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Liver > Liver symposium > Flashcards

Liver symposium Flashcards

1
Q

What does the liver do?

A

Protein synthesis
e.g. albumin, clotting factors
Glucose and fat metabolism
Detoxification and excretion: drugs, hormones, ammonia, billirubin
Defence against infection: reticuloendothelial system
Storage organs for fat in body

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2
Q

Bile

A

compound needed to digest fat and absorb vitamins A, D, E, K

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3
Q

Kuppfer Cells:

A

macrophages that reside in sinusoids in proximity to ECs.Theyserve a physiological function to remove senescentcellsand particulates, including bacteria and their products.

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4
Q

Liver lobules (Look at osmosis)

A

Normal liver is arranged in a regular way (acinar or lobular models).
Blood enters via the portal vein and hepatic artery, which lie together with a small bile duct within the portal tract

Blood flows into a system of sinusoids which bathe the liver cells, arranged in plates, with blood, before exiting via the hepatic vein (central vein).

Liver cells within the lobule can be divided into zones 1 to 3, which receive progressively less oxygenated blood.

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5
Q

Types of liver injury

A

Acute and chronic

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6
Q

Acute liver injury can lead to what?

A

Recovery or Liver failure

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7
Q

Chronic liver injury can cause what?

A

Recovery
Cirrhosis: scarring in liver – can be reversible now – right treatment of underlying condition
Liver failure: varices, hepatoma

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8
Q

What does acute liver injury lead to?

A

Damage and loss of cells
Cell death may occur by necrosis (associated with neutrophils), or apoptosis

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9
Q

Chronic damage leads to what?

A

Fibrosis.

In its severest form this is termed cirrhosis – wide fibrous septa join the portal tracts and central veins, leaving nodules of liver cells to attempt regeneration if the causative insult has been removed.

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10
Q

Causes of acute liver injury:

A

viral (A,B, EBV)
drug
alcohol
Vascular
Obstruction
Congestion

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11
Q

Causes of chronic liver injury:

A

alcohol
viral (B,C)
autoimmune
metabolic (iron, copper)

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12
Q

Typical presentation of acute liver failure:

A

malaise, nausea, anorexia, jaundice

Rarer:
confusion
bleeding
liver pain
hypoglycaemia

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13
Q

Presentation of chronic liver injury:

A

ascites, oedema
haematemesis (varices)
malaise,
anorexia,
wasting
easy bruising, itching
hepatomegaly,
abnormal LFTs
rarer: - jaundice - confusion

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14
Q

Serum liver function tests:

A

Serum bilirubin, albumin, prothrombin time:
Bilirubin low – high is signs of liver failure opposite for albumin
Elevated PT time – progressive chronic liver disease

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15
Q

Serum liver enzymes:

A

cholestatic: alkaline phosphatase, gamma-GT
hepatocellular: transaminases (AST, ALT)

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16
Q

What is Jaundice?

A

Raised serum billirubin

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17
Q

Types of Jaundice:

A

Unconjugated - “pre-hepatic”
- Gilberts, Haemolysis
Conjugated – “cholestatic”
-Liver disease “hepatic”
-Bile duct obstruction “post hepatic”

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18
Q

Jaundice classification:

A

Prehaptic (unconjugated) > Hepatic (conjugated) > Post Hepatic (conjugated)

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19
Q

Hepatitis causes:

A

viral, drugs immune, alcohol
Ischaemia – lack of oxygen in cells
Neoplasm
Congestion (CCF)

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20
Q

Gallstone causes:

A

bile duct, Mirizzi
Stricture: malignant, ischaemic, inflammatory

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21
Q

Pre hepatic jaundice features:

A

URINE: Normal
STOOLS: Normal
ITCHING: No
Liver Tests: Normal

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22
Q

Cholestatic (hepatic or post hepatic) features:

A

URINE: Dark
STOOLS: Pale - no billirubin
ITCHING: Maybe
Liver Tests: Abnormal

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23
Q

Questions to ask for Jaundice?

A

1.Dark urine, pale stools, itching?
2.Symptoms: biliary pain, rigors, abdomen swelling, weight loss?
3.Past history: biliary disease/intervention malignancy heart failure blood products autoimmune disease

  1. Drug history
  2. Social history
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24
Q

What tests need to be done for Jaundice?

A

Liver enzymes: Very high AST/ALT suggests liver disease, some exceptions

Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound

Need further imaging: CT Magnetic resonance cholangioram MRCP Endoscopic retrograde cholangiogram ERCP

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25
Q

Gall stone features:

A

Most form in gallbladder
Very common: 1/3 women over 60
70% Cholesterol, 30% pigment+/- calcium
Risk factors: Female, fat, fertile, forty (liver disease, ileal disease, TPN, clofibrate…)
Most are asymptomatic

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26
Q

Intrahepatic bile duct stones (hepatolithiasis)

A

Containing mainly brown pigment and cholesterol stones

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27
Q

Extrahepatic bile duct stones (choledocholithiasis)

A

Primary stones are mainly brown pigment stones, whereas secondary stones are mainly cholesterol stones

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28
Q

Gall bladder stones (cholecystolithiasis)

A

Containing cholesterol (or black pigment) stones

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29
Q

Gall stones presentation in gallbladder:

A

Bililary pain Yes
Cholecystitis: Yes
Obstructive Jaundice: maybe (Mirizzi)
Cholangitis: No
Pancreatitis: No

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30
Q

Gall stones presentation in bile duct:

A

Bililary pain : Yes
Cholecystitis: No
Obstructive Jaundice: Yes
Cholangitis: Yes
Pancreatitis: Yes

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31
Q

How do you manage gallbladder stones:

A

Laparoscopic cholecystectomy
Bile acid dissolution therapy (<1/3 success)

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32
Q

How do you manage bile duct stones:

A

-ERCP with sphincterotomy and: removal (basket or balloon)
crushing (mechanical, laser..) ‘
stent placement

  • Surgery (large stones)
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33
Q

What can present as gallstones (differential diagnosis)

A

Weight loss
Jaundice
Malignancy

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34
Q

Acute stone obstruction

A

Alk phos usually normal.
Initial ALT often >1000; rapidly falls

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35
Q

Drug-induced liver injury (DILI) incidence

A

About 1/10,000 patients/yr
0.1-3% of hospital admissions
30% of Acute Hepatitis
>65% of Acute Liver Failure
- 50% Paracetamol
- 15% idiosynchratic
Commonest reason for drug withdrawal from formulary

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36
Q

Types of DILI

A

Hepatocellular - ALT >2 ULN, ALT/Alk Phos ≥ 5
Cholestatic - Alk Phos >2 ULN or ratio ≤ 2
Mixed - Ratio > 2 but < 5

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37
Q

Diagnostic approach for DILI?

A

Not “what are you on”, but “what did you start recently”
Contact GP
Time course is critical:
- onset usually 1-12 weeks of starting
earlier is unusual (unless re-challenge)
may be several weeks after stopping

  • resolution: 90% within 3 months of stopping
    5-10%: prolonged
  • inadvertent re-challenge, seen in 6% (2% of these fatal)
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38
Q

Most likely to cause DILI?

A

32-45% Antibiotics (Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs)

15% CNS Drugs (Chlorpromazine, Carbamazepine Valproate, Paroxetine,

5% Immunosupressants

5-17% Analgesics/musculskeletal
(Diclofenac…)

10% Gastrointestinal Drugs (PPIs…)

10% Dietary Supplements

20% Multiple drugs

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39
Q

What drugs dont cause DILI?

A

Low dose Aspirin
NSAIDs other than Diclofenac
Beta Blockers
HRT
ACE Inhibitors
Thiazides
Calcium channel blockers

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40
Q

AC, 20 year old male
Admitted unwell, jaundiced, severe toothache
Analgesia taken over last 72 hours
ALT & AST in > 3000
Prothrombin time 32 seconds (n<10)
What has he taken?

A

Too much paracetamol

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41
Q

Paracetamol metabolism (toxic)

A

Paracetamol > Enzyme:CYP2E1(CYP3A4, CYP1A2)> Toxic metabolites (NAPQI) > Covalent binding oxidative stress > Hepatocyte damage

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42
Q

What is the management of paracetamol induced fulminant hepatic failure?

A

N acetyl Cysteine (NAC)
Supportive to correct:
-coagulation defects
-fluid electrolyte and acid base balance
-renal failure
-hypoglycaemia
-encephalopathy

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43
Q

Paracetamol-induced liver failure: severity indicators

A

Late presentation
(NAC less effective >24 hr)
Acidosis (pH <7.3)
Prothrommbin time > 70 sec
Serum creatinine ≥ 300 µmol/l

Consider emergency liver transplant - otherwise 80% mortality

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44
Q

Ascites cause what?

A

Chronic liver disease (most)
- +/- Portal vein thrombosis
- Hepatoma
- TB
Neoplasia (ovary, uterus, pancreas…)
Pancreatitis, cardiac causes

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45
Q

Where can you get varices?

A

Anywhere in portal system

46
Q

Pathogenesis of ascites:

A

Increased intrahepatic resistance – higher resistance in liver > Portal hypertension > Ascites < Low serum albumin

Systemic vasodilation:
Secretion of:
- Renin-angiotensin
- Noradrenaline
- Vasopressin
Leads to fluid retention > increased portal hypertension

47
Q

Management of Ascites:

A

Fluid and salt restriction
Diuretics Spironolactone
+/- Furosemide – side effect is low potassium

Large-volume paracentesis + albumin

Trans-jugular intrahepatic portosystemic shunt (TIPS)

48
Q

What does alcohol-related injury cause?

A

Hepatocyte ballooning and is mediated by neutrophils (acute alcoholic hepatitis).

Injured liver cells may accumulate a cytoskeletal protein which appears irregular and red on an H&E stain

49
Q

What is steatosis?

A

Alcohol changes the way that hepatocytes metabolise and produce fat. Fat accumulation within hepatocytes is termed steatosis.

It may be associated with acute liver injury, or as in the picture, chronic injury mediated by lymphocytes.

50
Q

Acute decompensation pathology:

A

Fatty Liver >1. Alcoholic hepatitis 2. Cirrhosis
1 + 2 > Acute decompensation

51
Q

Progression of Alcoholic Liver Disease

A

Normal liver > Steatosis (90% of heavy drinkers) > Alcoholic steatohepatitis/ fibrosis (20-40%) > Cirrhosis (8-20%) > Hepatocellular carcinoma (3-10%)

From alcoholic steatohepatitis + cirrhosis can goto alcoholic hepatitis which is better by abstinence, liver transplants, corticosteroids

52
Q

Risk factors for Alcoholic Liver Disease?

A

Females
Drinking pattern
Quantity consumed
Obesity
HCV
Genetics

53
Q

Incidence of Alcoholic Liver Disease (ALD)

A

Main cause of liver death in UK
Incidence increased 1960-2010
However, only 10-20% of heavy alcohol drinkers drinkers get serious ALD (? why)
Often not alcohol dependent (‘alcoholics’)
25% will stop drinking and 25% will reduce
Negative popular image
Poor outcome – 10 year survival 25%

54
Q

Causes of portal hypertension:

A

cirrhosis, fibrosis, portal vein thrombosis

55
Q

Pathology of portal hypertension:

A

increased hepatic resistance
increased splanchnic blood flow

56
Q

Consequences of portal hypertension:

A

varices (oesophageal, gastric…)
splenomegaly

57
Q

Male 48 years, wine merchant
Admitted with jaundice, ascites
120 units alcohol / wk for 10 yr
After 2 days: agitated, tremulous, wanted to leave hospital
Diagnosis?

A

Alcohol withdrawal
Treated with Lorazepam- improved
3 days later: very unwell, drowsy, BP 80/50

58
Q

Why do patients with chronic liver disease ‘go off’?

A

Constipation
Drugs - sedatives, analgesics
- NSAIDs, diuretics, ACE blockers
Gastrointestinal bleed
Infection (ascites, blood, skin, chest …)
HYPO: natraemia, kalaemia, glycaemia …
Alcohol withdrawal (not typically)
Other (cardiac, intracranial …)

59
Q

Why are liver patients so vulnerable to infection?

A
  • impaired reticulo-endothelial function
  • reduced opsonic activity
  • leucocyte function
  • permeable gut wall
60
Q

What is Spontaneous bacterial peritonitis?

A

Commonest serious infection in cirrhosis
Vague symptoms
based on neutrophils in ascitic fluid
Gram stain often neg; use blood culture bottles
After 1 episode:
- should have antibiotic prophylaxis
- consider liver transplantation

61
Q

What drugs cause renal failure in liver disease?

A

Drugs:
- Diuretics- NSAIDS- ACE Inhibitors - Aminoglycosides

62
Q

What other causes of renal failure in liver disease?

A

Infection
GI bleeding
Myoglobinuria
Renal tract obstruction

63
Q

What are the other consequences of liver dysfunction?

A

Malnutrition Coagulopathy
- impaired coagulation factor synthesis
- vitamin K deficiency (cholestasis)
- thrombocytopenia
Endocrine changes
- gynaecomastia
- impotence
- amenorrhoea
Hypoglycaemia (+/-)

64
Q

Drug prescribing in liver disease:

A

Analgesia: sensitive to opiates
NSAIDs cause renal failure
paracetamol safest

Sedation: Use short acting benzodiazepines
Diuretics: Excess weight loss, hyponatraemiam hyperkalaemia, renal failure
Antihypertensives: Can often stop, avoid ACE inhibitors
Aminoglycosides: Avoid

65
Q

Treatment of malnutrition in liver disease:

A

naso-gastric feeding

66
Q

Treatment of variceal bleeding in liver disease:

A

endoscopic banding
propranolol, terlipressin

67
Q

Treatment of encephalopathy in liver disease:

A

Lactulose

68
Q

Treatment of ascites/ oedema in liver disease:

A

Salt/ fluid restriction
Diuretics, paracentesis

69
Q

Treatment of infections in liver disease:

A

Antibiotics

70
Q

What do liver patients do when they ‘go off’?

A

1 ABC: Airway, Breathing, Circulation
2 Look at chart - vital signs, O2, BM(glucose), drug chart
3 Look at patient - focus of infection? bleeding?
4 Tests - FBC, U&E, blood cultures, ascitic fluid,clotting, LFTs

71
Q

What are the causes of chronic liver disease?

A

Alcohol
Non Alcoholic Steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune - autoimmune hepatitis
primary biliary cirrhosis
sclerosing cholangitis

Metabolic - Haemochromatosis, Wilson’s, alpha-1 antitrypsin deficiency
Vascular - Budd-Chiari

72
Q

Points in history in chronic liver disease?

A

Past history: alcohol problems, biliary surgery, autoimmune disease, blood products
Social history: alcohol, sexual
Drug history: All drugs
Family history

73
Q

Viral serology for chronic liver disease:

A

hepatitis B surface antigen, hepatitis C antibody

74
Q

Immunology investigation for chronic liver disease:

A

autoantibodies - AMA, ANA, ASMA, - coeliac antibodies - immunoglobulins

75
Q

Biochemistry investigations of chronic liver disease:

A

iron studies -
copper studies - caeruloplasmin - 24 hr urine copper
- 1-antitrypsin level
- lipids, glucose

76
Q

radiological investigations for chronic liver disease

A

USS / CT / MRI

77
Q

Differential diagnosis of hepatitis:

A

viral (A, B, C, CMV, EBV)
drug-induced
autoimmune
alcoholic

78
Q

What do we require for a hepatitis diagnosis?

A

Liver biopsy - appearance not always specific
Lymphocytes and plasma cells within portal tracts - resultant damage causes apoptosis or death in severe swathes causing massive necrosis

79
Q

Where does inflammation often occur in hepatitis?

A

Portal tracts with damage to adjacent or interface hepatocytes

80
Q

In Primary biliary cirrhosis where is the immune damage directed towards?

A

Small bile ducts

81
Q

Autoimmune hepatitis incidence

A

UK prevalence 1-2/10,000
70-75% women
40% present with ‘acute’ hepatitis
ANA, ASMA- positive in about 70%
Aggressive disease (usually fatal prior to 1970s) 30% have cirrhosis at presentation
90%: dramatic response to prednisolone  azathioprine
Diagnosis now based on points system
About 5% overlap with PBC

82
Q

Incidence of Primary biliary cirrhosis/cholangitis? (PBC)

A

Prevalence: 250X106 (Sheffield) 90% women
Pathogenesis unknown
+ve AMA in 95% of patients
Many patients have progressive disease
Mayo Clinic prognostic score: uses bilirubin albumin and prothrombin time

83
Q

How does PBC/ cholangitis present?

A

Asymptomatic lab abnormalities
Itching and/or fatigue
Dry eyes
Joint Pains
Variceal bleeding
Liver failure: ascites, jaundice

84
Q

Treatment of cholestatic itch

A

UDCA, antihistamines - little help
Cholestyramine helps in 50% of cases
Rifampicin effective; occasionally damages liver
Opiate antagonists
Liver transplantation

85
Q

How does the fatigue from PBC effect patients?

A

Can be disabling
Correlates with autonomic neuropathy
Not with disease severity or depression
Treatment: Modafinil (open studies)
No longer an indication for transplantation

86
Q

PBC associated diseases

A

Sjorgens
Thyroiditis
Scleroderma
Rheumatoid arthiritis
Lung disease
Coeliac disease

87
Q

Which acid works well in PBC?

A

Ursodeoxycholic acid

88
Q

Features of Ursodeoxycholic acid

A

Improvement in liver enzymes, bilirubin
Subtle reduction in inflammation; not fibrosis
Reduced portal pressure and rate of variceal development
Modestly reduced rate of death or liver transplantation

89
Q

What does Primary Sclerosing Cholangitis (PSC) present with?

A

Itching
Pain
Rigors
Jaundice

90
Q

Features of PSC

A

Leads to strictures (areas of narrowing) ± gallstones
Over 50% have inflammatory bowel disease
Raised Alk phos and GGT (like PBC)
10% develop cholangiocarcinoma (bile duct cancer)
Ursodeoxycholic Acid: unclear benefits
Good results from Liver Transplantation

91
Q

PSC histology

A

Disease of bile ducts
Concentric onion ring appearance
Lymphocytes present mediating damage

92
Q

What is haemochromatosis?

A

Genetic disorder
Autosomal recessive
Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
Mutation in HFE gene
When cirrhosis present, increased risk of hepatocellular carcinoma
Iron removal may lead to regression of fibrosis

93
Q

What does the diagnosis suggest for Haemochromatosis?

A

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

94
Q

Signs and sypmtoms of haemochromatosis?

A

Chronic fatigue
Hepatomegaly
Cirrhosis
Hepatocellular carcinoma
Diabetes
White nails
Joint pain
Skin dryness

95
Q

what is alpha1-antitrypsin deficiency?

A

2% of population carry Z allele of a1-antitrypsin gene. 0.04% homozygotes
Results in inability to export a1-antitrypsin from liver
Can lead to
-liver disease (protein retention in liver)
-emphysema (protein deficiency in blood)
No medical treatment
Will eventually lead to liver cirrhosis

96
Q

Who does hepatocellular carcinoma happen to most of the time?

A

Patients with cirrhosis

97
Q

Who is at risk of hepatocellular carcinoma?

A

highest for hepatitis B,C, haemochromatosis
lower: cirrhosis from alcoholic, autoimmune disease
Males >Females

98
Q

Presentation of hepatocellular carcinoma?

A

presents with decompensation of liver disease, wt loss ascites, or abdominal pain

50% produce alpha fetoprotein

99
Q

Treatments of hepatocellular carcinoma

A

Transplantation, resection or local ablative therapies Sorafenib recently shown to prolong life

100
Q

Risk factors for Non-alcoholic fatty liver (NAFL)?

A

Obesity
Diabetes
hyperlipidaemia

101
Q

Most common cause of mildly elevated LFTS

A

NAFL

102
Q

eFFECTIVE treatment for NAFL?

A

Still no effective drug treatments
Weight loss works - the more the btetter
Bariatric surgery

103
Q

Causes of hepatic vein occlusion?

A

thrombosis (Budd-Chiari syndrome)
may be underline thrombotic disorder
membrane obstruction
veno-occlusive disease (irradiation, antineoplastic drugs)
Congestion causes acute or chronic liver injury

104
Q

What can hepatic vein occlusion present as?

A

Abnormal liver tests
ascites
acute liver failure

105
Q

Treatment of hepatic vein occlusion?

A

Anticoagulation
transjugular intrahepatic portosystemic shunt
Liver transplantation

106
Q

Causes of chronic liver disease?

A

Alcohol
Non alcoholic steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune
Metabolic
Vascular

107
Q

Immune causes of chronic liver disease

A

autoimmune hepatitis
primary biliary cirrhosis
sclerosing cholangitis

108
Q

Metabolic causes of chronic liver disease

A

Haemochromatosis
Wilsons
alpha1 antitrypsin deficiency

109
Q

Vascular causes of chronic liver disease

A

Budd-Chiari

110
Q

History of those with chronic liver disease

A

Past history: Alcohol problems, biliary surgerym autoimmune disease, blood products
Social history - alcohol, sexual
Drug history
Family history

111
Q

investigation of chronic liver disease

A

Viral serology - hepatitis B surface antigen, hepatitis C antibody
Immunology - autoantibodies, immunoglobulins
Biochemistry - iron studies, copper studies

Liver (2 decks)

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