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Gastrointestinal > Liver - injury, jaundice, autoimmune hepatitis > Flashcards

Liver - injury, jaundice, autoimmune hepatitis Flashcards

1
Q

What are the 4 main functions of the liver?

A
  1. Protein synthesis - albumin, clotting factors
  2. Glucose and fat metabolism
  3. Detoxification and excretion - ammonia, bilirubin, drugs, hormones & pollutants
  4. Defence against infection - reticuloendothelial system
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2
Q

Describe the structure of the liver (macroscopic & microscopic) and blood flow into and out of the liver.

A

Macroscopically
The liver is roughly triangular and consists of two lobes: a larger right lobe and a smaller left lobe. The lobes are separated by the falciform ligament, a band of tissue that keeps it anchored to the diaphragm. A layer of fibrous tissue called Glisson’s capsule covers the outside of the liver. This capsule is further covered by the peritoneum, a membrane that forms the lining of the abdominal cavity.
This helps hold the liver in place and protects it from physical damage.

Microscopically, each liver lobe is seen to be made up of hepatic lobules. The lobules are roughly hexagonal, and consist of plates of hepatocytes, and sinusoids radiating from a central vein towards an imaginary perimeter of interlobular portal triads (containing the portal vein, hepatic artery and bile duct)

  • Blood enters the liver via the portal vein and hepatic artery which lie together with a small bile duct (cuboidal epithelium) within the portal tract
  • Blood flows into a system of sinusoids which bathe the hepatocytes with blood, before exiting via the hepatic vein (central vein).
  • Hepatocytes cytoplasm is very eosinophilic (pink) as they contain a lot of mitochondria.
  • Liver cells within the lobule can be arranged into zones 1-3 which receive progressively less oxygenated blood.
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3
Q

Name some causes of acute liver injury

A
  • Viral (Hepatitis A, B, Epstein-Barr Virus)
  • Drug
  • Alcohol
  • Vascular
  • Obstruction
  • Congestion
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4
Q

Name some causes of chronic liver injury

What is the most severe form of chronic liver injury known as?

A
  • Alcohol
  • Viral (Hepatitis B, C)
  • Autoimmune
  • Metabolic (iron, copper)

Most chronic form = cirrhosis.

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5
Q

What are the acute presentations of liver injury?

A
  • Malaise
  • Nausea
  • Anorexia
  • Jaundice
  • Rarer presentations → Confusion, bleeding, liver pain, hypoglycaemia
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6
Q

What are the more chronic presentations of liver injury?

What defines chronic liver injury from acute liver injury?

A
  • Been there for more than 6 months
  • Ascites, oedema
  • Haematemesis (varices)
  • Malaise, anorexia, muscle wasting
  • Easy bruising, itching
  • Hepatomegaly
  • Abnormal LFTs
  • Rarer presentations → Jaundice and confusion
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7
Q

Describe the pathway of bilirubin production, release and metabolism.

A
  1. RBCs are phagocytosed by macrophages (120days) - in spleen and lymph nodes
  2. Haemoglobin in RBC broken down → heme & globin
  3. Heme → biliverdin
  4. Biliverdin → Unconjugated bilirubin (UCB) - insoluble
  5. UCB bound to albumin → transported to liver hepatocytes
  6. Hepatocytes convert UCB → Conjugated bilirubin → soluble
  7. Conjugated bilirubin → gallbladder for storage → secreted in bile to gut
  8. Some conjugated bilirubin taken up by liver via enterohepatic circulation
  9. Rest is converted into urobilinogen by gut bacteria
  10. Urobilin either reabsorbed & excreted by kidneys (urine colour) or converted to stercobilin → turns faeces brown.
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8
Q

What is jaundice?

A

Yellowing of the skin, sclerae and mucosae due to raised serum bilirubin (visible at >60umol/L).

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9
Q

How is jaundice classified?

A

Jaundice is classified:

  1. based on the site of the problem (pre-hepatic, hepatic or post-hepatic) or
  2. based on the type of circulating bilirubin (conjugated or unconjugated).
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10
Q

What are the causes of pre-hepatic (unconjugated bilirubin) jaundice?
What effect on urine, stool and LFT would we expect?

A

Over-production of UCB:
- Haemolysis (eg. malaria, DIC, extravascular haemolytic anaemia, ineffective haematopoeisis)

Impaired hepatic uptake:

  • Gilberts syndrome where enzyme converting UCB to CB is low and therefore, cannot form as much CB and UCB build up (particularly during infection or stress where haemolysis increases)
  • Criglers Najjar syndrome - no enzyme to convert UCB to CB (brain deposits of UCB → fatal)

Effects:

  • As unconjugated bilirubin is not water soluble, it is not excreted into the urine - Normal urine, stools and no itching
  • LTFs normal
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11
Q

What are the causes of hepatic (conjugated bilirubin) jaundice?
What effect on urine, stool and LFT would we expect?

A
  • Hepatitis (viral, drugs, immune, alcohol)
  • Liver disease
  • Ischaemia
  • Neoplasm
  • Congestion (CCF)
  • Genetic defects = Dubin-johnson syndrome = where transporter protein moving CB into bile duct is defective so a new transport protein is formed which moves CB into blood rather than bile duct → increased CB in blood

Effects

  • normal urine
  • normal stools
  • no itching
  • normal LFTs
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12
Q

What are the causes of post-hepatic (cholestatic) jaundice?

What effect on urine, stool and LFT would we expect?

A

Post-hepatic Conjugated (Cholestatic)
Gallstones: Bile duct obstruction
- Pressure increase in bile duct → bile leaks into blood through tight junctions of hepatocytes → bile includes cholesterol, bile acids etc. so when these are moved into the blood → itchiness, hypercholesterolemia, xanthomas.
- Bile obstruction also leads to steatorrhea as bile is not released into gut → fat not absorbed → some vitamins wont be absorbed well either.
- Strictures: malignant, ischaemic, inflammatory

Effects:

  • Conjugated bilirubin is water soluble → Dark urine
  • Less conjugated bilirubin entering gut → pale stool
  • Itching and abnormal lft
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13
Q

What effect would damage to hepatocytes have on the levels of UCB and CB?

A

If there is damage to the liver cells, UCB will not be converted to CB or hepatocytes can be damaged and release their CB into the blood stream causing either UCB to increase, CB to increase or both.

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14
Q

What questions should we consider asking someone presenting with jaundice to help us decide what is going on?

A
  1. Dark urine, pale stools, itching of skin?
  2. Symptoms: biliary pain, rigors, abdomen swelling, weight loss?
  3. Past history: biliary disease or intervention, malignancy, heart failure, blood products, autoimmune disease?
  4. Drug history (herbs, OTC and drugs) - about 6 months history
  5. Social history - alcohol, potential hepatitis contact (irregular sex, IVDU, exotic travel, certain foods, tattoos)
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15
Q

What signs on examination could suggest chronic liver disease?

A
  • Hepatic encephalopathy
  • Lymphadenopathy (abnormal size lymph nodes)
  • Hepatomegaly
  • Splenomegaly
  • Ascites
  • Palpable gallbladder
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16
Q

What tests could we perform for jaundice?

A
  • *Liver enzymes**
  • very high AST/ALT suggests liver disease (some exceptions)
  • *Ultrasound**
  • Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound
  • Look for hepatic metastases or pancreatic mass?

If results aren’t clear, we can consider other imaging:

  • Magnetic resonance cholangiogram (MRCP)
  • Endoscopic retrograde cholangiogram (ERCP)
  • CT - if abdominal malignancy is suspected
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17
Q

What is the most common type of gallstone?

What are the risk factors for gallstones?

A

Cholesterol 70% (larger and often solitary)
Pigment 30% (brown and black - small caused by haemolysis)

  • Crohn’s disease.
  • Diabetes mellitus.
  • Diet —diets higher in triglycerides andrefined carbohydratesand low in fibre areassociated with gallstones.
  • Female gender— women have 2–3 times higher incidence of gallstones compared to men.
  • Genetic and ethnic factors.
  • Increasing age — incidence rises noticeably in people aged over 40 years, and is 4–10 times more likely in older people,peaking at 70–79 years.
  • Medication:
    • Somatostatin analogue octreotideimpairs gallbladder and small intestinal motility.
    • Glucagon-like peptide-1 analogues are associated with an increased risk of bile duct and gallbladder disease.
    • Ceftriaxone has been associated with pigment stone development due to precipitationin bile.
  • Non-alcoholic fatty liver disease.
  • Obesity — people with a Body Mass Index (BMI) over 30 are at greater risk of gallstone formation.
  • Prolonged fasting/weight loss —this causes gallbladder hypomotility and increases cholesterol excretion in bile.
    • Weight loss exceeding 1.5 kg a week— for example, people who have hadbariatric surgery areat increased riskdue tocholesterol supersaturation of bile from enhanced cholesterol mobilisation accompanied by decreased bile acid secretion.
  • Use of hormone replacement therapy (HRT).
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18
Q

What medication is the most common cause of drug induced liver injury?

A

Acetaminophen (paracetamol)

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19
Q

Drug induced liver injury accounts for what percentage of acute hepatitis?

A

30%

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20
Q

Name some drugs which are known to cause drug induced liver injury at normal doses

A
  • Antibiotics 32-45% (augemtin, flucloxacilin, erythromycin, septrin, TB drugs)
  • CNS drugs 15% (chlorpromazine, carbamazepine, valproate, paroxetine)
  • Immunosuppressants 5%
  • Analgesics 5-17% (diclofenac)
  • GI drugs (PPI) 10%
  • Dietary supplements 10%
  • Multiple drugs 20%
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21
Q

Some drugs which have not been shown to cause drug induced liver injury at normal doses?

A
  • Low dose aspirin
  • NSAIDs other than diclofenac
  • Beta blockers
  • HRT
  • ACEi
  • Thiazides
  • Calcium channel blockers
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22
Q

Describe the metabolism of paracetamol in the liver & how overdose causes toxicity in patients.

A
  1. Acetaminophen is metabolised in the liver → non toxic metabolites → excreted in urine
  2. Small amount of acetaminophen is metabolised by cytochrome P450 enzyme into → highly toxic substance NAPQI → in normal doses = glutathione conjugates with it to make it inactive
  3. In high doses → hepatocytes cannot breakdown all the acetaminophen → more metabolised by CP450 enzymes (CYP2E1) → more NAPQI production which builds up.
  4. NAPQI → cell death and acute hepatic necrosis
  5. Infants, elderly, malnutrition pts, those with glutathione synthesis deficiency = can experience toxic effects at therapeutic doses
  6. Chronic use of alcohol or medications = increase activity of CYP450 = more NAPQI produced.
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23
Q

Early and late symptoms of acetaminophen (paracetamol) overdose.

A
  • Early → Stomach pain, vomiting, nausea

- Later → jaundice, coagulatopathy, hepatic encephalopathy, acute renal failure.

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24
Q

Management of paracetamol overdose

What are the severity indicators for paracetamol overdose? What do we do if there is a high severity indicator?

A
  • N acetyl cysteine (NAC) ✅
  • replenishes glutathione stores
  • less effective if given more than 24 hours after overdose

Supportive treatment to correct:

  • Coagulation defects
  • Fluid electrolyte and acid base balance
  • Renal failure
  • Hypoglycaemia
  • Encephalopathy

Severity indicators:

  • Late presentation (less effective after 24 hours)
  • Acidosis ( pH <7.3)
  • Prothrombin time > 70 seconds
  • Serum creatinine >300umol/L
  • Consider emergency liver transplant (mortality rate 80%)
25
Q

Causes of chronic liver disease

A
  • Chronic alcohol use
  • Non alcoholic steatohepatitis (NASH)
  • Viral hepatitis (B,C)

Drugs

  • Amiodarone
  • Methyldopa
  • Methotrexate

Immune disorders

  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Sclerosing cholangitis

Genetic/metabolic disorders

  • Haemochromatosis
  • Wilson’s
  • a1 antitrypsin deficiency

Vascular (Budd-Chiari)

26
Q

Signs of chronic liver disease

A
  • Leuconychia (whitened nails)
  • Terry’s nails - white but distal 1/3rd is red from telengiectasias
  • Clubbing
  • Palmar erythema
  • Dupuytrens contracture
  • Spider naevi
  • Xanthelasma
  • Gynaecomastia
  • Atrophic testes
  • Loss of body hair
  • Parotid enlargement (alcohol)
  • Hepatomegaly or small liver in late disease
  • Ascites
  • Splenomegaly
27
Q

What is a normal amount of spider naevi to be present on someone? Why might someone have more?

A
  • Central arteriole from which numerous vessels radiate (spider looking)
  • Usually due to hyperoestrogenic cause (as in the case of chronic liver disease, OCP or pregnancy)
  • Normal to have about 5 in a person
  • Multiple spider naevi are a common sign of liver disease
28
Q

Causes of ascites?

A
  • Chronic liver disease (most common)
  • portal vein thrombosis
  • Hepatoma
  • TB
  • Neoplasia (ovary, uterus, pancreas)
  • Pancreatitis, cardiac causes
29
Q

Pathogenesis of ascites?

A

75% of patients with ascites have underlying cirrhosis.

Ascites formation is multifactorial with 2 main factors involved in pathogenesis:

  1. Sodium and water retention - due to systemic vasodilation which causes a decrease in effective arterial blood volume and a hyperdynamic circulation.
  2. Portal hypertension - due to structural changes in the liver in cirrhosis and increased splanchnic blood flow

The rapid and high inflow of arterial blood into the splanchnic microcirculation is the main factor increasing hydrostatic pressure in the splanchnic capillaries leading to an excessive production of splanchnic lymph over lymphatic return. Lymph leakage from the liver and other splanchnic organs is the mechanism of fluid accumulation in the abdominal cavity.

30
Q

Management for ascites

A
  • *Mild or moderate ascites**
  • Fluid restriction and no ‘added’ salt diet
  • Diuretics - spironolactone and furosemide

Severe or tense ascites
- Large-volume paracentesis + albumin to replace protein lost in fluid and prevent re-ocurrence of ascites
If ascites keeps coming back:
- Trans-jugular intrahepatic portosystemic shunt (TIPS), directs pressure into systemic circulation

31
Q

What is the main cause of liver death in the UK?
Is the incidence of this condition increasing or decreasing?
What age group are deaths highest in?

A

Alcoholic liver disease
Incidence is increasing
Death rates are highest in the 55-59 year olds.

32
Q

Does alcoholic liver disease more alcoholics or ‘non-alcoholics’?
What are some big risk factors for ALD?

A

Only 10-20% of heavy drinkers develop ALD
It is often not the alcohol dependent people who develop ALD.

Risk factors:
Long time overconsumption of alcohol
Overweight/obese (risk x2)
Female sex

33
Q

Pathology of ALD?

A
  • Increased hepatic resistance

- Increased splanchnic blood flow

34
Q

Pathogenesis of fatty liver disease?

A
  1. Alcohol is metabolised mainly in the liver, through 2 main pathways: alcohol dehydrogenase and cytochrome P-450 2E1.
  2. Alcohol dehydrogenase is a hepatic enzyme that converts alcohol → acetaldehyde, which is subsequently metabolised to acetate by acetaldehyde dehydrogenase.
  3. Alcohol dehydrogenase and acetaldehyde dehydrogenase reduce NAD to NADH.
  4. Excessive NADH in relation to NAD inhibits gluconeogenesis and increases fatty acid oxidation, which in turn promotes fatty infiltration in the liver.
  5. The cytochrome P-450 2E1 pathway generates free radicals through the oxidation of NADPH to NADP. Chronic alcohol use upregulates cytochrome P-450 2E1 and produces more free radicals.
  6. Chronic alcohol exposure also activates a third site of metabolism: hepatic macrophages, which produce tumour necrosis factor (TNF)-alpha and induce the production of reactive oxygen species in the mitochondria.
35
Q

What is alcoholic hepatitis?

A

Alcoholic hepatitis is inflammation of the liver caused by drinking alcohol.
It is most likely to occur in those who drink over many years however, not all heavy drinkers develop alcoholic hepatitis and the disease can occur in those who only drink moderately.

36
Q

What are mallory bodies?

A

Damaged intermediate filaments seen in alcoholic hepatitis due to infiltration of neutrophils

37
Q

What are the symptoms of alcoholic hepatitis?

A
  • Loss of appetite
  • N&V
  • Abdominal tenderness
  • Fever, often low grade
  • Fatigue and weakness
  • Malnutrition is common and most alcoholics get their calories from alcohol
  • In severe alcoholic hepatitis → ascites, confusion and behaviour changes, kidney and liver failure.
38
Q

Complications of alcoholic hepatitis?

A
  • Varices - blood that can’t flow freely through the portal vein backs up into the other blood vessels in the stomach and oesophagus. These blood vessels are much thinner and more likely to bleed if overfilled. Heavy bleeding is life-threatening
  • Ascites - fluid accumulation in abdomen can become infected and require antibiotics
  • Kidney failure - damaged liver affects blood flow to kidneys resulting in damage
  • Confusion, drowsiness, slurred speech - damaged liver cannot remove toxins as effectively and toxins can build up and cause damage.
  • Cirrhosis of the liver → liver failure
39
Q

Signs of alcohol withdrawal?

Treatment for alcohol withdrawal?

A
  • tremor
  • convulsions
  • confusion
  • increased pulse rate
  • hypotension
  • hallucinations

Treatment

  • Lorazepam or chlordiazepoxide (generous amount)
  • For chronic alcohol dependence you can use disulfiram which causes acetylaldehyde to build up and cause very unpleasant side effects (flushing, throbbing, headache, palpitations)
40
Q

What happens if someone with chronic LD is constipated?

A

Constipation - Ammonia is produced in the gastrointestinal tract by bacterial degradation of nutrients, and also through normal metabolic processes in intestinal cells. Normally, the liver breaks down ammonia into urea, which is safely excreted in urine. In constipation there is a build up of ammonia if not opening bowels and this can lead to hepatic encephalopathy which is where the liver stops functioning properly so it cannot detoxify the ammonia into urea or the blood from the gut bypasses the liver through porto-systemic shunt.

41
Q

What effect does chronic LD have on drugs?

A

Sedatives, analgesics, NSAIDs, diuretics, liver is more sensitive to the effects of drugs and will metabolise them slower.

42
Q

What are some reasons why patients with chronic liver disease deteriorate quickly?

A
  • Constipation (ammonia build up)
  • Drugs (slower metabolism leads to toxicity)
  • Gastrointestinal bleeds (DRE to check)
  • Infection (more prone to infection with LD)
  • Hypoglycaemia, hyponatraemia, hypokalaemia (electrolyte abnormalities are common in LD)
  • Alcohol withdrawal (not typically a cause for deterioration)
  • Cardiomyopathies, intracranial bleed if they’ve had a fal,.
43
Q

Why are those with liver disease more susceptible to infections?

A

Why they are more susceptible

  • They have impaired reticulo-endothial function.
  • Reduced opsonic activity
  • Leukocyte function
  • Permeable gut wall
44
Q

What are the susceptible sites of infection in chronic liver disease? (5)

A
  • Spontaneous bacterial peritonitis
  • Septicaemia
  • Pneumonia
  • Skin infection
  • UTI
45
Q

What is spontaneous bacterial peritonitis?

How is it diagnosed?

A

Spontaneous bacterial peritonitis (SBP) is the development of a bacterial infection in the peritoneum, despite the absence of an obvious source for the infection. It is specifically an infection of the ascitic fluid.

  • Commonest serious infection in cirrhosis
  • Vague symptoms
  • Based on neutrophil count in ascitic fluid
  • Gram stain often negative, use blood culture bottles
  • After 1 episode: should have antibiotic prophylaxis and consider liver transplant.
46
Q

How does renal failure affect prognosis in patients with liver disease?
What should you look at in patients who develop renal failure in liver disease?

A

It is associated with a poor prognosis
If a patient with liver disease develops renal failure, look at medications they are on:
- Diuretics
- NSAIDs
- ACE inhibitors
- Aminoglycosides
- Infection
- GI bleeding
- Myoglobinuria - if pt has been on floor for long time
- Renal tract obstruction - arrange USS of kidneys if worried
- Look at hydration of patient, are they drowsy, sleepy etc.

47
Q

What are some bedside tests for patients with encephalopathy?

A
  • Serial 7’s (ask them subtract 100-7)
  • WORLD backwards (spelling)
  • Animal counting in 1 minute (10 animals in 1 min)
  • Draw 5 point star
  • Number connection test (dot to dot)
48
Q

Is malnutrition common in liver disease patients?

A

Yes

They get a lot of their calories from alcohol so they are often malnourished.

49
Q 
How do we treat:
1. malnutrition
2. variceal bleeding
3. encephalopathy
4. ascites/oedema
5. infections
in liver disease?
A
  1. Naso-gastric feeding
  2. endoscopic banding, propanolol, terlipressin
  3. lactulose (acidifies bowel contents which draws ammonia into the bowel lumen and helps clear it)
  4. salt or fluid restriction, diuretics and paracentesis
  5. antibiotics
50
Q

What are 4 differential diagnosis for hepatitis?

A

Viral causes (A,B,C,CMV,EBV)
Drug induced hepatitis
Alcohol induced hepatitis
Autoimmune hepatitis

51
Q

What is autoimmune hepatitis?

A

Autoimmune hepatitis is an inflammatory condition of the liver of unknown cause characterised by abnormal T-cell function and autoantibodies directed against hepatocyte surface antigens.

52
Q

Who does autoimmune hepatitis most commonly affect?
What is a common presenting complaint?
How do we classify autoimmune hepatitis?

A

More commonly affects middle aged or young women (75% cases are women).
Amenorrhea is common and up to 40% present with acute hepatitis and signs of autoimmune disease (fever, malaise, urticarial rash, pleurisy, pulmonary. infiltration, glomerulonephritis)

Classification is by autoantibodies
70% present with ANA ASMA positive antibodies.

53
Q

What results on investigations would we expect to see for autoimmune hepatitis?

A

Serum bilirubin, AST, ALT, ALP all usually high
Hypergammaglobulinaemia (esp IgG)
Positive autoantibodies
Liver biopsy showing mononuclear infiltrate of portal and peripheral areas and necrosis

54
Q

How do we diagnose autoimmune hepatitis?

A
  • Exclude other causes
  • Diagnostic criteria based on IgG levels, autoantibodies and histology in the absence of viral disease
  • Sometimes it is challenging and there is overlap with other chronic liver conditions
55
Q

Treatment of autoimmune hepatitis?

A

Steroids - prednisolone with quite rapid improvements in AST and bilirubin levels

56
Q

What is primary biliary cholangitis?
What is the hallmark of the disease?
Does it most commonly affect men or women? What is the typical age of presentation?
Symptoms?

A

Interlobular liver bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis which may lead to fibrosis, cirrhosis and portal hypertension

Antimitochondrial antibodies (AMA) are the hall mark of PBC = present in 95% patients

Typically affects women (90%)
Typical age = 50

Symptoms:

  • Often asymptomatic and diagnosed after incidental finding
  • Lethargy and itching - 50/80%
  • Dry eyes - 10%
  • Joint pains - 10%
  • Variceal bleeding - 10-15%
  • Liver failure, ascites, jaundice - 5%
57
Q

What can be given to help manage cholestatic itch in PBC?

A

Cholestyramine helps in 50% cases
Rifampicin is effective but occassionally damages the liver
Opiate antagonists can be used
Liver transplant might be considered if itch is severely affecting QOL

58
Q

What other conditions can be associated with PBC?

A 
Sjorgens - 20-80%
Thyroiditis 10-20%
Scleroderma
Rheumatoid arthritis - 5-25%
Coeliac disease 5%
59
Q

What is the treatment for PBC?

A

Ursodeoxycholic acid

  • improves liver. enzymes. and bilirubin levels
  • subtle reduction in inflammation
  • reduces portal pressure and rate of variceal development
  • reduces rate of death or liver transplantation
  • doesn’t improve pruritis symptom.

Gastrointestinal (10 decks)

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