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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

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
Describe tissue distrobution of GLUTs
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
Explain causes of lactose intolerance
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
Describe consequences of lactose intolerance
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
State symptoms of lactose intolerance
1. Abdominal pain 2. Bloating 3. Diarrhoea 4. Discomfort 5. Nausea symptoms should appear 30 - 120 min following lactose consumption
29
Describe the diagnosis of lactose intolerance
1. Positive hydorgen breath test 2. Positive stool acidity tesy
30
Describe management of lactose intolerance
1. Decrease / elimination of lactose in diet 2. Consumptuon of lactase-treated foods / lactase supplements
31
Describe glucose requirements of tissues
1. 180g glucose needed per day in human body 2. Optimum blood glucose level 5mM 3.
32
Describe the 2 phases of glycolysis
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
Describe phase 1 of glycolysis
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
State regulatory points in glycolysis
Reaction 1 Reaction 3 Reaction 10 -ve delta G Highly exergonic Irreversible
35
Describe phase 2 of glycolysis
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
Diagram showing reactions 7-10 of glycolysis
37
Describe the causes, effects, diagnosis and management of PKD (Pyruvate Kinase Deficiency)
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
Glycolysis equation
39
Which reactions in glycolysis consume ATP and how many ATP molecules are consumed?
Reaction 1, Reaction 3 2 moles of ATPused per mole of glucose TO INITIATE THE PATHWAY
40
Which reactions in glycolysis synthesise ATP and how many ATP molecules are synthesised per molecule of glucose?
Reaction 7, Reaction 10 4 moles of ATP are produced per mole of glucose
41
Overall, what is the net number of ATP molecules produced in glycolysis
Net of 2 ATP per mole of glucose
42
43
Describe the role of anaerobic glycolysis
1. Allows for production fo ATP in absence of sufficient oxygen
44
State locations where anaerobic glycolysis occurs
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
State 2 common situations where anaerobic glycolysis is likely to occur
Vigorous exercise of muscle Poorly oxygenated tissue (tissues of GI tract)
46
Describe the reactions involved in anaerobic glycolysis
Involves 10 normal steps from glycolysis + 11th reaction: Pyruvate reduced to lactate via lactate dehydrogenase NADH+ re-oxidised
47
State overall reaction equation of anaerobic glycolysis
48
Describe what happens to the lactate that is produced in anaerobic glycolysis CORI CYCLE
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
Diagram of Cori Cycle with locations
FOCUS ON OTHER DIAGRAM - muscle - blood - liver
50
Describe lactate production in a physiological and pathological state
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
What factors determine the rate of plasma lactate concentration?
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
Hyperlactatemia
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
Lactic acidosis
Above 5mM in blood Above renal threshold - kidneys can not remove excess lactate Blood pH lower (acidosis)
54
State symptoms of lactic acidosis
Form of metabolic acidosis 1. Nausea 2. Vomiting 3. Muscle weakness 4. Deep breathing
55
State management for lactic acidosis
Restoration of oxygen

Med 2024-2028 (56 decks)

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