Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Metabolism > Liver and Gallbladder > Flashcards

Liver and Gallbladder Flashcards

1
Q

where is the liver

A
  • Liver is in the right upper quadrant of the abdomen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the blood supply to the liver

A
  • ¾ of the blood supply of the liver is from the portal system
  • The rest of the blood supply of the liver is arterial, carries oxygen supplied blood from the celiac axis which is a branch of the aorta
  • All of the portal blood drains into the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where does the portal system come from

A
  • Portal system comes from the gut, this means that if you eat anything it goes through the digestive system and is absorbed through the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do the sinusoids carry

A
  • Sinusoids carry a mixture of oxygen and nutrient rich blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where do the sinusoids go

A

the drain into the central vein, this goes into the hepatic veins which drain back into the IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what lines the sinusoids

A
  • They pass the hepatocytes which line the sinusoids, the hepatocytes take out what they need and put back in what they want to excrete
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what organ also drains into the liver

A

the spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are kupffer cells

A

these are macrophage like cells that are part of the overall immune function of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are cholangiocytes lined cells

A
  • There are cholangiocytes lined cells that line into bile ducts and this makes bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what vessels include the portal tract

A

biliary ductile, portal venule and hepatic arterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

almost all carbohydrate ..

A

reaches the liver as glucose

- All carbohydrates needs to be changed to glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what makes up sucrose

A

fructose + glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what makes up lactose

A

galactose + glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what makes up starches

A

maltose + glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does glycogensis mean

A

storing glucose as glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does glycolysis mean

A

breakdown of glycogen into glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what happens if there is too much glucose

A
  • If there is too much glucose the liver can store it as glycogen, when it is needed glycogen can be converted back to glucose and be converted to glycogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what happens if there is not enough glucose

A
  • If there isn’t enough glucose around, gluconeogenesis (production of new glucose from things such as amino acids and glycerol) takes place
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the effect of insulin on the liver

A
  • Signals the fed state
  • It promotes glycogen synthesis
  • Supresses gluconeogenesis
  • Accelerates glycolysis – increases fatty acid synthesis
  • Reduces blood sugar levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where does insulin primarily act

A
  • Insulin acts primarily on the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are amino acids

A
  • Amino acids are the building block of proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is amino acid metabolism

A

it is a bidirectional process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the two different types of amino acids

A

essential and non essential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are essential amino acids

A

mino acids need to have in our diet as we cannot synthesis them our selves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how can we make new Amino acids from ones that we already have

A

transamination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is transamination

A

Non-essential fatty acids can be made by the liver form other amino acids = transamination (transfer of amino group to a keto-acid) by transaminase enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is transamination catalysed by

A

aminotransferases (alanine and aspartate aminotransferases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what happens if alanine and aspartate aminotransferases are detected in the blood

A

if these are detected in the blood then there is damage to the hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is deamination

A

deamination of the amino acid, this is when you need to get rid of the amino acid as it is in excess
- therefore you remove the amine group and turn it into an ammonium ion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what happens if the ammonium ions are not removed

A
  1. Produces ammonia and this ammonium this pushes the equilibrium back the opposite way towards more proteins causing the cells to be depleted of ketoglutarate (important in Krebs cycle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does excess ammonia lead to

A

deplete cell of ketoglutarate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what happens if you have a depleted storage of ketoglutarate

A
  • this impairs energy producing activity
  • The ammonia in astrocytes leads to increased osmotic pressure and astrocyte swelling – increasing the volume of the cells in the skull this creates pressure in the brain and leads to herniation, and problems of neural exchange
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how is the ammonium ion reduced

A
  • Ammonia is produced by deamination and gut bacteria

- Ammonia is reduced to the ammonium ion and the ammonium ion is converted to urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

describe how the urea cycle works

A
  • Ammonium ions and carbon dioxide go into the urea cycle and makes urea
  • Urea removed by urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does a raised serum level indicate

A
  • Kidneys are not working therefore they are unable to absorbed and excrete the urea and therefore it builds up in the blood
  • Or the patient has a high protein in the blood this is caused by an internal bleed, leads to lots of albumin in the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what does a low serum level indicate

A
  • has no effect on liver disease

- enzymes won’t work leads to low serum urea urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is plasma

A

is the cell free component of the blood (has no red and white blood cells)

38
Q

what is serum

A

is plasma without clotting factors (important as clotting factors can get in the way of some testing)

39
Q

what does plasma contain

A
  • Albumin – reduced albumin liver failure
  • Globulin
  • Clotting factors – reduced clotting factors liver failure
  • Water/glucose/electrolytes
  • 90% of plasma proteins are form the liver
40
Q

what is the benefits of protein in the blood

A
  • Protein in the blood makes sure that the blood stays in the vascular space
  • If liver fails less protein in the blood vessels meaning that the osmotic pressure is low meaning that the blood vessels leak water out into the tissue this is called oedema
41
Q

lipids are not

A

water soluble

42
Q

what do triglycerides breakdown into

A

fatty acids and glycerol

43
Q

why are lipids energy rich

A
  • Energy rich molecule triglycerides are, lots of carbon-carbon bonds which release energy when they are broken down
44
Q

what is it called when fats are synthesised in the liver

A

de novo lipogenesis

45
Q

what inhibits the breakdown of lipids

A

insulin

46
Q

how are free fatty acids metabolised

A
  • Free fatty acids can be used for beta oxidation in the mitochondria and this feeds into the krebes ccycle
47
Q

in what form are fatty acids shuttled around the Body

A

these can be formed from dietary chylomicrons, these can be shuttled around the body

48
Q

what happens if the liver is resistance to insulin

A

if the liver is resistance to insulin this means that insulin is ineffective therefore there is high blood glucose level, therefore you activate de novo lipogenesis, this is the starting point of non-alcoholic liver disease

49
Q

what does liver insulin resistance lead to

A
  • increased glucose
  • inappropriate gluconeogensis
  • imparted glycogen synthesis
  • impaired suppression of lipolysis in adipocytes such as glycerol and FFA
50
Q

what causes increases glucose in liver insulin resistance

A

(activates ChREBP)
– De novo lipogenesis (SREBP1)
– Activates PKCe (inhibits IR tyrosine kinase

51
Q

what causes Inappropriate gluconeogenesis in liver insulin resistance

A

– Abnormal as high glucose level in the blood, make new glucose from lots of different sources when you don’t need to be this is caused by FOXO-1

52
Q

what causes increases glucose in liver insulin resistance

A

– Akt2-mediated

– Glycogen is not made from the glucose

53
Q

what converts excess glucose to fatty acids

A

– SREBP-1c

– ChREBP

54
Q

what is ketogensis

A
  • In the absence of glucose (starvation) there needs to be blood supply and energy supply to the brain, therefore ether Brian uses ketogensis
55
Q

what switches off ketogenesis

A

switched off by insulin

56
Q

describe how ketogensis takes place

A
  • Brains supply called ketones that go into the body, these are the breakdowns of lipids and proteins
  • The acytyle CoA produces ketone bodies Acetoacetate, D-β-Hydroxybutyrate
  • Turned back into Acetyl CoA in brain and this feeds the krebs ccyle
57
Q

what happens if inulin is missing

A
  • If insulin is missing that you are unable to turn off glycolysis and therefore you end up doing ketogenesis
  • These ketones eventually acidify the blood and cause confusion in the brain
  • This is diabetic ketoacidosis
58
Q

describe the billiard

A
  • Made out of the cystic duct, the gall bladder and hepatic ducts
  • Stuff from the liver drains into the biliary from the hepatic duct
  • Bile flows up the cystic duct into the gallbladder
  • The common bile duct drains into the duodenum
59
Q

what is bile

A
  • Bile is an emulsifier breaks down large fat molecules into smaller molecules
60
Q

where is bile secreted

A
  • Secreted by hepatocytes in canaliculi
61
Q

how much bile does the liver make

A
  • Liver makes Up to 800ml bile daily
62
Q

what is bile modified by

A
  • Modified by cholangiocytes – addition of HCO3
63
Q

what hormones control bile production

A
  • Cholecystokinin (CCK)

* Secretin

64
Q

when is CCK released

A

– Signal made in response of Fatty acids in lumen of duodenum
– Gall bladder contraction
– Sphincter of Oddi relaxation, this is so you get a squeeze at top and relaxation at bottom so it goes into the duodenum

65
Q

when is secretin released

A

– Made when Acid chyme that comes out of the stomach goes in duodenum
– Stimulates biliary ductal cells to make more bile

66
Q

what is the composition of bile

A
  • Water (>90%)
  • Bile Salts
  • Bilirubin
  • Cholesterol
  • Fatty acids
  • Lecithin
  • Na+ / K+ / Ca2+ / Cl- / HCO3- - some patients have biliary diversions that drain, patients are high risk of being dehydrated as they lose the electrolytes
67
Q

what are bile salts

A
  • These are breakdown products of cholesterol or they are synthesised from cholesterol
68
Q

what are the Amin bile salts

A
  • The main ones are Cholate or Chenodeoxycholate
69
Q

what are bile salts conjugated to and then secreted as

A
  • Conjugated to glycine or taurine

- They are then Secreted as sodium salts

70
Q

what is the action of bile salts

A
  • They act as Detergents this allows things that are fat soluble to be absorbed
71
Q

what are the substances that are absorbed when bile acts as a detergent

A
  • Fatty acids
  • Monoglycerides
  • Cholesterol
  • Fat soluble vitamins (A,D,E & K)
72
Q

what is the Enteroheptiatc circulation of bile

A
  • The important parts of the bile are reabsorbed once there function is done, this happens at the terminal ileum
  • This then goes back to the liver and is involved in making more bile
73
Q

what happens if you interpret the enterohepatic circulation of bile

A
  • If you interrupt this then you loose a lot of bile salts and this causes water to be drawn into the colon and produces watery diarrhoea
74
Q

describe how the FXR signalling pathway works

A

 Nuclear receptor for bile salts
 The bile salts which are agonists are brought in to the terminal ileum cells where they act of the FXR receptor
 They make FGF19
 This inhibits the synthesis of more bile salts in the liver
 This is the feedback mechanism
 works directly in the hepatocytes

75
Q

what reduces the bile effect on the FXR receptor

A

 The of bile effect on the FXR receptor is reduced by Acid synthesis, Reduced lipiogenesis, glyconeognesis and more liver cell regeneration this can be used clinically

76
Q

what is obeticholic acid

A

semi-synthetic bile acid

77
Q

what can semi-synthetic bile acids be used to treat

A

• Semi-synthetic bile acid that selectively activates FXR – this can cause much more activity of the FXR and drugs that can be used to treat patients with issues with their billary

78
Q

where can you get cholesterol from

A
  • Exogenous – diet

- Endogenous- liver

79
Q

what is the use of cholesterol

A
  • Cell membrane
  • Steroid hormones
  • Skin
  • Bile salts 80%
80
Q

what is the one step in cholesterol synthesis that you need to know

A
  • HMG-CoA is converted to mevalonate

- This is done by HMG-CoA reductase

81
Q

what inhibits HMG-CoA reductase

A

– statins inhibit this enzyme

- Statins are used to lower the cholesterol by stopping the production of cholesterol

82
Q

what Is bilirubin

A

• Bilirubin is made by the breakdown of RBC in spleen

83
Q

how is bilirubin excreted

A
  • Haem component is broken down it is converted to bilirubin
  • Bilirubin bound to albumin
  • Conjugated to glucuronate in the liver and secreted to the bile
84
Q

What happens if the flow of bile is obstructed

A
  • Less fat absorption
  • Less absorption of fat dependent vitamins as well
  • Less bile in the intestine and therefore the stool has a high content of fat but a low content of bile therefore you have pale stool
  • At the other end there is a build up of bilirubin this causes jaundice
85
Q

what is jaundice

A
  • Yellowing of skin and sclera due to excess bilirubin
86
Q

what are the causes of jaundice

A
  • Can be broken down into pre-hepatic, hepatic or post hepatic
  • Might be breaking down too much of there blood (pre hepatic)
  • The liver is unable to conjugate the bilirubin and excrete it (hepatic)
  • Might have a blockage in the gall bladder (post hepatic)
87
Q

describe how the liver acts as a storage

A 
•	Vitamins
–	A, D, B12
•	Iron
–	Apoferritin to ferritin (reversible)
–	Haemosiderin (insoluble)
88
Q

describe how the liver acts as drug metabolism

A 
•	Phase I – Modification
–	e.g. hydroxylation by cytochrome P450
Phase II – Conjugation
–	e.g. glutathione
•	Phase III - Further Modification / Excretion
89
Q

describe the steps of how paracetamol metabolism works

A
  • Acetaminophen (paracetamol) conjugated into sulphates or glucoconirde – renders it non-toxic in the liver
  • P450 system metabolises the drug into the toxic intermediate NAPQI, this is quickly converted in to glutathione rendering it non-toxic
  • If there is a large amount of paracetamol then NAPQI builds up which is toxic
  • Overdoses can lead to acute liver failure
  • In order to treat this
  • Give cysteine and mercapturic
90
Q

what happens in liver failure

A
  • Hypoglycemia
  • Reduced albumin
  • Impaired clotting
  • Jaundice
  • Hyperammonaemia (encephalopathy)

Metabolism (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions