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Liver Flashcards

1
Q

What is jaundice?

A

(1. ) Jaundice is the yellowish pigmentation of the skin and sclera and appears when total bilirubin levels exceed 2 mg/dL in adults.
(2. ) Total hyperbilirubinemia can be due to unconjugated or conjugated bilirubin and depends on where bilirubin metabolism is disrupted.
(3. ) Jaundice can be thought of as prehepatic, hepatocellular, or posthepatic

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2
Q

What is unconjugated bilirubin?

A

(1. ) UCB arises from haem of broken down RBC

(2. ) UCB is the form of bilirubin that’s lipid-soluble, meaning it’s not water-soluble.

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3
Q

What is conjugated bilirubin?

A

(1. ) UCB migrates to liver where it’s conjugated glucuronyl transferase (UGT), making it water soluble.
(2. ) It is then secreted out the bile canaliculi where it drains into the bile ducts and sent to the gallbladder for storage as bile.
(3. ) When you eat a donut or something, gallbladder secretes the bile and CB, it moves through the common bile duct to the duodenum and is converted to urobilinogen by intestinal microbes
(4. ) Some urobilinogen is reduced to stercobilin and excreted and responsible for brown faeces.

Some urobilinogen is reabsorbed into blood and oxidised into urobilin and sent to liver.

Some of urobilin goes to kidneys and is excreted this is responisble for the yellow-ness of urine.

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4
Q

What is a non-hepatocellular cause of prehepatic jaundice

A

(1. ) High levels of UNCONJUGATED bilirubin

(2. ) No evidence of liver dysfunction/injury. Could be due to haemolytic anemia, dyserythropoiesis

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5
Q

What is a hepatocellular cause of prehepatic jaundice

A

(1. ) Gilbert Syndrome
- Genetic condition that causes dec in uridine glucuronyl transferase, so liver is less effective at conjugating bilirubin.
- Usually asymptomatic, but triggers such as fasting - adipocytes release a lot of unconjugated bilirubin
- Usually resolves within 24 hours after resuming a normal diet.

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6
Q

What causes of intra-hepatic jaundice?

A

(1.) Intrahepatic disorders can lead to unconjugated or conjugated hyperbilirubinemia.

(2. ) Dubin-Johnsons Syndrome
- genetic condition where there is dec in bilirubin transport out of the hepatocyte
- So conjugated bilirubin levels are high

(3. ) Medications e.g. rifampin
- There is evidence of liver injury –> high AST and ALT levels

(4.) Hepatocellular disease: Viral infections (hepatitis A, B, and C), Chronic alcohol use, Autoimmune disorders

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7
Q

What causes post-hepatic jaundice?

A

(1. ) Conjugated bilirubin is high, high ALP
(2. ) Biliary obstruction due to stone, cholangiocarcinoma, pancreatic cancer or stricture formation (in primary sclerosing cholangitis).
(3. ) Choleostasis - retention of bilirubin in hepatocytes.

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8
Q

Why may pruritus be associated with obstructive jaundice?

A
  1. Blockage of common duct due to gallstones, mirizzi, pancreatic and cholangio carcinoma, stricture
    (2. ) Inc pressure of duct causes leakage of its content into the blood
    (3. ) Bile salt and acids, cholesterol in the blood causes pruritis, cholesterolemia, xanthoma, dark urine, steatorrhea.
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9
Q

What may you ask during Hx taking to help differentiate what type of jaundice a pt may be presenting?

A
  1. Associated Sx
    - Dark urine, pale stools, itching?
    - Biliary pain, rigors, abdomen swelling, weight loss?
  2. PMH - biliary disease/intervention, malignancy, heart failure, blood products, autoimmune disease
  3. Drug Hx - Over the counter, anything herbal?
  4. Social Hx - Alcohol, potential hepatitis contact (irregular sex, IVDU, exotic travel, certain foods)
  5. Family Hx/systemic review
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10
Q

What is choleostatic liver disease? Sx associated with it?

A

(1. ) Flow of bile from liver is reduced or blocked –> inc bilirubin.
(2. ) Two types of cholestasis: intrahepatic and extrahepatic cholestasis.
(3. ) Intrahepatic cholestasis originates within the liver
(4. ) Extrahepatic cholestasis is caused by obstruction of bile ducts such as gallstones, cysts, and tumours restrict the flow of bile.

(5.) Possible Sx depending on the cause= Fatigue, nausea, abdominal pain, Jaundice, Dark urine, Pale stools, Itching, Abnormal LFTs

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11
Q

What is Drug Induced Liver Injury? and its RF?

A

(1. ) An acute or chronic response to a natural or manufactured compound.
(2. ) RF = female, older age, inc BMI.

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12
Q

Types of DILI (5)

A
  1. Hepatocellular Injury - Elevation in transaminases (typically 3 times the upper limit) in comparison to the ALP level
  2. Cholestatic Injury
    - Elevation of ALP, typically 3 times the upper limit in comparison to transaminases
  3. Mixed - both the aminotransferases and ALP are 3 times upper limit
  4. Direct toxicity DILI - Mechanism is predictable from drugs known to cause liver injury e.g. Acetaminophen (paracetamol)
  5. Idiosyncratic DILI
    - Unpredictable and often occurs in susceptible patients e.g. Antibiotics, diclofenac (NSAID), Herbal and dietary supplements, CNS Drugs, immunosuppressants, Analgesics.
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13
Q

History and Presentation of DILI

A

(1. ) Tabulate the drugs taken
- Look for known offending drugs
- What did they start recently? Onset of illness: 4d to 8w (usually)
- Note: Challenge tests with drugs should be avoided
- Exclude other causes: Viral hepatitis, Biliary disease
- Consider liver biopsy

(2. ) Signs and Sx (may be acute of chronic)
- usually asymptomatic
- Jaundice
- Weakness
- abdominal pain (RUQ)
- dark stools or urine
- nausea
- pruritis (in cholestatic liver injury)

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14
Q

Investigations of DILI

A

(1. ) LFT
(2. ) INR - coagulopathy may be observed, indicating impaired liver function
(3. ) FBC, electrolytes, viral serologies, and autoantibodies
(4. ) Imaging Studies (abdominal ultrasound, MRI) - Can be helpful in cholestatic injury to exclude other biliary tract pathology.

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15
Q

Treatment and Management of DILI

A
  1. Removal of offending drug
  2. If paracetamol DILI –> N-acetyl-cysteine (NAC) - this metabolises it into stable, safe metabolites
  3. Supportive to correct:
    - coagulation defects
    - fluid electrolyte and acid base balance
    - renal failure
    - hypoglycaemia
    - encephalopathy
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16
Q

Clinical features and management of paracetamol induced liver failure

A

Clinical features:

  • Acidosis (pH <7.3) –> vomiting
  • Prothrommbin time > 70 sec –> liver damage, jaundice, encephalopathy
  • High serum creatinine –> acute kidney injury
  1. Acetylcysteine given <10-12h since overdose. It is not effective when given over 24h
  2. Consider emergency liver transplant - otherwise 80% mortality
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17
Q

What is Chronic Liver Disease? What are the most common causes? (6.)

A

(1.) Progressive deterioration of liver functions for >6m that ultimately leads to cirrhosis - final stage of CLD

Causes

(1. ) Alcoholic Liver Disease
(2. ) NAFLD and NASH
(3. ) Viral Hepatitis
(4. ) Genetic: AATD, haemochromatosis, Wilsons Disease
(5. ) Autoimmune: Autoimmune hepatitis, PBC, PSC
(6. ) Other: Drugs, Idiopathic, Vascular e.g. budd-chiari

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18
Q

Key Clinical features (ABCDEFGHIJ) and complications (6) of CLD

A

ABCDEFGHIJ

  • Asterixis, Ascites, Ankle oedema
  • Bruising
  • Clubbing/ Coagulopathy,
  • Dupuytren’s contracture
  • Encephalopathy / palmar Erythema
  • Fatigue, weakness due to malnutrition
  • Gynaecomastia
  • Hepatomegaly
  • Impotence + amenorrhoea (endo changes)
  • Jaundice
  • Others = spider naevi, hair loss

Complications

(1. ) Portal HTN = ascites, encephalopathy, varices
(2. ) Infection
(3. ) Coagulopathy
(4. ) Hypoglycaemia
(5. ) HCC

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19
Q

Stages of Alcoholic Liver Disease

A
  1. Alcoholic Fatty Liver or Steatosis
    a. At this stage, fat accumulates in the liver parenchyma.
    b. If the consumption of alcohol does not stop at this stage, it can lead to alcoholic hepatitis.
  2. Alcoholic Hepatitis
    a. Inflammation of liver, outcome depends on the severity of damage.
    b. Alcohol abstinence, nutritional support, treatment of infection, and prednisolone therapy can help
    c. With continued alcohol consumption, ALD progresses cirrhosis
  3. Alcoholic Cirrhosis
    a. Liver damage at this stage is irreversible and leads to complications of cirrhosis and portal HTN.
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20
Q

RF for ALD

A

(1. ) Drinking pattern
- quantity and duration of alcohol intake
- ‘continuous’ drinker rather than ‘binge’ drinking
- Exceeding 14units per week (PHE guideline)
- No correlation with alcoholism

(2. ) Women
(3. ) Obesity
(4. ) Genetics

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21
Q

Pathophysiology of ALD

A

(1. ) Alcohol metabolised by Alcohol dehydrogenase and Aldehyde dehydrogenase that converts it into acetaldehyde and acetate.
(2. ) Alcohol metabolism increases NADH production, leading to formation of glycerol phosphate, which combines with fatty acids and becomes triglycerides, which accumulate within the liver.
(3. ) lipolysis stops due to alcohol consumption so fats accumulation (steatosis) in the liver and lead to “fatty liver disease.”
(4. ) Continued alcohol consumption brings the immune system into play. Interleukins and neutrophils attack hepatocytes –> “alcoholic hepatitis”.
(5. ) Ongoing liver injury leads to irreversible liver damage –> cirrhosis.

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22
Q

Signs and Symptoms of ALD

A

Depending of severity and ALD stage

  • Spider naevi
  • Palmar erythema
  • Dupuytren contracture
  • Jaundice
  • Malnutrition
  • +/- hepatomegaly
  • Portal HTN –> ascites, encephalopathy, varices
  • HCC
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23
Q

Investigations of ALD

A

(1.) FBC: rule out the infection & look for complications of cirrhosis: anaemia, thrombocytopenia, hypoglycaemia

(2. ) LFTs
- raised AST
- hypoalbuminemia
- hyperbilirubinemia
- hypertriglyceridemia
- GGT raised, although not ALD-specific

(3. ) PT and INR
- Elevated value indicates severe disease
- PT and bilirubin can be used to calculate Maddrey’s Score/Glasgow score to assess severity of liver disease

Additional investigations

(4. ) Imaging: Tumours, biliary obstruction present?
(5. ) Endoscopy: look for oesophageal varices due to portal HTN.
(6. ) Liver biopsy: Determine severity, prognosis, staging, and treatment monitoring.
- H/E risk of complication, including life-threatening hemorrhage, so reserved for cases where results of a biopsy can make a difference in the treatment plan

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24
Q

Treatment and management of ALD

A

(1. ) Alcohol abstinence
(2. ) Nutritional support
(3. ) Screening for HCC every 6m
(4. ) Screening for esophageal varices in those with cirrhosis
(5. ) Limit dose of acetaminophen in chronic alcoholics
(6. ) Liver transplant may be considered
(7. ) Ascites Management
- Fluid and salt restriction - Diuretics
- Paracentesis + albumin
- Trans-jugular intrahepatic portosystemic shunt (TIPS), if ascites keep retuning

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25
Q

Complications of ALD

A
  1. Variceal Haemorrhage
  2. Ascites
  3. Spontaneous Bacterial Peritonitis (SBP) - ascites infection
  4. Hepatorenal syndrome (renal failure due to ALD)
  5. Hepatic Encephalopathy
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26
Q

What is NAFLD? and why may CV risk be monitored?

A

(1. ) Spectrum of conditions which are characterized by accumulation of fatty infiltration alone (steatosis) and absence of secondary causes of steatosis such as significant alcohol consumption, chronic use of medications
(2. ) NAFLD is considered to be a manifestation of metabolic syndrome as it is strongly associated with: Obesity, Dyslipidaemia, Type 2 diabetes, HTN
(3. ) Due to its close association with metabolic syndrome, NAFLD correlates with cardiovascular risk factors, which also contributes to mortality in these patients in addition to end-stage liver cirrhosis and HCC

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27
Q

What is Non-alcoholic steatohepatitis, NASH?

A

The presence of steatosis with inflammation.

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28
Q

Signs and Symptoms of NAFLD

A
  • Usually asymptomatic
  • Fatigue
  • Malaise
  • Mild RUQ discomfort
  • NASH = portal HTN: ascites, varices
29
Q

When would NAFLD be suspected and how would you differentiate this from ALD?

A

(1. ) Alcohol consumptions will differentiate between the two fatty liver disease
- A threshold of <20 g of alcohol per day in women and <30 g in men is usually used to allow a diagnosis of NAFLD

(2.) NAFLD suspicion if patient has RF for metabolic syndrome and if other common causes of abnormal LFTs have been excluded.

30
Q

Investigations of NAFLD

A

(1. ) Liver biopsy (gold standard)
(2. ) LFTs (not reliable indicator)
- mildly raised ALT but this tends to decline when disease progresses.
- 50% of patients can have normal ALT and AST levels
- Raised GGT can indicate alcohol use
(3. ) Imaging
- Visualise steatohepatitis

31
Q

Management and Treatment of NAFLD

A
  • Lifestyle Interventions = weight loss, diet, physical exercise
  • Screening and treatment of CV risk factors
  • Control of comorbidities if needed (BP, diabetes, lipids)
32
Q

What is autoimmune hepatitis and what are the two types?

A

(1.) Autoimmune hepatitis refers to chronic and progressive inflammation and subsequent fibrosis of liver from an unknown cause (may be genetic, environmental)

(2. ) Type 1
- Most common type
- Occurs at any age
- Associated coeliac disease, rheumatoid arthritis or ulcerative colitis
- Presence of ASMA +/- ANA antibodies

(3. ) Type 2
- Usually in children
- Prsences of Anti-LMK or Anti-LC

33
Q

Signs and Symptoms of AIH

A

Often asymptomatic and insidious onset unless acute AIH

  • fatigue
  • upper abdominal discomfort
  • arthralgias (joint pain)
  • mild pruritus, acne, hirsutism
  • jaundice
  • enlarged liver
  • nausea
  • amenorrhoea
  • spider angiomata.
  • hepatosplenomegaly

Acute presentation
- Extensive liver necrosis and liver failure

34
Q

Investigations of AIH

A

(1.) Diagnosis of AIH requires exclusion of viral, drug-induced and metabolic liver disease.

(2. ) Serological test for Autoantibodies
- Elevated serum IgG
- ANA, anti-SMA?

(3. ) Bloods: FBC, LFT
- AST and ALT elevated
- ALP is normal or mildly raised.
- Hypoalbuminaemia and prolongation of PT are markers of severe hepatic dysfunction

(4. ) Blood film
- may suggest the presence of active inflammation or necrosis. Not diagnostic.

(5. ) Liver biopsy
- required for AIH diagnosis
- ‘interface hepatitis’ = inflammation in portal tracts with damage to adjacent or interface hepatocytes

35
Q

Management of AIH (2)

A

Glucocorticoids are used for exacerbations and symptomatic AIH

(1.) Oral Prednisolone - gradually reduce dose as LFT improves

(2. ) Azathioprine -
- Maintenance Therapy once LFT and IgG levels are normal

36
Q

What is Primary Biliary Cholangitis

A

(1. ) Autoimmune condition where AMA antibodies and chronic granuloma inflammation causes destruction hepatic bile ducts.
(2. ) Damage to bile duct cells causes bile leakage into blood and other hepatocytes

(3. ) Bile leakage causes:
- inflammation
- fibrosis spreads from portal tract to liver parenchyma
- advanced stages can lead to cirrhosis

Remember BMWi = biliary, aMa, women, intrahepatic

37
Q

Signs and Sx of Primary Biliary Cholangitis

A

Often asymptomatic and diagnosed after incidental finding of inc ALP

(1. ) Fatigue
(2. ) Pruritus
(3. ) Jaundice (often in later stage) and Xanthomatous deposits around eyes
(4. ) RUQ discomfort
(5. ) Joint paint due to malabsorption of vitamins
(6. ) Steatorrhea - due to malabsorption
(7. ) Portal HTN - Mild hepatomegaly and splenomegaly, ascites, varices

38
Q

Investigations for Primary Biliary Cholangitis

A

(1. ) LFT
- Inc ALP, GGT and mild inc of AST, ALT
- Inc bilirubin, dec albumin, inc PT (in late disease)
- Mayoclinic prognostic score use bilirubin, albumin and PT.

(2. ) AMA +ve (in 95% of patients)
(3. ) Elevated IgM
(4. ) Ultrasound - Exclude extrahepatic cholestasis

39
Q

Treatment and Management of Primary Biliary Cholangitis (7)

A

(1. ) High dose UDCA: increases hepatic bile flow
(2. ) Colestyramine for pruritis
(3. ) Mondafinil for fatigue
- Fatigue is due to intracerebral changes from cholestasis not with disease severity or depression
(4. ) Fat soluble vitamin A, D, K, Ca replacement: for malabsorption
(5. ) Bisphosphonates
- If osteoporosis present due to malabsorption of vitamins
(6. ) Liver transplant
- If liver failure is indicated (serum bilirubin can be used to indicate liver function decline)
(7. ) Monitor regularly: LFT, ultrasound twice yearly if cirrhotic

40
Q

Complications of Primary Biliary Cholangitis

A

Due to cholestasis thus malabsorption of fat-soluble vitamins (A, D, E, K).

(1. ) Bone disease - osteoporosis, osteomalacia [rare].
(2. ) Coagulopathy.

41
Q

Pathophysiology of primary sclerosing cholangitis? RF? Complications?

A

(1. ) Inflammation of intrahepatic and extrahepatic bile systems causes stricture formation. ‘Beaded’ and fibrosus duct obstructs bile flow resulting in progressive cholestasis.
(2. ) Bile duct cells die + bile leaks into blood - causing elevated bilirubin, ALP and GGT.
(4. ) Fibrosis of wall can compress onto portal veins -> portal HTN. This can cause fluid to back up into the spleen and liver -> hepatosplenomegaly
(5. ) Constant damage to bile duct can lead to cirrhosis + liver failure, repeated infections, higher risk of cholangiocarcinoma. A liver transplant is the only known cure
(6. ) RF = male, IBD

42
Q

Signs and Sx of primary sclerosing cholangitis

A

(1. ) Pruritis
(2. ) Fatigue
(3. ) Intermittent jaundice
(4. ) Weight loss
(5. ) RUQ pain
(6. ) Portal HTN Sx
(7. ) If advanced = ascending cholangitis, cirrhosis, hepatic failure

43
Q

Investigation and Diagnosis of primary sclerosing cholangitis

A

Diagnostic criteria

  • Generalised beading and stenosis of the biliary system on cholangiography
  • Absence of choledocholithiasis (stones)
  • Exclusion of bile duct cancer

Investigations

(1. ) LFT
- Inc ALP, Inc bilirubin although fluctuates
- Modest elevation in transaminases
- Hypoalbuminemia and clotting abnormalities (later in disease)

(2. ) Autoantibodies
- May be ANA, ANCA +ve
- AMA -ve

(3. ) Serum Immunoglobulin
- Elevated IgM

(4. ) MRCP (Diagnostic tool)
- Reveals strictures and dilation

(5. ) ERCP
- Visualise narrow areas or blockages.

(6. ) Liver biopsy
- ‘onion skin’ fibrosis and inflammation around bile duct
- Portal oedema

44
Q

Treatment of primary sclerosing cholangitis

A
  • No Cure
  • UDCA may be used to reduce colon carcinoma risk
  • Cholestyramine for pruritus
  • Liver transplant
45
Q

What immunoglobulins and autoantibodies are associated with: AIH, Primary Biliary Cholangitis, primary sclerosing cholangitis ?

A
  1. AIH = IgG, ASMA, anti-LMK
  2. PBC = IgM, AMA
  3. PSC = Variable, ANCA (not specific)
46
Q

What is Hereditary Haemochromatosis? Causes? RF?

A

(1. ) Inherited disorder of iron metabolism which increases intestinal iron absorption.
(2. ) More iron is being absorbed by the body than being excreted
(3. ) Leading to iron deposits in joints, liver, heart, pancreas, pituitary glands, joints, skin.
(4. ) This damages cells via free radicals from ferritin, leading to cell death and necrosis
(5. ) 90% have mutations in HFE gene: C282Y, H63D
(6. ) RF = male, ~50yrs.

47
Q

Complications of Hereditary Haemochromatosis? (7)

A

(1.) Cirrhosis and liver Cancer - A lot of iron gets deposited in the liver, so damage over time and fibrosis due to free radical damage. This damage increases the risk of liver cancer.

(2. ) Type 1 Diabetes and Malabsorption
- Deposits in pancreatic cells, pts might develop type 1 diabetes mellitus from destruction of beta islet cells
- Patients might develop malabsorption from damage to the exocrine pancreas that helps us absorb nutrients.

(3. ) Bronze pigmented skin
- If the iron is absorbed into the skin, patients may have bronze pigmented skin.

(4. ) Cardiomyopathy/arrhythmias
- If it’s absorbed into the heart muscle or myocardium, patients can develop cardiomyopathy, which can later lead to arrhythmias.

(6.) Gonadal dysfunction - due to fibrosis, amenorrhea in women and and testicular atrophy in men.

(7. ) Degenerative joint diseases
- if it gets in the joints, it can cause degenerative joint diseases - due to fibrosis in the joint

48
Q

Signs and Symptoms of Hereditary Haemochromatosis?

A
  1. Chronic fatigue
  2. Hypopituitarism
  3. Cardiac rhythm disorders, Cardiac failure
  4. Diabetes
  5. Hepatomegaly, Cirrhosis, HCC
  6. Joint pain, osteoporosis
  7. Melanoderma, skin dryness
49
Q

Investigations of Hereditary Haemochromatosis?

A

Diagnosis = raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy

  • Inc LFTs
  • Inc serum ferritin
  • Inc transferrin % saturation (This measures binding sites occupied by Fe)
  • Liver biopsy and iron staining
  • HFE genotyping
  • Imaging of liver and cardiac for Fe overload
50
Q

Treatment of Hereditary Haemochromatosis?

A
  1. Phlebotomy, ‘blood letting’ - Until dec in ferritin, %saturation, iron load
  2. Deferoxamine - binds to free iron in the blood and makes it easier to get rid of via the urine, which again decreases the iron load
51
Q

Alpha-1- antitrypsin deficiency - normal vs deficiency, clinical features, investigations, treatment and management?

A

Normal

(1. ) Alpha-1 antitrypsin (aAT) is a serine protease inhibitor produced by the liver.
(2. ) It breaks down neutrophil elastase.
(3. ) aAT usually travels from your liver through your blood to protect your lungs and other organs.

Homozygous mutated aAT (on Z allele, PiZ or PiZZ types)

(1. ) Alpha-1- antitrypsin deficiency is an autosomal recessive condition
(2. ) Proteins aren’t the right shape so unable to leave the liver
(3. ) Low plasma aAT as it is accumulating within the liver
(4. ) This develops liver and pulmonary diseases

Clinical features

(1. ) Cholestatic jaundice
(2. ) Neonatal hepatitis, which can resolve spontaneously
(3. ) Cirrhosis and liver cancer in adults and in long-term HCC

Investigations

(1. ) Low plasma aAT
(2. ) Genotyping for presence of mutation

Treatment and Management
There is no specific treatment. Pts are advised not to smoke due to risk of emphysema.

52
Q

Budd-Chiari syndrome - pathophysiology, clinical features, investigations, treatment and management?

A

(1. ) Condition caused by thrombosis of the hepatic veins (veins that drain the liver).
(2. ) This blockage causes blood to back up into the liver resulting in hepatomegaly.
(3. ) Hepatic congestions affect centrilobular areas, this is followed by fibrosis and then cirrhosis

(4. ) Clinical features: Upper abdo pain, Ascites, Hepatomegaly, Features of cirrhosis and portal HTN may develop
(5. ) Investigations: LFT, Doppler US, reveal obliteration of hepatic veins or thrombosis, CT/ MRI, Liver biopsy

(6. )Management
(1. ) Thrombolysis w/ streptokinase, heparin, oral anticoagulation
(2. ) Angioplasty to open up vessels if strictures are present
(3. ) Trans-jugular intrahepatic portosystemic shunt TIPSS
(4. ) Transplant

53
Q

What is HCC? What RF are associated with it?

A

(1. ) Most common primary liver tumour
(2. ) Cirrhosis presents in 75-90% of individuals with HCC
(3. ) RF:
- hepatitis B, C, haemochromatosis (high risk)
- alcoholic, autoimmune hepatitis (lower risk)
- M>F.

54
Q

Presentation of HCC?

A

Deterioration in liver function

  1. Fatigue
  2. dec appetite and weight
  3. RUQ pain
  4. jaundice
  5. ascites, varices

Signs

  1. Hepatomegaly
  2. Abdominal bruit
  3. Hepatic rupture with intra- abdominal bleeding
55
Q

Investigations of HCC

A
  • 50% produce alpha-fetoprotein

- Imaging/ultrasound - identification of lesion.

56
Q

Treatment and Management of HCC

A

(1. ) Depends on presence of cirrhosis, tumour size, extent of liver disease, vascular invasion
(2. ) Hepatic resection
(3. ) Liver transplantation
(4. ) Ablation therapy (ethanol injection into tumour)
(5. ) Chemotherapy-Sorafenib

57
Q

Hepatitis A - how is it transmitted, RF, Sx, Investigations, Treatment and Management

A
  1. Faecal-oral route
  2. Short incubation period and sudden onset. Acute infection only.
  3. RF = travel, MSM, IV drug users

Signs and Sx

(1. ) fever
(2. ) malaise
(3. ) anorexia
(4. ) nausea
(5. ) jaundice
(6. ) abdo pain

Investigations

(1. ) LFT = elevated AST, ALT after 22-40d
(2. ) Serological tests = IgM and IgG. IgM rise after 25d and IgG detectable for life

Treatment and Management

(1. ) Usually self limiting
(2. ) Monitor LFT
(3. ) Supportive treatment
(4. ) Management of close contacts w/HNIG and vaccines
(5. ) 100% immunity after infection
(6. ) Liver transplant if develop liver failure/fulminant hepatitis

58
Q

Hepatitis B - how is it transmitted, Acute or Chronic? Investigations, Treatment and Management, Prevention

A
  1. Blood-borne (blood, bodily fluid, vertical transmission)
  2. Long incubation time
  3. (a.) 95% of HBV infection are symptomatic and resolve.
    (b. ) 5% may go on to develop chronic HBV infection –> cirrhosis –> carcinoma
    (c. ) 90% infected neonates develop chronic infection if not controlled
  4. Investigations
    (a. ) Anti-IgM
    (b. ) +ve hepatitis B surface antigen = infection present
  5. Treatment and Management
    (a. ) management of close contact w/HBV vaccine
    (b. ) Monitor LFT and supportive treatment
    (c. ) 48w pegylated interferon-α 2a - stimulates immune system
    (d. ) oral nucleos(t)ide analogues e.g. TDF, TAF, entecavir - inhibits viral replication
    (e. )
  6. Prevention
    (a. ) Antenatal screening (HBsAg testing) of pregnant mothers
    (b. ) HBV vaccination administered to baby at birth
    (c. ) tenofovir given to mother in pregnancy if high HBV DNA levels
59
Q

Hepatitis C - how is it transmitted, acute or chronic? Investigations, Treatment and Management, Prevention

A
  1. Blood-bourne
  2. Long incubation
  3. (a.) 70% chronic–> cirrhosis or HCC
    (b. ) 30% acute but also risk of re-infection
  4. Investigations
    (a. ) See if HCV antibody is present
    (b. ) Determine genotype from HCV RNA
  5. Treatment and Management
    (a. ) Directly-acting antiviral (DAA) therapy, one of the following:
    - Glecaprevir/Pibrentasvir
    - Elbasvir/Grazoprevir
    - Sofosbuvir/Velpatasir
    - Sofosbuvir/Velpatasir/Voxilaprevir
  6. Prevention
    - No vaccine
    - Previous infection does not confer immunity & can be re-infected
    - Screening blood products
    - Lifestyle modification, e.g. needle exchanges, alcohol etc.
    - Harm reduction & universal precautions handling bodily fluids)
60
Q

Hepatitis D - how is it transmitted, acute or chronic? Investigations, Treatment and Management

A
  1. Blood bourne
  2. Requires HBsAg to replicate (i.e. hepatitis B must be present in order for hep B to infect)
  3. Can be acquired simultaneously with HBV or
    after HBV
  4. Acute or Chronic infection
  5. Investigation
    (a. ) Hepatitis D antibody - if positive, test HDV RNA
    (b. ) Test for Hep B surface antigen
  6. Treatment and Management
    - 48-96 w pegylated inteferon-α
61
Q

Hepatitis E - how is it transmitted, acute or chronic? Investigations, Treatment and Management, Prevention

A
  1. Faecal-oral route, eating undercooked pig meat
  2. Short incubation and sudden onset
  3. 4 genotypes: G1,2,3,4. G3 and 4 are more common in UK
  4. Acute or chronic
  5. Investigations
    (a. ) Serology = Anti-IgG/IgM h/e not reliable in immunocompromised pts
  6. Treatment and Management
    (a. ) Usually self-limiting
    (b. ) Consider Ribavirin (antiviral)
    (c. ) If persists use pegylated-interferon-a
  7. Prevention
    - Avoid eating undercooked meat
    - Screening of blood donors
    - Vaccine in development
62
Q

Complications for viral hepatitis

A
  1. Fulminant hepatitis - complication of acute hepatitis B, D or E
  2. Cirrhosis
  3. Liver failure
  4. HCC
63
Q

Investigations for Viral Hepatitis

A

(1. ) Hepatitis serology to detect viral RNA
- or test for IgM antibodies if RNA PCR is not possible
- NOTE: IgM results may be unreliable in immunocompromised patients

(2. ) LFT
- ALT and AST levels may be increased
- Bilirubin may be elevated
- ALP < 2x the upper limit of normal, but higher if there is cholestasis
- PT may be prolonged

64
Q

Management for Viral Hepatitis

A
  1. Referral
    - Admit any patient if severely unwell
    - Patients with confirmed hepatitis B
  2. Symptom control
    - Advise patient to rest and stay hydrated
    - Pain relief – paracetamol, ibuprofen, or weak opioid
    - Nausea - metoclopramide or cyclizine
    - Pruritis - chlorphenamine
  3. Notify health protection unit for surveillance and contact tracing
  4. Ensure contacts of those with hepatitis B are offered immunisation
  5. Lifestyle
    - Avoid alcohol
    - Avoid attending school, work until no longer infectious
    - Maintain handwashing, good personal hygiene, avoid handling foods
    - Avoid sharing items that can be contaminated with blood such as toothbrushes, razors
  6. Safety-netting- advise patient to seek medical attention if symptoms worsen (particularly if they include vomiting and dehydration)
65
Q

What are the four main functions of the liver? (Formative Q)

A
  • Glucose and fat metabolism
  • Detoxification and excretion
  • Protein synthesis
  • Defence against infection
66
Q

Physical manifestations you might find in a patient with chronic liver disease? (Formative Q)

A
  • Ascites
  • Caput medusa (dilated vessels around umbilical region)
  • Telangiectasia
  • Hepatosplenomegaly
  • Peripheral oedema
  • Muscle wasting, cachexia
  • Spider naevi
  • Gynecomastia
67
Q

List causes of acute liver injury. (Formative Q) .

A
  • Viral
  • Drugs - illicit or medical
  • Obstruction (gallstones, strictures, masses/cancer)
  • Vascular (thrombosis)
  • Alcohol
  • Congestion (heart failure)
68
Q

Most common medication that people overdose on that causes liver failure? What medication do we use as an antidote? What blood tests are most important to measure as indicators of liver function? (Formative Q)

A
  1. Paracetamol.
  2. N-acetylcisteine is used as an anti-inflammatory for the liver and requires 21 hours for infusion.
  3. Prothrombin time is most useful (part of a clotting screen) and we monitor LFTs also
69
Q

Why are patients with chronic liver disease more prone to infections?

What infection must be ruled out when ascites is present and how would we test for this? (Formative Q).

A
  • Impaired reticulo-endothelial function
  • Reduced opsonic activity
  • Leucocyte function
  • Permeable gut wall

Must rule out spontaneous bacterial peritonitis by performing paracentesis or extraction of ascitic fluid which is then sent for analysis.
Routine ascitic analysis will include protein, cell count and culture.

GI (12 decks)

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