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PJ1311 Semester 2 > Liver Anatomy & Functions > Flashcards

Liver Anatomy & Functions Flashcards

1
Q

How much cardiac output does the liver produce

A

25%

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2
Q

Name the 4 lobes

A

Major- left and right
Minor - caudate and quadrate

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3
Q

List the main ducts in the liver

A

Common hepatic
Cystic
From gallbladder
- common bile duct/ joining pancreatic duct at hepatipancreatic ampulla

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4
Q

Where do the common bile duct and pancreatic duct join

A

Hepatopancreatic ampulla

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5
Q

Name the capsule of connective tissue surrounding the liver

A

Glisson’s capsule

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6
Q

What do the hepatic artery and portal vein supply

A

Artery- oxygen rich
Vein- nutrient rich

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7
Q

What does the celiac artery filter blood from

A

Stomach spleen and pancreas

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8
Q

What does the superior mesentric artery collect blood from

A

Pancreas
SI
Colon

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9
Q

What does the inferior mesentric artery collect blood from

A

Colon

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10
Q

Where does the portal vein deposit its contents

A

Sinusoids

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11
Q

Describe the structure of liver lobules

A

Hexagonal structure containing hepatocytes
Radiate outward from central vein
At each six corners is a portal triad
Contains sinusoids

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12
Q

Other terms for hepatic cells

A

Hepatocytes

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13
Q

Function of sinusoids

A

Specialised capillaries large and fenestrated

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14
Q

Function of kupffer cells

A

Fixed macrophages with phagocytic function

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15
Q

Function of stellate cells

A

Storage of vit A, when activated become fibrous

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16
Q

Function of basolateral membrane

A

Between hepatocytes and space of disse
Has microvilli

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17
Q

Function of apical membrane

A

Makeup bile canaliculi

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18
Q

Where is oxygen highest and metabolic pathways that occur

A

Periportal cells
Gluconeogenesis/ b oxidation
Nutrient/ oxygen

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19
Q

Where is o2 supply the lowest and metabolic pathways that occur

A

Central vein

Glycolysis
Lipogenesis
B catenin/ signalling

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20
Q

Liver injury at periportal cells

A

Autoimmune hep
Iron overload injury
Billiary cirhosis

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21
Q

Liver injury at central vein

A

Nafld
Drug alcohol toxicity
Parasite infection fibrosis

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22
Q

Describe the route of bile

A

Bile canaliculi to bile duct
Then common hepatic duct

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23
Q

Function of bile

A

Emulsify fats

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24
Q

What is stored in gallbladder and how is it stimulated

A

Bile not immediately needed for digestion, stimulated by CCK & secretin

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25
Q

What are bile acids derived from

A

Cholestrol

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26
Q

Mechanism of Action of bile- how does it work

A

In conjugation to taurine and glycine, increases polarity of molecules

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27
Q

Function of sinusoidql transporter ntcp

A

Bile acid transporter, symport with sodium

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28
Q

Function of oatp sinusoidal transporter

A

Organic anion transporter protein
Into hepatocyte and blood

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29
Q

Function of oct

A

Into hepatocyte and blood

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30
Q

Function of mrp4

A

Transport drug metabolite back into blood

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31
Q

Function of biliary transporter mrp2

A

Bilirubin transported to bile

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32
Q

Function of biliary transporter abcg

A

Cholestrol

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33
Q

Function of biliary transporter mdr3

A

Pc

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34
Q

Function of biliary transporter bsep

A

Bile salts

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35
Q

Function of biliary transporter mdr1

A

Drug and metabolites

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36
Q

Function of biliary transporter bcrp

A

Steroid derivatives

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37
Q

Function of mdr1, abcb1 (p gylcoprotein) in the body

A

Found in liver gi tract kidneys and brain
Pump materials out of brain,
Activity can be both induced and inhibitted

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38
Q

Enzyme which activates bilirubin

A

Uridine glucournayl transferase

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39
Q

Methods of excretion for bile

A

Feces
Urine
Enterohepatic circulation

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40
Q

Functions of liver

A

Metabolic
Synthesis
Breakdown
Storage of vitamins
Excretion of waste products from blood stream to bile

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41
Q

Carbohydrate and lipid metabolism

A

Gluconeogenesis
Glycogenolysis
Glycogenesis

Cholestrol synthesis
Lipogenesis

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42
Q

At basal state what happens to blood sugar levels

A

Decreased glucose and insulin
Increased glucagon

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43
Q

At starved state what happens to blood sugar levels

A

Decreased insulin and glucose
Increased glucagon
Acetyl CoA supply straight to the brain

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44
Q

Hormones involved in glycogen mobilisation

A

Insulin
Glucagon
Adrenaline

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45
Q

Target organs involved in glycogen mobilisation

A

Liver and muscle

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46
Q

Key enzymes regulated from glycogen mobilisation

A

Glyogen synthase and phosphorylase

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47
Q

Function of glycogen phosphorylase

A

Removal of glucose residues

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48
Q

How is glycogen phosphorylase controlled

A

Kinase - active
Phosphatase- inactive

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49
Q

Why is glycogen synthase switched off

A

Stop a futile cycle

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50
Q

Function of glycogen synthase

A

Regulate synthesis of glycogen

51
Q

Why do we need protein synthesis

A

Amino acids
Albumin
A/b globulins
Tranferrin
Hormones

52
Q

Why do we need aa for breakdown

A

Bd insulin and other hormones
Amino acid metabolism
Ammonia to urea
Drug metabolism

53
Q

Enzymes used in amino acid formation

A

Transaminase
Aminotransferase

54
Q

Function if glutamate dehydrogenase

A

Release ammonia
And generate nadph

55
Q

Enzyme for glutamine synthesis

A

Glutamine synthetase

56
Q

Enzyme for glutamine hydrolysis

A

Glutaminase

57
Q

What can increased urea levels cause

A

Cerebral oedema

58
Q

Function of orthinine transcarbamylase

A

Turns carbsmoyl phosphate and orthinie into citrulline

59
Q

Effect of OTc deficiency in urea cycle

A

Build up of toxic ammonia levels= hyperammonemia

60
Q

Definition of drug metabolism

A

Process by which biochemical reactions alter drugs into the body

61
Q

Another term for drug metabolism

A

Drug biotransformation

62
Q

What can cause a loss of pharma activity in liver

A

Change in structure

63
Q

What are pro drugs and toxic metabolites a product of

A

Change ins structure

64
Q

Why are substances excreted by liver

A

Lipophillic xenobiotics are not elimintaed efficiently by kidney

65
Q

What does the process of biotransformation do

A

Parent drug turned imore polar

66
Q

Difference between phase 1 and phase 2 reactions

A

Phase 1 unmasks chemical reactive functional group
phase 2 conjugates endogenous molecule onto functional group

67
Q

Examples of phase 1 reactions

A

Oxidation
Reduction hydrolysis

68
Q

Examples of phase 2 reaction

A

Sulphation
Glucuronidation
Acetylation
Methylation

69
Q

Describe cytochrome p450

A

Haem proteins that catalyse monooxygenase reactions

70
Q

What does cytochrome p450 play an important role in

A

Primary mediators of phase 1 reactions

71
Q

Requirements for p450 catalytic cycle

A

Molecular oxygen
Nadph
Lipid- membrane bound endoplasmic reticulum

72
Q

How do we classify isoforms of cyp p450

A

Homology of primary amino acid sequence

73
Q

Why are cytochromes considered first defence against xenobiotics

A

High catalytic versatility
Broad substrate specificity

74
Q

What do the different overlapping substrates cause in CYP

A

Different rates of metabolism

75
Q

In a phase two reaction, what will all enzymes be

A

Transferases

76
Q

What is the effect of phase 11 metabolism

A

More polar = more water soluble

77
Q

In a glucuronidation reaction what are the reactants

A

Glucuronic acid WITH
OH
COOH
NH2
SH
Forming an amide ester or thiol bond

78
Q

In a glutathione reaction, what does glutathione perixidase convert glutathione into

A

Reduced to oxidised

79
Q

In a glutathione reaction, what does glutathione reductase convert glutathione into

A

Oxidised to reduced

80
Q

In general terms, explain the steps of phase 1 and phase 11 reactions

A

Drug ——derivative———conjugate

81
Q

What will drug metabolism affect

A

Drug concentration

82
Q

What useful parameters are used for pharmacokinetics

A

Half life
Area under the curve

83
Q

Definition of half life

A

Time taken for concentration of drug to fall by half

84
Q

Definition of cmax

A

Highest concentration of drug in blood

85
Q

Definition if cmin

A

Lowest concentration of drug in blood

86
Q

Factors affecting drug metabolism

A

Disease-liver
Genetic factors-
Polymorphic distribution

87
Q

Definition of poor metaboliser

A

Lackijg active gene allele

88
Q

Definition of intermediate metaboliser

A

Homozygous for 2 reduced activity gene alleles
OR
Heterozygous for inactive allele

89
Q

Definition for extensive metaboliser

A

Normal complemenet of 2 fully active gene alleles
Expect response to standard dose

90
Q

Definition of ultrarapid metaboliser

A

More than 2 copies of active gene alleles

91
Q

Three types of activation

A

Induction
Auto induction
Heteroinduction

92
Q

Concerns regarding clinical implications of cyp induction

A

Reduction in pharma effect
Induction leads to toxicity

93
Q

3 types of inhibitors

A

Competitors
Non competitive inhibitors
Irreversible inhibitors

94
Q

Effect of comp inhibitor

A

Most common
Como for active site

95
Q

Effect of non comp inhib

A

Form inactive intermediate with enzyme = decreased enzyme activity

96
Q

Effect of irreversible inhib

A

Substrate inactivates enzyme
Time dependent loss of enzyme activity
Aka suicide inhibitors

97
Q

What is the effect of administering a cyp inhihitor with a drug

A

Slower rate of clearance

98
Q

Propranolol and metoprolol can have interaction with:

A

Fluoxetine
Paroxetine
Antidepressants
Quinine
Cyp2d6 inhibitors

99
Q

What can st johns wart interact with

A

Enzyme inducers
Inducing hepatic cyt p450 and intestinal p glycoproteins

100
Q

Increased blood levels of calcium and statins naturally is due to

A

Grapefruit juice containing furancoumarins which inhibit cyp3a4 in gut wall and liver

101
Q

Steatosis

A

Fatty liver due to alcohol
Nonalcoholic fatty liver due to diabetes

102
Q

Cholestasis

A

Blockage of bile flow leading to jaundice

103
Q

Cirrhosis

A

Loss of lobular structure

104
Q

Causes of cirhosis

A

Alcohol abuse
Hep b c
Errors of metab
Adverse drug reaction

105
Q

Symtoms of cirrhosis

A

Blockage of venous flow leading to hypertension
Biliary obstruction leading to jaundice
Liver cell failure - decreased metabolism

106
Q

Symptoms of portal hypertension

A

Hypersplenism
Neutropenia
Thrombocytopenia
Marked ascites

107
Q

List Treatment of cirrhosis

A

Prevention of fibrosis
Limit fluid retention/encephalopathy
Avoid alcohol
Ascites if present reduce salt intake and diuretics

108
Q

Causes of hepatitis

A

Liver inflammation leading to celullar necrosis
Due to viral/alcohol/drugs

109
Q

Symptoms of acute viral hepatitis

A

Less than 6 months
Nausea/vomiting
Increased bilirubin

110
Q

Symptoms of chronic viral hep

A

More than 6 months
Asymptomatic
Fever/fatigue

111
Q

Treatment of viral hepatitis

A

Rest
Low fat diet
No alcohol
Avoid contact

112
Q

Acute alcoholic hepatitis

A

Hep inflammation and necrosis
Similer symp to HAV
No alcohol

113
Q

Treatment for Drug induced hep mimick acute viral hep

A

Drug withdrawal

114
Q

Gallbladder disorder
Treatment methods

A

Cholangitis
Bile duct inflamed
Vomiting and pain
Antibacterial/IV fluids
Surgery

115
Q

Cholecystisis
Different types
With treatment methods

A

Inflammation of gall bladder
Acute and chronic
Retained bile in gallbladder
Pain/jaundice
Opioid analgesics
Antibac drugs

116
Q

Overdose of paracetamol can lead ti

A

Hepatotoxicity

117
Q

Explain the effect of taking paracetamol overdose

A

Glucuronide saturation = sulphate/gsh conjugate depletion

=== increased toxicity’s

118
Q

List sinusoidal transporters

A

Ntcp
Oatp
Oct
Mrp4

119
Q

List biliary transporters

A

MRP2
Abcg 5/8
Mdr3
Bsep
Mdr1
Bcrp

120
Q

What enzyme activates glycogen synthase

A

Protein kinase a

121
Q

What stops glycogen syntahse

A

Phosphoproteun phosphatase 1

122
Q

What can CYP450 be also known as

A

Mixed function oxidase

123
Q

Requirements for mixed function oxidase

A

Molecular oxygen
Nadph
Lipid (membrane bound endoplasmic reticulum)

PJ1311 Semester 2 (6 decks)

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