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Year 3 Gastrointestinal > Liver disease > Flashcards

Liver disease Flashcards

1
Q

What are the three stages of alcoholic liver disease?

A

Fatty changes (steatosis), alcoholic hepatitis and chronic cirrhosis.

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2
Q

What is alcoholic hepatitis?

A

Inflammatory liver injury caused by chronic heavy intake of alcohol.

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3
Q

What is the aetiology of alcoholic hepatitis? (x3)

A
  1. Fatty liver infiltration occurs from build-up of NADH caused by reduction of alcohol, by alcohol dehydrogenase and acetaldehyde dehydrogenase, by inhibiting gluconeogenesis and increasing fatty acid oxidation.
  2. Alcohol is also metabolised by cytochrome P450 which produces free radicals and damages tissue
  3. Chronic alcohol exposure also activates hepatic macrophages which produce TNF-a leading to inflammation
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4
Q

What is the pathophysiology of alcoholic hepatitis? (x6)

A

Liver histopathology shows:

  • Centrilobular ballooning degeneration and necrosis of hepatocytes
  • Steatosis (abnormal fat retention)
  • Neutrophilic inflammation
  • Cholestasis (flow of bile reduced or blocked)
  • Mallory hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments)
  • Giant mitochondria
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5
Q

What are the risk factors of alcoholic hepatitis? (x6)

A

Alcohol, hepatitis C, female (develops more rapidly and in lower drinking levels), overweight, smoking, Hispanic.

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6
Q

What is the epidemiology of alcoholic hepatitis: Percentage of heavy drinkers?

A

10-35% of heavy drinkers.

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7
Q

What are the symptoms of alcoholic hepatitis? (x4 and x5)

A
  • May remain asymptomatic
  • Symptoms can range from: nausea, malaise, epigastric/right hypochondrial pain, low-grade fever to…
  • Jaundice, abdominal discomfort, distension, swollen ankles, GI bleeding (haematemesis or meleana)
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8
Q

How do patients often present with alcoholic hepatitis?

A

Asymptomatic and with a trigger event e.g., aspiration pneumonia or injury.

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9
Q

How may a woman present differently with alcoholic hepatitis?

A

More florid (red, flushed complexion) illness than a man.

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10
Q

What are the signs of alcoholic EXCESS? (x10)

A

Malnourished, palmar erythema, Dupuytren’s contracture, facial telangiectasia, parotid enlargement, spider naevi, gynaecomastia, testicular atrophy, hepatomegaly, easy bruising.

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11
Q

What are the signs of severe alcoholic hepatitis? (x8)

A
  • Febrile
  • Tachycardia
  • Jaundice
  • Bruising
  • Encephalopathy. Clinical features of this include hepatic foeter, liver flap (asterixis), drowsiness, unable to copy a five-pointed star, disorientated.
  • Ascites
  • Hepatomegaly
  • Splenomegaly
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12
Q

What is hepatic foeter?

A

Condition seen in portal hypertension where portosystemic shunting allows thiols to pass directly into the lungs, producing a sweet faecal odour.

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13
Q

What is hepatic encephalopathy?

A

Altered level of consciousness as a result of liver dysfunction or portosystemic shunting.

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14
Q

What are the blood investigations for alcoholic hepatitis? (x4)

A
  • FBC would show low Hb, high MCV, high WCC, low platelets
  • LFTs: high transaminases (ALT, AST), AST:ALT ratio more than 2 (reversal of ratio = viral or non-alcoholic fatty liver disease), high bilirubin (reflects cholestasis and impaired metabolic function of liver), low albumin (impaired liver function), high AlkPhos (reflects cholestasis), high gamma-GT
  • U&E: urea and potassium low, unless significant renal impairment. Elevated urea in the presence of normal creatinine suggest active GI bleed.
  • Clotting: prolonged PT is a sensitive marker of significant liver damage
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15
Q

What are the other investigations for alcoholic hepatitis? (x4)

A
  • USS: to exclude other causes of liver impairment such as malignancy
  • Upper GI endoscopy: investigate for varices
  • Liver biopsy: percutaneous or trans-jugular to differentiate from other causes of hepatitis
  • Electroencephalogram: for slow-wave activity indicative of encephalopathy
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16
Q

How is alcoholic hepatitis managed acutely? (x7)

A
  • Thiamine, vitamin C and other multivitamins (initially parenterally)
  • Monitor and correct K+, Mg2+ and glucose abnormalities
  • Ensure adequate urine output
  • Treat encephalopathy with oral lactulose and phosphate enemas
  • Ascites managed by diuretics or therapeutic paracentesis
  • Glypressin and N-acetylcysteine for hepatorenal syndrome
  • Alcohol withdrawal – look at separate notes
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17
Q

How is alcoholic hepatitis managed with nutrition? (x2)

A

Increased calorie intake. Protein restriction should be avoided unless patient is encephalopathic. Nutritional supplementation and vitamins should be started parenterally initially and continued orally after.

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18
Q

Why is protein restriction indicated in encephalopathy?

A

Ammonia is a key factor in the disease pathogenesis. Ammonia is produced in the metabolism of proteins.

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19
Q

!!! What is the pathogenesis of hepatic encephalopathy? (x2)

A
  1. FAILURE TO METABOLISE NITROGEN-CONTAINING COMPOUNDS: As the liver fails, nitrogenous waste (as ammonia) builds up in the circulation and passes to the brain, where astrocytes clear it (by processes involving the conversion of glutamate to glutamine). This excess glutamine causes an osmotic imbalance and a shift of fluid into these cells—hence cerebral oedema.
  2. PORTOSYSTEMIC SHUNTING: In portal hypertension, some of the portal circulation is shunted into the systemic circulation. As such, nitrogenous waste in the portal system escapes into the systemic system and can access the brain.
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20
Q

How is alcoholic hepatitis medically managed?

A

Steroid therapy

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21
Q

What are the complications of alcoholic hepatitis? (x3)

A

Acute liver decompensation, hepatorenal syndrome (renal failure secondary to advanced liver disease) and cirrhosis.

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22
Q

What is the prognosis of alcoholic hepatitis?

A

Mortality in first month = 10%. 40% in first year. If alcohol intake continues, progression to cirrhosis within 1-3 years.

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23
Q

What are two prognostic scores in alcoholic hepatitis?

A

(1) Maddrey’s discriminant function = (bilirubin/17) + (prolongation of PT x 4.6). If MDF is higher than 32, this indicates over 50% 30-day mortality. (2) Glasgow alcoholic hepatitis score = allocates a score based on age, WCC, urea, PT ratio and bilirubin. If GCS higher than or equal to 9, there is an over 50% 30-day mortality risk.

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24
Q

What is cirrhosis?

A

End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.

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25
Q

What is a decompensated liver?

A

Decompensated alcohol related liver disease occurs when there is a deterioration in liver function in a patient with cirrhosis which presents with jaundice, coagulopathy, ascites, GI bleeding and hepatic encephalopathy.

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26
Q

What are the causes of cirrhosis? (x9)

A
  • Alcohol
  • Chronic viral hepatitis
  • Autoimmune hepatitis
  • Drugs such as methotrexate and hepatotoxic drugs
  • Inherited: alpha1-antitrypsin deficiency, haemochromatosis, Wilson’s disease, galactosaemia, CF
  • Vascular: Budd-Chiari syndrome or hepatic venous congestion
  • Chronic biliary diseases: PSC
  • Cryptogenic (unknown origin): 5-10%
  • Non-alcoholic steatohepatitis (NASH): associated with OBESITY (obesity is one of the main causes of cirrhosis in the Western world), diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs
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27
Q

What are the factors that can precipitate liver decompensation? (x9)

A

Infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol, drugs, tumour development, portal vein thrombosis.

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28
Q

What is the epidemiology of cirrhosis: Incidence mortality?

A

Top 10 leading causes of death in the world.

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29
Q

What are the symptoms of cirrhosis? (x5, x3, x4, x4)

A
  • EARLY: anorexia, nausea, fatigue, weakness, weight loss
  • REDUCED LIVER SYNTHETIC FUNCTION: easy bruising, abdominal swelling, ankle oedema
  • REDUCED DETOXIFICATION FUNCTION: jaundice, personality change, altered sleep pattern, amenorrhoea
  • PORTAL HYPERTENSION: abdominal swelling, haematemesis, PR bleeding or melaena
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30
Q

What are the signs of cirrhosis? (x5 +11)

A
  • ABCDE
  • Asterixis
  • Bruises
  • Clubbing
  • Dupuytren’s contracture
  • Erythema (palmar)
  • Jaundice, gynaecomastia, leukonychia (hypoalbuminemia), parotid enlargement (alcoholic), spider naevi, excoriations, ascites, hepatomegaly (shrunken in later stage), testicular atrophy, caput medusa, splenomegaly.
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31
Q

!!! Hepatic failure, cirrhosis and symptoms?

A

Hepatic failure in cirrhosis leads to coagulopathy, encephalopathy, hypoalbuminemia (oedema), sepsis, spontaneous bacterial peritonitis and hypoglycaemia.

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32
Q

!!! Portal hypertension, cirrhosis and symptoms?

A

Portal hypertension in cirrhosis leads to ascites, splenomegaly, portosystemic shunt and caput medusa.

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33
Q

What are the blood investigations for cirrhosis? (x9)

A
  • FBC would show low Hb, high MCV, high WCC, low platelets (hypersplenism)
  • LFTs: high transaminases (ALT, AST), high bilirubin (reflects cholestasis and impaired metabolic function of liver), low albumin (impaired liver function), high AlkPhos (reflects cholestasis), high gamma-GT
  • Clotting: prolonged PT is a sensitive marker of significant liver damage
  • Serum AFP (alpha-fetoprotein): increased but can also suggest carcinoma.
  • U&E: low sodium associated with ascites.
  • Serology: viral serology of HBsAg (Hep B surface antigen), HBsAb (Hep B), HCV ab (Hep C), antinuclear antibodies (autoimmune hepatitis), antimitochondrial antibodies (primary biliary cholangitis), anti-smooth muscle antibodies (autoimmune hepatitis)
  • Iron studies: serum ferritin, iron, total iron binding capacity (hemochromatosis)
  • Alpha1-antitrypsin: hepatic inflammation
  • Caeruloplasmin: low in Wilson’s disease
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34
Q

What are other investigations for cirrhosis? (x4)

A
  • Ascitic tap: microscopy, culture and sensitivity, biochemistry (protein, albumin, amylase) and cytology. If neutrophils are over 250/mm^3, this indicates spontaneous bacterial peritonitis.
  • Liver biopsy: percutaneous or transjugular if clotting deranged or ascites present.
  • Imaging: USS, CT or MRI to detect complications such as ascites, carcinoma or hepatic/portal vein thrombosis, to exclude biliary obstruction
  • Endoscopy: examine for varices, portal hypertensive gastropathy
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35
Q

What is assessed in a liver biopsy for cirrhosis? (x3) Grade and stage?

A

Histopathology: periportal fibrosis, loss of normal liver architecture and nodular appearance. Grade refers to the assessment of degree of inflammation, whereas stage refers to the degree of architectural distortion, ranging from mild portal fibrosis to cirrhosis

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36
Q

What is Child-Pugh grading in cirrhosis?

A

Class A is score 5-6, Class B is score 7-9 and Class C is score 10-15.

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37
Q

How is cirrhosis managed? (x3)

A
  • Treat the cause
  • Nutrition
  • Treat the complications
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38
Q

How are the complications of cirrhosis treated? (x3)

A
  • Encephalopathy: treat infections, lactulose, phosphate enemas and avoid sedation
  • Ascites: diuretics, dietary sodium restriction, therapeutic paracentesis, fluid restriction in patients with hyponatraemia. Monitor daily weight and aim for 0.5kg loss per day.
  • SBP: antibiotics
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39
Q

How is cirrhosis surgically managed? (x2) But?

A

Consider insertion of TIPS (Transjugular intrahepatic portosystemic shunt) to relieve portal hypertension although it may precipitate encephalopathy. Only curative measure = transplant.

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40
Q

What are the complications of cirrhosis? (x5)

A

Portal hypertension with ascites, encephalopathy or variceal haemorrhage, SBP, hepatocellular carcinoma, renal failure (hepatorenal syndrome), pulmonary hypertension (hepatopulmonary syndrome)

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41
Q

How does cirrhosis lead to renal failure?

A

Reduced hepatic clearance of immune complexes leads to trapping in kidneys.

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42
Q

What is the prognosis of cirrhosis: 5-year survival? Ascites 2-year survival?

A

Poor: 5-year survival is 50%. In the presence of ascites, 2-year survival is 50%.

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43
Q

What is the difference between cirrhosis and fibrosis?

A

Fibrosis leads to cirrhosis.

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44
Q

What is liver failure?

A

Aka ACUTE LIVER FAILURE. Severe liver dysfunction defined by jaundice, encephalopathy and coagulopathy.

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45
Q

What are the classifications of liver failure? (x4)

A
  • Defined as presentation of encephalopathy relative to jaundice
  • Hyperacute: jaundice with encephalopathy occurring in LESS THAN 7 DAYS
  • Acute: jaundice with encephalopathy occurring from 1 to 4 WEEKS OF ONSET
  • Subacute: jaundice with encephalopathy occurring 4 to 12 WEEKS OF ONSET
  • Acute-on-chronic: acute deterioration (decompensation) in patients with chronic liver disease (cirrhosis)
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46
Q

What are the causes of liver failure? (x10)

A
  • VIRAL: Hepatitis A, B, D, E, ‘non-A-E hepatitis’, yellow fever
  • DRUGS: paracetamol overdose, idiosyncratic drug reactions (such as anti-TB therapy)
  • AUTOIMMUNE: autoimmune hepatitis
  • Budd-Chiari syndrome: hepatic vein thrombosis
  • Pregnancy
  • Malignancy e.g., lymphoma
  • Haemochromatosis
  • Mushroom poisoning (Amanita phalloides)
  • Wilson’s Disease
  • PSC or PBC
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47
Q

What is the pathogenesis of liver failure? (x3)

A
  • Jaundice from decreased secretion of conjugated bilirubin
  • Encephalopathy from increased delivery of gut-derived products into the systemic circulation and brain, arising from decreased extraction of nitrogenous products by liver and portal systemic shunting. Ammonia may play a role hence management includes protein-restriction.
  • Coagulopathy: decreased synthesis of clotting factors. Decreased synthesis of platelets from hypersplenism if chronic portal hypertension. Platelet functional abnormalities associated with jaundice or renal failure.
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48
Q

What is the histopathological pathophysiology of liver failure?

A

Most cases are characterised by massive hepatocyte necrosis and apoptosis may coexist.

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49
Q

What is the pathophysiology of liver failure in paracetamol overdose?

A

Paracetamol is predominantly metabolised in the liver through glucuronidation and sulfation, with a small amount metabolised by the cytochrome P450 system. A toxic intermediate, NAPQI, generated via the P450 pathway is subsequently conjugated by glutathione. In the setting of paracetamol overdose, glutathione stores may become depleted, resulting in direct hepatocyte injury via NAPQI.

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50
Q

What are the risk factors for liver failure? (x6)

A

Alcohol, barbiturates, poor nutritional status, age over 40 years, female gender, pregnancy.

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51
Q

How do alcohol, barbiturates and nutritional deficiency contribute to liver failure?

A

Induction of the P450 system through chronic alcohol use or barbiturates and depletion of glutathione stores in settings such as nutritional deficiency may result in a greater propensity to develop paracetamol hepatotoxicity.

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52
Q

What is the epidemiology of liver failure: Cause?

A

Paracetamol overdose accounts for 50% of acute liver failure in the UK.

53
Q

What are the symptoms of liver failure? (x4)

A
  • May be asymptomatic
  • Fever
  • Nausea and vomiting
  • Jaundice
  • Abdominal pain and RUQ tenderness
54
Q

What are the signs of liver failure? (x8 (x3))

A
  • Jaundice
  • Encephalopathy
  • Liver asterixis
  • Fetor hepaticus (smell of ‘pear drops’)
  • Ascites (less common in (hyper)acute)
  • Splenomegaly (less common in (hyper)acute). Seen more commonly in chronic liver disease and cirrhosis.
  • Bruising or bleeding from puncture sites or GI tract
  • Signs indicative of secondary causes such as bronze skin colour (haemochromatosis), Kayser-Fleischer rings (copper depositions in cornea from Wilson’s disease), pyrexia (infection or liver necrosis)
55
Q

What are the biggest differentials between liver failure and chronic liver disease? (x4)

A

Chronic liver disease (and cirrhosis), unlike liver failure, is associated with splenomegaly, spider naevi, palmar erythema and depression.

56
Q

What are the signs of hepatic encephalopathy?

A

Spectrum of neurological signs ranging from impaired awareness, anxiety, lethargy, and sleep alterations, to asterixis, marked confusion, hyperreflexia and rigidity.

57
Q

What is negative myoclonus?

A

Myoclonus is irregular twitching (different from clonus which is regular). Negative myoclonus is caused by brief lapses of contraction. Asterixis is a type of negative myoclonus.

58
Q

What are the blood investigations for liver failure? (x7)

A
  • LFTs: hyperbilirubinemia (defining feature). Paracetamol overdose associated with high AST and ALT. ALT/AST:AlkPhos >5 is sensitive for drug-induced liver failure.
  • PT/INR: test for coagulopathy. Will also see low FV.
  • U&E: elevated urea, creatinine and deranged potassium – hepatorenal failure.
  • FBC: leucocytosis (infective cause), anaemia (esp. in Wilson’s and GI bleed), thrombocytopenia
  • Arterial blood: metabolic acidosis and arterial lactate elevated. Elevated in paracetamol overdose.
  • Serology: viral hepatitis and autoimmune hepatitis
  • Serum ceruloplasmin (copper-carrying protein): decreased in Wilson’s
59
Q

What are the other investigations for liver failure? (x7)

A
  • Urine toxicology screen: determine paracetamol levels
  • Urinary copper: elevated in Wilson’s disease
  • Urinary catheterisation to assess fluid output for renal failure
  • Pregnancy test
  • CXR: assess aspiration pneumonia – with hepatic encephalopathy
  • Abdominal USS: hepatic vessel thrombosis, hepatomegaly, splenomegaly
  • Electroencephalogram: to monitor encephalopathy
60
Q

What are the principles of liver failure management? (x6)

A
  • Resuscitation
  • Treat the cause: for example, N-acetylcysteine for paracetamol overdose
  • Treatment and prevention of complications
  • Treat renal failure: hemofiltration and nutritional support
  • Surgical: liver transplant
  • Avoid sedatives and other drugs with hepatic metabolism
61
Q

How are complications of liver failure treated/prevented? (x6)

A
  • Encephalopathy: lactulose and phosphate enemas
  • Antibiotic and antifungal prophylaxis
  • Hypoglycaemia treatment
  • Coagulopathy treatment: IV Vitamin K, FFP, platelet infusions if required.
  • Gastric mucosa protection: PPIs or sucralfate – prophylaxis against stress ulceration
  • Cerebral oedema: IV mannitol to decrease intracranial pressure and hyperventilate
62
Q

What criteria is used for liver transplantation? ((x2))

A

King’s College Hospital criteria: IF DUE TO PARACETAMOL OVERDOSE – arterial pH less than 7.3, PT over 100s, creatinine over 300 and severe encephalopathy; IF DUE TO OTHER CAUSES (three out of five) – less than 10y/o or older than 40, bilirubin > 300um, caused by non-A, non-E viral hepatitis or drugs, interval from jaundice onset to encephalopathy > 7 days, or PT over 100s.

63
Q

What are the complications of liver failure? (x10)

A

Infection, coagulopathy, hypoglycaemia, electrolyte disturbances, acid-base disturbances, CVS disturbances, hepatorenal syndrome (concurrent hepatic and renal failure), cerebral oedema, increased intracranial pressure and respiratory failure.

64
Q

What is the prognosis of liver failure?

A

Poor prognostic indicators are outlined in the King’s College Hospital criteria.

65
Q

What is portal hypertension?

A

Hypertension in the hepatic portal system – that drain most of the intestines to the liver. Defined as a hepatic venous pressure gradient of 10mmHg or more.

66
Q

What is the aetiology of portal hypertension? (x2 mechanisms)

A

Increased vascular resistance due to liver fibrosis and regenerative nodules (from myofibroblast and hepatic stellate cell activation) produces contractile elements in the liver’s vascular bed leading to portal hypertension. Increased portal venous blood flow from splanchnic vasodilation and humoral vasodilatory agents (including NO and glucagon) exacerbates portal hypertension. Additionally, there is activation of hepatic stellate cells and myofibroblasts. The

67
Q

What are the causes of portal hypertension? (x4, x6 and x3)

A
  • Pre hepatic causes i.e., originating in portal venous system before it reaches liver): portal vein thrombosis, splenic vein thrombosis, splenomegaly, hypersplenism
  • Hepatic causes: cirrhosis, PSC, chronic pancreatitis, Schistosomiasis, fibrosis, hepatitis
  • Post hepatic causes (between liver and heart): IVC obstruction, right-sided HF and Budd-Chiari syndrome
68
Q

What are the symptoms of portal hypertension? (x3)

A
  • Abdominal pain from ascites
  • GI bleeding
  • Consider chronic symptoms of liver failure including encephalopathy
69
Q

What are the signs of portal hypertension? (x5)

A
  • Ascites with abdominal tenderness/oedema
  • Splenomegaly
  • Thrombocytopenia
  • Anaemia (from GI bleeding)
  • Caput medusa
70
Q

What are the investigations for portal hypertension?

A

Doppler US: shows dilated portal vein, slow velocity and identification of collaterals

71
Q

How is portal hypertension managed? (x5)

A
  • PORTOSYSTEMIC SHUNTS: shunts inserted between non-intestinal portal veins to systemic veins (while leaving intestinal venous drainage to pass through the liver) so that portal blood that doesn’t contain encephalopathic compounds can enter the systemic circuit and take pressure off the portal system. Examples include splenic to renal vein.
  • TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS): artificial channel produced between the inflow portal vein and outflow hepatic vein
  • VARICEAL BLEEDING MANAGEMENT: vasoactive drugs, endoscopic banding ligation and balloon tamponade.
  • ASCITES: salt restriction, diuretics (spironolactone), paracentesis.
  • HEPATIC ENCEPHALOPATHY: lactulose, phosphate enemas.
72
Q

Why must ascites management be gradual?

A

Avoids sudden changes in systemic volume status which can precipitate encephalopathy and kidney failure.

73
Q

What are the complications of portal hypertension? (x3)

A

Intestinal bleeding, oesophageal bleeding (oesophageal varices) and ascites.

74
Q

How does portal hypertension lead to oesophageal varices?

A

Leads to formation of collaterals between the portal and systemic systems. These varices and increased pressure gradients increase bleeding risk.

75
Q

Where can varices be found in portal hypertension?

A

Oesophagus, stomach, umbilicus region and rectum.

76
Q

What is non-alcoholic fatty liver disease?

A

NAFLD: Excessive build-up of fat in the liver without a clear cause such as alcohol.

77
Q

What are the two types of NAFLD?

A

Non-alcoholic fatty liver (NAFL) and non-alcohol steatohepatitis (NASH).

78
Q

What is NASH?

A

Characterised histologically by macrovesicular hepatic steatosis and inflammation in those who do not consume alcohol enough to cause HARM to the liver.

79
Q

What is hepatic steatosis?

A

Called FATTY CHANGE: abnormal retention of fats within a cell.

80
Q

What is macrovesicular steatosis?

A

Excess lipid accumulates in vesicles that displace the cytoplasm. When the vesicles are large enough to distort the nucleus, this is called macrovesicular steatosis.

81
Q

What is the difference between NASH and NAFL?

A

NAFL is accumulation of fat (hepatic steatosis) without disturbing liver function. NAFL progresses to NASH, where steatosis exists with inflammation and sometimes fibrosis.

82
Q

What is the epidemiology of NASH: Prevalence? Location? Age? Gender?

A

Affects 20-40% of the Western world. Less common in Asian and Pacific regions. Age between 40-60. Equal gender distribution.

83
Q

What are the risk factors for NASH? (x6)

A
  • Obesity
  • Insulin resistance/diabetes
  • Dyslipidaemia
  • Hypertension
  • Metabolic syndrome including hyperglycaemia, HTN, obesity and dyslipidaemia
  • Rapid weight loss
  • Hepatotoxic medications such as amiodarone and tamoxifen
  • Total parenteral nutrition
84
Q

What is the pathophysiology of NASH?

A
  • There are several theories:
  • Insulin resistance leading to excessive triglyceride accumulation in the liver and subsequent development of hepatic steatosis
  • Once steatosis is present, additional oxidative injury
85
Q

What are the signs and symptoms of NASH? (x5 +5)

A
  • PRESENCE OF RISK FACTORS: obesity, insulin resistance, hyperlipidaemia, hypertension etc.
  • Fatigue and malaise (can also be a manifestation of encephalopathy in more advanced disease)
  • Hepatosplenomegaly
  • RUQ abdominal discomfort
  • Jaundice and pruritus due to compromised liver function and decompensation (uncommon)
  • Uncommon: spider naevi, palmar erythema, Dupuytren’s contracture, bruising, petechia
86
Q

What are the LFT investigations for NASH? (x5)

A
  • Mildly elevated AST and ALT. ALT>AST but reverses in more advanced disease
  • Elevated bilirubin in decompensated disease
  • Elevated AlkPhos
  • Elevated GGT associated with fibrosis
  • Low albumin
87
Q

What are the other blood investigations for NASH? (x5)

A
  • FBC: anaemia or thrombocytopenia
  • Metabolic panel: hyponatraemia due to increased levels of ADH. Urea and creatinine may be elevated due to declining renal function.
  • Lipid profile: high LDL, low HDL
  • Elevated PT
  • Insulin: elevated
88
Q

What other investigations are there for NASH? (x3 +3)

A
  • Biopsy: ultimate requirement for diagnosis
  • USS: diffuse hyperechoic echotexture, compared with kidneys and vascular blurring. Deep attenuation too.
  • CT/MRI: low attenuation liver from increase fat content
  • Assess for complications: endoscopy to monitor for varices, EEG for encephalopathy and portal venous pressure measurements for portal HTN
89
Q

How is NASH managed? (x5)

A
  • Lifestyle: lose weight, improve diet and exercise with calorie restriction
  • Anti-diabetics may help with liver fat loss
  • Insulin sensitisers such as metformin to treat insulin resistance
  • Statins improve liver histology and markers of liver biochemistry
  • Surgery: bariatric surgery
90
Q

What are the complications of NASH? (x5)

A

Fibrosis, cirrhosis, hepatic carcinoma, CVD, chronic kidney disease.

91
Q

What is a liver abscess?

A

Purulent collection in liver parenchyma that results from bacterial, fungal or parasitic infection.

92
Q

What are the two types of liver abscess?

A

PYOGENIC (refers to bacterial causes or fungal infection in immunosuppressed individuals), or AMOEBIC (refers to parasite infection caused by Entamoeba histolytica).

93
Q

What is the aetiology of liver abscesses? (x3 points)

A
  • Pyogenic (producing pus) abscess is often polymicrobial, most commonly associated with E. coli, Klebsiella, enterococcus, Bacteroides, Streptococci, Staphylococci species.
  • 60% caused by biliary tract disease such as gallstones, strictures.
  • Amoebic by Entamoeba histolytica
94
Q

What is the pathophysiology of liver abscesses?

A

Form by spread of infection from biliary tree, portal vein, hepatic vein or penetrating trauma.

95
Q

What are risk factors for liver abscess? (x7)

A
  • Biliary tract disease
  • Diabetes mellitus
  • Cancer
  • Cirrhosis
  • Prior liver transplant
  • Cardiopulmonary disease
  • Immunocompromised
96
Q

What is the epidemiology of liver abscess: Incidence? Where? Age? Gender?

A

Rare: 3.6 per 100,000. Most cases of amoebic infections occur in Central and Sourth America, Africa and Asia. Incidence increased with age. Higher risk in men.

97
Q

What are the symptoms and signs of liver abscess? (x9)

A
  • Fever and chills
  • Fatigue
  • N&V
  • Chest symptoms: cough, SOB, pleuritic pain or right shoulder tip pain if diaphragm affected
  • RUQ tenderness
  • Jaundice
  • Diarrhoea
  • Hepatomegaly: right lobe affected more commonly than left.
  • Dullness to percussion and decreased breath sounds at right base of lung, caused by reactive pleural effusion.
98
Q

What is the difference in symptoms between pyogenic and amoebic liver abscess?

A

Amoebic is acute; pyogenic is insidious.

99
Q

What are the investigations for liver abscess? (x5)

A
  • BLOOD: FBC shows mild anaemia, leucocytosis. LFTs show raised AlkPhos and bilirubin. Increased ESR and CRP. PT is usually normal. Serology for Entamoeba histolytica.
  • STOOL MICROSCOPY: for E. histolytica
  • LIVER USS/CT/MRI: localises structure
  • CXR: right pleural effusion or atelectasis, raised hemidiaphragm
  • ASPIRATION AND CULTURE OF THE ABSCESS MATERIAL: for gram staining and culture
100
Q

What is a liver cyst?

A

Fluid-filled sac in liver parenchyma, distinct from abscess as it is not pus-filled and not caused by bacteria or fungi.

101
Q

What is the aetiology of liver cysts? (x2)

A

Hydatid cyst from Tapeworm Echinococcus granulosis. Other causes may be Tuberculosis.

102
Q

What is meant by ‘hydatid cyst’?

A

Parasitic infection of humans caused by E. granulosis.

103
Q

What is the epidemiology of liver cysts?

A

Hydatid disease is common in sheep-rearing countries.

104
Q

What are the signs and symptoms of liver cysts? (x9)

A
  • ACUTE ONSET as cyst grows slowly but not painful until enlarged.
  • Fever and chills
  • Fatigue
  • N&V
  • Chest symptoms: cough, SOB, pleuritic pain or right shoulder tip pain if diaphragm affected
  • RUQ tenderness
  • Jaundice
  • Diarrhoea
  • Hepatomegaly: right lobe affected more commonly than left.
  • Dullness to percussion and decreased breath sounds at right base of lung, caused by reactive pleural effusion.
105
Q

What are the investigations for liver cysts? (x4)

A
  • BLOOD: FBC shows mild anaemia, leucocytosis and INCREASED EOSINOPHILS. LFTs show raised AlkPhos and bilirubin. Increased ESR and CRP. Can also look for hydatid serology.
  • STOOL MICROSCOPY: for tapeworm eggs
  • LIVER USS/CT/MRI: localises cyst
  • CXR: right pleural effusion or atelectasis, raised hemidiaphragm
106
Q

What is the anatomy of liver lobules?

A

Portal triad of portal vein, artery and bile duct is also known as the portal tract.

107
Q

How are liver lobules divided into zones?

A

.

108
Q

What is Hepatitis A, B, C, D, E?

A
  • A and E: infection with RNA HAV or HEV that follows an ACUTE course without progression to chronic carriage.
  • B and D: infection with DNA HBV which may follow an acute OR chronic course. HBD is an RNA virus that can only propagate in the presence of HBV. It may only co-infect with HBV or superinfect persons who are already carriers of HBV
  • C: infection with RNA HCV that follows a CHRONIC cause in 80% of cases
109
Q

What defines chronic hepatitis?

A

Viraemia and hepatic inflammation continuing for at least 6 months.

110
Q

What is the aetiology of Hepatitis A, B, C, D, E?

A
  • A and E: HAV is a picornavirus and HEV a calicivirus – small non-enveloped single-stranded linear RNA viruses with FAECAL-ORAL TRANSMISSION. Intubation period is 3-6 weeks. A and E are VOWELS, so come from the BOWELS
  • B and D: HBV is an enveloped, partially ds-DNA virus with SEXUAL, BLOOD and VERTICAL TRANSMISSION. HDV has the same methods of transmission. Intubation period 3-6 months
  • C: small, enveloped RNA of the flavivirus family with PARENTERAL TRANMISSION e.g., blood products, IVDU, tattooing and those on haemodialysis. Sexual and vertical transmission is uncommon.
111
Q

What is the pathophysiology of Hepatitis A, B, C, D, E?

A
  • A and E: virus replicates in hepatocytes and secreted into bile. Liver inflammation and hepatocyte necrosis is caused by the immune response, with targeting of infected CELLS by CD8+ T cells and NK cells. There is inflammatory cell infiltration of the portal tracts, zone 3 necrosis and bile duct proliferation
  • B and D: antibody- and cell-mediated immune responses are mounted leading to a spectrum of mild through to severe inflammation and cirrhosis. Various viral proteins are produced against HBV including core antigen (HBcAg), surface antigen (HBsAg), and e antigen (HBeAg). HDV is coated with HBsAg which it utilises for entry into hepatocytes
  • C: immune responses to HCV leads to hepatic inflammation and necrosis. Chronic hepatitis and characterised by lymphoid follicles (lymphocyte aggregates) in the portal tracts on biopsy, with fatty changes and cirrhosis.
112
Q

What are the risk factors for Hepatitis B and D? (x5)

A

IVDU, unscreened blood products, infants of HBeAg-positive mothers, sexual contact with HBV carriers. Babies more likely to be carriers of HBV.

113
Q

What is the epidemiology of Hepatitis?

A
  • A and E: highest rates in developing world where it is endemic
  • B and D: common in SE Asia, Africa and Mediterranean. Uncommon in the UK
  • C: highest rates in developing world, with varying genotypes in different geographical locations (HCV is highly mutant as RNA virus)
  • Most common in UK is C, most common in world is B.
114
Q

What are the signs and symptoms of Hepatitis A, B, C, D, E?

A
  • A and E: PRODROMAL PERIOD of malaise, anorexia (distaste for cigarettes in smokers), fever, N&V. ICTERIC PHASE: dark urine, pale stools, jaundice lasting 3 weeks, with tender hepatomegaly, and splenomegaly/cervical lymphadenopathy in some. Occasionally itching and jaundice in last weeks of HAV owing to cholestatic hepatitis
  • B and D: PRODROMAL PERIOD of malaise, anorexia, N&V, headache, diarrhoea and RUQ pain. May also suffer serum-sickness-type illness such as fever, arthralgia, polyarthritis, rash. ICTERIC PHASE: same as A and E. CHRONIC CARRIAGE may be diagnosed after routine LFTs or if cirrhosis or decompensation appears.
  • C: 90% are asymptomatic with 10% presenting with jaundice and flu-like illness. Chronic disease may be diagnosed after routine LFTs or if cirrhosis or decompensation appears. Less common extra-hepatic manifestations include skin rash caused by cryoglobulinemia causing small vessel vasculitis, and renal dysfunction caused by glomerulonephritis.
115
Q

What are the LFTs for Hepatitis A, B, C, D and E?

A
  • A and E: LFTs have ^^ AST and ALT, ^ Bilirubin, ^ AlkPhos
  • C: ^ AST and ALT, mild ^ bilirubin. Chronic leads to ^^ AST and ALT, often fluctuating over time
116
Q

What is viral serology for Hepatitis A, B, C, D and E?

A
  • A: Anti-HAV IgM (during acute, disappearing after 3-5 months)
  • B: acute phase: HbsAg+ and IgM anti-HbcAg; chronic phase: HbsAg+, IgG anti-HbcAg, HbeAg+ (may be negative in precure mutant variant)
  • C: IgM in acute, IgG in chronic or past exposure.
  • D: IgM or IgG against HDV too
  • E: Anti-HEV IgM (1-4 weeks after onset of illness) and IgG
117
Q

When is liver biopsy indicated in hepatitis?

A

If clotting is deranged or ascites present

118
Q

What additional tests can be used for Hepatitis B?

A

PCR for most sensitive detection of HBV DNA

119
Q

What additional tests can be used for Hepatitis C?

A

Reverse-transcriptase PCR for detection of HCV RNA, recommended in patients with suspected HCV but negative serology.

120
Q

What is a marker of disease activity in Hepatitis B?

A

HbeAg.

121
Q

How is hepatitis managed? (x3, x1 and x2)

A
  • ACUTE: supportive care; avoid alcohol, fluid replacement, cholestyramine if pruritis
  • All are notifiable diseases
  • CHRONIC: IFN-alpha therapy (augments natural antiviral mechanisms) or nucleoside/tide analogues (such as adefovir, entecavir in B/D and ribavirin in C)
122
Q

What additional management is there for Hepatitis B?

A

Passive immunisation with Hep B immunoglobulin for acute management

123
Q

What are the indications for treatment of chronic hepatitis B? (x2)

A

Compensated cirrhosis and HBV DNA over 2000 IU/mL, or decompensated cirrhosis and detectable HBV DNA by PCR.

124
Q

Hepatitis: prevention control? (x3)

A
  • Safe water, sanitation, food hygiene for Hepatitis A and E
  • Safe sex practices and instrument sterilisation in Hepatitis B and D
  • Immunisation for Hepatitis A and B. HAV vaccine has 10-year protection and attenuated virus is administered. HBV vaccine, in three doses, gives life-long protection and recombinant HbsAg is given – the vaccine also protects against HDV. No vaccines available for C, D or E
125
Q

What is viral serology after Hepatitis A and B vaccines?

A

.

126
Q

What are the complications of hepatitis? (x5)

A
  • Fulminant hepatic failure (more common in HBV and HEV)
  • Post-hepatitis syndrome: continued malaise for weeks/months
  • Hepatocellular carcinoma in Hepatitis B, C and D, not in A or E
  • Cholestatic hepatitis after HAV
  • Extrahepatic immune complex disorders in B and D such as glomerulonephritis, polyarteritis nodosa
127
Q

What is fulminant hepatitis?

A

Rapid necrosis of liver parenchyma.

128
Q

What is the prognosis of fulminant hepatitis?

A

80% mortality

Year 3 Gastrointestinal (29 decks)

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