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Phase 2a > Liver and co. > Flashcards

Liver and co. Flashcards

1
Q

What are the functions of the liver?

A
  • Glucose + fat metabolism.
  • Detoxification + excretion.
  • Protein synthesis (albumin, clotting factors).
  • Defence against infection.
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2
Q

What do liver function tests measure?

A
  • Serum bilirubin, albumin + prothrombin time.
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3
Q

What enzyme raises in…

i) Cholestatic liver disease?
ii) Hepatocellular liver disease?

A
  • Alkaline phosphatase (ALP).

- Transaminases (AST, ALT).

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4
Q

What occurs in pre-hepatic jaundice? What are the urine + stools like?

A
  • Increased breakdown of erythrocytes results in increased levels of unconjugated bilirubin.
  • Urine + Stools normal, no itching, LFTs normal.
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5
Q

What occurs in cholestatic jaundice? What are the urine + stools like?

A
  • Can be due to liver disease (hepatic) or bile-duct obstruction (post-hepatic).
  • Raised conjugated bilirubin.
  • Dark urine + pale stools, itching, abnormal LFTs.
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6
Q

What are the symptoms of jaundice?

A

Biliary pain, rigors (indicative of obstructive), weight loss.

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7
Q

PARACETAMOL OVERDOSE

What occurs in the therapeutic dose of paracetamol?

A
  • Mostly metabolised via sulfate/glucuronic acid conjugation pathway (Phase II).
  • If stores are low, undergoes phase I oxidation forming highly reactive toxic compound NAPQI which is immediately conjugated with glutathione + excreted.
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8
Q

PARACETAMOL OVERDOSE

What happens in paracetamol overdose?

A
  • Large amounts of paracetamol oxidised to NAPQI due to Phase II saturation.
  • Liver glutathione stores depleted, NAPQI persists > hepatotoxicity + kidney injury.
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9
Q

PARACETAMOL OVERDOSE

What are the clinical features of paracetamol overdose?

A

Asymptomatic for first 24h.
Liver damage peaks 72h after…
- Jaundice, metabolic acidosis, hypoglycaemia.

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10
Q

PARACETAMOL OVERDOSE

What is the treatment for paracetamol overdose?

A
  • Gastric decontamination with activated charcoal.

- IV N-acetyl-cysteine (replenishes cellular glutathione stores).

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11
Q

LIVER FAILURE

What is the pathophysiology of liver failure?

A
  • Destruction of hepatocytes + development of fibrosis in response to chronic inflammation.
  • The destruction of the architecture of the nodules of the level removes the ability of the liver to adequately perform functions, repair + regenerate.
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12
Q

LIVER FAILURE

What is fulminant hepatic failure? How does it come about?

A
  • Massive necrosis of liver cells leading to severe impairment of liver function.
  • Can be acute or progress from a chronic liver disease.
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13
Q

LIVER FAILURE

What is the aetiology of fulminant hepatic failure?

A
  • Infection (Hep B/C, CMV).
  • Induced (alcohol, drug toxicity).
  • Autoimmune hep, metabolic liver diseases.
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14
Q

LIVER FAILURE

What is the clinical presentation of fulminant hepatic failure?

A
  • Jaundice.
  • Hepatic encephalopathy (drowsiness/confusion).
  • Clubbing.
  • Ascites.
  • Asterixis.
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15
Q

LIVER FAILURE

What is hepatic encephalopathy?

A
  • Liver unable to remove ammonia + so it’s able to cross BBB causing cerebral oedema.
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16
Q

LIVER FAILURE

What are the investigations for fulminant liver failure?

A
  • Bloods – hepatitis, CMV + EBV serology, raised bilirubin, low glucose.
  • Abdominal USS.
  • Doppler flow studies of portal vein.
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17
Q

LIVER FAILURE

What is the treatment for fulminant liver failure?

A
  • Nutrition + supplements.
  • Treat complications (lactulose, mannitol for hepatic encephalopathy)
  • Liver transplantation.
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18
Q

ALCOHOLIC LIVER DISEASE

What are the three stages of alcoholic liver disease?

A
  • Fatty change.
  • Alcoholic hepatitis.
  • Alcoholic cirrhosis.
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19
Q

ALCOHOLIC LIVER DISEASE

Explain the fatty change stage.

A
  • Biopsy finding, hepatocytes contain macrovesicular droplets of triglycerides.
  • Fat disappears on cessation of alcohol intake.
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20
Q

ALCOHOLIC LIVER DISEASE

Explain the alcoholic hepatitis stage.

A
  • Ballooned hepatocytes that contain eosinophilic material called Mallory bodies, surrounding by neutrophils.
  • Fibrosis + foamy degeneration of hepatocytes possible, usually co-exists with cirrhosis.
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21
Q

ALCOHOLIC LIVER DISEASE

Explain the alcoholic cirrhosis stage.

A
  • Final stage of alcoholic liver disease where there’s destruction of liver architecture + fibrosis.
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22
Q

ALCOHOLIC LIVER DISEASE

What are the clinical presentations of alcoholic hepatitis and alcoholic cirrhosis?

A 
Hepatitis...
- Rapid onset jaundice.
- Nausea, fever, ascites.
- Encephalopathy.
Cirrhosis...
- Spider naevi, loss of body hair.
- Clubbing, palmar erythema, white nails.
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23
Q

ALCOHOLIC LIVER DISEASE

What are the investigations for alcoholic liver disease?

A

Bloods = macrocytic anaemia.

Liver biochemistry = AST + ALT raised (AST>ALT ratio), GGT v raised.

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24
Q

ALCOHOLIC LIVER DISEASE

What is the treatment for alcoholic liver disease?

A
  • Alcohol cessation.

- Treat malnutrition from alcohol (thiamine).

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25
Q

CIRRHOSIS

What is the pathophysiology of cirrhosis?

A
  • Cirrhosis results form necrosis of liver cells followed by fibrosis + nodule formation, the end result is impairment of liver cell function + gross distortion of the liver architecture leading to portal HTN.
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26
Q

CIRRHOSIS
What is…
i) compensated cirrhosis?
ii) decompensated cirrhosis?

A

i) When the liver can still function effectively + there are no/few noticeable symptoms.
ii) Liver is damaged to point it cannot function adequately + clinical complications present. Events causing this can be infection, portal vein thrombosis + surgery.

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27
Q

CIRRHOSIS

What is the aetiology of cirrhosis?

A

Chronic liver diseases…

  • Alcohol misuse (commonest in western world).
  • Hep B/C (commonest worldwide).
  • Obesity/T2DM.
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28
Q

CIRRHOSIS
What is the clinical presentation of
i) Chronic liver disease?
ii) Secondary to portal HTN + liver failure?

A

i) Spider naevi + loss of body hair, clubbing, palmar erythema, white nails.
ii) Ascites, abdominal pain, variceal haemorrhage, encephalopathy, jaundice.

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29
Q

CIRRHOSIS

What are the major complications with cirrhosis?

A
  • MAJOR = hepatocellular carcinoma, screen for it every 6 months with ultrasound + serum alpha-fetoprotein, AFP.
  • Hepatic encephalopathy.
  • Abnormal bleeding (portal HTN > variceal haemorrhage).
  • Ascites.
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30
Q

CIRRHOSIS

What are the investigations for cirrhosis?

A
  • Bloods, FBC = thrombocytopenia witih leukopenia + anaemia later.
  • Liver ultrasound + duplex.
  • Liver biopsy = diagnostic.
  • Ascitic tap.
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31
Q

CIRRHOSIS

What is the treatment for cirrhosis?

A
  • Treat underlying.
  • Symptom relief = spironolactone for ascites, lactulose/mannitol for hepatic encephalopathy.
  • If ascites, prohylactic ciprofloxacin.
  • Liver transplant most effective.
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32
Q

PORTAL HYPERTENSION

What is the pathophysiology of portal HTN?

A
  • Inflow of portal blood can be partially/completely obstructed leading to high pressure proximal to obstruction.
  • Endothelin-1 production is increased + NO production is decreased in cirrhosis so there’s more vasoconstriction, increasing portal pressure.
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33
Q

PORTAL HYPERTENSION

What is the aetiology of portal HTN?

A
  • Pre-hepatic (blockage of portal vein) = thrombosis or portal/splenic vein.
  • Intrahepatic (distortion of liver architecture) = cirrhosis (UK), schistosomiasis (worldwide).
  • Post-hepatic (venous blockage outside liver) = Budd-Chiari syndrome.
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34
Q

PORTAL HYPERTENSION

What is Budd-Chiari syndrome?

A
  • Vascular disease associated with occlusion of hepatic veins that drain liver.
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35
Q

PORTAL HYPERTENSION

What are the complications tha can occur in portal HTN?

A
  • Varices can occur due to diversion of blood into portosystemic collaterals (gastro-oesophageal junction) to relieve the pressure where they are superifical + liable to rupture, causing massive GI haemorrhage.
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36
Q

PORTAL HYPERTENSION

What is the clincial presentation of portal HTN?

A

Oesophago-gastric varcies…

  • Haematemesis.
  • Pallor.
  • Shock (hypotensive, tachycardic).
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37
Q

PORTAL HYPERTENSION

What are the investigations for portal HTN?

A
  • Upper GI endoscopy.
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38
Q

PORTAL HYPERTENSION

What are the treatment for portal HTN?

A 
Medical (reduce portal pressure)...
- Beta blocker to reduce CO.
- Nitrates + ADH analogue.
Surgical...
- Band ligation.
- Trans-jugular intrahepatic portosystemic shunt (TIPSS).
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39
Q

ACUTE PANCREATITIS

What is the pathophysiology of acute pancreatitis?

A
  • Inflammatory process with release of inflammatory cytokines (TNF-alpha, IL-6) + pancreatic enzymes (trypsin, lipase) which destroys the pancreas.
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40
Q

ACUTE PANCREATITIS

What are the three types of pancreatitis?

A
  • Oedematous (acute fluid collection).
  • Necrotising.
  • Haemorrhagic.
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41
Q

ACUTE PANCREATITIS

What is the aetiology of acute pancreatitis?

A

I GET SMASHED…

  • Idiopathic.
  • Gallstones.
  • Ethanol (alcohol).
  • Trauma.
  • Steroids.
  • Mumps.
  • Autimmune.
  • Scorpion stings.
  • Hyperlipidaemia.
  • ERCP (endoscopic retrograde cholangiopancreatography).
  • Drugs.
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42
Q

ACUTE PANCREATITIS

What are the symptoms of acute pancreatitis?

A
  • Severe epigastric abdominal pain (radiates to back, sitting forward may relieve).
  • May be gradual/sudden onset.
  • Vomiting.
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43
Q

ACUTE PANCREATITIS

What are the signs of acute pancreatitis?

A
  • Periumbilical or flank bruising (Cullen’s + Grey Turner’s signs respectively) from blood vessel autodigestion + retroperitoneal haemorrhage.
  • Jaundice.
  • Shock.
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44
Q

ACUTE PANCREATITIS

What are the investigations for acute pancreatitis?

A

Diagnosis on 2/3…

  • Characteristic severe epigastric pain radiating to back.
  • Raised serum amylase (3-fold upper limit).
  • Abdominal CT scan pathology.
  • Serum lipase is more sensitive + specific.
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45
Q

ACUTE PANCREATITIS

What is criteria is used for predicting acute pancreatitis severity?

A 
Modified Glasgow Criteria, PANCREAS ≥3 suggests severe...
PaO2 < 8kPa.
Age >55y/o
Neutrophilia
Calcium <2mmol/L.
Raised urea >16mmol/L.
Elevated enzymes.
Albumin <32g/L.
Sugar, blood glucose >10mmol/L.
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46
Q

ACUTE PANCREATITIS

What is the treatment for acute pancreatitis?

A
  • Analgesia, IV fluids (maintian electrolyte balance).
  • Oxygen.
  • Treat cause.
  • Abx? Gallstone removal (progressive jaundice)? Drain oedematous fluid, surgery.
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47
Q

CHRONIC PANCREATITIS

What is the pathophysiology of chronic pancreatitis?

A
  • Chronic inflammation of the pancreas leads to irreversible damage.
  • Pancreatic duct obstruction leads to activation of pancreatic enzymes leading to necrosis + subsequent fibrosis.
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48
Q

CHRONIC PANCREATITIS

What is the aetiology of chronic pancreatitis?

A
  • Most excessive alcohol consumption as proteins precipitate in ductal lumen causing obstruction.
  • Smoking, autoimmune.
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49
Q

CHRONIC PANCREATITIS

What is the clinical presentation of chronic pancreatitis?

A
  • Epigastric pain radiating to back (relieved sitting forward).
  • Weight loss.
  • Steatorrhoea (excretion of abnormal quantities of fat).
  • DM.
  • Nausea + vomiting.
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50
Q

CHRONIC PANCREATITIS

What are the investigations for chronic pancreatitis?

A
  • Ultrasound ± CT shows pancreatic calcifications.
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51
Q

CHRONIC PANCREATITIS

What is the treatment for chronic pancreatitis?

A 
Lifestyle = smoking + alcohol cessation, ?low fat diet.
Drugs = analgesia, pancreatic enzyme replacement, steroids if autoimmune.
Surgery = local resection.
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52
Q

BILIARY COLIC

What is the pathophysiology of biliary colic?

A
  • RUQ pain due to gallstone blocking bile duct temporarily.
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53
Q

BILIARY COLIC

What is the aetiology of biliary colic?

A

Gallstones…

- Cholesterol, bile pigment + phospholipids are components seen.

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54
Q

BILIARY COLIC

What is the clinical presentation of biliary colic?

A
  • Recurrent episodes of severe, persistent RUQ pain (back radiation).
  • Triggered by heavy, faty meal.
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55
Q

BILIARY COLIC

What are the investigations of biliary colic?

A
  • Basis of history + ultrasound showing gallbladders.
  • Serum ALP + bilirubin increases during attack.
  • Absence of inflammatory features differentiates from acute cholecystitis.
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56
Q

BILIARY COLIC

What is the treatment for biliary colic?

A
  • Analgesics + elective cholecystectomy.
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57
Q

ACUTE CHOLECYSTITIS

What is the pathophysiology of acute cholecystitis?

A
  • Inflammation of the gallbladder following the impaction of a stone in the cystic duct/neck of gallbladder, obstruction to bile emptying.
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58
Q

ACUTE CHOLECYSTITIS

What is the aetiology + risk factors for acute cholecystitis?

A
  • Gallstones.

- Fat, Forty, Female, Fertile.

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59
Q

ACUTE CHOLECYSTITIS

What is the clinical presentation of acute cholecystitis?

A
  • Sever RUQ pain associated with fever, vomiting.
  • Gallbladder mass.
  • NO jaundice.
  • Murphy’s sign (tenderness worse on inspiration when 2 fingers on RUQ).
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60
Q

ACUTE CHOLECYSTITIS

What are the complications of acute cholecystitis?

A
  • Empyema (pus) + perforation with peritonitis.
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61
Q

ACUTE CHOLECYSTITIS

What are the investigations of acute cholecystitis?

A
  • Bloods = FBC shows increased WCC.
  • Liver function tests to exclude liver/bile duct pathology.
  • Abdominal USS shows gallstones + distended gallbladder w/ thickened wall.
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62
Q

ACUTE CHOLECYSTITIS

What are the treatments for acute cholecystitis?

A

Supportive = nil-by-mouth, IV fluids, pain relief.

Laparoscopic cholecystectomy.

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63
Q

ASCENDING CHOLANGITIS

What is the pathophysiology of ascending cholangitis?

A
  • Gallstone is stuck in the common bile duct + because flow of bile can no longer prevent intestinal bacteria from migrating up the biliary tree there is infection + inflammation.
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64
Q

ASCENDING CHOLANGITIS

What is the aetiology of ascending cholangitis?

A
  • Gallstones.

- Infection (E. coli, klebsiella, enterococcos, group D strep).

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65
Q

ASCENDING CHOLANGITIS

What is the clinical presentation of ascending cholangitis?

A
  • Charcot’s triad = fever, RUQ pain + jaundice (cholestatic).
  • Reynold’s pentad w/ hypotension + confusion.
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66
Q

ASCENDING CHOLANGITIS

What are the investigations for ascending cholangitis?

A 
Bloods – WCC increased, blood cultures, positive, LFTs raised.
MR cholangiopancreatography (MRCP) visualises site + Cause of obstruction.
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67
Q

ASCENDING CHOLANGITIS

What is the treatment for ascending cholangitis?

A
  • Fluid resuscitation, Abx.

- ERCP for biliary drainage, stone removal + bile sample for culture.

68
Q

PBC

What is the pathophysiology of primary biliary cholangitis (PBC)?

A
  • Interlobular bile ducts (intrahepatic) are damaged by chronic autoimmune granulomatous inflammation causing cholestasis which can lead to fibrosis, cirrhosis + portal HTN.
69
Q

PBC

What is the epidemiology + aetiology of PBC?

A
  • F:M = 9:1, positive family Hx gives 10-fold risk.

- Unknown triggers, associated with other autoimmune diseases like coeliac.

70
Q

PBC

What is the clinical presentation of PBC?

A
  • Asymptomatic but may have pruritus, fatigue.

- Signs = jaundice, skin hyperpigmentation, hepatosplenomegaly.

71
Q

PBC

What are the investigations for PBC?

A

Blood…

  • LFTs, increased ALP.
  • Serum autoantibodies, antimitochondrial antibodies (AMA, IgM).
  • Serum antibodies (IgM) increased.
72
Q

PBC

What are the treatments for PBC?

A
  • Colestyramine for pruritus.
  • Vitamin A, D, E + K supplementation.
  • Liver transplantation.
73
Q

PSC

What is the pathophysiology of primary sclerosing cholangitis?

A
  • Progressive cholestasis characterised by strictures + fibrosing inflammatory destruction of both intra + extrahepatic bile ducts.
74
Q

PSC

What is the aetiology of PSC?

A
  • Secodary to infection, thrombosis, trauma.
  • 75% association with ulcerative colitis.
  • Cancers more common.
75
Q

PSC

What is the clinical presentation of PSC?

A
  • Pruritus ± fatigue.

- Cirrhosis + hepatic failure if advanced (jaundice, fever).

76
Q

PSC

What are the investigations for PSC?

A
  • Serum autoantibodies like Anti-neutrophil cytoplasmic antibody (ANCA, not specific).
  • ERCP/MRCP show duct anatomy.
  • Liver biopsy.
77
Q

PSC

What are the treatments for PSC?

A
  • Colestyramine for pruritus.
  • Vitamin A, D, E + K supplementation.
  • Liver transplantation.
78
Q

ASCITES

What is ascites?

A
  • Accumulation of fluid in peritoneal cavity leading to abdominal distention.
79
Q

ASCITES

Why does ascites occur in cirrhosis?

A

In cirrhosis, peripheral arterial vasodilation leads to reduction in effective blood volume, with activation of sympathetic nervous system + RAAS prompting renal salt + water retention.
- Formation of oedema encouraged by hypoalbuminaemia + mainly localised to peritoneal cavity due to portal HTN.

80
Q

ASCITES

What is the aetiology of ascites?

A

Exudative (cloudy)…
- Local inflammation (peritonitis).
Transudate (clear)…
- Leaky vessels (imbalance between hydrostatic/oncotic pressures [H>O] Hp increased due to portal HTN + RAAS).
- Low flow (cirrhosis, thrombosis, cardiac failure).
- Low protein (hypoalbuminaemia decreases oncotic pressure).

81
Q

ASCITES

What is the clinical presentation of ascites?

A
  • Distended abdomen.
  • Shifting dullness.
  • Flank swelling.
  • Bulging flanks.
82
Q

ASCITES

What is the major complication of ascites?

A

Spontaneous bacterial peritonitis…

  • Complication of ascites w/ cirrhosis.
  • Causes = E. coli, klebsiella, enterococcus.
  • Ascitic tap shows raised neutrophils.
  • Mange by cefotaxime, ciprofloxacin prophylaxis.
83
Q

ASCITES

What are the investigations for ascites?

A
  • Ultrasound/CT/MRI abdomen.
  • LFTs, serum albumin.
  • Ascitic tap.
84
Q

ASCITES

What is the treatment fo ascites?

A
  • Treat cause, limit dietary sodium + fluids.
  • Paracentesis (drainage).
  • Diuretics like spironolactone.
85
Q

AUTOIMMUNE HEPATITIS

What is the pathophysiology of autoimmune hepatitis?

A
  • Inflammatory liver disease characterised by abnormal T-cell function + autoantibodies directed against hepatocyte surface antigens.
86
Q

AUTOIMMUNE HEPATITIS

What is the clinical presentation of autoimmune hepatitis?

A
  • Insidious w/ anorexia, malaise, nausea, fatigue.

- Signs of chronic liver disease (spider naevi, jaundice etc).

87
Q

AUTOIMMUNE HEPATITIS

What are the investigations for autoimmune hepatitis?

A

Circulating autoantibodies, IgG
- Type 1 = antinuclear antibody (ANA), anti-smooth muscle antibody (ASMA).
- Type 2 = anti-liver kidney microsome.
Liver biopsy.

88
Q

AUTOIMMUNE HEPATITIS

What are the treatments for autoimmune hepatitis?

A
  • Immunosuppresion with prednisolone.

- Liver transplantation if failure of medical therapy.

89
Q

VIRAL HEPATITIS

What are the pathological features of hepatitis? What is the difference between acute + chronic hepatitis?

A
  • Liver cell necrosis + inflammatory cell infiltration.
  • Acute = most commonly hepatitis viruses, often self-limiting with return to normal structure + function.
  • Chronic = sustained inflammatory disease of liver lasting >6 months.
90
Q 
VIRAL HEPATITIS
What is the aetiology of...
i) Acute infective
ii) Acute non-infective
iii) Chronic ifnective

hepatitis?

A

i) Hepatitis A–E, EBV, CMV.
ii) Alcohol, drugs, toxins, autoimmune.
iii) Hepatitis B–D, E in immunocompromised.

91
Q

VIRAL HEPATITIS A

What type of virus is hepatitis A? How is it spread? How long does it take to incubate?

A
  • RNA virus, 100% acute w/ immunity after.
  • Faeco-oral, normally w/ travel history, contaminated food/water.
  • 2–6 weeks.
92
Q

VIRAL HEPATITIS A

What are the symptoms of hepatitis A?

A
  • Fever, malaise, anorexia, nausea then jaundice + hepatosplenomegaly.
93
Q

VIRAL HEPATITIS A

What are the investigations for hepatitis A?

A

AST + ALT rise.
Serology…
- Anti-HAV IgM rises initially = recent infection.
- Anti-HAV IgG detectable for life.

94
Q

VIRAL HEPATITIS A

What is the treatment for hepatitis A?

A
  • Preventative = vaccination for travellers.

- Supportive, avoid alcohol, manage close contacts.

95
Q

VIRAL HEPATITIS B

What type of virus is hepatitis B? How is it spread?

A
  • DNA virus (replicates in hepatocytes), acute.

- Blood-borne like IV drug users, sexual, needle-stick (highly infectious).

96
Q

VIRAL HEPATITIS B

What is the first stage in the natural history of hepatitis B?

A

Immune tolerance phase = unimpeded viral replication leads to high HBV DNA levels.

97
Q

VIRAL HEPATITIS B

What is the second stage in the natural history of hepatitis B?

A

Immune clearance phase = immune system stimulated by HBV proteins, liver inflammation + high ALT.

98
Q

VIRAL HEPATITIS B

What is the third stage in the natural history of hepatitis B?

A

Inactive HBV carrier phase = HBV DNA levels low, ALT levels normal, no liver inflammation.

99
Q

VIRAL HEPATITIS B

What is the last stage in the natural history of hepatitis B?

A

Reactivation phase = ALT + HBV DNA levels are intermitted + inflammation is seen on liver > fibrosis.

100
Q

VIRAL HEPATITIS B

What are the symptoms of hepatitis B?

A
  • Fever, malaise, arthralgia, then jaundice, hepatosplenomegaly.
101
Q

VIRAL HEPATITIS B

What are the investigations for hepatitis B?

A

Viral serology…

  • HBV surface antigen detected 6w–3m.
  • Anti-HBV core IgM after 3m.
102
Q

VIRAL HEPATITIS B

What is the treatment for hepatitis B?

A
  • Supportive, monitor liver function, manage contacts.
  • Pegylated interferon alpha 2a (boosts immune system).
  • Follow up at 6m to see if HBV surface antigen cleared, if not chronic.
  • Prevention via vaccination (small amount of inactive HBsAg), HBVs IgG present in vaccinated.
103
Q

VIRAL HEPATITIS B

What are the consequences of hepatitis B?

A
  • Cirrhosis.
  • HCC.
  • Fulminant hepatic failure.
104
Q

VIRAL HEPATITIS C

What type of virus is hepatitis C? How is it spread?

A
  • RNA virus, 70% progress to chronic.

- Blood-borne like materno-foetal transmission.

105
Q

VIRAL HEPATITIS C

What are the investigations for hepatitis C?

A

Viral serology…

  • Anti-HCV antibodies (IgM/G) confirms exposure.
  • HCV-PCR confirms ongoing infection.
106
Q

VIRAL HEPATITIS C

What are the treatments for hepatitis C?

A
  • Ribavirin + pegylated interferon alpha 2a.
107
Q

VIRAL HEPATITIS D

What sort of virus is hepatitis D and how does it spread? What are the investigations for hepatitis D?

A

Defective RNA virus, needs HBV for assembly as it needs HBsAg for protection.
Blood-borne transmission, esp. IVDU.
Viral serology…
- Anti-HDV antibody if HBsAg +ve also.

108
Q

VIRAL HEPATITIS D

What is the treatment for hepatitis D?

A
  • Complete prevention if HBV vaccination.

- Liver transplantation.

109
Q

VIRAL HEPATITIS E

What type of virus is hepatitis E? How is it spread?

A
  • Small RNA virus, acute but risk of chronic in immunocompromised.
  • Faeco-oral, contaminated food/water, undercooked pork in UK.
110
Q

VIRAL HEPATITIS E

What are the investigations + treatment for hepatitis E?

A

Viral serology…
- Anti-HEV IgM rises initially + means recent infection.
- Anti-HEV IgG detectable for life.
Vaccine, good food hygiene.

111
Q

NAFLD

What is the pathophysiology of non-alcoholic fatty liver disease (NAFLD)? What is non-alcoholic steatohepatitis (NASH)?

A
  • Represents increased fat in hepatocytes visualised that cannot be attributed to other causes like alcohol.
  • If inflammation is present = NASH.
112
Q

NAFLD

What are the risk factors + investigations for NAFLD?

A
  • Metabolic syndrome, T2DM.

- Rule out other causes of liver disease, enhanced liver fibrosis test (for advanced liver fibrosis).

113
Q

NAFLD

What is the treatment for NAFLD?

A
  • Control risk factors (lose weight, exercise more, avoid alcohol).
  • Address CV risk, monitor for complications.
114
Q

LIVER ABSCESS

What is the pathophysiology of liver abscess?

A
  • Pus-filled mas inside liver post-infection, appendicitis or haematogenous spread via portal vein.
115
Q

LIVER ABSCESS

What is the aetiology of liver abscess?

A
  • Elderly (biliary sepsis).
  • Trauma.
  • E. coli (most common), klebsielle pnuemoniae
116
Q

LIVER ABSCESS

What is the clinical presentation, investigations + treatment of liver abscess?

A
  • Fever, vomiting, RUQ pain.
  • Bloods = ALP, ESR/CRP raised, CT abdomen, ultrasound to detect + sample.
  • Aspiration under USS, anitbiotics like co-amoxiclav, metronidazole.
117
Q

AMOEBIC ABSCESS

What is the pathophysiology of amoebic abscess?

A
  • Entamoeba histolytica can be carried from bowel to liver in portal venous system leading to portal inflammation + development of abscesses.
118
Q

AMOEBIC ABSCESS

What is the clinical presentation of amoebic abscess?

A
  • Fever, abdominal pain, tender hepatomegaly, night sweats.

- Signs of effusion or consolidation.

119
Q

AMOEBIC ABSCESS

What are the investigations + treatment of amoebic abscess?

A
  • Serological test for amoeba (ELISA).
  • USS abdomen + cyst aspiration shows ‘anchovy sauce’ pus.
  • Metronidazole, aspiration.
120
Q

DIARRHOEA

What is diarrhoea? What is acute + chronic diarrhoea?

A
  • Abnormal passage of loose or liquid stool ≥3x daily.
  • Acute = usually due to infection/dietary indiscretion.
  • Chronic = defined as diarrhoea >14d.
121
Q

DIARRHOEA

What three things leads to decreased stool consistency?

A
  • Osmotic = large quantities of non-absorbed hypertonic substances in bowel draw fluid into intestine (malabsorption, laxatives).
  • Secretory = active intestinal secretion of fluid + electrolyes as well as decreased absorption.
  • Inflammatory = damage to intestinal mucosal cells leads to loss of fluid, blood + defective absorption of fluid + electrolytes.
122
Q

DIARRHOEA

What is the aetiology of diarrhoeal infection?

A
  • Traveller’s diarrhoea, viral, bacterial, helminths.
  • Enterohaemorrhagic E.coli cause bloody diarrhoea + has shiga like toxin.
  • Enteropathogenic E. coli causes large volumes of watery diarrhoea.
123
Q

DIARRHOEA

What are the aetiology of non-infectious diarrhoea and risk factors?

A
  • Gastritis/peptic ulceration/acute cholecystitis/peritonitis.
  • Risks = food handlers, health care workers, children at nursery.
124
Q

DIARRHOEA

What is the clinical presentation of infective, inflammatory + helminths diarrhoea?

A
  • Sudden onset bowel frequency w/ crampy abdominal pains + fever = infective
  • Bowel frequency with loose, blood-stained stools = inflammatory.
  • Fever, eosinophilia, diarrhoea, cough, wheeze = helminths.
125
Q

DIARRHOEA

What are the investigations for diarrhoea?

A
  • Stool samples (culture + sensitivity), faecal calprotectin, faecal occult test.
  • Blood/mucous?
  • Family Hx?
  • Abdominal pain?
  • Foreign travel?
  • Bloating/weight loss?
126
Q

DIARRHOEA

What are the preventative measures for diarrhoea?

A
  • Access to clean water.
  • Good sanitation + hand hygiene.
  • Don’t let food handlers go to work without negative stool sample
  • Close wards.
127
Q

DIARRHOEA

What are the treatments for diarrhoea?

A
  • Treat cause, oral rehydration ± electrolyte replacement.

- Anti-motility agents.

128
Q

TRAVELLER’S DIARRHOEA

What is the pathophysiology + aetiology of traveller’s diarrhoea?

A
  • Increased secretion of Cl- into intestinal lumen, water follows down osmotic gradient.
  • Enterotoxigenic E. coli (ETEC), campylobactera jejuni, Giardia lamblia.
129
Q

TRAVELLER’S DIARRHOEA

What are the varying clinical presentations for traveller’s diarrhoea?

A
  • ETEC = watery diarrhoea preceded by cramps + nausea.
  • Giardia = upper GI symptoms (bloating, belching).
  • C. jejuni = colitic symptoms, urgency, cramps.
130
Q

TRAVELLER’S DIARRHOEA

what are the investigations + treatment for traveller’s diarrhoea?

A
  • > 3 unformed stools/day + abdominal pain, cramps, nausea or vomiting.
  • Occurs within 3 days of arrival in new country, lasts week.
  • Oral rehydration + anti-motility agents.
131
Q

INFECTIVE DIARRHOEA

What is the epidemiology of infective diarrhoea?

A
  • 2nd leading cause of death in children <5y/o globally (after pneumonia).
132
Q

INFECTIVE DIARRHOEA

What is the aetiology of infective diarrhoea?

A 
Viral causes most...
- Children = rotavirus.
- Adults = norovirus (cruises, hospitals, restaurants).
Bacterial causes...
- C. jejuni (poultry association).
- Children = E. coli, salmonella, shigella.
- Anitbiotic association.
- Parasitic (Giardia lamblia)
133
Q

INFECTIVE DIARRHOEA

What antibiotics are associated with Costridium difficile diarrhoea?

A

Rule of Cs…

  • Clindamycin.
  • Ciprofloxacin (quinolones).
  • Co-amoxiclav (penicillins).
  • Cephalosporins.
134
Q

INFECTIVE DIARRHOEA

What is C. diff? How does it present? What are the risk factors? How do you treat it?

A
  • Gram +ve spore forming bacteria.
  • Pyrexia, colic, raised inflammatory markers.
  • Elderly, long hospital stay, acid suppression.
  • Metronidazole, oral vancomycin.
135
Q

INFECTIVE DIARRHOEA

How does Giardia lamblia cause diarrhoea + how is it treated?

A
  • Diarrhoea due to alteration of intestinal villi = decreased absorption.
  • Metronidazole.
136
Q

INFECTIVE DIARRHOEA

What are the clinical presentations for infective diarrhoea?

A
  • Blood indicates bacterial infection.
  • Vomiting, abdominal cramping.
  • Fever, fatigue, headache = virus.
137
Q

INFECTIVE DIARRHOEA

What are the investigations of infective diarrhoea?

A
  • Bloods = find alternative cause, raised WCC if parasitic, raised ESR/CRP indicate infection.
  • Stool culture.
  • Sigmoidoscopy with biops.y
138
Q

INFECTIVE DIARRHOEA

What is the treatment of infective diarrhoea?

A
  • Treay cause, oral rehydration, anti-emetics, anti-motility + Abx.
139
Q

CHOLERA

What causes cholera + how do you investigate this?

A
  • Infection from vibrio cholerae (gram-ve aerobic ‘comma-shaped’ rod) found in faecal contaminated water.
  • Stool culture sample.
140
Q

CHOLERA

What is the clinical presentation + treatment of cholera?

A
  • Rice-water stool (diarrhoea), vomiting + dehydration, metabolic acidosis.
  • Biggest preventer = safe-drinking water, oral rehydration salts, doxycycline.
141
Q

HAEMOCHROMATOSIS

What is the pathophysiology of haemochromatosis?

A

Inherited disorder of iron metabolism in which an increase in intestinal iron absorption leads to iron accumulation/deposition in several places (joints, heart, pancreas).

142
Q

HAEMOCHROMATOSIS

What is the aetiology of haemochromatosis?

A
  • AR associated with HFE gene leading to deficiency in the iron regulatory hormone hepcidin.
143
Q

HAEMOCHROMATOSIS

What is the clinical presentation of haemochromatosis?

A
  • Slate-grey skin pigmentation.
  • DM (‘bronze’ diabetes from pancreatic iron deposition).
  • Cardiomyopathy.
144
Q

HAEMOCHROMATOSIS

What are the investigations + treatment of haemochromatosis?

A
  • Bloods = increased LFTs, ferritin, transferrin saturation ratio.
  • Confirm by HFE genotyping by PCR.
  • Excess tissue iron removed by venesection, desferrioxamine, may need insulin.
145
Q

WILSON’S DISEASE

What is the pathophysiology of Wilson’s disease? What is the aetiology?

A
  • Disorder of copper metabolism where ther eis excessive deposition of copper in the liver + CNS.
  • AR disorder of a copper transporting ATPase.
146
Q

WILSON’S DISEASE

What is the clinical presentation of Wilson’s disease?

A
  • Fayser-Fleischer rings = copper in iris.

- Neurological signs (tremor, dysphagia, dyskinesias) due to copper in CNS.

147
Q

WILSON’S DISEASE

What are the investigations + treatment of Wilson’s disease?

A
  • Low total serum copper, increased 24h urinary copper.

- Lifetime penicillamine to excrete copper, reduce intake (shellfish, liver, chocolate).

148
Q

ALPHA-1-ANTITRYPSIN DEF

What is the pathophysiology + aetiology of alpha-1-antitrypsin (A1AT) deficiency?

A
  • Results in protein retention in the liver + eventually cirrhosis.
  • Deficiency of serine protease inhibitor A1AT (SERPINA1) gene), AR.
149
Q

ALPHA-1-ANTITRYPSIN DEF

What is the clinical presentation of A1AT deficiency?

A
  • COPD symptoms due to alveoli damage + emphysema.

- Jaundice, hepatitis, cirrhosis.

150
Q

ALPHA-1-ANTITRYPSIN DEF

What are the investigations + treatment in A1AT deficiency?

A
  • Serum A1AT levels.

- Manage COPD (stop smoking), liver transplantation is a cure.

151
Q

LIVER CANCERS

What is the pathophysiology of liver cancers?

A
  • Mostly secondary (90%) as they have metastasisted from the GI tract, breast + bronchus.
152
Q

LIVER CANCERS

What are the two benign liver cancers?

A
  • Haemangiomas = commonest, often incident on USS/CT, don’t require treatment.
  • Adenomas = common, anabolic steroids, OCT, pregnancy, only treat if symptomatic.
153
Q

LIVER CANCERS

What is the epidemiology of the two primary liver cancers?

A
  • Hepatocellular carcinoma (HCC) = 90%, China/Africa.

- Cholangiocarcinoma = 10%.

154
Q

LIVER CANCERS

What is the aetiology of liver cancers?

A 
HCC...
- Most occur in chronic liver disease, cirrhosis, viral hep B/C.
- Alcohol + anabolic steroids.
Cholangiocarcinoma...
- Flukes biliary cysts, viral hep B + C.
155
Q

LIVER CANCERS

What is the clinical presentation of liver cancers?

A

HCC…
- Weight loss, fever, abdominal pain, ascites, hepatomegaly.
Cholangiocarcinoma…
- Fever, abdominal pain (± ascites).

156
Q

LIVER CANCERS

What are the investigations for liver cancers?

A

HCC…
- Bloods (serum AFR may be raised), USS/CT to identify lesions, biopsy.
Cholangiocarcinoma…
- Bloods = increased bilirubin, big incresaedin ALP.
- ERCP for biopsies.

157
Q

LIVER CANCERS

What is the treatment for liver cancers?

A 
HCC...
- Prevention with HBV vaccination.
- Surgical resection, liver transplant.
Cholagniocarcinoma...
- Mostly inoperable, stent to relieve symptoms.
158
Q

PANCREATIC CANCERS

What is the pathophysiology of pancreatic cancers?

A
  • Mostly ductal adenocarcinoma (metastasise early, present late).
  • 60% arise from head, 25% body, 15% tail.
  • Some arise in ampulla of Vater (ampulllary tumour) or pancreatic islet cells (insulinoma, gastrinoma, glucagonomas etc).
159
Q

PANCREATIC CANCERS

What is the aetiology of pancreatic cancers?

A
  • Hereditary (dominant susceptibility gene) + environemtnal factors (smoking, obesity) contribute).
  • Chronic pancreatitis is pre-malignant.
160
Q

PANCREATIC CANCERS

What is the clinical presentation of pancreatic cancers?

A

Male, >70y/o.
Head/ampulla…
- Painless obstructive jaundice, palpable gallbladder.
Body + tail…
- Epigastric pain (radiates to back, relieved by sitting forward), weight loss, anorexia.

161
Q

PANCREATIC CANCERS

What are the investigations + treatment for pancreatic cancers?

A
  • USS/CT scan to show pancreatic mass.
  • ERCP/MRCP.
  • Whipple’s procedure for head of pancreas, laparoscopic excision for tail lesions, combined chemo/radiotherapy.
162
Q

PERITONITIS

What is the difference between localised + generalised peritonitis?

A
  • Localised = occurs with all acute inflammatory conditions of GI tract.
  • Generalised = occurs as a result of rupture of an abdominal viscus (duodenal ulcer, appendix).
163
Q

PERITONITIS

What is the aetiology of peritonitis?

A

Bacterial…
- Perforated organ, spontaneous bacterial peritonitis, secondary to peritoneal dialysis.
Non-infective…
- Bile leak, blood from ruptured ectopic.

164
Q

PERITONITIS

What is the clinical presentation of peritonitis?

A
  • Pain, tenderness, systemic symptoms (nausea, chills, rigor).
165
Q

PERITONITIS

What are the investigations + treatment of peritonitis?

A
  • Abdominal examination = guarding, rebound, rigidity, erect CXR = gas under diaphragm.
  • Localised = treat underlying cause, generalised = antibiotics, supportive measures.

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