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Liver diseases Flashcards

1
Q

Types of jaundice?

A

Pre- hepatic
Hepatocellular/ hepatic
Post hepatic

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2
Q

Pre- hepatic?

A

Excess red cell breakdown overwhelms liver

More unconjugated

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3
Q

Hepatocellular/ hepatic jaundice?

A

Liver cells injured/ dead
Liver loses conjugating ability
Can be mixed conjugated and unconjugated

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4
Q

Post- hepatic jaundice?

A

Obstruction biliary drainage
Bile cannot escape into bowel
Still conjugated in the liver

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5
Q

Normal urine + normal stool but jaundice?

A

Pre- hepatic cause

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6
Q

Dark urine + pale stools?

A

Post hepatic cause

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7
Q

Gilbert’s syndrome?

A

Mild disorder of bilirubin processing in liver
Mutation decreases activity of liver enzyme that processes bilirubin
Increased unconjugated bilirubin in blood with normal LFT’s

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8
Q

Haemolytic anaemia?

A

Abnormal breakdown of RBC’s
Fatigue, SOB
Jaundice

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9
Q

Acute hepatocellular jaundice?

A

Posioning e.g. paracetamol
Infection e.g. Hep A, B
Liver ischaemia

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10
Q

Chronic hepatocellular jaundice?

A 
AFLD
NASH
Cirrhosis
Chronic infection (Hep B, C)
PBC
Pregnancy
AI hep
PSC< haemochromatosis, Wilsons
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11
Q

Obstructive jaundice?

A

Gallstones
Strictures
Tumours
Congenital biliary atresia

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12
Q

How does liver injury occur?

A

Hepatic stellate cells in space of Disse usually in quiescent state are activated by injury and cause fibrosis

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13
Q

NAFLD?

A

Non alcoholic fatty liver disease

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14
Q

NAFL ?

A

Steatosis - no inflammation or fibrosis

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15
Q

NASH?

A

Non- alcoholic steatohepatitis

- Steatosis & inflammation and scarring

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16
Q

Pathway from steatosis to cirrhosis?

A

Steatosis –> Steatohepatitis –> steatohepatitis with fibrosis –> cirrhosis

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17
Q

2 hit pathogenesis of liver disease?

A

1st = excess lipid accumulation in liver
2nd = Oxidative stress and lipid peroxidation
Pro- inflammatory cytokine release, lipopolysaccharide, ischaemia

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18
Q

NAFLD?

A 
4 stages:
1 - Simple fatty liver (steatosis) (most common)
2 - NASH
3 - Fibrosis
4 - Cirrhosis
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19
Q

Clinical features/ history of NAFLD?

A 
Asymptomatic
Fatigue
RUQ pain
Alcohol, drugs, sexual activity
Obesity 
Slightly deranged LFT's 
Diabetes
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20
Q

Diagnosis of NAFLD?

A

Usually incidentally
Suspect if abnormal USS or LFT derangement > 3 months
Usually diagnosed by ultrasound
Biopsy for staging
Signs of advanced liver disease? - jaundice, ascites, spiders

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21
Q

Ultrasound finding for NAFLD?

A

Steatosis in absence of injurious causes e.g. alcohol

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22
Q

Risk factors for NAFLD?

A

Obesity
Hypertension
Type 2 diabetes
Hyperlipidaemia

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23
Q

Treatment of NAFLD?

A

Weight loss, exercise
Nutrition
Vitamin E
Liver transplantation

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24
Q

NASH diagnosis?

A

Liver biopsy:

  • Mallory bodies
  • Ballooning
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25
Q

Risks of NASH?

A

Can progress to cirrhosis

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26
Q

Treatment of NASH?

A

Weight loss, exercise

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27
Q

Alcoholic liver disease?

A

Result of chronic, heavy alcohol consumption

Inc release of fatty acids and TAGs in hepatocytes

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28
Q

What is responsible for damage in ALD?

A

Acetaldehyde (ethanal)

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29
Q

Microscopic appearance of fatty liver?

A

Fat vacuoles in hepatocyes

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30
Q

Microscopic appearance of alcoholic hepatitis?

A

Hepatocytes necrosis
Neutrophils
Mallory bodies
Fibrosis

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31
Q

Microscopic appearance of alcoholic fibrosis?

A

Collagen laid down around cells

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32
Q

Microscopic appearance of alcoholic cirrhosis?

A

Micro- nodular

Bands of fibrosis separating regenerating nodules

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33
Q

Alcoholic fatty liver disease history/ clinical features?

A 
Fatigue
RUQ pain 
Alcohol, drugs, sexual activity
Obesity
Clear history if excess alcohol
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34
Q

Diagnosis of AFLD?

A

May be asymptomatic
LFTs
Liver screen - rule out other causes
USS/ fibro scan, MRI, CT

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35
Q

Treatment of AFLD?

A

NO ALCOHOL
Corticosteroids may be used in acute inflammation
Benzodiazepenes (acute withdrawal)
Transplant (6-12 months abstinence)

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36
Q

Complications of AFLD?

A 
Many e.g.
Acute liver failure
Cirrhosis
Hepatocellular carcinoma
Oesophageal varices
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37
Q

Cirrhosis?

A

Final common end point of liver disease
Irreversible
Bands of fibrosis separating regenerative nodules of hepatocytes

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38
Q

Common causes of cirrhosis?

A 
Alcohol
NAFLD
Hep C
PBC
AI Hepatitis
Hep B
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39
Q

Chronic liver disease?

A

> 6 months

Can lead to cirrhosis

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40
Q

Signs and symptoms of cirrhosis? - Liver dysfunction

A 
Spider nevi
Palmar erythema
Gynecomastia
Ascites
Shrunk, large liver
Jaundice
Itching
Acute kidney injury
Abnormal bruising
Hypogonadism
Encephalopathy etc
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41
Q

Signs and symptoms of cirrhosis? - Portal hypertension

A

Splenomegaly
Oesophageal varices
Caput medusa
Anorectal varices

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42
Q

Cirrhosis history?

A
  • Chronic alcohol abuse
  • NAFLD
  • Chronic infection
  • AI, inherited disorders
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43
Q

Cirrhosis diagnosis?

A

Liver biopsy - regenerating nodules of hepatocytes, fibrosis/ connective tissue between nodules
Liver screen
LFTs
USS (elastography)

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44
Q

How does fibrosis lead to portal hypertension?

A

Fibrosis leads to destruction of other structures within liver (sinusoids, space of Disse, vascular structures) –> leads to inc resistance and inc portal pressure

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45
Q

Compensated cirrhosis?

A

Asymptomatic stage
LFTs show damage
Some back pressure may be visible
Palmar erythema, clubbing, gynecomastia, hepato/ splenomegaly

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46
Q

Decompensated cirrhosis?

A 
Symptomatic - 
Ascites
Jaundice
Variceal haemorrhage 
Easy bruising
Hepatic encephalopathy
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47
Q

Grading cirrhosis?

A

CHILD PUGH score

MELD

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48
Q

Cirrhosis management?

A

Cannot be reversed - stop progression and complications

Healthy diet, no alcohol

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49
Q

Symptom management cirrhosis - ascites?

A

Diuretics - spironolactone 1st line, furosemide

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50
Q

Symptom management cirrhosis - itch?

A

Bile salt resins e.g. cholestyramine

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51
Q

Symptom management cirrhosis ?

A

Caution with meds e.g. paracetamol
Treat cause to prevent progression
Transplantation

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52
Q

Liver transplant?

A 
Event based (ascites, varies)
Liver funciton based
UKELD score (49 = min)
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53
Q

Portal hypertension?

A

Portal hepatic pressure gradient >5
Inc in hydrostatic pressure within portal vein or tributaries
Results from inc resistance to portal flow and inc portal Venous inflow

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54
Q

What is portal vein made from?

A

Superior mesenteric vein
Splenic vein
Gastric vein
Part from inferior mesenteric veins

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55
Q

Portal blood supply?

A

Carries deoxygenated blood from gut to liver

Drains blood from organs, back through liver for processing

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56
Q

Hepatic blood flow?

A

Twin/ dual blood supply
O2 blood from hepatic artery (circulation)
Nutrient rich, deox blood from hepatic portal vein

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57
Q

Pathway of hepatic blood flow?

A

O2 blood from hepatic artery and deox, nutrient blood from hepatic portal vein –> liver sinusoids –> central vein –> IVC –> RA of heart

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58
Q

What happens to blood supply in portal hypertension?

A

Anastomosis in portal venous system (w/ systemic blood supply) become enlarged, dilated, varicosed & rupture

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59
Q

Effect on blood pathway in portal hypertension?

A

Inc pressure in portal vein –> inc pressure in portal circulation –> inc pressure in systemic circulation –> blood flows at inc volume down anastomosis –> dilate –> rupture

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60
Q

Pre- hepatic causes of portal hypertension?

A

Blockage of portal vein before the liver

Due to - portal vein thrombosis, occlusion secondary to congenital portal vein abnormalities

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61
Q

Intra- hepatic causes of portal hypertension?

A

Due to distortion of liver architecture

  • Pre- sinusoidal (schistomasis)
  • Post sinusoidal (cirrhosis)
  • Budd chair syndrome, veno- occlusive disease
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62
Q

Budd chairi syndrome?

A

Occlusion of hepatic veins which drain the liver

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63
Q

Budd chairi syndrome clinical features?

A 
Assoc. w/ pregnancy
Sudden RUQ pain
Rapid ascites
Hepatomegaly
Jaundice
Acute kidney injury +/- fulminant liver failure
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64
Q

Diagnosis of Budd Chairi?

A 
LFTs - mild elevation
Urea and creatine - renal impairment?
Coagulation profile
USS, CT, MRI
venography
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65
Q

Definitive management of Budd Chairi?

A

Liver transplant

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66
Q

Veno- occlusive disease?

A

Small veins in liver are obstructed

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67
Q

Clinical presentation of Veno- occlusive disease?

A

RUQ pain
Painful hepatomegaly
Ascites
Abnormal LFT’s

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68
Q

Diagnosis of Veno- occlusive disease?

A

Anyone who has undergone HCT then develops liver dysfunction

Clinical ground - Modified Seattle Criteria

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69
Q

Pharmacological treatment of BCS and VOD?

A

Correct underlying disorder
Anticoagulation - enoxaparin and SC warfarin
Thrombophilia
Symptoms control - furosemide

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70
Q

Surgical treatment of BCS and VOD?

A

VOD - prevention, pharmacologic prophylaxis w/ ursodeoxycholic acid or low dose heparin
Supportive care
- Radiologic intervention (UVC balloon, hepatic angioplasty, TIPS),surgical shunting, liver transplant

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71
Q

Acites?

A
  • Pathological accumulation of fluid in peritoneal cavity
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72
Q

How do ascites occur?

A

Cirrhosis causes portosystemic shunting –> inc hydrostatic pressure in splanchnic vessels –> release of vasodilators (NO mediated) –> vasodilation causes dec blood volume (baroreceptors) –> RAAS, sympathetic system and ADH –> sodium and water retention

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73
Q

Spontaneous bacterial peritonitis?

A

Neutrophil >250 cells/mm3
Bacterial infection in peritoneum, no obvious source
Diagnostic paracentesis tap promptly as acute management & check cell count
E. coli - most common cause
Broad spectrum antibiotic

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74
Q

Diagnosis of ascites?

A

Shifting dullness
USS
Diagnostic tap for pts with undetermined cause of ascites

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75
Q

Treatment for ascites?

A 
SPIRONOLACTONE 1st line
Treat underlying disease
Infection?
Furosemide
No NSAIDS
Paracentesis
TIPPS if long term recurrent
Transplant
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76
Q

Hepatorenal syndrome?

A

Result of cirrhosis/ portal hypertension
Kidney failure in those with severe liver damage
Look for altered liver function, abnormalities in circulation and kidney failure
Treat - transplant, TIPPS

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77
Q

Mechanism for hepatorenal syndrome?

A

Portal hypertension –> splanchnic vasodilation –> decreased effective circulatory volume –> activation of RAAS –> renal vasoconstriction –> hepatorenal syndrome

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78
Q

Hepatic encephalopathy?

A

Decline in brain function due to severe liver disease

Liver failure causes hyperammonaemia - toxic to CNS

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79
Q

Symptoms of Hepatic encephalopathy?

A 
LIVER FLAP
Confusion
Non- coordination, shaking
Drowsiness, coma
Slurred speech
Seizures
Cerebral oedema
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80
Q

Treatment of Hepatic encephalopathy?

A

Lactulose - decreases colonic pH, prevents absorption of NH3, NH3 can be converted to NH4 and excreted
Antibiotics - neomycin, rifaxamin (suppress colonic flora, inhibits ammonia)

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81
Q

Causes of Hepatic encephalopathy?

A

Drugs, infection renal, GI bleed, electrolyte disturbances

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82
Q

Acute liver failure?

A

Any insult to liver causing damage in previously normal liver
< 6 months duration
Causing encephalopathy & impaired protein synthesis

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83
Q

Clinical features of acute liver failure?

A 
None
Jaundie
Lethargy, arthralgia
N&amp;V, anorexia
RUQ pain
Itch
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84
Q

Diagnosis of acute liver failure?

A
  • Physical exam (jaundice, ascites).
  • History
  • Infections, alcohol, pregnancy.
  • Mental changes, coagulopathy.
  • Abnormal LFTs.
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85
Q

Investigations for acute liver failure?

A 
Alcohol? Drugs, paracetamol?
Possible toxins
LFTs
Virology
Investigations for chronic liver disease
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86
Q

Treatment of acute liver failure?

A 
Rest - 3-6 months recovery
Fluids
No alcohol
Inc calorie intake
Regular observation
Monitor and supplement
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87
Q

How can NSAIDs damage the liver?

A

Decrease renal PGE synthesis
Worsens renal impairment by increasing renal vasoconstriction and sodium retention
Increase risk of hepatorenal syndrome

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88
Q

How can diuretics damage the liver?

A

o Furosemide – Decreases intravascular volume – hypokalaemia, hepatorenal syndrome.
o Thiazide – Same as furosemide.
o Spironolactone. Combats secondary aldosteronism.

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89
Q

Oesophageal varices?

A

Abnormally swollen veins in oesophagus
Formed when blood flow in liver is compromised
Band ligation during acute bleeding
BB for prophylaxis

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90
Q

Hepatitis A?

A

Faecal oral spread
Most common viral hep worldwide
Poor hygiene, overcrowding
No chronic state, only acute

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91
Q

Clusters in which Hep A is prevalent?

A

Gay men

PWID

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92
Q

Clinical features of hepatitis A?

A

Acute hepatitis
Older children, young adults
Unwell with no specific symptoms - nauseam anorexia, headache, myalgia arthralgia

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93
Q

Jaundice in Hep A?

A

Pts may recover and not become jaundice (lifetime immunity/ aninteric infection)
After 1-2 weeks some become jaundice (most infectious just before jaundice)

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94
Q

Lab marker on Hep A?

A

Acute infection - Hep A IgM (HAV IgM) (acute infection)

IgG HAV - present in those who have been vaccinated

LFTs - serum bilirubin reflects jaundice, serum AST and ALT rise before onset of jaundice

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95
Q

Management?

A

Stop alcohol consumption
Supportive treatment
Vaccine
Hygiene

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96
Q

Hep E?

A 
Similar to HEP A
Tropical countries
Faecal oral 
- Pigs 
- Contaminated water
Acute infection will only progress to chronic in some immunocompromised
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97
Q

Clinical presentation of Hep E?

A 
Almost identical to Hep A
Nausea and anorexia
Jaundice 
Vomiting
Altered mental state
Enlarged liver, splenomegaly
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98
Q

Investigations for Hep E?

A

Hep E Viral RNA (HEV RNA) - detected by PCR in stool or serum

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99
Q

Management of HEP E?

A

Stop alcohol

Supportive treatment

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100
Q

Hep B transmission ?

A

3 B’s
Bone (sex)
Blood
Baby (mother to child)

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101
Q

When is chronic Hep B infection more likely to result?

A

If first exposure is in childhood

102
Q

Clinical features of Hep B?

A 
May be asymptomatic
V similar to Hep A
Illness more severe
Itchy rashes
Arthritis
Fever
Diarrhoea, abdo pain
103
Q

Hep B surface antigen (HBsAg)

A

In all infectious individuals

- If > 6 months = chronic

104
Q

Hep B e antigen (HBeAg)?

A

Present in highly infectious individuals
Also indicates acute infection
Continues infectious state
Allows for replication of virus in blood

105
Q

Hep B virus DNA (HBV DNA)?

A

Present in highly infectious individuals

Also used to measure response to anti-viral therapy

106
Q

Hep B IgM?

A

Recently infected cases

107
Q

Anti Hbs?

A

Present in immunity (vaccine, previous infection)

108
Q

Hep B c IgM titre levels?

A

High titre - acute/ recent infection

Low titre - Chronic infection

109
Q

Hep B IgG?

A

Past exposure to Hep B (vaccine)

HBsAg will be negative

110
Q

Anti HBs?

A

Hep B surface antibody (HbsAb) - recovery/ immunity to HBV

Successful vaccination

111
Q

Best indication of Hep B prognosis?

A

HBV DNA

112
Q

Control of Hep B?

A

Minimise exposure
Pre- exposure vaccines (children, older children and adults)
Post exposure prophylaxis - vaccine and plus HBIG

113
Q

Prognosis?

A

Self resolving most of the time
Full recovery
Or chronic infection

114
Q

Management of HBV?

A

If symptomatic
Constant HBV marker monitoring
Antivirals (only suppress, don’t cure)
Antecavir, tenofavir, in v ill

115
Q

Hep D?

A

Only found with HBV
Unable to replicate on it own - activated by HBV
Parasite of a parasite
Exacerbates HBV infection

116
Q

Hep C?

A

Chronic infections more common

Transmission - blood, sex and mother to child (BBB)

117
Q

Clinical features of Hep C?

A

Acute - asymptomatic, mild flu- like, jaundice, raised amino transferases

Chronic - more common

118
Q

Investigations for HCV?

A

Initially test for antibody (anti- HCV)
If positive - either past infection or active

Test for HCV RNA by PCR - determines if active or past

119
Q

HCV RNA?

A

Tests usually positive 1-8 weeks after infection
Current active infection
Dec –> recovering
Levels stay same –> chronic?

120
Q

Management of Hep C?

A

Continually monitor HCV- RNA
If viral load falls - treatment may not be req
Spontaneous clearing
If not - anti- viral therapy during acute phase

121
Q

General treatment of acute Hepatitis infection?

A 
If symptomatic
No antivirals
Monitor for encephalopathy
Monitor for resolution 
Notify public health
immunisation of contacts
122
Q

Chronic hepatitis?

A

Caused by HBV and HCV

123
Q

When to treat chronic HBV infection?

A

Raised ALT and high HBV DNA

124
Q

When to treat chronic HCV infection?

A

Always straight away

Patients with advanced fibrosis and cirrhosis first

125
Q

Therapy for chronic HBV?

A

Suppressive anti viral drug
- E.g. entecavir, tenofavir

Peginterferon alone

126
Q

Chronic HVC therapy?

A

Aim for undetectable HCV RNA 12 weeks after treatment completion

Direct antivirals - sofosbuvir, ledipasvir

Reg screen for hepatocellular carcinoma

No alcohol

127
Q

Autoimmune hepatits?

A

Females > males
T cells directed against hepatocyte surface antigens
Type 1 & 2

128
Q

Type 1 Ai hepatitis?

A

Age 10-20, 45-70

Teen girls, young women

129
Q

Type 2 AI hepatitis?

A

Young kids/ adults

130
Q

Young female with deranged LFT’s taking oral contraceptive?

A

Think AI hepatitis

131
Q

Clinical features of AI hepatitis?

A

Hepatomegaly
Jaundice
Signs of chronic liver disease
May present similarly to acute onset hepatitis

132
Q

Investigations for AI hepatitis?

A

Antibodies
Raised LFTs?
Raised IgG
Liver biopsy to confirm severity

133
Q

Antibodies for type 1 AI hepatitis?

A

ASMA and ANA positive

134
Q

Antibodies for type 2 AI hepatitis?

A

LKM positive

ASMA and ANA negative

135
Q

Management of AI hepatitis?

A

Corticosteroids and azathioprine

Eventual liver transplant

136
Q

Benign focal lesions of the liver?

A

Haemangioma
Focal nodular hyperplasia
Adenoma
Liver cysts

137
Q

Malignant lesions of liver?

A

Primary liver cancers (hepatocellular carcinoma, cholangiocarcinoma)
Metastases

138
Q

Haemangioma?

A 
Most common liver tumour
Female > male
Hypervascular tumour
Well demarcated capsule
Asymptomatic
139
Q

Diagnosis of haemangioma?

A
  • USS: echogenic spot, well demarcated
  • CT: venous enhancement from periphery to center
  • MRI: high intensity area
140
Q

Treatment for haemangioma?

A

No treatment

141
Q

Focal nodular hyperplasia ?

A

Benign
Central scar containing large artery, radiating branches to periphery
Middle aged women
ASympto, some pain

142
Q

Diagnosis of FNH?

A
  • US: Nodule with varying echogenicity
  • CT: Hypervascular mass with central scar
  • MRI: Iso or hypo intense
  • FNA: Normal hepatocytes and Kupffer cells with central core
143
Q

Treatment of FNH?

A

None

144
Q

Features of FNH?

A 
Hypervascular
Contains all liver ultrastructure (RES and bile ductules)
Pain
Central scar
No malignant risk
145
Q

Hepatic adenoma?

A

Benign neoplasm composed of normal hepatocytes no portal tract, central veins or bile ducts
Right lobe&raquo_space;
Females
Contraceptive hormones, anabolic steroids

146
Q

Symptoms of hepatic adenoma?

A

Incidental finding
Asymptomatic
RUQ pain, bleeding

147
Q

Diagnosis of hepatic adenoma?

A
  • US: Filling defect
  • CT: Diffuse arterial enhancement
  • MRI: Hypo or hyper intense lesion
  • FNA: May be needed
148
Q

Treatment of hepatic adenoma?

A

Stop taking oral contraceptive, hormones, steroids
Weight loss
Males = surgical excision (as malignant transformation risk higher)
Females = (<5cm or reducing, annual MRI)
(>5cm, surgical excision)

149
Q

Cystic lesions in liver?

A 
Simple
Hyatid
Atypical
Polycystic
Pyogenic or amoebic abscess
150
Q

Simple cyst?

A

Liquid collection lined by epithelium

151
Q

Symptoms of simple cyst?

A

Most asymptomatic but may include:

  • RUQ pain
  • Fever
152
Q

Investigations for simple cyst?

A

USS - 1st line

Follow up imaging in 3-6 months if in doubt

153
Q

Treatment of simple cyst?

A

None

If symptomatic/ uncertain diagnosis - surgical intervention may be req

154
Q

Hyatid cyst?

A

Caused by tapeworm echinococcus granulosus
Live stock
Farming communities
Cysts can erode into adjacent structures

155
Q

Clinical features of hyatid cysts?

A

Often asymptomatic

May cause dull ache and swelling in right hypochondrium

156
Q

Investigations for heated cysts?

A

Serology (check for anti- echinococcus antibodies)
AXR - cyst calcification
US/ CT - cysts and daughter cysts = diagnostic sign

157
Q

Management of hyatid cysts?

A 
Surgery
- Conservative (open cystectomy, marsupialization)
- Radical (peri-cystectomy, lobectomy)
Medical - Albendazole anti worm meds
Percutaneous drainage (PAIR)
158
Q

Polycystic liver disease?

A

Numerous cysts throughout liver parenchyma

3 types - VMC, polycystic liver disease, autosomal dominant polycystic kidney disease

159
Q

Von Meyenburg complexes (VMC)?

A

Benign cystic nodules throughout the liver

Incidental finding

160
Q

Polycystic liver disease (PCLD)?

A

o Liver function preserved and kidneys functioning normally
o Symptoms depend on size of cysts – may cause RUQ pain and distension
o PCLD gene – PRKSCH and SEC63

161
Q

Autosomal dominant polycystic kidney disease

A

o Renal failure due to polycystic kidneys and non- renal extra- hepatic features common
Massive hepatic enlargement
o Marked reduction in kidney function but liver function should be preserved
o ADPKD genes – PDK1 and PDK2

162
Q

Clinical features of polycystic liver disease?

A
  • Abdominal pain
  • Abdominal distension
  • Atypical symptoms
  • Signs of liver failure
163
Q

Investigations of polycystic liver disease?

A
  • Gene studies
  • Polycystic disease shown clearly on CT
  • Kidney function tests
164
Q

Management of polycystic liver disease?

A 
-	Conservative treatment 
o	Halt cyst growth
o	Allow abdo decompression
o	Ameliorate symptoms
-	Surgical procedures if advanced PCLD, ADPKD, liver failure:
o	Aspiration/ defenestration
o	Liver transplantation 
-	Pharmacologic therapy:
o	Somatostatin analogues (sandostatin) 
- Symptomatic relief
- Reduce liver volume
165
Q

Liver abscess?

A

Pus filled mass in the liver

Can be pyogenic (pus forming) or caused by protozoa

166
Q

Clinical features of liver abscess?

A
  • High fever
  • Leukocytosis
  • Abdominal pain
  • Complex liver lesion
  • Nausea and vomiting
  • Jaundice:
    o If so may be pleural rub in right lower chest
  • Malaise lasting several months
167
Q

History for liver abscess?

A
  • Abdominal or biliary infection

- Dental procedure

168
Q

Investigations for liver abscess?

A
  • Check for leucocytosis
  • CXR may show a raised right hemi-diaphragm
  • US – detects an abscess
  • CT – more useful in complex and multiple lesions
  • Echocardiogram
169
Q

Management for liver abscess?

A

Broad spectrum antibiotics (amoxicillin, metronidazole gentamicin) IV

ASpiration/ drainage percutaneously

Echocardiogram

Operation - open drainage, resection

4 weeks repeat antiB, repeat imaging

170
Q

Primary tumours in liver?

A

Rare

171
Q

Secondary tumours in liver?

A

More common than primary

172
Q

Hepatocellular carcinoma?

A

Most common primary cancer
Men»
Malignant

173
Q

Risk factors for hepatocellular carcinoma?

A

Cirrhosis
Carriers of HBV, HCV
Male

174
Q

Clinical features of hepatocellular carcinoma?

A
  • Weight loss and RUQ pain (most common)
  • Malaise, fever, anorexia
  • Asymptomatic
  • Worsening of pre- existing chronic liver disease
  • Acute liver failure
  • Known liver cirrhosis + rapid symptoms
175
Q

Examination for hepatocellular carcinoma?

A
  • Signs of cirrhosis
  • Hard enlarged RUQ mass
  • Liver bruit (rare)
176
Q

Investigations for hepatocellular carcinoma?

A

Serum alpha- fetoprotein (AFP) - may be raised (HCC tumour marker)

USS - filling defects

CT - HCC

MRI - if smaller than 1cm

177
Q

Treatment of hepatocellular carcinoma?

A 
1 - Resection (if possible)
2 – Liver transplantation
3 – Local ablation if assoc. disease means liver transplant not possible, temp measure
4 – TACE (early cirrhosis)
5 – Systemic therapies - 
sorafenib
178
Q

Fibrolamellar carcinoma?

A 
Young
Not related to cirrhosis
AFP = normal
CT - stellate scar with radial septa
Surgical resection or transplantation
TACE if unresectable
179
Q

Secondary liver mets?

A

Most common site for blood Bourne mets
Colon, breast, lung, stomach, pancreas, melanoma
Mild cholestatic picture
Imaging or FNA

180
Q

Haemochromatosis?

A

Inherited disease characterised by excess iron deposition in liver
Defect in iron absorption and metabolism
Autosomal recessive

181
Q

Common inherited gene for Haemochromatosis?

A

HFE gene on chromosome 6

182
Q

Clinical features of Haemochromatosis?

A

Early - lethargy, arthralgia
Classic triad = bronze skin, hepatomegaly, diabetes mellitus
Cardiac arrhythmias, HF
Liver fibrosis, failure, cirrhosis

183
Q

Investigations for haemochromatosis?

A

Serum iron >30
LFT’s - normal
1st degree fam - screened

184
Q

Management of haemochromatosis?

A

Avoid iron rich foods
Venesections (2x weekly until adequate iron removed)
Desferrioxamine (iron chelation therapy)

185
Q

Wilson’s disease?

A

Autosomal recessive disorder leading to reduced ceruloplasmin (copper transporter) –> copper accumulates in liver and brain

186
Q

Gene defect in Wilson’s disease?

A

ATP78 gene defect on chromosome 13

187
Q

Symptoms of Wilson’s disease?

A

Kayser Fleischer rings
Signs of liver disease
CNS signs - tremor, involuntary movements
(Vomiting, weakness, abdominal fluid, leg swelling, yellowish skin and itchiness)

188
Q

Investigations for Wilson’s disease?

A

LFTs
Ceruloplasmin (reduced)
Serum copper - reduced

189
Q

Management of Wilson’s disease?

A

Penicillamine

190
Q

Alpha- 1 antitrypsin deficiency?

A

Autosomal recessive

AAT = mainly produced by liver

191
Q

Signs and symptoms of AAT deficiency?

A

o Lung – emphysema

o Liver – cirrhosis and HCC

192
Q

Investigations for AAT deficiency?

A

Alpha-1 antitrypsin levels = low

Spirometry = obstructive

193
Q

Management of AAT deficiency?

A

Never smoke, drink
COPD treatment if lung involved
AAT deficiency augmentation therapy
Organ transplan

194
Q

Fulminant hepatic failure?

A

Jaundice and encephalopathy in someone with previously normal liver

195
Q

Causes of FHF?

A

Drug overdose

Viral

196
Q

Management of paracetamol overdose?

A

o Acetylcysteine
o <8 hours can add activated charcoal
o Anti- emetic (odansetron)
o Liver transplant

197
Q

Bile?

A

When chyme enters duodenum –> CCK stimulates gallbladder to contract and release bile
Bile is secreted via sphincter of ODDI at D2

198
Q

Types of gallstnes?

A

Cholesterol (usually)
Pigmented black stones (too much bilirubin in bile)
Brown stones (parasitic infection)

199
Q

Cholelithiasis ?

A

Gallstones

200
Q

Cholecystolithiasis ?

A

gallstone in gallbladder

201
Q

Choledocholithiasis ?

A

Gallstones in bile duct

202
Q

Uncomplicated gallstones - clinical features?

A 
Colicky pain --> back and shoulder
Worse after eating fatty meal
Nausea &amp; vomiting
Itch
Dark urine, pale stool and/ or jaundice
203
Q

Investigations for uncomplicated gallstones?

A

LFTs - raised ALP and GGT
USS
MRCP

204
Q

Management of uncomplicated gallstones?

A

Supportive
Ursodoxycholic acid for itch
ERCP

205
Q

Biliary colic?

A

Temporary obstruction of cystic/ common bile duct by a gallstone
2-6 hours (crescendo of pain then plateaus)
Pain caused by contraction around stone

206
Q

Signs and symptoms of biliary colic?

A

RUQ/ epigastric colicky pain (sharp, localized GI pain) - may radiate to right shoulder
Assoc. w/ indigestion and high fat foods
Mid-evening, early morning, lying flat
Nausea and vom

207
Q

Investigations for biliary colic?

A

Clinical diagnosis

USS

208
Q

Management of biliary colic?

A

Lifestyle modifications
Paracetamol, NSAIDs
Diclofenac IM (severe pain)
Stone will either pass in faeces orgs back into GB

209
Q

Gallstone ileus?

A

Form of bowel obstruction caused by gallstones lumen of small bowel
Large stone
Thinning of GB wall
Fistulas form

210
Q

Signs, symptoms of gallstone ileus?

A

Abdo distension
N&V
Recurrent RUQ pain (due to chronic cholecystitis)
Dehydration

211
Q

Investigations for gallstone ileus?

A
  • Rigler’s triad (via radiography)
    o Pneumobilia (air in biliary tree)
    o Evidence of small bowel obstruction
    o Evidence of gallstone outside gallbladder
212
Q

Management of gallstone ileus?

A

IV fluid resuscitation
NG tube
Gallstone removal

213
Q

Cholangitis?

A

Cholangitis means inflammation of bile duct system

214
Q

Ascending cholangitis

A

Inflammation of bile duct due to bacterial infection on obstruction of biliary tree

215
Q

Clinical features of Ascending cholangitis?

A
  • Charcot’s triad:
    o Fever, jaundice, RUQ pain
  • Reynold’s pentad:
    o Fever, jaundice, RUQ pain, hypotension, confusion
216
Q

Causes of ascending cholangitis?

A 
Anything causing blockage
Gallstones
Iatrogenic in surgery
chronic pancreatitis
Malignancy
217
Q

Investigations for ascending cholangitis?

A
  • ERCP - gold standard
  • Bloods - raised WCC, raised CRP
  • LFTs - raised ALP, bilirubin, GGT (consistent with obstruction)
  • Blood culture
  • USS
  • MRCP
218
Q

Management of ascending cholangitis?

A
  • IV Abx amoxicillin, metronidazole and gentamicin (Vancomycin, metronidazole and gentamicin if penicillin allergic)
  • |Step down to oral Co-trimoxazole and metronidazole
219
Q

Complications of ascending cholangitis ?

A

Sepsis

220
Q

Cholecystitis?

A

Inflammation of gallbladder

221
Q

Clinical features of cholecystitis?

A
  • RUQ pain spreading to back/ shoulder
  • RUQ tenderness
  • Fever
  • Nausea and vomiting
    • Murphy’s sign
  • Obstructive jaundice
222
Q

Murphys sign?

A

Take in and hold deep breath while palpating right subcostal area
If pain occurs on inspiration - inflamed gallbladder comes into contact with hand = positive

223
Q

Causes of cholecystitis?

A
  • Anything causing a blockage
  • Gallstones
  • PSC
  • Iatrogenic during surgery
  • Malignancy
224
Q

Investigations for cholecystitis?

A 
History
High ALP
Abdo USS - stones, thickened GB wall?
MRCP
ERCP
225
Q

Management of cholecystitis (GB inflammation)?

A

Symptoms <72 hours - cholecystectomy (GB removal)
>72 hours - medical management, follow up for cholecystectomy

& days oral Ab - amici, metronidazole, gentamicin

226
Q

Complications of cholecystitis?

A

perforation
Fistula
Peritonitis
Sepsis

227
Q

Acalculous cholecystitis?

A

Inflammation of GB in absence of gallstone

228
Q

signs and symptoms of acalculous cholecystitis?

A

Same as calculous

229
Q

Investigations for acalculous cholecystitis?

A

Raised ALP
High CRP
USS - thickened GB wall, no stones

230
Q

Management of calculous cholecystitis ?

A 
Cholecystectomy
Percuataneous cholecystostomy (stoma in GB)
231
Q

Primary biliary cholangitis/ cirrhosis?

A

Autoimmune condition - T cells attack small bile ducts in liver causing bile to leak into interstitium –> chronic inflammation of bile ducts

232
Q

Clinical features of PBC?

A 
Middle aged women, 45- 60
Asymptomatic
Symptoms:
- Fatigue
- Itch, no rash
- Jaundice
- Joint pain
- Xanthelasma and xanthoma
- Abdo pain
233
Q

Associated doseases with PBC?

A

Sjogren’s
rheumatoid arthritis
Hypothyroidism

234
Q

Investigations for PBC?

A

2/3:

  • Positive AMA (anti- mitochondiral antibody)
  • Cholestatic LFTs (raised ALP, GGT)
  • Liver biopsy

(USS< MRCP, high IgM, cholesterol High)

235
Q

Treatment for PBC?

A

First line = urseodoxycholic acid

2nd = obeticholic acid

236
Q

Primary sclerosing cholangitis?

A

Long term progressive disease of liver and gallbladder - inflammation and scarring of bile ducts (normally allow bile to drain into GB)

237
Q

Cholestasis?

A

decrease in bile flow

238
Q

Clinical features of PSC?

A 
Male
Asymptomatic
History of UC
Abdo - RUQ pain
Itch
Fatigue
Jaundice
Weight loss
Acute presentation of hepatitis- like infection - fever, jaundice, cholangitis
239
Q

Investigations for PSC?

A 
Examination - jaundice, weight loss?
Lots - raised ALP and GGT
USS
MRCP - standard for diagnosis (beaded appearance)
ERCP - biopsy, onion skin
May have ANCA bodies
240
Q

Management of PSC (if symptomatic)?

A

Liver transplant
Manage symptoms
good diet
Endoscopic interventions - ERCP for balloon dilation or stent placement

241
Q

Biliary strictures?

A

Narrowing of bile duct

242
Q

Congenital biliary atresia?

A

Condition babies born with –> absence or deficiency of extra- hepatic biliary tree
Leads to cholestasis and eventual liver cirrhosis from back pressure of bile

243
Q

Symptoms of congenital biliary atresia?

A

3 months of birth

  • Jaundice
  • Dark urine, pale stools
  • Growth delay
244
Q

Investigations for congenital

A

Blood tests - LFTs, bilirubin
USS - fibrous tissue, change to hepatic blood flow
HIDA scan

245
Q

Management for congenital biliary atresia?

A

Excision of fibrous tissue

Liver transplant

246
Q

Cholangiocarcinoma?

A

Cancer of bile duct

Intrahepatic (less) or extra hepatic

247
Q

Most common form of cholangiocarcinoma?

A

Hilar cholangiocarcinoma

248
Q

Risk factors for cholangiocarcinoma?

A

Age (>65)
SE Asia
Prev biliary disease e.g. PSC, gs, cysts
Genetic predisposition

249
Q

Symptoms of cholangiocarcinoma?

A 
Asymptomatic
Jaundice (dark urine, pale stools)
Abdo pain
Weight loss, fatigue, loss of appetite
Symptoms of cholangitis - Charcot's triad and Reynolds pentad
RUQ pain, jaundice, fever
250
Q

Investigations for cholangiocarcinoma?

A

LFTs - abnormal bilirubin, marked elevation of ALP and GGT

Contrast MRI!!!
CT for staging

251
Q

Management of cholangiocarcinoma?

A

Surgical resection
Stenting
Adjuvant chemotherapy and radiotherapy

252
Q

carcinoma of ampulla of vater?

A

Rare cancer - forms at junction of CBD and main pancreatic duct
Extensive surgery

GI (9 decks)

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