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BRS/POM MOCKS > POM MOCK 2- Cholesterol, microbial infection, cell metabolism > Flashcards

POM MOCK 2- Cholesterol, microbial infection, cell metabolism Flashcards

1
Q

What can cause steatorrhea?

A

Lack of bile salts.

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2
Q

Why are lipids transported as lipoproteins?

A

Lipids are hydrophobic and so to transport in aqeuous plasma they have to be transported within proteins.

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3
Q

VLDL role?

A

Endogenous fat transport

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4
Q

HDL role

A

Reverse cholesterol transport

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5
Q

What does cholesterol in membranes do?

A

Alter membrane stiffness depending on temperature and nature of membrane.

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6
Q

Describe the structure of a lipoprotein

A

Phospholipid monolayer containing cholesterol and apoproteins surrounding core of triacylglycerols and cholesterol esters.

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7
Q

Where are cholesterol esters produced and how?

A

Produced in the plasma by transfer of an acyl chain from phosphatidylcholine (lecithin) catalyzed by lecithin:cholesterol acyltransferase.

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8
Q

How are LDL’s formed?

A

Addition of cholesterol esters to IDL (intermediate lipoprotein) from HDL to form LDL.

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9
Q

Explain lipoprotein transport pathways.

A

Liver produces VLDL which transports fatty acids produced in the liver to tissues to become a lipid depleted remnant. The remnant then loses its apoprotein to HDL and become IDL which gets cholesterols esters from HDL to form LDL. LDL then transports cholesterol to tissues and is uptaken by macrophages or the liver. HDL is involved in reverse cholesterol transport and takes cholesterol from tissues back to liver.

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10
Q

Familial hypercholesterolaemia mechanism?

A

Defect in gene that codes for LDL receptor.

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11
Q

How do statins work?

A

They reduce total cholesterol by inhibiting HMG-CoA reductase.

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12
Q

How do resins work?

A

Bind to bile acid cholesterol complexes preventing their reabsorption by the intestine.

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13
Q

What cancer does human papilloma viruses cause?

A

Cervical cancer.

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14
Q

Key points of prokaryotes

A

Don’t have internal membranes. Single copy of chromosome (haploid). Contain peptidoglycan in cell wall. Divide by binary fission. Poorly defined cytoskeleton.

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15
Q

Why are mutations expressed immediately in prokaryotes?

A

Only contain one copy of the gene.

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16
Q

What gives bacteria its shape?

A

Peptidoglycan in cell wall.

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17
Q

What kind of bacteria is Neisseria meningitidis?

A

Harmless commensal bacterium. Under certain conditions can become a potentially lethal disease that can cause sepsis and acute meningitis.

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18
Q

How does shigella spread?

A

Using host cell actin.

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19
Q

H. pylori (Heliobacter pylori) can cause what?

A

Peptic ulcer and gastric cancer.

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20
Q

Why are mutations more common in bacteria than humans?

A

Generation time is much quicker and haploid organism so only require one gene to have effect.

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21
Q

How does malaria and leishmaniasis replicate?

A

Formation of trophozoites inside a cell

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22
Q

What are protozoa?

A

Unicellular eukaryotes.

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23
Q

What are helminths?

A

Multicellular eukaryotes.

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24
Q

Which organism has greatest point mutation rate?

A

Viruses.

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25
Q

Why can’t glucose-6-phosphate diffuse out of cell?

A

Cause of the negative phosphate group. Makes molecule more reactive and can’t bind to glucose carriers.

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26
Q

What key enzyme regulates entry of sugars into glycolysis pathway?

A

Phosphofructokinase.

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27
Q

Deficiency in what glycolytic enzyme is fatal?

A

Triose phosphate isomerase.

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28
Q

Why is glycolysis described as substrate level phosphorylation?

A

Phosphate group is directly being transferred from a substrate (sugar intermediate) to ADP.

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29
Q

Why is pyruvate converted to lactate?

A

Allows continuation of glycolysis as NAD+ is regenerated by converting pyruvate into lactate and oxidising NADH to produce NAD+.

30
Q

Where is NAD+ needed in glycolysis?

A

Dehydrogenation of glyceraldehyde 3-phosphate into 1,3-bisphosphoglycerate.

31
Q

Why are molecules called high energy intermediates?

A

Hydrolysis of phosphate bond has high delta G. Very energetically favourable.

32
Q

How is pyruvate converted to acetyl CoA?

A

Decarboxylation. Addition of co enzyme A. NADH produced.

33
Q

What catalyses pyruvate to acetyl CoA?

A

pyruvate dehydrogenase complex

34
Q

Where are fatty acids converted into acetyl CoA?

A

Mitochondrial matrix.

35
Q

What else is produced in the conversion of fatty acids to acetyl CoA?

A

One molecule of FADH2 and NADH.

36
Q

What does one turn of the krebs cycle produce?

A

Three NADH molecules, One GTP molecule, one molecule of FADH2 and two molecules of CO2.

37
Q

What is produced from glycolysis?

A

Two molecules of pyruvate, 2 molecules of ATP and 2 molecules of NADH.

38
Q

What does creatine phosphate do?

A

Acts as a buffer for demand for phosphate.

39
Q

What allows acetyl CoA to donate the acetate group?

A

High energy thioester bond (C-S Bond) so it is readily hydrolysed.

40
Q

Why is thiamine required for proper PDH function?

A

Required for thiamine pyrophosphate which is a cofactor in PDH.

41
Q

Pyruvate to acetyl CoA products?

A

Acetyl CoA, NADH and CO2.

42
Q

Why does NADH high energy electrons need to enter the matrix of the mitochondria?

A

So that they can be used in oxidative phosphorylation and to regenerate NAD+ for glycolysis.

43
Q

In the glycerol phosphate shuttle what is the final destination for the electrons transferred to?

A

FAD and then to co-enzyme Q (part of electron transport chain).

44
Q

Where is the glycerol phosphate shuttle used in the body?

A

Skeletal muscle and brain

45
Q

Where is the malate aspartate shuttle used?

A

Liver, Kidney and heart

46
Q

What transports malate and aspartate across the mitochondrial membrane?

A

Antiporter. (As one molecule goes in another molecule leaves).

47
Q

What is the warburg effect?

A

Mutations in genes of Fumerase, Succinate, Isocitrate Dehydrogenase, decreases Kreb’s Cycle activity which enhances anaerobic glycolysis. Generation of lactate from glucose even in increased O2 availability.

48
Q

Where does the first step of B oxidation occur?

A

Outer mitochondrial membrane.

49
Q

How is acyl CoA transported into the mitochondrial matrix?

A

Carnitine shuttle. Acyl group binds to carnitine and acyl carnitine is transported in via a translocase. Acyl group is then transferred to a CoA molecule and carnitine is transported back out.

50
Q

Why are ketone bodies made?

A

Acetyl CoA produced from b oxidation of fatty acids can only be used if there is enough oxaloacetate. The body needs a plan b as oxaloacetate is used in gluconeogenesis and can sometimes be low in quantity. Also brain can’t use fatty acids and so they can only use glucose or ketone bodies.

51
Q

Where does fatty acid synthesis take place?

A

Cytoplasm.

52
Q

Enzymes in fatty acid synthesis?

A

Acetyl CoA carboxylase and fatty acid synthase.

53
Q

What carrier is used in b fatty oxidation?

A

CoA.

54
Q

What carrier is used in fatty acid synthesis?

A

ACP (Acyl carrier protein).

55
Q

Reducing power in fatty acid synthesis?

A

NADPH.

56
Q

Reducing power in b fatty oxidation?

A

FAD/NAD+

57
Q

Where does fatty acid elongation to increase fatty acid chain length above 16 carbons occur?

A

Mitochondria and endoplasmic reticulum.

58
Q

What class of enzymes catalyses conversion of saturated fatty acids to unsaturated fatty acids?

A

Desaturases.

59
Q

Why can’t red blood cells use ketone bodies?

A

They don’t have mitochondria.

60
Q

What energy sources can the brain not use?

A

Fatty acids.

61
Q

How is gluconeogenesis made energetically favourable?

A

Six phosphoanhydride bonds are broken (atp bonds).

62
Q

What occurs during anaerobic exercise?

A

Where there is a high demand for ATP, glucose transport from the blood can’t keep up with the high demand for glucose. Glycogen is therefore broken down. Lactate increases to allow continuation of glycolysis. Liver uses lactate to form glucose (gluconeogenesis lactate to pyruvate to glucose).

63
Q

Why does FADH2 produce less ATP than NADH?

A

FADH2 bypasses complex I when it is reoxidised. NADH therefore pumps more H+ ions into the intermembrane space and so produces more ATP.

64
Q

What does cyanide and azide target?

A

Haem group in cytochrome oxidase complex (Complex IV).

65
Q

How does cyanide and azide stop ATP production?

A

Blocks flow of electrons.

66
Q

How does malonate act as a metabolic poison?

A

Acts as a competitive inhibitor of complex II. Slows flow of electrons from succinate to ubiquinone.

67
Q

What happens during non shivering thermogenesis?

A

UCP-1 is activated. ATP synthase is bypassed and energy from H+ gradient is released as heat instead of producing ATP.

68
Q

How does Rotenone act as a metabolic poison?

A

Blocks transfer of electrons from complex I to co enzyme Q. Limits synthesis of ATP.

69
Q

How does oligomycin act as a metabolic poison?

A

Blocks protons from flowing down ATP synthase and so ATP can’t be produced in oxidative phosphorylation.

70
Q

How does DNP act as a metabolic poison?

A

Can move H+ ions across cell membrane reducing the concentration gradient of H+ ions. Reduces ATP synthesis.

BRS/POM MOCKS (23 decks)

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