MEH Flashcards

1
Q

How do you calculate BMI?

A
  • Weight/ height in metres squared= kg/msquared
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2
Q

If a patients BMI is 31.9kg/m squared what would you class them as?

A
  • Obese
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3
Q

What is the energy requirement for sedentary males?

A
  • <12,000 kj/day
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4
Q

If carbohydrates, protein and fat do not add up to a total daily energy intake, what else could be the extra source of energy?

A
  • Alcohol
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5
Q

What part of a patients diet would give you cause for concern?

A
  • Lipid content is too high
  • protein content is too low
  • alcohol too high
  • low vitamin, mineral and fibre intake
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6
Q

If someone went on a crash diet and this involved extended periods of fasting what would be the order in which potential fuel molecules would be mobilised and utilised?

A
  • Glucose from glycogen
  • Glucose from gluconeogenesis
  • Fatty acids from glycerol and adipose tissue
  • Ketone bodies from fatty acids via acetyl co-a
  • Glucogenic and ketogenic amino acids from muscle protein
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7
Q

How can an overdose of paracetemol cause damage to the liver?

A
  • With high levels of paracetemol the normal metabolic pathway is saturated so metabolism switches to a pathway which produces toxic products (NAPQI)
  • NAPQI has direct toxic effects to hepatocytes
  • NAPQI undergoes conjugation with glutathione and depletes hepatocytes of this important antioxidant
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8
Q

What is homeostasis?

A
  • The control of the internal environment within set limits
  • A dynamic equilibrium
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9
Q

What is the Basal Metabolic Rate?

A
  • Energy required to maintain life
  • For the functioning of various tissues of the body at physical, digestive and emotional rest
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10
Q

What can effect BMR?

A
  • Body weight
  • gender
  • Body temperature
  • Thyroid status
  • Pregnancy and lactation
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11
Q

Breifly describe how uncoupling proteins (UCPs) are involved in heat generation in the body

A
  • UCPs allow a leak of protons across the membrane
  • Reducing te p.m.f and the energy is dissipated as heat rather than ATP production
  • UCP1 is expressed in brown adipose tissue and is involved in thermogenesis
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12
Q

What is anabolism?

A
  • Building up of larger molecules from smaller ones
  • Requires energy
  • Reductive
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13
Q

What is Catabolism?

A
  • The breakdown of larger molecules into smaller ones releasing energy
  • Oxidative
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14
Q

Give an example of a catabolic pathway?

A
  • Glycolysis
  • Pentose phosphate pathway
  • Glycogenolysis
  • Lipolysis
  • Fatty acid oxidation
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15
Q

Give an example of an anabolic pathway?

A

Gluconeogenesis

Glycogenesis

Fatty acid synthesis

Ketogenesis

Cholesterol synthesis

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16
Q

Give an example of a high energy signal

A
  • ATP
  • NADH
  • NADPH
  • FAD2H
17
Q

Why is catabolism generally activated by low energy signals?

A
  • Low energy signals indicate that cell had inadequate energy levels for its immediate needs to catabolism needs to occur to release energy from fuel molecules
18
Q

State three anabolic processes that the TCA cycle provides precursors for

A
  • Amino acid synthesis
  • Haem synthesis
  • Fatty acid synthesis
  • Glucose synthesis
19
Q

Why are there no known human genetic defects causing complete deletion of an enzyme involed in the TCA cycle?

A
  • TCA cycle is essential for life in humans with respect to catabolism such that a genetic defect causing an enzyme deletion would be lethal
20
Q

Where, how and why is lactate produced?

A
  • Where- Tissues carrying anaerobic glycolysis e.g. exercising skeletal muscle, RBC, WBC, Kidney medulla
  • How- Lactate dehydrogenase converts pyruvate to lactate
  • Why- To enable NADH to be oxidised back to NAD so that glycolysis (When NAD-NADH) can continue, so some energy produced fro tissues without oxygen
21
Q

How is lactate utilised by the body?

A

Circulated in the blood and taken up by the heart muscle and liver

Lactate is converted to pyruvate by LDH

Pyruvate is catabolised in the heart

Pyruvate is used in gluconeogenesis in liver and kidney

22
Q

Why is a pateint with heart failure particularly prone to muscle cramping in exercise?

A
  • Muscle cramps are caused by acidosis
  • Patients heart failure means imparied oxygen supply to all tissues due to poor perfusion
  • Therefore increased anaerobic metabolism espeically in skeletal muscle during exercise which leads to increased lactate produced
  • the diseased heart may be unable to utilise the lactate
  • Disease heart may produce lactate
23
Q

Name two molecules that can cause metabolic acidosis and explain why

A
  • Ketone bodies
  • Pyruvate
  • lactate
  • Fatty acids
  • Amino acids
  • All contain acidic groups
24
Q

State two tissues in which glycogen is stored and state what these stores are used for in each tissue?

A
  • Liver- used to maintain blood glucose
  • Skeletal muscle- used to provide Glucose 6 phosphate to be catabolised via glycolysis to provide energy
25
Q

What enyzme controls Glygoen synthesis (Glycogenesis)?

A

Glycogen synthase

26
Q

What enzyme controls Glycogen degradation (glycogenolysis)?

A

Glycogen phosphorylase

27
Q

What features make tricylglycerol an efficient energy storage molecule?

A
  • Triacylglycerol is hydrophobic and so can be stored in an anhydrous form
  • Fatty acids in triacylglycerol are in highly reduced state so yield a lot of energy when oxidised
28
Q

Outline the hormonal signal, enzyme and resulting products in the mobilization of triacylglycerol from fat stores?

A
  • Glucagon or adrenaline stimulate the enzyme hormone sensitive lipase in adipose tissue to hydrolyse triacylglcerol yielding fatty acids and glycerol
29
Q

Briefly describe the process of oxidative phosphorylation

A
  • Reduced coenzymes are re-oxidised
  • Electrons are passed along electron transport chain to O2 releasing energy
  • Energy drives H+ transport across membrane
  • H+ gradient produced
  • H+ reenter via ATP synthase
30
Q

Briefly describe the effect of DNP on oxidative phosphorylation

A
  • DNP increases the permeability of the mitochondria membrane to H+
  • This uncouples electron transport from ATP
31
Q

Briefly describe why the effect of an inhibitor of a key enzyme in the electron transport chain such as cyanide is different to DNP?

A
  • An enzyme inhibitor such as cyanide disrupts the electron transport chain so that energy is not available to dribe the pumping protons to produce p.m.f
  • Without the p.m.f ATP is not produced and heat is not produced
  • Uncouplers such as DNP increase the permeability of the inner mitochondrial membrane to protons which collapses the p.m.f so ATP is not produced but potential energy of the p.m.f is dissipates as heat
32
Q

What are the differences between oxidative phosphorylation and substrate level phosphorylation?

A