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Y2 NnD > Liver and LFTs > Flashcards

Liver and LFTs Flashcards

1
Q

What are the two blood supplies of liver

A

portal vein and hepatic arter
75% portal vein

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2
Q

Where is bile formed from and what is its passage out of the liver

A

Bile is formed from the hepatocytes, flows through bile canaliculi to bile duct (⇒ flow is opposite to blood)

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3
Q

Where does blood in central veins go to

A

Blood collected in central veins goes to sublobular veins, then to collecting veins, and then hepatic veins leaving the liver

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4
Q

What maintain pressure within common bile duct

A

Ampulla of vater/ sphincter body
Pressure there should usually be higher than that of gallbladder

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5
Q

What causes gallbladder contraction (what hormone is involved)

A

Cholecystokinin release from mucosa in duodenum during feeding causes gallbladder contraction, reduced sphincter pressure on bile and allows bile to flow from gall bladder to duodenum

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6
Q

What are cholangiocytes

A

Bile duct epethelia, contribute to cell function

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7
Q

What forms the sieve plate in liver

A

Endothelial cells

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8
Q

Sinusoidal vs lateral faces in hepatocytes

A
  • Microvilli are present on sinusoidal face to project sparsely into bile canaliculi
  • A portion of the lateral faces of hepatocytes is modified to form bile canaliculi
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9
Q

Where are glycogen granules stored in hepatocytes

A

In association with SER

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10
Q

Difference between periportal and perivenous/pericentral zone in liver acinus

A

Periportal has good o2 supply and nutrient rich, involved in gluconeogenesis, glycogenolysis and bile salt formation, perivenous involved in glycolysis, lipolysis, glucuronidation, glycogenesis and cytochrome p450 reaction. Low in nutrients and relatively hypoxic

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11
Q

Three phases of biotransformation

A

I - oxidation, reduction and hydrolysis by CYP450
II- Conjuation in cytoplasm with endogenous substances like glucuronic acid to form inactive conjugates
III- secretion into bile, excretion mediated by ATP

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12
Q

What can conjugate with drugs in phase II metabolism

A

Gluthatione for oxidated species
or sulfur, acetyl or glucuronide for hydrolysed species

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13
Q

Glutathione conjugation in paracetamol metabolism??

A

Bonds with NAPQI to form non-toxic conjugates

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14
Q

What does N-acetyl cysteine do

A

Increases Glutathione to mop up NAPQI

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15
Q

What causes alcohol flush response

A

Deficiency in ALDH-2 ( Aldehyde dehydrogenase) that results in increased acetylaldehyde and catecholamine release

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16
Q

What happens to insulin and glucagon after feeding and main actions in liver

A

Increased insulin and decreased glucagon
- Hepatic glucose uptake
- Glycogen deposition in hepatocytes
- Glucose converted into glycerol and fatty acids

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17
Q

What happens to insulin and glucagon in fasting and main actions in liver

A

Reduced insulin and increased glucagon
- Glycogen breakdown in periportal hepatocytes
- Gluconeogenesis from lactate, pyruvate, AA, glycerol

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18
Q

Synthesis of lipids in liver

A

Liver also synthesizes VLDL and HDL
Also synthesises cholesterol and phospholipids, some of which is secreted into bile and some is converted into bile acids

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19
Q

What transport proteins are synthesised in liver

A

ceruloplasmin to transport copper and transferrin which transports iron

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20
Q

Which enzymes synthesized in liver require vitamin K

A

II, VII, IX, X are post-translational modified by Vitamin K dependent enzymes ⇒ synthesis impaired by VItamin K deficiency

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21
Q

How is unconjugated bilirubin formed

A

from breakdown of heme in spleen

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22
Q

Where does bilirubin get conjugated and by what

A

By glucuronyl billirubin transferase in liver

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23
Q

What does direct bilirubin get converted to and where

A

To urobilinogen in duodenum by microbiome, then to stercobilin

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24
Q

What vitamins stored in large amounts in liver

A

A, D, B12

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25
Q

What does an isolated rise in bilirubin suggest
What does rise suggest

A

Gilbert’s syndrome ⇒ problems with processing of bilirubin
Haemolysis
Rise - Biliary problems

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26
Q

What is prothrombin time an indicator of

A

Synthetic function

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27
Q

How is PT in ALF and cirrhosis

A

usually very good, also rarely abnormal in cirrhosis

28
Q

PT in paracetamol overdose

A

Very high, 100 instead of 10 or 12

29
Q

What do ALT and AST show

A

Increases when hepatocytes die ⇒ Leak out and give indication of how many died the previous day

30
Q

ALT in Hep C vs NAFLD

A

150 in Hep C vs75-100 in NAFLD

31
Q

Is ALT or AST usually higher and what does the ratio so

A
  • ALT usually higher than AST
    • In ALD, AST is higher
    • In NAFLD, AST goes up relative to ALT due to mitochondrial dysfunction as a result of scarring ( as AST leaks from Mito.)
      • Indicator of advancing fibrosis
32
Q

What does high Alkaline Phosphatase mean

A

Need to chek GGT if ALP is high, to see if ALP is from liver, if it is, suggests irritation of bile ducts => assess cholestasis ) stoppage of bile flow)

Biliary disease eg. stones, pancreatic cancer , PBC (Cholestatic LFTs, liver biopsy with granulomas, +ve AMA)

33
Q

What does high GGT suggest

A
  • Increases by induction,not damage
    • i.e. Enzyme induction by drugs
      • Alcohol, phenytoin, carbamazipine
    • Obesity, NAFLD cirrhosis
34
Q

What can affect albumin levels

A

Dehydration raises it, dilution or reduced synthesis reduces it . Can be low in pregnancy due to increased volume in circulation

35
Q

When are albumin levels often low in liver disease and why

A
  • In liver disease, retains salt and water and also dilutes albumin down.
    • Often normal in cirrhosis until liver is failing
36
Q

Mild ALT vs high ALT

A

Mild ALT
- NASH ⇒ Inflammation and scarring, cirrhosis
- AFLD ⇒ Fatty liver (umbrella term)
- HepC
- ALD, including ALcoholic Hep
High ALT⇒ Hepatitis including drug damage
- Inflammation of liver

37
Q

What does isolated high GGT suggest

A

Usually high GGT suggests alcoholism or drugs, or inactive cirrhosis (NAFLD)

38
Q

Serum markers of liver function include?

A

ALbumin, Pt, Bilirubin

39
Q

does space of disse have a basal lamina

A

no

40
Q

Is bilirubin high in cirrhosis

A

yes

41
Q

What vitamins and minerals are stored in the liver

A
  • Vit- A, D, B12, some K
  • Folate
  • Metabolises Vit D3 to 25-OH…
  • Iron in ferritin and haemosiderin
  • copper
42
Q

Which autoimmune diseases target the:
Hepatocytes
Small bile ducts
Larger bile ducts

A
  • Autoimmune hep
  • PBC
  • PSC, IgG4-related cholangitis
43
Q

Which AI Liver/ Biliary diseases are more likely to affect:
50-60 yo
20-40 yo
Any Age

A
  • PBC, IgG4
  • PSC
  • AIH
44
Q

Which AI Liver/ Biliary diseases are more likely to affect:
Males
Females

A
  • PBC and AIH
  • PSC and IgG4
45
Q

AMA high- what AI disease?

A

PBC

46
Q

MRCP findings in PBC

A

Normal ducts since only small ducts are affected

47
Q

How to diagnose and confirm PBC

A
  • +ve AMA tgt with alk phos and GGT, can confidently diagnose PBC)
  • If -ve AMA, biopsy liver
48
Q

Can PBC lead to Cirrhosis?

A

Yes, if not treated over 2 decades

49
Q

Staging disease ?severity in PBC

A

Transient elastography for liver fibrosis stage

50
Q

Common Sx of PBC

A
  • Itch or fatigue if Sx present, otherwise usually aSx with slowly increasing LFTs
    -May have RUQ discomfort
51
Q

Tx for PBC (first and second line)

A
  • UDCA
  • Obeticholic acid and bezafibrate
52
Q

Multifocal stricturing and beading of bile ducts and even intra-hepatic ducts - what cause and what Ix?

A

PSC, MRCP

53
Q

What disease is PSC assoc with and what diseases are these pts at higher risk for

A
  • IBD, esp UC
  • High risk of colorectal, bile duck and gallbladder cancers
  • Risk of cirrhosis of liver
54
Q

Px of pts with PSC

A
  • Fevers and rigors in infxn in bile duct
  • (Intermittent) Jaundice ( later on)
  • Itch
  • RUQ pain
  • Fatigue, weight loss
55
Q

Medical therapy for PSC

A

None, only transplant can help. But may given cipro for acute cholangitis attacks, and ERCP to relieve obstruction through balloon dilatation
Annual colonscopies if IBD , and annual gallbladder US

56
Q

Px of AIH

A

Malaise and jaundice,fatigue and joint pains but may be aSx apart from raised ALT. Decompensated cirrhosis may be first px

57
Q

What antibodies may be raised in AIH

A

ANCA, AMA, IgG4, LKM and SLA

58
Q

How to confirm Dx of AIH

A

Liver biopsy to confirm and stage fibrosis

59
Q

Tx for AIH

A
  • Steroids like predni or budesonide for non-cirrhotic pts for 6-12 mo
  • Azathioprine as maintenance therapy
60
Q

How to diagnose IgG4 cholangipathy

A

Histology - IgG4 producing lymphocytes, plasma cells and fibrosis

61
Q

Ix for IgG4 Cholangiopathy

A
  • Serum IgG4
  • Biopsy
  • MRCP: No stricturing unlike PSC
  • Consider steroid trial
62
Q

Px of IgG4 cholangiopathy

A
  • May mimic PSC or hilar cholangiocarcinoma
  • May have obstructive jaundice due to either hilar stricturing/intrahepatic sclerosing cholangitis or a low bile duct stricture
63
Q

What drug may induce AIH

A

Nitrofurantoin

64
Q

What demographic is PBC more common amongst

A

Cigarette smokers

65
Q

What diseases are PBC assoc with

A

Assoc with thyroid disease, coeliac and systemic sclerosis

66
Q

What antibodies commonly found in serum of pts with PSC

A

ANCA

67
Q
A

Y2 NnD (10 decks)

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