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Laboratory Medicine > The Hepatic and Biliary Systems > Flashcards

The Hepatic and Biliary Systems Flashcards

1
Q

Describe the pathology of acute viral hepatitis, and name causitive organisms

A

Hepatocyte necrosis, usually around hepatic veins associated with neutraphil infiltration. Major causitive organisms:

  • Hepatitis A & E, B
  • CMV
  • EBV
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2
Q

What are the non-viral causes of acute hepatitis?

A

Non viral causes of acute hepatitis include:

  • Infection e.g. toxoplasmosis
  • Drugs e.g. paracetamol
  • Alcohols
  • Poisons
  • Others: pregnancy, Wilson’s disease
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3
Q

Describe the pathology of chronic hepatitis. What are the main causative organisms of chronic viral hepatitis?

A

Chronic (>6 month) inflammatory cell infiltrate, comprising plasma cells and sometimes lymphoid follices. There is a varying degree of liver fibrosis, starting around the portal tracts and eventually linking to form nodules.

Causitive organisms:

  • Hepatitis B and C
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4
Q

What is the presentation of acute viral hepatitis?

A

Generally presents with non-specfiic symptoms including:

  • Malaise / low grade fever / arthralgia / nausea
  • Jaundice (if severe)
  • Hepatomegaly (1-2 cm, soft edge)
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5
Q

In the absence of jaundice, acute hepatitis is often diagnoses using liver function tests. What would be the expected findings in levels of:

  • Albumin
  • AST / ALT
  • Bilirubin
A
  • Albumin: Normal
  • AST / ALT - Raised due to hepatic necrosis
  • Bilirubin - Elevated. In severe acute hepatitis urobilinogen may be absent from urine representing cholestasis, but reappears as hepatitis resolves
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6
Q

The most common cause of viral hepatitis is Hep. A. Describe the clinical features of disease including transmission, incubation period, and clinical signs

A
  • Transmission: fecal-oral, saliva
  • Incubation: short (2-3 weeks)
  • Clinical symptoms
    • nonspecific nausea, and anorexia.
    • Jaundice may develop 1 - 2 weeks post-infection
    • Urine may become dark and stools pale due to intrahepatic cholestasis

Note: there is no chronic stage in hepatitis A infection - prognosis is good, and infection resolves in 3 - 6 weeks

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7
Q

How is a diagnosis of hepatitis A infection made?

A
  • Anti-HAV IgG antibodies common in geneal population older than 40, an anti-HAV IgM signals acute infection
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8
Q

Hepatitis B is a cause of both acute and chronic hepatitis. Describe the transmission and incubation period of HBV infection

A
  • Transmission: Blood (needlestick injury, IVDU), vertical (mother-child), saliva, sexual contact (particularly male-male)
  • Incubation: Long - 1-5 months
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9
Q

Acute HBV may be subclinical, or may produce symtpoms similar to acute HAV infection. However, approximately 10% of patients may progress to a chronic phase. What are the clinical features and investigations performed in chronic hepatitis?

A
  • Clinical features
    • May present as mild, slowly progressive hepatitis, or established chronic liver disease
    • Increased risk of cirrhosis
    • Increased likelihood of hepatocellular carcinoma
  • Investigations
    • Moderate rise in AST / ALT
    • Moderate rise in ALP
    • Bilirubin often normal
    • HBsAg and HBV DNA often present in serum.
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10
Q

There are several markers that can be used in HBV infection to aid in diagnosis of infection:

A
  • HBsAg - Surface antigen. Present in acute or chronic infection
  • HBeAg / HBcAg - HBV ‘Core’ antigen (or the surface form of the antigen, in the case of HBeAg) - indicator of viral replication and continued infectious state of host
  • HBV DNA - Implies viral replication
  • Anti-HBs - Immunity to HBV, previous exposure or vaccination
  • Anti-HBc
    • IgM - acute infection
    • IgG - past infection (cleared if HBsAg negative)
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11
Q

Describe the transmission, timecourse and clinical presentation of HCV infection

A
  • Transmission: IVDU and unscreened blood products (pre-1990)
  • Timecourse - Long - acute hepatitis usually asymptomatic, usually not possible to date start of infection
  • Clnical features:
    • Often asymptomatic with disease discovered following routince biochemical tests showing ALT elevation
    • Progression to chronic liver disease and cirrhosis may occur
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12
Q

When is treatment indicated for chronic hepatitis (either HBV of HCV)

A
  • Evidence of liver damage - cirrhosis, chronic liver failure
  • Both have potential to progress to hepatocellular carcinoma - approx 1% p/a with concurrent cirrhosis
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13
Q

What is cirrhosis? Describe the pathogenesis

A

Cirrhosis results from necrosis of liver cells followed by fibrosis and nodule formation. Diffusely abnormal liver architecture interferes with blood flow and function, leading to portal hypertension and impaired cell function.

Fibrosis results from chronic inflammation and necrosis. It is initiated by stellate cells, a main source of fibrous tissue, and stimulated by Kuppfer and other inflammatory cells.

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14
Q

What are the main causes of cirrhosis?

A

Most common / Less common

  • Alcoholic liver disease
  • Hepatitis B or C
  • Non-alcoholic fatty liver disease
  • Metabolic disorders: Wilson’s disease, hereditary haemochromatosis, alpha-1 anti-trypsin deficiency
  • Autoimmune hepatitis
  • Primary biliary cirrhosis, primary sclerosing cholangitis
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15
Q

Cirrhosis is often clinically silent until complications develop. Investigations show reduced prothrombin time and abnormal biochemistry, often with a raised ALP in line with cholestasis due to inflammation. What additional tests should be performed to assess severity?

A
  • Imaging
    • Ultrasound may demonstrate change in size and shape, fatty change and fibrosis may produce change in echogenicity.
    • CT shows hepatosplenomegaly
    • Endoscopy is used for the treatment of varices and portal hypertensive gastropathy
  • Liver Biopsy
    • Necessary to confirm type and severity of disease. Defined by diffuse nodularity surrounded by fibrous tissue.
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16
Q

What are the main complications of cirrhosis?

A
  • Portal hypertension and gastrointestinal haemorrhage
  • Ascites
  • Portosystemic encepalopathy
  • Hepatocellular carcinoma
  • Bacteraemia, infection
  • Renal failure
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17
Q

What is the managemet of cirrhosis?

A
  • Treat underlying cause
  • 6 monthly ultrasound to detect early development of hepatocellular carcinoma
  • Reduced salt intake
  • Avoid aspirin and NSAIDS
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18
Q

What is portal hypertension? How are the causes subdivided?

A

Portal hypertension is raised pressure within the portal vein, caused by resistance to portal flow. Causes may be:

  • Pre-hepatic: (blockage of portal vein before liver) portal vein thrombosis
  • Intra-hepatic: (distortion of liver architecture) primary biliary cirrhosis, cirrhosis, Budd-Chiari syndrome
  • Post-hepatic: (venous blockage outside of liver - rare) right sided heart failure, constrictive pericarditis
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19
Q

What are the clinical features and presenting features of portal hypertension?

A

Patients are often asymptomatic - the only clinical evidence is splenomegaly and often chronic liver disease. Presenting features include:

  • Haematemesis or melaena from rupture of gastro-oesophageal varices of portal hypertensive gastropathy
  • Ascites
  • Encephalopathy
  • Breathlessness due to porto-pulmonary hypertension or hepatopulmonary syndrome
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20
Q

Patients with portal hypertension are at risk of variceal haemorrhage. How is this managed?

A
  • Acute management: resuscitation, urgent endoscopy and variceal banding to stem bleeding
  • Long term management: non-selective betablocade to reduce resting heart rate, repeated courses of variceal banding to prevent bleeding.
21
Q

Ascites are a common complication of cirrhosis. What are they, and what is the pathogenic mechanism?

A

Ascites are fluid within the peritoneal cavity, due to sodium and water retention:

  • A reduction in pressor systems promotes salt and water retention
  • Portal hypertension exerts local hydrostatic pressure
  • Low serum albumin (a consequence of impaired liver function) further contributes by a reduction in plasma oncotic pressure.
22
Q

What is the management of ascites?

A

Aim is to reduce sodium intake and increase renal sodium excretion, producing a net reabsorption of fluid from the ascites into the circulating volume.

  • Reduce sodium intake from diet
  • Diuretic of first choice is aldosterone antagonist spironolactone
23
Q

A major complication of ascites is spontaneous bacterial peritonitis (SBP). What is this?

A

Occurs in approximately 8% of individuals with ascites with cirrhosis. Infectious organisms access the peritoneum by haematogenous spread, leading to peritonitis. SBP is an indication to refer to liver transplant.

24
Q

Hepatic failure may occur as the end-stage of chronic liver disease, following 80-90% loss of functional capacity of the liver. It is often due to an additional insult, resulting in decompensation. What are the clinical features?

A
  • Jaundice
  • Peripheral oedema (due to hypoalbuminaemia)
  • Fetor hepaticus (sweet and sour smell on breath)
  • Coagulopathy
  • Hepatic encephalopathy
  • Renal failure

High mortality without liver transplantation

25
Primary liver tumours may be benign or malignant, but the most common are malignant. Worldwide, hepatocellular carcinoma (HCC) is the fith most common cancer, however, it is rarer in the West than in Africa. Why is this?
* HCC usually occurs on a background of cirrhosis if there is any cause * The high incidence of HBV and HCV infection in Africa leads to a much higher disease burden * In the west, alcoholism leading to cirrhosis is a more likely cause of HCC
26
Describe the clinical features of HCC?
HCC does not have a characteristic presentation however, there may be: * Abdominal pain/mass, fatigue, weight loss, malaise * Enlarged liver on palpation * Elevated serum-apha feroprotein in around 50% (neither sensitive nor specific for HCC) Rapid development of these features in a cirrhotic patient is strongly suggestive of HCC
27
What is the prognosis of HCC?
Generally a poor prognosis, as only 10-20% suitable for surgery. Without treatment, survival is 6-12 months, although improved in those with a non-cirrhotic liver. Surgical resection of liver transplantation may be curative.
28
Liver tumours are a relative common clinical finding. Are they usually a primary or seconday?
The majority of liver tumours are secondary, particularly from the GI tract (due to the distribution of the portal blood supply), breast or bronchus. They are usually multiple. Presentation is with weight loss, malaise, upper abdominal pain and hepatomegaly, with or without jaundice.
29
Describe the clinical spectrum of alcoholic liver disease
* Fatty change: with large amounts of alcohol, hepatocytes become swollen with fat (steatosis), though this resolves on cessation of drinking. * Alcoholic hepatitis: in addition to fatty change, there is PMN infiltration and hepatocyte necrosis. Dense cytoplasmic inclusions (Mallory bodies) may be seen in hepatocytes, and mitochondria are enlarged * **Alcoholic cirrhosis**
30
What are the risk factors for the development of alcoholic liver disease?
* Quantity of alcohol consumed * Gender - women more susceptible * Concomitant HCV infection * Genetic factors - Cytochrome p450 and ethanol dehydrogenase polymorphisms * Malnutrition - particularly vit. A and E deficiency
31
What investigations and results are indicative of alcoholic liver disease?
* An elevated **MCV** often indicates heavy drinking * LFTs demonstrate raised aminotransferase. An increased **GGT** is helpful to determine whether the patient is taking alcohol * Aditionally, in alcoholic hepatitis there will be elevated serum **bilirubin**, **ALP** and an **increased prothrombin time**
32
What is the management of alcoholic liver disease?
* Patient must s**top drinking:** delirium tremens may be treated by diazepam and IV thiamine may be given to prevent Wernicke-Korsakoff encephalopathy * In fatty liver disease, changes are reversable, biochemistry will return to normal as long as consumption is controlled * Repeated episodes of hepatitis are likely to lead to cirrhosis -\> reduced liver function and associated complications
33
Cirrhosis may also be caused by non-alcoholic fatty liver disease (NAFLD). What are the causes of NFALD?
* Associated with obesity, dyslipidaemia, insulin resistance, diabetes * May be caused by drugs (amiodarone, tamoxifen) * Pathogenesis unknown, increasing with obesity epidemic
34
What is the basis of diagnosis of non-alcoholic fatty liver disease? What is the management
* Largely asymptomatic, often detected because of abnormal LFTs * Diagnosis of exclusion: fatty liver demonstrated on ultrasound, other causes of liver injury (eg. alcohol) excluded * Treated with: * Weight loss * Exercise * Strict control of hypertension, diabetes and lipid levels
35
What is haemochromatosis, what are the primary and secondary causes
Haemochromatosis is iron overload, leading to deposition of iron within multiple organs. It may be: * Primary: hereditary due to a mutation in HFE involved in uptake of dietary iron from the gut. There is no direct pathyway of Fe2+ excretion in the body - only regulation is uptake. HFE mutation leads to increased uptake * Secondary causes include: * Parenteral iron overload (e.g. multiple blood transfusion) * Ineffective erythropoiesis (thalassemia) * Increased oral intake of iron
36
What is the prevalence and aetiology of hereditary haemochromatosis?
Autosomal recessive, 1/9 heterozygotes, 1/220 homozygotes. However, only 20% penetrance. Occurs more commonly in men, as menstrual blood losses compensate in women.
37
Describe the clinical features of haemochromatosis
* **Iron is deposited** throughout body in liver, pancreas, myocardium (leading to restrictive cardiomyopathy) and many endocrine glands * **Cirrhosis** occurs due to iron deposition * May be **diabetes and malabsorption** * Classic triad of bronze skin pigmentation (due to **melanin deposition**) **hepatomegaly** and **diabetes mellitus** only present in cases of gross overload.
38
What investigations would be performed in supected haemochromatosis, and what would the results demonstrate?
* **Serum iron** is elevated, with saturated transferrin * **Serum ferritin** is elevated * Diagnosis is confirmed by **elevated hepatic iron concentration**
39
What is the treatment for haemochromatosis?
* Regular venesection used to remove free Fe2+ from serum and stimulate erythropoiesis * Iron chelation with desferioxamine mesilate - increase urinary iron excretion * Avoidance of high iron food (e.g. red meat)
40
What is the prognosis for haemochromatosis?
* Prognosis is excellent if identified and treated early. * Morbidity and mortality related to end organ damage: * Cirrhosis * Hepatocellular Carcinoma * Pancreatic insufficiency * Cardiomyopathy
41
What is primary biliary cirrhosis, and what is it caused by?
Chronic disorder in which there is **progressive destruction** of the **small bile duct**, eventually leading to cirrhosis. Frequently affects **middle aged women** (6:1 M:F, peak onset 40-50) Has an autoimmune aetiology - serum **anti-mitochondrial antibodies** (AMA) found in almost all patients with PBC, causing **inflammatory destruction of intra-hepatic bile ducts**
42
What are the clinical features of primary biliary cirrhosis?
* Often has an insidious onset, with **pruritis** and **fatigue** the first symptoms * Years later, **jaundice** will follow with **hepatomegaly** * There is a gradual progression to **cirrhosis** and **liver failure** * May see pigmented xanthelasma on eyelids or other deposits of cholesterol in the creases of the hands
43
What investigations are performed in suspected primary biliary cirrhosis, and what are the results?
* Anti-mitochondrial antibodies measured in 95% of patients * Elevated ALP and cholesterol * In late stages there may be elevated bilirubin * Serum IgM may be very high
44
What is the histological presentation of primary biliary sclerosis following liver biopsy?
* There is inflammation of the portal tract, with bile duct injury and eventual destruction * Hepatic granulomas are a non-specific sign of PBC - also present in sarcoidosis, tuberculosis, parasitic infection etc * Eventual fibrosis and cirrhosis of liver * Cholestasis leads to bile accumulation in liver - the liver may be green macroscopically.
45
What is the treatment for primary biliary sclerosis?
* Ursodeoxycholic acid reduces cholestasis by reducing cholesterol uptake from gut * Pruritis may be controlled by cholestyramine * Supplementation of fat soluble vitamins is required (A,D,E,K) * Bisphosphonates are required to reduce osteoporosis
46
What is primary sclerosing cholangitis? The cause is unknown, but what is the main association?
* Chronic cholestatic liver disease characterized by fibrosing inflammatory destruction of intra- and extrahepatic bileducts * In 75% of patients it is associated with IBD, usually ulcerative collitis * Male predominance (2:1), onset usually between 20 and 40 years
47
Describe the clinical features of primary sclerosing cholangitis.
* Due to increased screening of patients with IBD, PSC is often detected in an asymptomatic phased by **elevated ALP** * Symptomatic presentation is usually with **fatigue, pruritis, jaundice and fat malabsorption**
48
How is primary sclerosing cholangitis diagnosed?
* Typical biliary changes may be diagnosed using MRCP, showing characteristinc narrowed segments of biliary tree * Bilirubin and ALP is usually elevated * The autoantibody pANCA (anti-neutrophil cytoplasmic antibody) is usually raised, but not diagnostic
49
What is the management of primary sclerosing cholangitis?
* Management with ursodeoxycholic acid (to reduce bilirubin and aminotransferase levels) and cholestyramine (reduce pruritis) * Liver transplantation considered * Mortality due to cirrhosis / liver failure. There is also an increased risk of cholangiocarcinoma, thought to occur in up to 15% of patients

Laboratory Medicine (7 decks)

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