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Semester 4 > PBL 5 > Flashcards

PBL 5 Flashcards

1
Q

The end product of glycolysis is different in aerobic and anaerobic conditions, what are these?

A

Aerobic - pyruvate produced

Anaerobic - lactate produced

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2
Q

How does glucose enter hepatocytes?

A

Via facilitated diffusion through the GLUT-2 transporter

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3
Q

How is glucose ‘trapped’ when it first enters hepatocytes?

A

It is converted to glucose-6-phosphate by hexokinase, this phosphorylation traps glucose in the hepatocytes

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4
Q

What reaction does hexokinase catalyse?

A

Conversion of glucose to glucose-6-phosphate

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5
Q

How does hexokinase IV differ in activity to hexokinase I-III?

A

Hexokinase I-III: activated at very low concentrations of glucose, and is a relatively slow enzyme

Hexokinase IV: only activated which glucose levels are high, but the speed of the enzyme is much higher. It increases in activity as the concentration of glucose increases

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6
Q

What is the rate limiting step in glycolysis?

A

The conversion of fructose-6-phosphate to fructose 1,6-bis-phosphate by phosphofructokinase 1 (PFK-1)

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7
Q

What is known as the point of no return in glycolysis and why?

A

The conversion of fructose-6-phosphate to fructose 1,6-bis-phosphate by phosphofructokinase 1 (PFK-1)

This reaction is irreversible

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8
Q

How is the enzyme phosphofructokinase 1 (PFK-1) regulated?

A

Activated by AMP and fructose 2, 6 bisphosphate

Inhibited by ATP and citrate

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9
Q

What reaction in glycolysis does PFK-2 regulate?

How?

A

The conversion of fructose-6-phosphate to fructose 1,6-bis-phosphate by phosphofructokinase 1 (PFK-1)

It regulates the activation of fructose 2,6-P, which is an activator on this reaction

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10
Q

How is the activity of PFK-2 regulated by glucagon?

How does this effect glycolysis?

A

Glucagon binds to hepatocytes causing cAMP signalling
This activates PKA which phosphorylates PFK-2
Phosphorylated PFK-2 is inactive
PFK-2 cannot stimulate fructose,2,6-P
Fructose 2,6-P cannot stimulate the action of PFK-1
This inhibits glycolysis, and stimulates Gluconeogenesis

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11
Q

How is the activity of PFK-2 regulated by insulin?

How does this effect glycolysis?

A

High insulin inhibits glucagon signalling
This means PFK-2 cannot be phosphorylated
Unphosphorylated PFK-2 is active
Active PFK-2 stimulates fructose,2,6-P
Fructose 2,6-P can then stimulate the action of PFK-1
This causes increased glycolysis

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12
Q

How many ATP are generated in glycolysis?

A

2 ATP

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13
Q

How is glucose converted to glycogen?

A

Glucose-6-phosphate converted to glucose 1-phosphate by phosphoglucomutatase

Glucose 1-phosphate converted to glycogen by glycogen synthase

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14
Q

How is glycogenesis regulated by glucagon?

A

Glucagon activates cAMP signalling which activates PKA
PKA phosphorylates glycogen synthase (branching enzyme) causing it to become inactive
This results in decreased glycogenesis

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15
Q

How does glucagon regulate glycogenolysis

A

Glucagon activates cAMP signalling which activates PKA
PKA phosphorylates glycogen phosphorylase (a debranhing enzyme) causing it to become active
This increases glycogenolysis

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16
Q

What happens when glycogen synthase is phosphorylated?

A

It becomes inactive

Glycogenesis is inhibited

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17
Q

What happens when glycogen phosphorylase is phosphorylated?

A

It becomes active

Glycogenolysis is activated

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18
Q

How does glucagon regulate Gluconeogenesis?

A

Represses pyruvate kinase - increasing the amount of PEP
Increasing expression of PEP carboxykinase - increasing PEP
Repressing F-2,6-BP by PFK-2: represses glycolysis

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19
Q

What cycle is pyruvate fed into following glycolysis?

A

The TCA cycle

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20
Q

How are express carbohydrates and proteins stored in the body?

A

As fatty acids (triacylglycerols) in adipocytes

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21
Q

What is the rate limiting step of fatty acid synthesis?

A

Conversion of acetyl-coA to malonyl-coA by acetyl co A carboxylase (ACC)

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22
Q

How is the conversion of acetyl-coA to malonyl-coA by acetyl co A carboxylase (ACC) regulated?

A

Activated by citrate
Inhibited by fatty acyl-CoA: negative feedback mechanism

Inhibited by glucagon: causes phosphorylation of ACC
Activated by insulin: inhibits glucagon

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23
Q

Through what process can energy be derived from stored fats in the presence of oxygen?

A

Beta oxidation

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24
Q

What compound are fatty acids most likely to be stored as?

A

Palmitoyl CoA (16 carbon chains)

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25
Q

How can energy be derived from stored fats in the absence of oxygen?

A

Through the production of ketone bodies

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26
Q

What are the two main ketone bodies?

A

Acetoacetate

3-hydroxybutyrate

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27
Q

Why can you get ketoacidosis in type I diabetes?

A

Absence of insulin, so glucagon cannot be suppressed
You get fasting signals despite being well fed
Fasting signals promote ketone body production for energy
Ketone bodes are highly acidic

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28
Q

What is the only nutrient that cannot be stored in the liver?

A

Protein - it has no storage form

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29
Q

Some amino acids are fed into ketone body production. They are either partially or fully ketogenic. Which amino acids are these?

A

Partially ketogenic - Phe, Try, Trp

Fully ketogenic - Leu, Lys

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30
Q

What reaction does alanine transaminase (ALT) catalyse?

A

Conversion of:
alanine + alpha-ketoglutamic acid > pyruvate + glutamate

ALSO DOES REVERSE REACTION

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31
Q

What reaction does aspartate transaminase (AST) catalyse?

A

Conversion of:
Aspartate + alpha-ketogenic acid > oxaloacetate + glutamate

ALSO DOES REVERSE REACTION

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32
Q

Compare ALT and AST and their specificity and amounts they are found in the liver?

A

ALT: more specific to the liver, found in small amounts
AST: less specific to the liver, found in large amounts

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33
Q

How is does peripheral excess ammonia get fed into the urea cycle

A

Excess ammonia is put into glutamine which is transported to the liver
Glutamine is converted into glutamate
Glutamate conversion into alphaketoglutarate by AST gives off aspartate
Aspartate is fed into the urea cycle

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34
Q

What does it mean if a drug has a small or large volume distribution?

A

Small volume distribution - drug tends to stay in bloodstream bound to plasma proteins, so is not widely distributed in the body
Large volume distribution - drug is more widely distributed in the body and is not bound to plasma proteins. Drug is probably more lipid soluble

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35
Q

What are the two phases of drug metabolism?

A

Phase I - functionalisation

Phase II - conjugation

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36
Q

What is the aim of drug metabolism?

A

To convert a drug from a lipid soluble to a water soluble form so it can be excreted in urine

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37
Q

What happens in phase I metabolism?

A

A drug is metabolised to produce or uncover a chemically reactive functional groups

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38
Q

At what stage of metabolism are pro drugs activated?

A

Phase I (functionalisation)

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39
Q

What are the most prominent enzymes of phase I metabolism?

A

Cytochrome p450

40
Q

What happens in phase II metabolism

A

A drug is conjugated to make it more water soluble and easier to excrete

41
Q

What is the role of the liver in the recirculating of some drugs?

A

Enterohepatic circulation

  • Addition of glucuronide to a drug by glucuronyl transferase in the liver
  • This is excreted in bile and into the GI tract
  • hydrolysis by beta-glucuronidase in the GI tract causes it to be reabsorbed
42
Q

Through what process can the liver extend the half life of a drug?

A

Enterohepatic circulation

43
Q

Which drugs are particularly susceptible to enterohepatic circulation?

A

Oestrogens
Rifampicin
Chloramphenicol
Morphine

44
Q

How does metabolism enzyme activity alter with age?

A

As you get older, it decreases, so may need to give lower dosages

45
Q

Why does drug metabolism increase during pregnancy?

A

Increased blood flow to kidneys and liver

Increased expression of metabolic enzymes

46
Q

What is the difference between a type A and type B adverse drug reaction?

A

Type A - exaggerated response to a drugs normal actions when given at a usual dose
Type B - a bizzare reaction to a drug that was not expected upon known pharmalogical actions of the drug

47
Q

How can cigarette smoking and alcohol effect drug metabolism?

A

It increases the metabolism of many drugs

48
Q

Name some dietary factors that effect metabolism

A

Metabolism inducers - BBQ meat, Brussels sprouts

Metabolism inhibitors - grapefruit juice

49
Q

What are the 3 types of liver toxicity?

A

Hepatocellular -
Cholestatic - bile obstruction
Mixed hepatocellular and cholestatic

50
Q

What are the immune cells of the liver called?

A

Kupffer cells

51
Q

What are bile acids synthesised from?

A

Cholesterol

52
Q

How do bile acids become bile salts?

What are the different types of bile salts?

A

They are conjugated

BA-Z (conjugated with taurine and glycine)
BA-Y (conjugated with sulphate and glucuronate)

53
Q

By what transporters are the different bile acids and bile salts secreted at the apical membrane into the canaliculi?

A

Bile salt export pump (BSEP) - secretes BA-Z and BA- (unconjugated bile acid)

Multidrug resistance associated protein 2 (MRP2) - secretes BA-Y

54
Q

What family of transport proteins do the BSEP and MRP2 belong to?

A

ABC (ATP binding cassette) transporter family

55
Q

How and where are bile acids reabsorbed in the intestines?

A

Unconjugated bile acids are reabsorbed all along the intestine in a passive manner

Conjugated bile acids are active reabsorbed in the terminal ileum

56
Q

How are the different bile acids and salts taken up by hepatocytes once they are reabsorbed?

A

BAH - simple diffusion
BA- (unconjugated bile acid): exchanged for chloride (OATP)
BA-Z (conjugated bile acid): co transport with sodium (NTCP)

57
Q

What is bilirubin?

A

It is a major end product of haemoglobin degradation - formed by the four pyrrole nuclei of heme

The colour is what gives bile its colour

58
Q

How is bilirubin taken up by hepatocytes and excreted in the bile canaliculi?

A

Free bilirubin is taken up by OATP (organic anion transport polypeptide) into hepatocytes

Bilirubin is conjugated and transported into canaliculi by MRP2 (Multidrug resistance protein 2)

59
Q

What is the fate of bilirubin once it enters the intestine?

A

Converted to urobilinogen - some of this is reabsorbed and excreted as urobilin (yellow) in urine

Some urobilinogen is converted into stercobilin (brown) - excreted in the feces

60
Q

What makes urine yellow?

A

Urobilin

61
Q

Why is bilirubin measured?

A

To assess liver function

62
Q

What is bilirubin usually conjugated with in the liver?

A

Glucuronide

63
Q

What is Jaundice a result of?

A

Excessive levels of serum bilirubin due a problem in the breakdown and excretion of bilirubin from the body

64
Q

What are the 3 types of jaundice and what are they caused by?

A

Pre-hepatic: problem with breakdown of haemoglobin
Intra-hepatic: problem with breakdown of bilirubin in liver
Postheaptic: problem with excretion of bilirubin from bile duct

65
Q

What is the pathogenesis of viral hepatitis?

A

Hepatitis infects hepatocytes in the liver
Antigen recognition of viruses by cytotoxic T cells
This results in destruction/apoptosis of hepatocytes

66
Q

Why are younger patients less likely to have symptoms of hepatitis?

A

Their immune system is underdeveloped, therefore the immune response to viral infection is reduced

The symptoms are due to the immune response

67
Q

What are the symptoms of hepatitis?

A 
Fatigue
Itching 
Nausea 
Jaundice
Right upper quadrant pain and tenderness
68
Q

How is hepatitis A spread?

A

Faecal-oral route

69
Q

What family of viruses does Hep A belong to

A

Picornavirus

RNA virus

70
Q

What type of hepatitis virus can occur due to indigestion of contaminated shellfish?

A

Hep A

71
Q

What is the most common hepatitis virus?

A

Hep A

72
Q

What is the pathophysiology of Hep A infection?

A

Replicates in liver
Acute infection
Tends to be self limiting and normally gets better in a couple of weeks

73
Q

What is the serological course of antibodies following Hep A infection?

A

Acute infection: IgM antibodies for hep A

Recovery or vaccinated state: IgG antibodies for hep A

74
Q

What is the vaccination called for hep A

A

Harvix

75
Q

How is hep E transmitted?

A

Faeco-oral route

76
Q

What type of virus is Hep E

A

Herpesvirus

RNA

77
Q

What are the different genotypes for Hep E and where are they found?

A

Genotype 1,2: water borne

Genotype 3,4: zoonotic, associated with undercooked pork

78
Q

What types of viral hepatitis can be spread by blood and bodily fluids?

A

B,C,D

Somewhat E

79
Q

What type of virus is Hep B

A

DNA

80
Q

How does the pathophysiology of hep B differ on the age of contraction of the virus?

A

If you are exposed early in life - this can lie dormant for some time and lead to a chronic infection
If you are exposed later in life - this can cause symptomatic infection

81
Q

What is the course of hep B infection if exposed early in life?

A

Immune tolerant stage - virus sits there as immune system is underdeveloped
Immune clearance stage - immune system develops and tries to clear virus
Inactive carrier stage - virus becomes inactive
Reactivation - cycles of inflammation and repair occur, leading to fibrosis

82
Q

What are the different viral proteins found in hep B diagnosis and what do they mean?

A

HBsAg (Hep B surface antigen) - this shows infection present
HBeAg (Hep B e antigen) - this shows virus is in a replicative state

83
Q

What defines chronic hep B infection?

A

If surface hep b antigen (HBsAg) is present for more than 6 months

84
Q

What are the host antibodies produced against Hep B infection?

A

Anti-Hbe - hepatitis B e antibody
Anti HBc (IgM, IgG) - hepatitis B core antibody
Anti HBs - hepatitis B surface antibody

85
Q

What type of antibody will be present if you have been vaccinated against Hep B

A

Anti-HBs: hepatitis b surface antibody

86
Q

What are the two approved NICE treatments for chronic Hep B infection?

A

Interferon (pegylated interferon)

Tenofovir/Entecavir

87
Q

How does interferon work in Hep B treatment?

How effective is it?

A

Stimulates the immune system

Has low efficacy (less than 25% of people benefit)
However when it does work it works well

88
Q

How do Tenofovir and Entecavir work in Hep B treatment?

Why are they lifelong treatments?

A

Act as nucleoside analogues which inhibit DNA polymerase

They cannot clear the cccDNA, therefore if you stop taking drugs then the virus will just return

89
Q

What type of virus is Hepatitis Delta?

A

RNA

90
Q

Which other hepatitis virus does hepatitis Delta require for replication?

A

Hepatitis B

91
Q

What type of virus is Hepatitis C

A

RNA

Flavivirus

92
Q

How likely is Hep C virus infection to become chronic?

A

25% clear virus

75% get the chronic infection

93
Q

How is hepatitis C infection treated?

A

Direct acting antivirals (DAAs) - target enzymes in HCV life cycle

Ribavirin - nucleoside Inhibitor, prevents viral RNA synthesis

94
Q

What kind of drug is sofosbuvir?

What is the mechanism of action?

A

It is a direct acting antiviral drug (DAA)

It inhibits the HCV NS5B RNA dependant RNA polymerase

95
Q

How does cortisol effect glucose levels?

A

Increases glucose levels by inducing:
Gluconeogenesis
Lipolysis

96
Q

Which hepatitis virus is associated with 20% mortality rate in pregnant women?

A

Hep E

97
Q

How much bile is secreted each day?

A

250mL - 1000mL

Semester 4 (10 decks)

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