis, removed from body via spleen)

EFFECTS:
- Haemolytic anaemia (premature destruction of RBCs)

SYMPTOMS
- pallor (white skin)
- jaundice
- weakness

DIAGNOSIS
- Direct enzyme assays
- Genetic tests
- FBC (full blood count)

MANAGEMENT
- Folic acid
- Blood transfusion
- Splenectomy (remove spleen)

38
Q

Glycolysis equation

A
39
Q

Which reactions in glycolysis consume ATP and how many ATP molecules are consumed?

A

Reaction 1, Reaction 3
2 moles of ATPused per mole of glucose
TO INITIATE THE PATHWAY

40
Q

Which reactions in glycolysis synthesise ATP and how many ATP molecules are synthesised per molecule of glucose?

A

Reaction 7, Reaction 10
4 moles of ATP are produced per mole of glucose

41
Q

Overall, what is the net number of ATP molecules produced in glycolysis

A

Net of 2 ATP per mole of glucose

42
Q
A
43
Q

Describe the role of anaerobic glycolysis

A
  1. Allows for production fo ATP in absence of sufficient oxygen
44
Q

State locations where anaerobic glycolysis occurs

A

RBCs - small no of mitochondria
Kidney medulla
Testes - small no of mitochondria
Lens + cornea
WBC - small no of mitochondria

are these examples of tissues which do not have mitochondria? yes they all are

45
Q

State 2 common situations where anaerobic glycolysis is likely to occur

A

Vigorous exercise of muscle
Poorly oxygenated tissue (tissues of GI tract)

46
Q

Describe the reactions involved in anaerobic glycolysis

A

Involves 10 normal steps from glycolysis + 11th reaction:

Pyruvate reduced to lactate
via lactate dehydrogenase
NADH+ re-oxidised

47
Q

State overall reaction equation of anaerobic glycolysis

A
48
Q

Describe what happens to the lactate that is produced in anaerobic glycolysis

CORI CYCLE

A
  1. Lactate released into blood
  2. Metabolised in liver, heart, kidney.
  3. Here, converted to pyruvate (pyruvate used to obtain energy)
  4. In liver, lactate used in gluconeogenesis, glucose produced from this is then released into blood. Glucose used by exercising muscle to produce ATP via CORI CYCLE
49
Q

Diagram of Cori Cycle with locations

A

FOCUS ON OTHER DIAGRAM
- muscle
- blood
- liver

50
Q

Describe lactate production in a physiological and pathological state

A

Physiological state:
1. Without exerctise: 50g / day
2. Strenuous exercise: 30g / 5 min

Pathological state:
Involving hypoxia:
- SHOCK
- CONGESTIVE HEART DISEASE
- ARTERIAL DISEASE
- BURNS
Other
-CANCER
-DRUG/TOXIN-RELEATED (metformin, alcohol)
-DEFECT IN METABOLIC PATHWAY

51
Q

What factors determine the rate of plasma lactate concentration?

A
  1. Lactate production
  2. Lactate utilisation (lower in liccer disease, vit thiamine, enzyme defiencies, high alcohol intake)
  3. Clearance (kidney) - kidney can clear lactate
52
Q

Hyperlactatemia

A

Plasma lactate conc too high
2-5mM in blood
No change in blood pH
Below renal threshold - kidneys can still remove the excess lactate

53
Q

Lactic acidosis

A

Above 5mM in blood
Above renal threshold - kidneys can not remove excess lactate
Blood pH lower (acidosis)

54
Q

State symptoms of lactic acidosis

A

Form of metabolic acidosis

  1. Nausea
  2. Vomiting
  3. Muscle weakness
  4. Deep breathing
55
Q

State management for lactic acidosis

A

Restoration of oxygen

Med 2024-2028 (56 decks)

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