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Medicine Year 2 > GI Topic 5 - Liver > Flashcards

GI Topic 5 - Liver Flashcards

1
Q

What LFT results would suggest cholestasis?

A

High ALP and GGT

AST <3, ALP >2

High bilirubin

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2
Q

Describe the microanatomical organisation of the liver

A
  • Arranged into lobules - structural units
    • 1-2mm hexagonal lobules, centred on a central vein (terminal hepatic venule)
    • At periphery of each - arteriole, venule + bile duct = portal triad
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3
Q

How are acini zones functionally distinct?

A
  • Zone 1 - closest to blood supply, carries out processes which require oxygen e.g. synthesis of glycogen and plasma proteins
  • Zone 2 - intermediate zone
  • Zone 3 - vascular periphery, furthest from blood supply, hepatocytes sensitive to hypoxia
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4
Q

List the lobes of the liver

A
  • R lobe (biggest)
  • L lobe
  • Quadrate lobe - next to gallbladder
  • Caudate lobe - above quadrate, between right and left lobes
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5
Q

List the causes of hepatitis

A
  • Alcohol
  • Metabolic disease
  • Viral infection
  • Autoimmune disease
  • Biliary disease
  • Drugs/toxins
  • Cryptogenic
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6
Q

What are AST/ALT levels used to indicate?

A

Hepatocellular injury markers - intermediates in gluconeogenesis

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7
Q

What test should be done if ALP and GGT are raised?

A
  • Ultrasound or CT to visualise the biliary ducts
  • Dilated ducts = stones/strictures
  • Non-dilated ducts = primary biliary cholangitis
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8
Q

Describe the pathological changes which cause Reye-Like acute onset liver failure

A

Microvesicular steatosis

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9
Q

Describe the typical clinical history of fatty liver disease

A
  • Usually asymptomatic
  • Rarely, if severe - acute cholestasis and liver failure
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10
Q

What LFT results would suggest hepatocellular injury?

A

High AST and ALT

AST >3, ALP <2

High bilirubin

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11
Q

Describe the origins of the hepatic portal vein

A

HPV formed from the union of the superior mesenteric and splenic veins at the neck of the pancreas (splenic mesenteric confluence)

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12
Q

How is the biliary system of the liver organised?

A
  • Bile canaliculi - between hepatocytes, direction of flow opposite to blood supply (towards bile duct)
  • Bile ducts lined with columnar epithelium with thick nuclei
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13
Q

How does exchange of materials occur in the liver?

A

Hepatocytes arranged in plates and cords exchange material with blood at the sinusoidal surface

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14
Q

List the complications of liver cirrhosis

A
  1. Portal hypertension
  2. Liver failure
  3. Liver cancer
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15
Q

Describe the attachments of the coronary ligament

A

Attaches the liver to the inferior surface of the diaphragm

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16
Q

Describe the innervation of the liver

A
  • Glisson’s capsule - branches of the lower intercostal nerves
  • Parenchyma - hepatic plexus
    • Sympathetic = coeliac plexus
    • Parasympathetic = vagus nerve
    • Enter liver at porta hepatis, follow branches of hepatic artery and portal vein
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17
Q

How are sinusoids specialised?

A

Fenestrated endothelium, lack complete basement membrane

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18
Q

Describe the microscopic pathological changes seen in alcoholic hepatitis

A
  • Signs of fatty liver disease +
    • Hepatocyte ballooning
    • Mallory bodies in cytoplasm
    • Hepatocyte death (necrosis)
    • Neutrophil polymorph inflammation
    • Fibrosis (scarring) - initially perivenular and pericellular - progresses to cirrhosis
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19
Q

What is the function of sinusoids?

A
  • Specialised capillary
  • Optimise exchange of material between blood and hepatocytes
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20
Q

Describethe functional organisation of the liver

A
  • Acini = functional units
    • Triangular structures, portal tracts at base and terminal hepatic venule at apex
    • Divided into 3 zones
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21
Q

What does high conjugated bilirubin indicated?

A

Inherited/acquired defects in hepatic excretion

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22
Q

Describe the attachments and structure of the lesser omentum

A
  • Attaches the liver to the lesser curvature of the stomach and the 1st part of the duodenum
  • Hepatoduodenal ligament - duodenum to liver, surrounds the portal triad
  • Hepatogastric ligament - lesser curvature of stomach to liver
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23
Q

What causes liver cirrhosis?

A
  • Result of chronic inflammation (hepatitis) - injury causing agent present for a long time
  • Can be reversed up to a certain point - if injury causing agent is removed, eventually irreversible
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24
Q

What is the role of accessory hepatic portal veins?

A

Drain directly into liver from the GI tract/spleen/pancreas without joining the hepatic portal vein

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25
Q

Describe the presentation of Reye-Like acute onset liver failure

A
  • Neonatal to 3 years old
  • History of episodic vomiting (since neonatal), failure to thrive, family history?
  • Clinical features - encephalopathy, acidosis, hypoglycaemia, no ketosis, high transaminases, prolonged prothrombin time, low serum albumin, leukocytosis
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26
Q

How does the liver function in amino acid metabolism/disposal of urea?

A
  • Nitrogen produced by amino acid metabolism is converted to urea in the liver and excreted by the kidneys
  • Liver failure - encephalopathy due to increasing ammionia levels in the brain (drowsy, confused)
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27
Q

List the processes carried out in zone 1 of acini

A
  • Respiratory chain
  • Citric acid cycle
  • Fatty acid oxidation
  • Gluconeogenesis
  • Urea synthesis - ammonia detoxification
  • Production and excretion of bile
  • Cholesterol synthesis
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28
Q

List the ligaments of the liver

A
  1. Falciform ligament
  2. Coronary ligament
  3. Triangular ligament
  4. Lesser omentum
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29
Q

Which areas are drained by the hepatic portal vein?

A

Drains from just below the gastroesophageal junction to the upper 2/3 of the rectum, as well as the spleen and pancreas

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30
Q

What is primary biliary cholangitis?

A
  • Autoimmune disease of the liver
  • Slow, progressive destruction of the bile ducts of the liver
  • Symptoms - tiredness, pruritis, jaundice, cirrhotic symptoms in advanced disease
  • Cholestatic LFTs, anti-mitochondrial antibodies
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31
Q

What should the patient be asked if their LFTs are abnormal

A
  • Symptoms
    • Weight loss?
    • Anorexia?
    • Vomiting?
    • Pain?
    • Myalgia?
    • Jaundice?
    • Pruritis?
    • Urine/stool
  • Exposure to hepatoxins? - alcohol, medication etc.
  • Family history - viral hepatitis, heritable liver disease?
  • Exposure to viruses - sexual transmission? Travel? Transfusion? IV drug use?
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32
Q

What causes liver cirrhosis?

A
  • Long-term hepatitis, including viral
    • Specifically - alcohol, non-alcoholic steatohepetitis (NASH), biliary disease
  • Haemochromatosis
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33
Q

How is alcohol metabolised in the liver?

A
  • 2 main pathways, both oxidise alcohol to acetaldehyde, which is converted to acetate then acetyl coA which is used in the tricarboxylic acid cycle to produce fatty acids
  • Reduces the liver’s capacity to oxidise other molecules
  • Pathways = cytoplasma alcohol dehydrogenase and microsomal ethanol oxidising system
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34
Q

List the external surfaces of the liver

A
  • Diaphragmatic (has bare area)
  • Visceral - in contact with right kidney, adrenal gland, colic flexure, transverse colon, 1st part of gallbladder, oesophagus and stomach)
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35
Q

What is Gilbert’s syndrome?

A
  • Autosomal dominant disease
  • Deficiency of UDP-glucuronyl transferase
  • Test to confirm - unconjugated bilirubin
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36
Q

What does it mean if ALP is high without a corresponding rise in GGT?

A

Bone disease e.g. fractures, Paget’s disease, osteomalacia, bony metastasis

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37
Q

Where do vascular structures enter/exit the liver?

A
  • R and L hepatic ducts, R and L branches of hepatic artery and portal vein enter/exit at the porta hepatitis
  • From anterior to posterior - duct, artery, vein
38
Q

What markers are tested in liver function tests?

A
  • Bilirubin
  • Albumin
  • Alanin/aspartate aminotransferase (ALT/AST)
  • Alkaline phosphatase
  • Gamma glutamyl transferase (GGT)
  • Total protein
    • viral markers, serum autoantibodies, serum immunoglobulins?
39
Q

When will total protein levels be high in LFTs?

A

Viral hepatitis

40
Q

Describe the process of lipogenesis

A
  • Acetyl choline (from steroids, amino acids or breakdown products of glucose) is converted to fatty acids (can then be converted to triglycerides or cholesterol / prostaglandins / phospholipids / glycolipids)
  • Amino acids can be converted to pyruvate, which is converted to acetyl choline
  • Glycerol from glucose breakdown can be converted to triglycerides
41
Q

What causes fatty liver disease (steatosis)?

A
  • Alcohol
  • Obesity
  • Type 2 diabetes
  • Nutritional imbalance - after intestinal surgery or coeliac disease
  • Drugs e.g. methotrexate, steroid-related drugs
42
Q

Where do portosystemic shunts and varices typically form in portal hypertension?

A
  • Gastroesophageal junction
  • Rectum
  • Left renal vein
  • Diaphragm
  • Retroperitoneum
  • Anterior abdominal wall via the umbilical vein
43
Q

Describe the cause of alcoholic hepatitis

A
  • Related to volume and duration of alcohol excess
  • Develops after 3-5 years of alcohol abuse but only occurs in 1/3 of alcoholics
  • Females at greater risk
  • Genetic susceptibility
44
Q

Describe the path of blood through the liver

A
  • Incoming from hepatic artery or hepatic portal vein
  • Travels through liver parenchyma to reach hepatic veins
  • Sinusoids (specialised capillaries in parenchyma) connect incoming and outgoing blood flow
45
Q

Define cirrhosis

A
  • Endstage liver disease
  • Characterised by diffuse nodules and fibrosis
46
Q

What are the potential complications of splenomegaly in liver cirrhosis?

A

Fewer clotting factors (liver dysfunction) and fewer platelets (splenomegaly) - portosystemic varices vulnerable to rupture and bleeding - causes haematemesis and malena/haematochezia

47
Q

What are the consequences of hepatic detoxification?

A

Can generate toxic/carcinogenic metabolites

48
Q

What causes centrilobular necrosis?

A
  • Caused by sepsis, shock induced ischaemia, congestive heart failure, toxicity from drugs/poisons
  • Made worse by malnutrition, infection, fasting and exercise
49
Q

What function does the liver have in blood coagulation?

A

Formation of clotting factors - fibrinogen, prothrombin, accelerator globulin, factor VII (requires Vitamin K)

50
Q

What causes metabolic liver disease?

A
  • Congenital deficiencies of enzymes
  • Nutritional deficiency/excess
  • Toxic damage to organelles
  • Hypoxic/ischaemic insult
  • Secondary to metabolic effects of disease
51
Q

Describe the epidemiology of hepatocellular carcinomas

A
  • 85% of malignant primary liver tumours
  • 80% in males
  • 80% in cirrhotic livers
52
Q

What is the portal triad?

A

Bile ducts, hepatic artery, portal vein

53
Q

What does high unconjugated bilirubin indicate?

A

Increased bilirubin production or defects in hepatic uptake/conjugation

E.g. Gilbert’s disease (lack of UDP-glucuronyl transferase)

54
Q

Describe the breakdown of fatty acids to produce ATP

A
  • Fatty acids to fatty acyl coA to acyl carnitine
  • Acyl carnitine transported into mitchondrial matrix by carnitine shuttle
  • Acyl carnitine to fatty acyl coA, undergoes beta oxidation to acetyl coA
  • Acetyl coA goes through citric acid cycle to produce NADH and FADH2, which produce ATP
55
Q

How does alcohol consumption increase hepatic lipids?

A
  • Alcohol changes hepatocyte fat metabolism - increases lipid synthesis, catabolism impaired, accummulation of cholesterol esters and fatty acids
  • Raised peripheral fat metabolism
  • Decreased lipoprotein synthesis
56
Q

List the processes carried out in zone 3 of acini

A
  • Glycolysis
  • Glutamine synthesis
  • Xenobiotic metabolism
  • Lipogenesis
  • Ketogenesis
57
Q

What indicates hepatocellular carcinoma?

A

High serum alpha-fetoprotein

58
Q

What causes Reye-Like acute onset liver failure?

A

Inherited metabolic disease - inborn errors of metabolism

59
Q

How are lipids produced in the liver transported around the body?

A
  • Initially transported as VLDL (very low density lipoprotein) in the bloodstream, lipoprotein lipase releases fatty acids and monoglycerides for uptake by tissues
  • VLDL is converted to IDL (intermediate density lipoprotein) and LDL (low density lipoprotein) in the bloodstream
  • LDL transports lipids in the bloodstream, lipids (cholesterol) move from high to low concentration through capillary walls into interstitial fluids
  • Excess cholesterol diffuses out of cells back into the bloodstream, absorbed by HDL (high density lipoprotein)
  • HDL transports lipids back to the liver, excess excreted in bile salts
60
Q

List the types of parenchymal liver cells

A
  • Hepatocytes (majority) - cuboidal epithelial cells, have microvilli
  • Endothelial cells
  • Kupffer cells (macrophages) - immune
  • Perisinusoidal (fat-storing) cells - storage of fat-soluble vitamins A, D, E, K
  • Liver associated lymphocytes - immune
61
Q

Describe the functions of the liver involved in carbohydrate metabolism

A
  • Stores glycogen, releases glucose (through glycogenolysis or gluconeogenesis)
  • Uses glucose for energy in glycolysis, citric acid cycle and fatty acid/triglyceride synthesis
  • Converts fructose/galactose to glucose phosphates (for use in respiration)
62
Q

What is the effect of mitochondrial damage to the liver

A
  • No beta oxidation of fatty acids - micro-vesicular steatosis
  • No oxidative phosphorylation - insufficient ATP generation
  • No respiratory chain - excess reactive oxygen species with lipid peroxidation
  • Increased permeability transition - cell death
63
Q

Describe the structural arrangement of the liver

A

Portal tracts and parenchyma

64
Q

Describe the anatomical location of the liver

A
  • R hypochondrium, epigastrum and L hypochondrium
  • Just below diaphragm, lower edge at level of costal margin - usual not palpable unless hepatomegaly
  • Inferior part passes xiphoid process
  • Up to level of nipples
65
Q

What is the treatment for Reye-Like acute onset liver failure

A

Correct hypoglycaemia, acidosis, bleeding tendency and hyperammonaemia

66
Q

Describe the coverings of the liver

A
  • Covered by fibrous membrane - Glission’s capsule
  • Partially covered by peritoneum
67
Q

What should be checked in a physical examination if LFTs are abnormal?

A
  • BMI
  • Nutritional status
  • Jaundice
  • Ascites, pleural effusion, ankle oedema
  • Hepatomegaly, splenomegaly, other abdominal masses
  • Spider naevi - swollen vessels under the skin surface, central red spot and red extensions
  • Palmar erythema
68
Q

How is the inferior vena cava secured to the liver?

A

By hepatic veins and fibrous tissue

69
Q

Hepatic mitochondrial dysfunctions include inborn enzyme deficiencies involving…

A
  • Fatty acid oxygenation
  • Organic acids
  • Lactate metabolism
  • Oxidative phosphorylation
  • Urea cycle
70
Q

Where is alkaline phosphatase found?

A

Mostly liver and bone (+ intestines, placenta during pregnancy)

71
Q

Describe the venous drainage of the liver

A
  • Caudate lobe drains directly into the inferior vena cava
  • Other lobes drain into central veins, which drain to collecting veins then hepatic veins, which then join the inferior vena cava
72
Q

Describe the development and consequences of portal hypertension

A
  • Increased resistance to blood flow due to fibrosis
  • Blood escapes back to systemic circulation at portocaval anastomoses
  • Leads to portosystemic shunts and varices, ascites and splenomegaly
73
Q

What is the effect of metabolic disease of the liver?

A

Dysfunction of:

  • Synthesis - plasma proteins etc.
  • Detoxification/degradation e.g. ammonia
  • Regulation e.g. blood glucose
74
Q

How does the liver produce bile acids?

A

Bile acids are derivatives of cholesterol, which is recycled in the enterohepatic circulation

75
Q

How is the liver involved in protein metabolism?

A
  • Albumin and glycoprotein synthesis
  • Glycation of proteins
76
Q

Describe the conjugation of bilirubin in the liver

A
  • Unconjugated bilirubin from the breakdown of haemoglobin is transported to the liver bound to albumin
  • Ligandin presents unconjugated bilirubin to glucaronic acid
  • Conjugated by UDP-glucuronyl transferase
77
Q

Describe the blood supply of the liver

A
  • Hepatic artery
    • 30-40%
    • Incoming blood supply - rich in oxygenated blood, high pressure
  • Hepatic portal vein
    • 60-70%
    • Incoming blood supply - rich in nutrients from gut, low pressure
78
Q

Describe the attachments of the triangular ligament

A

Left and right triangular ligaments attach the liver to the diaphragm

79
Q

Compare the cytoplasma alcohol dehydrogenase pathway to the microsomal ethanol oxidising system

A
  • CAD - main route, not inducible
  • MEOS - in smooth endoplasmic reticulum, uses cytochrome P450, is inducible (increased by alcoholism), affects metabolism of drugs e.g. paracetamol
80
Q

Describe the connective tissue of the liver

A
  • Liver capsule
  • Portal tracts
  • Parenchymal reticulin - basement membrane, collagen type I + III
81
Q

Describe the process of detoxification which occurs in the liver

A
  • Phase 1 reactions
    • In the smooth endoplasmic reticulum, mediated by cytochrome P450
    • Produces hydroxylated or carboxylated compounds
  • Phase 2 reactions
    • Subsequent conjugation with glucaronic acid, acetyl or methyl radicals, glycine/taurine or sulphate
82
Q

Why is GGT used as a marker for liver function?

A
  • Microsomal
  • Transfers glutamyl from alpha glutamyl pepides to other peptides/amino acids
  • In liver, hepatobilliary tree, heart, kidneys, lungs, pancreas and seminal vescicles
  • Poor specificity for liver disease - good for raised ALP of liver origin or chronic alcohol consumptions
  • Rasied GGT may be due to liver damage/alcohol consumption - not definite
83
Q

List the types of inherited metabolic diseases of the liver

A
  • Essential product deficit e.g. glucose-6-phosphate deficiency (Glycogen storage 1)
  • Precursor accummulation e.g. ornithine transcarbamylase deficiency (hyperammonaemia)
  • Alternative pathway activation e.g. amino-acidopathy
  • Or combination
84
Q

List the functions of the liver

A
  1. Amino acid, carbohydrate and lipid metabolism
  2. Plasma protein and enzyme synthesis
  3. Bile production
  4. Detoxification - drugs etc.
  5. Storage of proteins, glycogen, vitamins and metals
  6. Immune function
85
Q

Define ascites

A

Abnormal build-up of fluid in the abdominal cavity, sign of cirrhosis

86
Q

Describe the pathogenesis of cirrhosis

A
  • Hepatocyte injury
    • Causes inflammation, which leads to fibrosis
    • Also leads to hepatocyte regeneration, forming hyperplastic nodules
  • Nodules and fibrosis cause architectural abnormality, leading to ischaemia which causes further hepatocyte injury
  • Shunts form - allowing blood to flow between arteries and veins and reducing the oxygenation of tissues
87
Q

How does the liver function in lipid metabolism?

A
  • Mitochondrial beta oxidation of short chain fatty acids
  • Synthesis of fatty acids, triglycerides, cholesterol, phospholipids and lipoproteins
88
Q

Compare AST and ALT

A
  • AST
    • Cytosolic and mitochondrial
    • In liver, cardiac/skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes and RBC
    • Low sensitivity/specificity for the liver
  • ALT
    • Cytosolic
    • More specific to liver
89
Q

Describe the microscopic pathological changes seen in fatty liver disease

A
  • Lipid droplets in hepatocytes
    • Initially small - microvesicular
    • Coalesce to form macrovesicular
  • Seen after 2 days of alcohol excess
  • Rapid reversal
90
Q

Describe the blood pressure of the hepatic portal vein

A

Low pressure (below 10mmHg) already through the gut capillary bed

91
Q

Describe the structure of the falciform ligament

A
  • Attaches to the anterior abdominal wall, divides the left and right lobes
  • Free edge = ligamentum teres, remnant of the umbilical cord

Medicine Year 2 (41 decks)

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