Week 5 - Metabolism Flashcards Preview

(BMED) Formatives > Week 5 - Metabolism > Flashcards

Flashcards in Week 5 - Metabolism Deck (69):
1

A 32-year old male comes to see you in a GP surgery. He is concerned that his father died at the age of 50 from a heart attack and wants his blood cholesterol checked. You arrange for a fasting blood sample to be taken. The lab reports the following results:
• total serum cholesterol = 12 mmol/L (reference range = 3.5 – 6.5 mmol/L)
• serum triacylglycerol = 1.0 mmol/L (reference range 0.7 – 2.0 mmol/L)
• serum lipoprotein profile = increased amounts of LDL particles
What other analysis should you request and why?

Blood glucose to check for diabetes

2

What is the link between diabetes and cholesterol?

Diabetes raises LDL cholesterol

3

What is hyperlipoproteinemia?

Any condition resulting in raised blood cholesterol or triglycerides after a 12-hour fast

4

What is the prevalence of familial hypercholesterolemia?

1/250

5

What class of lipoprotein would not be present in a normal fasting blood sample?

Chylomicrons

6

What classes of lipoprotein would be present in a normal fasting blood sample?

LDL, VLDL, and HDL

7

Outline 2 pathways by which tissues obtain the cholesterol they need.

1. Direct synthesis from acetyl CoA within the tissues themselves
2. Obtain cholesterol synthesized by LDLs in the liver

8

Name 3 treatment options for a patient presenting with high cholesterol.

1. Reduce dietary cholesterol intake
2. Statins to reduce synthesis of LDL in the liver
3. Bile salt sequestrants to increase disposal of cholesterol in the liver

9

What are the two main signs and/or symptoms treated by Paracetamol?

1. Pain
2. Fever (i.e., high body temperature)

10

Describe how paracetamol overdose damages the liver.

Normal phase II pathway is saturated ->
Switch to phase I pathway of drug metabolism ->
Production of NAPQI ->
Conjugation of NAPQI with glutathione (GSH) ->
Hepatocytes deprived of an important anti-oxidant defence

11

Compare necrosis and apoptosis.

Necrosis = unprogrammed cell death
Apoptosis = programmed cell death

12

Define homeostasis.

The control of the internal environment to achieve a DYNAMIC EQUILIBRIUM

13

Define the basal metabolic rate.

Energy required to maintain life at rest

14

Explain the mechanism of penicillin.

Prevents cross-linking of peptidoglycan (the main component of cells walls), leaving cells unable to grow and divide
Note: only affects gram-positive bacteria.

15

Compare gram-positive and gram-negative bacteria.

Gram-positive: thick cell wall, weaker (analogy: winter coat)
Gram-negative: thin cell wall, stronger (analogy: bulletproof vest)

16

List 4 mechanisms by which bacteria become resistant to penicillin.

1. Degradation of penicillin enzymes (i.e., β-lactamase)
2. Mutation of target site (i.e., penicillin binding proteins)
3. Increased efflux (due to rise in efflux pumps)
4. Decreased penetration (due to change in porins)

17

Describe how uncoupling proteins (UCPs) generate heat.

Allow protons to leak across the mitochondrial membrane ->
Dissipation of proton gradient ->
No ATP production ->
Excess energy released as heat

18

The presence of ___ in brown adipose tissue triggers thermogenesis.

UCPs (uncoupling proteins)

19

Lactate is produced by tissues carrying out ___ respiration.

Anaerobic

20

Anaerobic respiration is carried out by tissues low in ___.

Oxygen

21

List 4 areas where lactate is produced.

1. Red blood cells
2. White blood cells
3. Skeletal muscle
4. Kidney

22

How is lactate produced?

LDH (lactate dehydrogenase) reduces pyruvate

23

Lactate is reduced from pyruvate. How does this process allow glycolysis to resume?

Pyruvate accepts electrons from NADH ->
NADH is oxidised back to NAD+ ->
Glycolysis (where NAD+ -> NADH) can resume

24

Oxidation involves ___ electrons.

Losing

25

Which 3 parts of the body contain high concentrations of LDH (lactate dehydrogenase)?

1. Heart muscle
2. Liver
3. Kidney

26

How is LDH (lactate dehydrogenase) circulated through the body?

Via blood

27

List 5 molecular forces involved in maintaining protein structure.

1. Hydrogen bonds
2. Covalent bonds
3. Ionic forces
4. Hydrophobic forces
5. Van der Waals forces

28

List the 3 components of a protein’s structure that determine its ionisation state.

1. R-group
2. Carboxyl-group
3. Amino-group

29

Compare the histological appearance of skeletal and cardiac muscle.

Skeletal: multinucleated, nuclei flat, nuclei peripheral, tissue organised into fascicles, largest cells
Cardiac: 1-2 nuclei, tissue branching, presence of intercalated discs

30

A 57-year old man with a predisposition to coronary heart disease complains of intense muscle cramps following rigorous exercise. You discover he has elevated levels of lactate in his blood. Describe why this patient is particularly prone to muscle cramps during exercise.

Heart disease ->
Poor circulation of blood (and thus oxygen) ->
Body relying on anaerobic respiration ->
Lactic acidosis ->
Muscle cramps

31

Molecules containing ___ groups can cause metabolic acidosis.

Acidic

32

List 6 molecules that can cause metabolic acidosis.

1. Ketones
2. Fatty acids
3. Amino acid
4. Pyruvate
5. Lactate
6. ATP (releases H+ when hydrolyzed)

33

Compare anabolism to catabolism.

Anabolism: building larger molecules from smaller ones, requires energy
Catabolism: breaking larger molecules into smaller ones, releases energy

34

In a reduction reaction, energy is ___.

Required
Remember: energy follows electrons

35

In an oxidation reaction, energy is ___.

Released
Remember: energy follows electrons

36

Gaining electrons ___ energy.

Requires
Remember: energy follows electrons

37

Losing electrons ___ energy.

Releases
Remember: energy follows electrons

38

List examples of anabolic and catabolic pathways.

Anabolic: gluconeogenesis, glycogenesis, ketogenesis, fatty acid synthesis, cholesterol synthesis
Catabolic: glycolysis, glycogenolysis, lipolysis, fatty acid oxidation, pentose phosphate pathway

39

List 4 high energy signals.

1. ATP
2. NADH
3. NADPH
4. FAD2H

40

What do low energy signals indicate?

Cell needs more energy for its immediate needs

41

Why is catabolism generally activated by low energy signals?

Catabolism releases energy from fuel molecules

42

Describe how skeletal muscle increases in mass as a result of exercise or steroid use.

Satellite cells divide and fuse with myofibres, leading to hypertrophy

43

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

Crucial cycle for sustaining life; enzyme deletion would be lethal

44

List 4 signs of very high blood cholesterol.

1. Corneal arcus
2. Xanthelasma
3. Xanthoma
4. High blood pressure

45

What is corneal arcus?

Blue, grey, or white ring around the cornea

46

What is xanthelasma?

Yellowish deposit of cholesterol around the eye

47

What is xanthoma?

Yellowish deposit of cholesterol under the skin

48

Glycogen is stored in small ___ in the cytoplasm.

Granules

49

List two tissues where glycogen is stored.

1. Liver
2. Skeletal muscle

50

What is the function of glycogen in the liver?

Regulate blood glucose

51

What is the function of glycogen in in skeletal muscle?

Provides glucose 6-phosphate to be metabolized via glycolysis for energy

52

Glycolysis as the first step for aerobic and ___ respiration.

Anaerobic

53

Which enzyme controls the synthesis of glycogen from glucose subunits?

Glycogen synthase

54

Which hormone activates glycogen synthase? (Hint: glycogen synthase converts glucose subunits to glycogen.)

Insulin

55

Which enzyme controls the degradation of glycogen to glucose subunits?

Glycogen phosphorylase

56

Which 2 hormones activate glycogen phosphorylase? (Hint: glycogen phosphorylase converts glycogen to glucose subunits.)

1. Glucagon
2. Adrenaline

57

What is the major energy storage molecule in animals?

Triacylglycerol (TAG)

58

Why is triacylglycerol (TAG) a more efficient energy storage than glycogen?

It is more reduced, so it releases more energy when metabolized

59

List 5 non-disease related causes of skeletal muscle atrophy.

1. Lack of use
2. Ageing
3. Malnutrition
4. Long-term steroid use
5. Injury (causing loss of innervation)

60

In response to low glucose, TAG in adipose tissue is hydrolyzed to yield which 2 sources of energy?

1. Fatty acids
2. Glycerol

61

Which protein transports fatty acids?

Albumin

62

Glycerol can feed into which pathway to produce energy?

Glycolysis

63

Describe the process of oxidative phosphorylation.

NADH and FADH2 re-oxidized to NAD+ and FAD ->
Release their electrons ->
Electrons passed down electron transport chain to form water with O2 ->
Release of energy ->
Energy used to pump H+ to the intermembrane space ->
Electrochemical gradient ->
H+ ions flow back to the mitochondrial matrix via ATP synthase ->
Addition of Pi to ADP ->
ATP produced

64

List the 2 main functions of oxidative phosphorylation.

1. Re-oxidize NADH and FADH2
2. Synthesize ATP

65

Briefly describe the effect dinitrophenol (DNP) has on oxidative phosphorylation

UNCOUPLES oxidative phosphorylation (i.e., allows protons to leak across the mitochondrial membrane -> dissipation of proton gradient -> no ATP production -> excess energy released as heat)

66

Describe the effect an inhibitor of a key enzyme in the electron transport chain (e.g., cyanide) would have on oxidative phosphorylation.

Electrons are unable to pass down the chain to form water with O2 ->
No energy to pump H+ to the intermembrane space ->
No electrochemical gradient ->
O2 deprivation + no ATP production

67

List 2 pathways involving substrate level phosphorylation.

1. Glycolysis
2. Krebs cycle

68

Describe substrate level phosphorylation.

Transfer of a phosphate from a substrate to ADP in coupled reaction

69

List 3 differences between oxidative phosphorylation and substrate level phosphorylation.

1. Location: electron transport chain vs. Krebs and citric acid cycles
2. Coenzymes: oxidation of NADH and FADH2 vs. reduction of FAD and NAD
3. Correlation: indirect phosphorylation vs. direct phosphorylation