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Liver symposium Flashcards

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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
Gall stone features:
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
26
Intrahepatic bile duct stones (hepatolithiasis)
Containing mainly brown pigment and cholesterol stones
27
Extrahepatic bile duct stones (choledocholithiasis)
Primary stones are mainly brown pigment stones, whereas secondary stones are mainly cholesterol stones
28
Gall bladder stones (cholecystolithiasis)
Containing cholesterol (or black pigment) stones
29
Gall stones presentation in gallbladder:
Bililary pain Yes Cholecystitis: Yes Obstructive Jaundice: maybe (Mirizzi) Cholangitis: No Pancreatitis: No
30
Gall stones presentation in bile duct:
Bililary pain : Yes Cholecystitis: No Obstructive Jaundice: Yes Cholangitis: Yes Pancreatitis: Yes
31
How do you manage gallbladder stones:
Laparoscopic cholecystectomy Bile acid dissolution therapy (<1/3 success)
32
How do you manage bile duct stones:
-ERCP with sphincterotomy and: removal (basket or balloon) crushing (mechanical, laser..) ' stent placement - Surgery (large stones)
33
What can present as gallstones (differential diagnosis)
Weight loss Jaundice Malignancy
34
Acute stone obstruction
Alk phos usually normal. Initial ALT often >1000; rapidly falls
35
Drug-induced liver injury (DILI) incidence
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
36
Types of DILI
Hepatocellular - ALT >2 ULN, ALT/Alk Phos ≥ 5 Cholestatic - Alk Phos >2 ULN or ratio ≤ 2 Mixed - Ratio > 2 but < 5
37
Diagnostic approach for DILI?
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)
38
Most likely to cause DILI?
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
39
What drugs dont cause DILI?
Low dose Aspirin NSAIDs other than Diclofenac Beta Blockers HRT ACE Inhibitors Thiazides Calcium channel blockers
40
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?
Too much paracetamol
41
Paracetamol metabolism (toxic)
Paracetamol > Enzyme:CYP2E1(CYP3A4, CYP1A2)> Toxic metabolites (NAPQI) > Covalent binding oxidative stress > Hepatocyte damage
42
What is the management of paracetamol induced fulminant hepatic failure?
N acetyl Cysteine (NAC) Supportive to correct: -coagulation defects -fluid electrolyte and acid base balance -renal failure -hypoglycaemia -encephalopathy
43
Paracetamol-induced liver failure: severity indicators
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
44
Ascites cause what?
Chronic liver disease (most) - +/- Portal vein thrombosis - Hepatoma - TB Neoplasia (ovary, uterus, pancreas...) Pancreatitis, cardiac causes
45
Where can you get varices?
Anywhere in portal system
46
Pathogenesis of ascites:
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
Management of Ascites:
Fluid and salt restriction Diuretics Spironolactone +/- Furosemide – side effect is low potassium Large-volume paracentesis + albumin Trans-jugular intrahepatic portosystemic shunt (TIPS)
48
What does alcohol-related injury cause?
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
What is steatosis?
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
Acute decompensation pathology:
Fatty Liver >1. Alcoholic hepatitis 2. Cirrhosis 1 + 2 > Acute decompensation
51
Progression of Alcoholic Liver Disease
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
Risk factors for Alcoholic Liver Disease?
Females Drinking pattern Quantity consumed Obesity HCV Genetics
53
Incidence of Alcoholic Liver Disease (ALD)
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
Causes of portal hypertension:
cirrhosis, fibrosis, portal vein thrombosis
55
Pathology of portal hypertension:
increased hepatic resistance increased splanchnic blood flow
56
Consequences of portal hypertension:
varices (oesophageal, gastric…) splenomegaly
57
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?
Alcohol withdrawal Treated with Lorazepam- improved 3 days later: very unwell, drowsy, BP 80/50
58
Why do patients with chronic liver disease ‘go off’?
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
Why are liver patients so vulnerable to infection?
- impaired reticulo-endothelial function - reduced opsonic activity - leucocyte function - permeable gut wall
60
What is Spontaneous bacterial peritonitis?
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
What drugs cause renal failure in liver disease?
Drugs: - Diuretics- NSAIDS- ACE Inhibitors - Aminoglycosides
62
What other causes of renal failure in liver disease?
Infection GI bleeding Myoglobinuria Renal tract obstruction
63
What are the other consequences of liver dysfunction?
Malnutrition Coagulopathy - impaired coagulation factor synthesis - vitamin K deficiency (cholestasis) - thrombocytopenia Endocrine changes - gynaecomastia - impotence - amenorrhoea Hypoglycaemia (+/-)
64
Drug prescribing in liver disease:
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
Treatment of malnutrition in liver disease:
naso-gastric feeding
66
Treatment of variceal bleeding in liver disease:
endoscopic banding propranolol, terlipressin
67
Treatment of encephalopathy in liver disease:
Lactulose
68
Treatment of ascites/ oedema in liver disease:
Salt/ fluid restriction Diuretics, paracentesis
69
Treatment of infections in liver disease:
Antibiotics
70
What do liver patients do when they 'go off'?
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
What are the causes of chronic liver disease?
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
Points in history in chronic liver disease?
Past history: alcohol problems, biliary surgery, autoimmune disease, blood products Social history: alcohol, sexual Drug history: All drugs Family history
73
Viral serology for chronic liver disease:
hepatitis B surface antigen, hepatitis C antibody
74
Immunology investigation for chronic liver disease:
autoantibodies - AMA, ANA, ASMA, - coeliac antibodies - immunoglobulins
75
Biochemistry investigations of chronic liver disease:
iron studies - copper studies - caeruloplasmin - 24 hr urine copper - 1-antitrypsin level - lipids, glucose
76
radiological investigations for chronic liver disease
USS / CT / MRI
77
Differential diagnosis of hepatitis:
viral (A, B, C, CMV, EBV) drug-induced autoimmune alcoholic
78
What do we require for a hepatitis diagnosis?
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
Where does inflammation often occur in hepatitis?
Portal tracts with damage to adjacent or interface hepatocytes
80
In Primary biliary cirrhosis where is the immune damage directed towards?
Small bile ducts
81
Autoimmune hepatitis incidence
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
Incidence of Primary biliary cirrhosis/cholangitis? (PBC)
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
How does PBC/ cholangitis present?
Asymptomatic lab abnormalities Itching and/or fatigue Dry eyes Joint Pains Variceal bleeding Liver failure: ascites, jaundice
84
Treatment of cholestatic itch
UDCA, antihistamines - little help Cholestyramine helps in 50% of cases Rifampicin effective; occasionally damages liver Opiate antagonists Liver transplantation
85
How does the fatigue from PBC effect patients?
Can be disabling Correlates with autonomic neuropathy Not with disease severity or depression Treatment: Modafinil (open studies) No longer an indication for transplantation
86
PBC associated diseases
Sjorgens Thyroiditis Scleroderma Rheumatoid arthiritis Lung disease Coeliac disease
87
Which acid works well in PBC?
Ursodeoxycholic acid
88
Features of Ursodeoxycholic acid
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
What does Primary Sclerosing Cholangitis (PSC) present with?
Itching Pain Rigors Jaundice
90
Features of PSC
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
PSC histology
Disease of bile ducts Concentric onion ring appearance Lymphocytes present mediating damage
92
What is haemochromatosis?
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
What does the diagnosis suggest for Haemochromatosis?
Diagnosis suggested by raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy
94
Signs and sypmtoms of haemochromatosis?
Chronic fatigue Hepatomegaly Cirrhosis Hepatocellular carcinoma Diabetes White nails Joint pain Skin dryness
95
what is alpha1-antitrypsin deficiency?
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
Who does hepatocellular carcinoma happen to most of the time?
Patients with cirrhosis
97
Who is at risk of hepatocellular carcinoma?
highest for hepatitis B,C, haemochromatosis lower: cirrhosis from alcoholic, autoimmune disease Males >Females
98
Presentation of hepatocellular carcinoma?
presents with decompensation of liver disease, wt loss ascites, or abdominal pain 50% produce alpha fetoprotein
99
Treatments of hepatocellular carcinoma
Transplantation, resection or local ablative therapies Sorafenib recently shown to prolong life
100
Risk factors for Non-alcoholic fatty liver (NAFL)?
Obesity Diabetes hyperlipidaemia
101
Most common cause of mildly elevated LFTS
NAFL
102
eFFECTIVE treatment for NAFL?
Still no effective drug treatments Weight loss works - the more the btetter Bariatric surgery
103
Causes of hepatic vein occlusion?
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
What can hepatic vein occlusion present as?
Abnormal liver tests ascites acute liver failure
105
Treatment of hepatic vein occlusion?
Anticoagulation transjugular intrahepatic portosystemic shunt Liver transplantation
106
Causes of chronic liver disease?
Alcohol Non alcoholic steatohepatitis (NASH) Viral hepatitis (B, C) Immune Metabolic Vascular
107
Immune causes of chronic liver disease
autoimmune hepatitis primary biliary cirrhosis sclerosing cholangitis
108
Metabolic causes of chronic liver disease
Haemochromatosis Wilsons alpha1 antitrypsin deficiency
109
Vascular causes of chronic liver disease
Budd-Chiari
110
History of those with chronic liver disease
Past history: Alcohol problems, biliary surgerym autoimmune disease, blood products Social history - alcohol, sexual Drug history Family history
111
investigation of chronic liver disease
Viral serology - hepatitis B surface antigen, hepatitis C antibody Immunology - autoantibodies, immunoglobulins Biochemistry - iron studies, copper studies

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