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Clinical Biochemistry: Introduction to Clinical Biochemistry > Structure and Function of the Liver > Flashcards

Structure and Function of the Liver Flashcards

1
Q

What is the Blood Supply for Liver?

A

Dual blood supply:

  • 2/3 from Portal Vein which drains from the gut. Everything from the gut comes straight to the liver
  • Remainder from the Hepatic Artery
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2
Q

What makes up the vessels in the Liver Structure?

A

Portal Triad

  • Hepatic Artery
  • Portal vein
  • Biliary Duct

Central Vein

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3
Q

What is the function of the Liver?

A
  • Carbohydrate metabolism
  • Fat Metabolism
  • Protein Metabolism
  • Hormone Metabolism
  • Toxin/Drug: Metabolism and Excretion
  • Storage: Glycogen, Vitamin A/B12, Iron
  • Bilirubin: Metabolism and Excretion
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4
Q

How does the liver perform Carbohydrate metabolism?

A

Gluconeogenesis

  • Amino acids/lactate/glycerol → glucose

Glycogen synthesis (glycogenesis)

  • Excess glucose → glycogen

Glycogen Metabolism (Glycogenolysis)

  • Glycogen → glucose
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5
Q

How does the Liver perform Fat Metabolism?

A

Catabolism

  • Triglyceride oxidation → energy (ketogenesis)

Anabolism

  • Lipoprotein synthesis
  • Excess carbohydrate & fat → Fatty acid synthesis→ fatty acids & triglycerides → stored in adipose tissue
  • Cholesterol (& phospholipid) synthesis & excretion
  • Bile Acid synthesis
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6
Q

How does the Liver perform Protein Metabolism?

A
  1. Deamination and transamination of amino acids. Urea synthesis and nitrogen removal
    • Non-nitrogenous part → glucose or lipid
    • Nitrogenous part → ammonia → urea
  2. Plasma Protein Synthesis
    • Albumin
    • Fibrinogen/Prothrombin (& other clotting factors)
    • Lipoproteins/Caeruloplasmin/Transferrin/
    • CRP/α1AT/αFP
  3. Synthesis of non-essential amino acids
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7
Q

Which hormones are metabolised by the liver?

A
  • Insulin-like Growth Factor-1 (IGF-1)
  • Angiotensinogen
  • Thrombopoeitin
  • Hepcidin
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8
Q

How does drug/toxin metabolism occur?

A

Phase I reactions: Intro/unmask functional group

  • Oxidation (Cytochrome P450)
  • Reduction
  • Hydrolysis

Phase II reactions:

  • Glucuronide/Acetyl/Methyl
  • Glutathione
  • Glycine/Sulphate

Usually necessary to achieve renal excretion

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9
Q

Describe how Bilirubin is metabolised and excreted?

A
  • Haem catalysed by haem oxygenase to Bilverdin
  • Bilverdin catalysed by Bilverdin Reductase to Unconjugated Bilirubin
  • Unconjugated Bilirubin catalysed by UDP-Glucoronyl Transferase to Conjugated Bilirubin (dissolvable in solvent to be excreted in urine and faeces)
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10
Q

How is Liver function Assessed?

A
  • Clinical assessment
  • Imaging
  • Biopsy (Time, Analysis & interpretation)
  • Biochemical tests (Blood (plasma/serum) & urine)
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11
Q

What are some clinical signs of Liver Disease?

A
  • Dupuytren’s Contracture
  • Palmar Erythema
  • Ascites
  • Jaundice
  • Spider Naevi
  • Male gynaecomastia
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12
Q

What can liver disease lead to?

A
  • Cirrhosis
  • Oesophageal Varices
  • Hepatic Encephalopathy
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13
Q

What are the uses of Liver Function tests?

A
  • Screening for the presence of Liver disease
  • Assessing Prognosis
  • Measuring the efficacy of treatments for Liver Disease
  • Monitoring disease progression
  • Assessing severity, especially in patients with cirrhosis
  • Stratifying the differentials between hepatic and cholestatic disease
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14
Q

What are some Liver Functions tests?

A

LFTs allow differentiation of patterns of liver disease between hepatocellular injury and cholestasis

  • Serum bilirubin
  • AST or ALT (indicators of hepatocellular damage)
  • ALP (indicate a cholestatic picture)
  • Serum albumin (determine chronicity of disease and synthetic function)
  • PT or INR (determine synthetic function and identify severity of disease)
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15
Q

How can abnormal LFTs present outside of primary hepatic disorders?

A
  • Heart failure
  • Sepsis
  • Infection/inflammation
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16
Q

What is the function of Albumin in the LFTs?

A
  • Crude indicator of synthetic capacity of liver. Half-life ~20 days so may not present initially
  • Maintains plasma oncotic pressure
  • Binds several hormones, drugs, anions and fatty acids
  • Decreases in the acute phase response (APR)
17
Q

How is Bilirubin used in the LFTs?

A
  • Total Bilirubin
  • Direct/Conjugated Bilirubin
  • Differentiate between intra-hepatic (liver mets, hepatitis) and extrahepatic obstruction (gallstones, carcinoma of head of pancreas)
18
Q

When is Jaundice visible?

A

Visible when bilirubin >50 µmol/L

19
Q

What is Kernicterus?

A

Unconjugated bilirubin crossing blood brain barrier in neonates

20
Q

Describe the features of Unconjugated Bilirubin

A
  • Not water soluble=protein bound
  • Not filtered at the glomerulus hence does not reach the urine
21
Q

What are the pathological states that lead to increased Unconjugated Bilirubin?

A
  • Haemolytic states
  • Gilbert’s (inherited defect in UDP glucuronyltransferase)
22
Q

Describe the features with conjugated Bilirubin?

A
  • Water soluble
  • Filtered at the glomerulus hence reaches the urine = bilirubinuria
23
Q

Which pathological states lead to increased Conjugated Bilirubin?

A

Intra or extra hepatic obstruction

24
Q

How is Urobilinogen produced and excreted?

A
  • When bilirubin reaches the gut, it is converted to urobilinogen by gut bacteria
  • It gets absorbed from the distal small intestine
  • It is then excreted in the urine
25
Q

How is Urobilinogen pathologically significant?

A
  • If urobilinogen present in urine, shows that bilirubin is reaching the gut
  • High plasma bilirubin & No urobilinogen in urine = bilirubin is not reaching the gut (cholestasis)
26
Q

What is ALP and when is it raised?

A
  • Secreted by cells lining biliary tract
  • Enhanced synthesis/inducible enzyme
  • Raised in bone disease (↑osteoblast activity)
  • Raised during growth, pregnancy (different reference ranges apply)
27
Q

What is ALT and its use?

A

Alanine aminotransferase (ALT)

  • Catalyses transfer of amino group from alanine residues
  • Cytosolic and present in wide range/All tissues
28
Q

What is AST and its use?

A

Aspartate aminotransferase (AST)

  • Catalyses transfer of amino group from aspartate residues
  • Cytosolic (20%) and mitochondrial (80%). It is present in wide range/all tissues.
  • There are high levels in heart, liver, skeletal muscle, kidney, lung & red blood cells. Also found in significant amounts in brain, gastric mucosa & adipose tissue
29
Q

What are the uses of Transaminases?

A
  • Indicators of hepatocellular damage
  • ALT more specific for liver than AST
  • ALT:AST ratio often used

High AST also seen in MI, muscle injury & CCF

30
Q

What is GGT?

A
  • Located in cell membrane of various tissues; mainly kidney, liver, biliary tract & pancreas. Found in hepatocytes & biliary epithelial cells
  • Catalyses transfer of gamma glutamyl group from peptides to appropriate acceptors
  • Kidney contains largest amount but is not released into plasma
31
Q

How is GGT used clinically?

A

Indicator of obstruction (intrahepatic/biliary)

  • Enhanced synthesis/inducible enzyme: Alcohol & anticonvulsants

Useful in conjunction with ALP

  • e.g ↑ALP - ?liver/bone/other
  • ↑ALP & ↑GGT – suggests hepatic cause
  • ↑GGT & N ALP – alcohol intake
32
Q

What is Liver Fibrosis?

A
  • Continuous inflammation can lead to fibrosis due to altered remodelling of the extracellular matrix. Complex and dynamic process
  • In healthy tissue, ECM remodelling is tightly controlled and synthesis of ECM proteins is relatively slow
  • Chronic wound healing causes immune cells to infiltrate the interstitial matrix resulting in a pro-fibrogenesis environment
33
Q

What is Liver Cirrhosis?

A
  • Slow deterioration of the liver until unable to function normally
  • Scar tissue replaces normal rissue and partiall blocks blood flow
  • There are 2 forms of liver cirrhosis: Compensated and Decompensated
  • Insidious involvement
  • Liver may in theory be able to regenrate to some extent

Clinical Biochemistry: Introduction to Clinical Biochemistry (11 decks)

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