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Block 32 GI and surgery > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

what are the functions of the liver?

A

metabolism of carbohydrates, lipids, proteins, ammonia, vitamins, bilirubin

storage of carbohydrate, vitamin, minerals,

Coagulation

Endocrine function

Immune and inflammatory response (kupffer cells)

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2
Q

describe the role of the liver in carbohydrate metabolism?

A

Glucose homeostasis and maintenance of blood sugar

In periods of prolonged starvation ketone bodies and fatty acids are used instead

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3
Q

describe the role of the liver in protein metabolism?

A
  • Synthesis and storage of proteins
  • amino acids from intestine and muscles.
  • Controls rate of gluconeogenesis and transamination
  • controls albumin levels
  • Synthesises coagulation factors and complement system
  • Stores vitamins
  • Degradation – nitrogen excretion. Ammonia, converted to urea and exctreted by the kidneys
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4
Q

describe the role of the liver in lipid metabolism?

A

Metabolising lipoproteins
• VLDL synthesis and HDL
• HDL substrate for conversion of free cholesterol to cholesterol ester
• Triglyceride removed from IDL to produce LDL
• Oxidation or de novo synthesis of FFA occurs in the liver
• Cholesterol can be dietary or produced from acetyl coa – free or esterified with FA. Occurs via LCAT enzyme which is reduced in liver disease, increasing free cholesterol to ester, altering membranestructures.

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5
Q

what should you ask about in a patient with a history of liver disease?

A
  • Timing and duration of symptoms and associated symptoms
  • Patients concerns
  • RF: blood transfusion, IV drug use, surgery, contacts – sex, chemical exposure
  • Med hx: prescribed, OTC, herbal/alternative
  • FH
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6
Q

in general what can diseases of the liver be classified as?

A
  • functional abnormalities

- pathological manifestations

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7
Q

what are the functional abnormalities that can cause problems with the liver?

A
  • Metabolism – protein, carb, lipid, bile acid, bilirubin, hormone and drug
  • Removal of microbes/toxin
  • Excretion
  • Immunological function
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8
Q

what are the pathological manifestations causing disease of the liver?

A
  • acute hepatitis
  • chronic hepatitis
  • jaundice
  • cirrhosis
  • hepatocellular carcinoma
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9
Q

describe the features of acute hepatitis (causes and consequences)?

A 
Toxic Drugs – paracetamol poisoning
Viruses (hep A, B, C, D, E)
Alcohol
Vascular damage
Biliary Obstruction – gall stones, tumours
Metabolic
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10
Q

describe the features of chronic hepatitis (causes and consequences)?

A

Toxic, drugs – 24% alcohol related
Hep (B, C, D) – 57% Hep C
AI Disease (AI hepatitis)
Biliary Disease – primary biliary cirrhosis, sclerosing cholangitis, graft vs host disease, transplant rejection
Steatohepatitis (NASH – non-alcohol SH)
Steatosis is fatty infiltration of the liver. When inflammation is associated with fatty change, the term steatohepatitis is used.
RF: obesity, DM, hyperlipidaemia, jejunoileal bypass surgery

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11
Q

what are the causes of jaundice?

A 
Drugs
Viruses
Alcohol
AI Disease (primary biliary cirrhosis, Primary sclerosis cholangitis)
Biliary obstruction
Sepsis
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12
Q

what are the causes of crirrhosis?

A 
Drugs
Viruses
Alcohol
amyloidosis
Biliary obstruction
Others: haemochromatosis
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13
Q

what are the most common conditions associated with elevated LFTs?

A

hep C

NAFLD

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14
Q

what tests make up LFTs?

A
  • Albumin
  • Bilirubin (total and conjugated)
  • Serum aminotransferases (AST and ALT)
  • Alkaline phosphatase (APT)
  • PT
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15
Q

what are synthetic liver function tests?

A
  • Bilirubin
  • PT
  • Albumin
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16
Q

what is albumin?

A

– main protein synthesised by the liver and circulates in blood. Production is controlled by multiple factors including nutritional status, serum oncotic pressure, cytokines, and hormones. A serum albumin may be reflection of the synthetic function of the liver. Ability to make this and other proteins is affected in chronic liver disease.

Total protein - albumin and other in blood

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17
Q

what is bilirubin and why is it important clinically?

A

bile its yellow/green colour.

Used to determine liver’s ability to clear endogenous/exogenous substances from the circulation.

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18
Q

what are the types of bilirubin and when are these raised?

A

Indirect (unconjugated) bilirubin - Elevated with haemolysis, hepatic disease

Direct (conjugated) bilirubin - Elevated with biliary obstruction and hepatocellular disease.

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19
Q

what level does bilirubin need to be at for jaundice to develop?

A

≥ 3 mg/dL

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20
Q

what are aminotransferase enzymes?

A

Aminotransferase enzymes are intra-cellular enzymes
Also released from hepatocytes with hepatocellular injury.
examples: AST and ALT

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21
Q

what is the normal AST/ALT ratio and what is it in alcoholic hepatitis?

A

normal is 0.8

In alcoholic hepatitis, is usually > 2

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22
Q

what is ALT?

A

helps process proteins.
Large amounts occur in liver cells. When liver is injured or inflamed the blood level of ALT rises = hepatitis
ALT is usually considered more specifically related to liver problems than AST

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23
Q

what is AST?

A

enzyme in liver cells
involved in amino acid metabolism
High levels= liver is injured – hepatic necrosis.
AST can also be released if heart, liver, kidney, pancreas or skeletal muscle is
damaged – MI, CHF.

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24
Q

what is alkaline phosphatase?

A

a group of enzymes that catalyze the hydrolysis of a large number of organic phosphate esters.
In liver, believed to play an active role in down-regulating the secretory activities of the intrahepatic biliary epithelium.

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25
Q

what is gamma glutamyltranspeptidase?

A

induced by drugs and alcohol.
ALP normal and GGT raised = alcohol intake.
Mild GGT common with small alcohol consumption and fatty liver disease. In cholestasis ALP and GGT raised. Poor specificity. Sensitive huge.

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26
Q

what are the clotting factors that the liver synthesises?

A 
Factor I (fibrinogen)
Factor II (prothrombin)
Factor V
Factor VII
Factor IX
Factor X
Factors XII and XIII
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27
Q

what is raised IgG suggestive off?

A

autoimmune hepatitis

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28
Q

what is raised IgM suggestive of?

A

primary billiary cirrhosis

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29
Q

what is raised IgA suggestive of?

A

alcoholic liver disease

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30
Q

in general what is the pattern of LFTs in patients with hepatocellular injury?

A

Very high AST, ALT with mild/moderately elevated alkaline phosphatase.

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31
Q

in general what is the pattern of LFTs in patients with cholestasis?

A

mild/moderately elevated AST/ALT with very high alkaline phosphatase
Bilirubin can be elevated with both combinations

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32
Q

What other specific blood tests can be performed in a patient with liver disease?

A
  • Viral serology
  • Blood alcohol
  • Drug levels
  • Liver auto antibodies
  • Cu/Fe/a-1 anti-trypsin studies
  • Unconjugated bilirubin, reticulocytes, hepatoglobulins/coombes test
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33
Q

what test is useful to perform for primary biliary cirrhosis?

A

anti-mitochondrial antibody

raised IgM

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34
Q

what test is useful to perform for autoimmune hepatitis?

A

anti-nuclear, smooth muscle(actin)
liver/kidney microsomal antibody
raised IgG

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35
Q

what test is useful to perform for hepatitis A, B, C, D, E

A

viral markers

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36
Q

what test is useful to perform for hepatocellular carcinoma?

A

alpha fetoprotein

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37
Q

what test is useful to perform for hereditary haemchromatosis?

A

serum iron, transferrin saturation, serum ferritin

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38
Q

what test is useful to perform for wilson’s disease?

A

serum and urinary copper

serum caeruloplasmin

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39
Q

what test is useful to perform for cirrhosis?

A

alpha1 antitrypsin

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40
Q

what test is useful to perform for primary sclerosing cholangitis?

A

anti nuclear cytoplasmic antibodies

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41
Q

what test is useful to perform for non alcoholic fatty liver disease and hepatits C?

A

markers of liver fibrosis

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42
Q

what test is useful to perform for HFE gene (hereditary haemochromatosis)?

A

genetic analysis

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43
Q

what steps need to be taken in diagnosing a patient with acute hepatitis?

A
  1. history and examination
  2. IgM anti HAV (if positive= hep A)
  3. HBsAg and IgM anti-HBc (if positive hepB then do anti HDV if risk factors)
  4. anti HCV (if positive=hep C)
  5. if all these are negative consider wilsons, EBV, CMV, autoimmune hepatitis, congestive heart failyre, biliary tract disease, metastases
  6. consider biopsy
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44
Q

what investigations would be performed in a patient with elevated ALT?

A
  1. history and examination
  2. HBsAg->IgM anti-HBc [if +ve=acute hep B] [If -ve=chronic hep B]
  3. anti-HCV->hepatitis C
  4. if above -ve consider wilsons, haemochromatosis, autoimmune hepatitis, alpha 1 antitrypsin deficiency, coeliac disease
  5. if all above -ve US or CT for fatty liver or biopsy
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45
Q

what investigations should be performed in a patient with mild diffuse LFT abnormalities?

A
  1. history and examination
  2. obesity, diabetes, hyperlipidaemia (non alcoholic fatty liver)
  3. viral hepatitis risk factors (serological tests)
  4. autoimmune features (serum globulins and auto antibodies)
  5. other considerations (test for haemochromatosis, wilsons disease, alpha 1 antitrypsin deficiency, coeliac disease)
  6. if all above consider US, CT, MRCP, ERCP, liver biopsy or transient elastography as suggested by results
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46
Q

what investigations should be performed in a patient with elevated alkaline phosphatase?

A
  1. history and examination
  2. GGT or isoenzymes normal ->extra hepatic source
  3. elevated = hepatobiliary disesae
  4. abdominal US (if normal->AMA, ACE level, serological tests for viral hepatitis, alpha fetoprotein.) gallstones, focal lesion, biliary tract abnormalities
  5. if all above negative consider biopsy, transient elastography
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47
Q

when would you take a liver biopsy?

A
  • Acute and chronic liver dysfunction
  • Hepatomegaly
  • Space occupying lesions
  • To find cause and severity (stage of progression)
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48
Q

what action would be taken if work up is negative and AST/ALP remain elevated?

A

Observe:
o Patients with two-fold or less increase in AST/ALT and no hyperbilirubinemia

Liver Biopsy
o Patients with > two-fold increase in AST/ALT, or abnormalities of other liver function tests

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49
Q

what causes hepatocellular injury?

A 
viral hepatitis
hepatitis due to other viruses 
drug induced liver injury
toxins
metabolic
vascular events
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50
Q

what other viruses can cause hepatitis?

A

herpes viruses 1,2 and 6
adenovirus
epstein barr virus
CMV

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51
Q

what toxins can cause liver injury?

A

Amanita phalloides (death cap)

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52
Q

what metabolic issues can result in hepatocellular injury?

A

acute fatty liver of pregnancy

reye’s syndrome

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53
Q

what vascular issues can result in hepatocellular injury?

A

Acute circulatory failure
Budd-Chiari syndrome (occlusion of hepatic veins)
Veno-occulsive disease
Heat stroke

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54
Q

what other conditions can result in hepatocellular injury?

A

Wilson disease
Autoimmune hepatitis
Massive tumour infiltration
Liver transplant with primary graft dysfunction

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55
Q

describe the role of the liver in drug metabolism?

A
  • Liver major site of drug metabolism
  • between the splanchnic and systemic circulations and large amount of enzymes that are capable of transforming drugs into active compounds or degrading for elimination
  • Converted from fat soluble to water soluble substances that are excreted in urine or bile
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56
Q

what is a phase I drug reaction?

A

oxidative and reductive processes

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57
Q

what is a phase II drug reaction?

A

oxidation, reduction and hydrolysis are couple with endogenous substrates such as glucuronic acid, sulfuric acid, glutathione. Render polar lipophilic compounds. Excreted in bile if molecules are large or in urine if small

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58
Q

what is a phase III drug reaction?

A

reactions actively transported from cell.

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59
Q

what are the 6 mechanisms that drugs can cause liver damage?

A
  • Disruption of intracellular calcium homeostasis
  • Disruption of bile canalicular transport mechanisms
  • Formation of non-functioning adducts
  • Present on surface of hepatocyte as new immunogens – attacked by T cells
  • Induction of apoptosis -Inhibit mitochondrial function
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60
Q

describe drug induced hepatotoxicity?

A
  • Intrinsic hepatotoxins = paracetamol
  • Idiosyncratic (abnormal physical reaction to something) hepatotoxins = hypersensitivity and metabolic Can lead to hepatitis, cholestasis, fatty change and fibrosis
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61
Q

what affect can paracetamol have on the liver?

A
  • Undergoes conjugation with glucuronide and sulphate. Remainder is metabolised by microsomal enzymes to produce toxic derivatives. Detoxified by conjugation with glutathione.
  • Larger doses ingested, pathway becomes saturates and toxic derivative is produced at faster rate, binds to cell membranes. Can produce liver necrosis
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62
Q

what affect can halothane and other volatile anaesthetics have on the liver?

A
  • Produces hepatitis in those having repeated exposures

* Hypersensitivity reaction

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63
Q

what affect can steroid compounds have on the liver?

A
  • Cholestasis caused by natural and synthetic oestrogens

* Interfere with biliary flow

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64
Q

what affect can phenothiazines have on the liver?

A
  • Cholestatic picture

* Hypersensitivity reaction

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65
Q

what affect can anti TB chemo have on the liver?

A

• Elevated AMT
• Hepatic necrosis with jaundice
• Rifampicin produces hepatitis, pyrazinamide
produces abnormal liver tests

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66
Q

what affect can amiodarone have on the liver?

A

steatohepatitis?

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67
Q

describe acetaminophen overdose?

A

• Toxicity is likely to occur with single ingestions greater than 250 mg/kg or those greater than 12 g over a
24-hour period
• AST/ALT elevation is first sign of liver damage (usually 24-hours after ingestion)

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68
Q

what is acute hepatitis and how does it present?

A
  • Definition: Rapid development of hepatic synthetic dysfunction
  • Presentation: jaundice, bleeding, confusion, abnormal LFTs
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69
Q

what is the aetiology of acute hepatitis?

A
  • Drugs – isoniazid – first line treatment for TB
  • Halothane (general anaesthetic)
  • Viruses – hepatitis A, B, C, EBV, CMV, Adenovirus, Herpes
  • Alcohol
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70
Q

what is the commonest cause of liver disease worldwide?

A

acute viral hepatitis

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71
Q

what effective vaccines are available for acute viral hepatitis?

A

o Enterically transmitted: HAV, HEV

o Blood borne: HBV, HCV, HDV, HGV

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72
Q

what are the symptoms of acute viral hepatitis?

A
  • Asymptomatic

* Health screen in at risk populations

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73
Q

Is hepatitis A acute or chronic?

A

acute

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74
Q

what part of the history are important in a patient with hepatitis A?

A 
travel
recent outbreak
nausea
vomiting 
jaundice
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75
Q

what labs are useful to diagnose hepatitis A?

A

hepatitis A IgM

frequent elevated bilirubin

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76
Q

is hepatitis B acute or chronic

A

can be both?

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77
Q

what part of the history are important in a patient with hepatitis B?

A

See if patient from Asia, Subsaharan Africa; Sexual history, Drug use

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78
Q

what labs are useful to diagnose hepatitis B?

A

hepatitis B surface antigen
surface antibody
core antibody

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79
Q

what part of the history are important in a patient with hepatitis C?

A

IV drug abuse, blood transfusion prior to 1992, Sexual history, Tattoos

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80
Q

what labs are useful to diagnose hepatitis C?

A

Hepatitis C antibody (Hepatitis C viral load if HIV positive or immunocompromised)

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81
Q

what labs are useful to diagnose infectious mononucleosis (acute EBV)?

A

monospot

EBV IgM

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82
Q

what would LFTs show in a patient with HIV?

A

isolated elevated aminotransferases

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83
Q

what labs are useful to diagnose HIV?

A

HIV antibody test

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84
Q

what part of the history are important in a patient with HIV?

A

sexual history

IV drug use

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85
Q

what is the transmission of hepatitis A?

A

faecal oral

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86
Q

where are outbreaks of hepatitis A common?

A

schools

institutions

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87
Q

what is the incubation period of hepatitis A?

A

28 days (between 15-50)

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88
Q

describe the onset and symptoms of hepatitis A?

A 
abrupt onset
fever
malaise
anorexia
nausea
abdominal discomfort
dark urine
jaundice
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89
Q

how does age affect the symptoms presenting in a patient with hepatitis A?

A

age related
<6yrs 70% asymptomatic
>15yrs 70% icteric

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90
Q

what test is used to make a diagnosis of hepatitis A?

A

hep A IgM

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91
Q

what is the first sign of hepatitis A in smokers?

A

going of the fags

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92
Q

what is an effective way of preventing hepatitis A/

A

vaccination

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93
Q

describe the pre-icteric phase?

A

prodromal illness days to weeks
• Icteric = jaundice
• A prodromal phase from days to more than a week
• Characterised by appearance of symptoms like loss of appetite, fatigue, abdominal pain, N&V, fever,
diarrhoea, dark urine and pale stools (cholestatic phase)
• Malaise
• Anorexia
• Flu-like and GI like symptoms
• Few signs except for enlarged liver and jaundice

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94
Q

what is the icteric phase?

A
  • Jaundice
  • Pale stools and dark urine
  • Improvement in symptoms
  • DDx: surgical jaundice
95
Q

what is post hepatitis syndrome?

A

• Malaise, depression, anorexia
• DDx: chronic hepatitis, liver biopsy after 6 months
• Fulminant hepatic failure: acute liver failure is broad that encompasses fulminant hepatic failure and
subfulminant hepatic failure = late onset. FHF describes the development of encephalopathy within 8 weeks
of the onset of symptoms in a patient with previously healthy liver.
• SHF is reserved for patients with liver disease for up to 26 weeks before the development of hepatic
encephalopathy

96
Q

describe the hepatitis A virus?

A

icosahedral capsid ssRNA

97
Q

describe the hepatitis B virus?

A

enveloped dsDNA

98
Q

describe the hepatitis C virus?

A

enveloped ssRNA

99
Q

describe the hepatitis D virus?

A

enveloped ssRNA

100
Q

describe the hepatitis E virus?

A

unenveloped ssRNA

101
Q

which hepatitis are spread via fecal-oral route?

102
Q

what hepatitis are spread via blood, close contact?

103
Q

what is the incubation period of hepatitis A?

104
Q

what is the incubation period of hepatitis B?

105
Q

what is the incubation period of hepatitis C?

A

2-26 weeks

106
Q

what is the incubation period of hepatitis D?

107
Q

what is the incubation period of hepatitis E?

108
Q

which types of hepatitis are linked to hepatocellular carcinoma?

109
Q

which types of hepatitis become chronic?

A

B (5-10%)
C (.>50%)
D (coinfection-5% / superinfection-80%)

110
Q

how is hepatitis B usually transmitted?

A

mother to baby
in blood
via sex

111
Q

if contracted at birth what percentage develop chronic hepatitis B infection?

112
Q

what percentage of patients with hepatitis A get fulminant hepatitis and what is this?

A

20-25%
rare and fatal form of acute hpe B, radpily deteriorates with
hepatic encephalopathy, necrosis of parenchyma, renal failure and coma

113
Q

describe the serology of hepatitis B?

A
  • HBsAg – hallmark of infection
  • Anti HBs – immunity
  • Anti HBc (core) previous exposure
  • HBeAg marker of viral replication
  • HBV DNA – direct marker
114
Q

how can hepatitis B be treated?

A
  • Interferon – as hep C – unpleasant
  • Lamivudine – mutation risk
  • Prevention better than cure – vaccinate household contacts, vaccinate babies (active +/- passive)
115
Q

who gets hepatitis C?

A
  • 60% of drug users +ve

* >40% of prison population

116
Q

describe chronic hepatitis C infection?

A

Chronic hepatitis (85%) > cirrhosis > Hepatocellular carcinoma > death or stable cirrhosis

fulminant hepatitis rare

117
Q

what are the symptoms for hepatitis C?

A
  • Nothing to everything
  • RUQ pain
  • Brain fog
  • Depression
  • Alcohol intolerance
118
Q

how can hepatitis C be treated?

A
  • PEGylated interferon and ribavirin

* Significant SE: arthralgia, myalgia, alopecia, neutropenia, thyroid and AI disorders, rashers, pregnancy

119
Q

what are the symptoms and signs of chronic hepatitis?

A
  • Stigmata of CLD
  • Jaundice
  • Splenomegaly
  • Portal hypertension late
  • ALT (mild <100 mod 100-400 severe >400) Ig’s
  • ALK, Phos, Bili, ALB ofte normal
120
Q

what is seen histologically in chronic hepatitis?

A
  • Necroinflammaotory and fibrosis score
  • eAG = e antigen
  • IFN = interferon
  • ANA = anti-nuclear antibody
  • Anti-sm = anti-smith antibody
121
Q

what are the causes of chronic hepatitis?

A

drugs
viruses
Al D
wilsons D

122
Q

describe HBV and chronic hepatitis

  1. men or women more
  2. age
  3. making a diagnosis
  4. treatment
A
  1. men
  2. any age
  3. HbsAg e Ag PCR
  4. IFN iamivudine
123
Q

describe HCV and chronic hepatitis

  1. men or women more
  2. age
  3. making a diagnosis
  4. treatment
A
  1. men=women
  2. any age
  3. anti-HCV and PCR
  4. IFN ribavirin
124
Q

describe autoimmune chronic hepatitis

  1. men or women more
  2. age
  3. making a diagnosis
  4. treatment
A
  1. women
  2. 10-20 and post menopause
  3. ANA anti-Sm Igs
  4. prednisolone
125
Q

describe drugs causing chronic hepatitis

  1. men or women more
  2. age
  3. making a diagnosis
  4. treatment
A
  1. women
  2. middle age onwards
  3. isoniazid. furantoin
  4. withdrawl drugs
126
Q

describe wilson’s disease and chronic hepatitis

  1. men or women more
  2. age
  3. making a diagnosis
  4. treatment
A
  1. Men=women. rare, haemolysis. neurological disease
  2. 10-30
  3. Kayser-fleischer rings. serum Cu and caeruloplasmin
  4. chelation
127
Q

what liver changes occur in alcoholic Liver disease?

A

• Fatty change (steatosis)
• Steatohepatitis: spotty liver cell necrosis, focal. Neutrophils, mallory’s hyaline (accumulation of eosinophilic
material in cytoplasm of damaged liver cells), perivenular fibrosis (around the vein), micronodular cirrhosis.

128
Q

what are the symptoms of alcoholic liver disease?

A
  • Asymptomatic to dull RUQ pain
  • Mildly elevated ALT
  • Hepatomegaly
  • Resolves with abstinence
  • 10% develop cirrhosis
129
Q

what is the prevalence of alcohol use above recommended levels

A

25% men

18% women

130
Q

what conditions is excess alcohol use associated with?

A

Directly associated with cirrhosis, epilepsy, pancreatitis, dementia and foetal abnormalities
• Contributes to chronic conditions: CAD, stroke and cancers

131
Q

what are the acute harms associated with excess alcohol use?

A

RTAs
drowning
assaults

132
Q

what is one unit of alcohol?

A

10G = one unit = 1/2pint = glass of wine

133
Q

how much alcohol use leads to cirrhosis?

A

> 80g/day for 10 years = cirrhosis

134
Q

what are the clinical features in a patient with alcoholic liver disease?

A

• AST > ALT (rarely greater than 300 IU/L)
• GGT – high level is associated with heavy alcohol drinking. Involved in the break down and clear alcohol from
the body
• Hypokalaemia – alcohol is a diuretic, so will lose more potassium through kidneys
• Hyperuricaemia – high uric acid levels, alcohol increases uric acid
• Hyperlipidaemia
• Macrocytosis – near constant hb, enlarged RBC. MCV > 100femtolitres
• Dupuytren’s contracture
• Blood or urinary alcohol levels (or breath test)
• Liver biopsy – steatosis, neutrophilic infiltrate, pericellular zone 3 fibrosis

135
Q

what are the clinical features in a patient with asymptomatic (mild hepatitis or fatty liver) alcoholic liver disease?

A
  • Raised ALK phos/AST

* Smooth hepatomegaly

136
Q

what are the clinical features of acute alcoholic hepatitis?

A
  • Pyrexia
  • Tachycardia
  • Shaking
  • Anorexia/weight loss/malnutrition
  • Nausea/ vomiting/ diarrhoea
  • Tender abdomen
  • Hepatomegaly
  • Spider naevae
  • Dupuytren’s contracture
  • Icterus
137
Q

what are the signs of liver failure or cirrhosis?

A

• Ascites, bleeding, encephalopathy, hypoglycaemia

138
Q

what would laboratory tests show in a patient with alcoholic liver disease?

A
  • LFTS: raised AST and ALK phos and bilirubin and low albumin
  • FBC: Leucocytosis (raised WBC) and thrombocytopaenia (decreased levels of platelets)
  • U&Es: Hypokalaemia
  • Clotting profile: increase in PTT
139
Q

what is the treatment for patients with alcoholic liver disease?

A
  • Sedation and supportive care
  • Sedation – chlormethiazole/hemineverin/chlordiazepoxide
  • Prevent delirium tremens
  • IV fluids 5% dextrose and KCL and antiemetics
  • Vitamins (bit B and C as pabrinex, vit k)
  • Calories
  • Treat accompanying medical problems: GI bleeds, sepsis, ascites, encephalopathy, hepatorenal failure
  • Steroids if marked coagulopathy and jaundice
  • Treat addiction and complications
140
Q

what causes Non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver (NAFL)?

A
  • DM
  • Drugs
  • Parenteral nutrition
  • Intestinal by-pass surgery
141
Q
  1. what does exposure of drugs, DM etc to a healthy liver lead to?
  2. what does severe exposure lead to?
  3. once at these stages what does continued exposure lead to?
A
  1. steatosis
  2. hepatitis
  3. cirrhosis
142
Q

what damage occurs in hepatitis?

A

liver cell necrosis
inflammation
mallory bodies
fatty change

143
Q

what damage occurs in cirrhosis?

A 
fibrosis
hyperplastic nodules
• Micronodular cirrhosis
• Diffuse liver disease with fibrosis and nodule
• Lobular architecture is destroyed and parenchyma is converted into structurally abnormal nodules of liver cells
separated by bands of fibrosis.
• Irreversible condition = ESLF
• Formation due to regeneration
144
Q

what damage occurs in steatosis?

A

fatty change

perivenular fibrosis

145
Q

what is the presentation of NASH and NAFL?

A

• Bland steatosis to fibrosis/cirrhosis
• 40-60% of obese individuals have NAFLD
• 80% steatosis
• 20% steatohepatitis
• 25% progress to cirrhosis over 8yrs
• Classic patient: ALT 98, aetiology screen negative, BMI 33, HT/Diabetes +/-, USS = hyperechoic liver in keeping
with fatty infiltration.
• Increase in AST/ALT are usually less than 4-fold. Ratio of AST/ALT is usually < 1
• History: Female, obesity, diabetes
• Labs:
o Labs to rule out other causes of hepatitis
o Abdominal Ultrasound: look for fatty infiltration of liver

146
Q

what is the treatment for NASH and NAFL?

A
  • Previously thought to be benign
  • Lose weight
  • Good DM control – glitazone
  • Control RF
147
Q

what are the symptoms of drug toxication?

A
  • Varies from ALF to mild hepatitis
  • Often idiosyncratic
  • Isoniazid and Augmentin
  • Hepatitic picture: paracetamol, methotrexate, tetracyclines
  • Statins common reason for referral. Discuss and consider change in agent if 2-3X ULN ALT
148
Q

what is the aetiology of cirrhosis?

A

• Alcoholic LD – 60-70%
• NAFLD
• Viral Hepatitis
• AI hepatitis
• Chronic cholestatic LD
• Metabolic: Iron and copper overload = haemochromatosis and wilson’s
• Drugs and toxins – a-1 antitrypsin deficiency, amiodarone and methotrexate
• Idiopathic
• Paediatric disease – glycogenosis (glycogen storage disease)
• Hepatic venous outflow obstruction: budd chiari syndrome (hepatic vein obstruction is a blockage of the hepatic
vein, carries blood away from the liver. This blockage > liver disease. Constrictive pericarditis – LT inflammation
of sac covering heart with thickening, scarring and muscle tightening.
• Prolonged cholestasis: hepatocellular failure, portal HT, compensated or decompensated, child-pugh
classification – assess the prognosis of CLD, mainly cirrhosis

149
Q

what are the consequence of liver cirrhosis?

A

• Impaired liver function
• Hypoalbuminaemia
• Reduced coagulation factor synthesis
• Decreased metabolism of endogenous oestrogens
• Failure of detoxification – encephalopathy, hepatorenal syndrome: progressive kidney failure with cirrhosis.
• More prone to bleeding, brain disease due to increased levels of ammonia crossing BBB
• Portal HT
• Leads to sodium and water retention: pooling of blood in VD splanchnic circulation, reduced effective
circulating BV, renin release from kidney, hyperaldosteronism
• Ascites: increased transudation due to increased hydrostatic pressure in portal vein, low plasma oncotic
pressure (hypoalbuminaemia), sodium and water retention and extravasation of hepatic lymph
• Infection: kupffer cell dysfunction – macrophages, reduced synthesis of immunoregulatory proteins,
spontaneous bacterial peritonitis
• Hepatocellular carcinoma

150
Q

what are the clinical features of cirrhosis?

A
  • Leukonychia (white nails)
  • Spider naevae
  • Clubbing
  • Palmar erythema
  • Dupuytren’s contracture/parotid gland enlargement
  • Gynaecomastia
  • Testicular atrophy
  • Loss of body hair
  • Malnourished
  • Oedema
  • Ascites
  • Caput medusa (engorged distended paraumbilical veins, radiate from the umbilicus across the abdomen
  • Hepatosplenomegaly
151
Q

What acute vascular changes can occur in a patient with cirrhosis?

A
  • Hypotension
  • RCHF
  • Hepatic venous outflow obstruction (budd-chiari)
152
Q

what chronic vascular changes can occur in a patient with cirrhosis?

A

• Right sided CF
• Venocclusive disease: condition in which some of the small veins in the liver are obstructed. Complicatons of
high dose CT and marked by weight gain due to fluid retention, increased liver size and raised bilirubin levels. (Alkaloids, Alcoholic liver disease, Blood disorders, RT, Cytotoxic drugs, Tumours, Membrane obstruction

153
Q

what are the types of benign liver tumours?

A
  • Focal nodular hyperplasia
  • Liver cell adenoma
  • Bile duct adenoma
  • Haemangioma
154
Q

what are the types of metastatic liver tumours?

A
  • Hepatocellular carcinoma (hepatoma)
  • Cholangiocarcinoma
  • Angiosarcoma
155
Q

who gets hepatocellular carcinoma?

A

M>F
africa and orient
frequency increasing in the west

156
Q

what is a tumour marker of hepatocellular carcinoma?

A

alpha fetoprotein

157
Q

what are the complications of hepatocellular carcinoma?

A

liver failure, bleeding, hypoglycaemia, mets

poor prognosis

158
Q

what is cholangiocarcinoma?

A
  • Tumour of bile ducts
  • Multifocal
  • Associated with chronic biliary irritation: gall stones, liver fluxes, sclerosing cholangitis, cysts
  • Obstructive
  • Poor prognosis
159
Q

what is hepatic angiosarcoma?

A
  • Rare
  • Multifocal haemorrhagic tumours
  • Associated with: occupational exposure to vinyl chloride, arsenic, thorotrast
  • Poor prognosis
160
Q

what would labs show in a patient with hereditary hemochromatosis?

A

• Serum iron, TIBC

  • Calculate iron saturation = serum iron/TIBC (total iron binding capacity)
  • If iron saturation > 45%, check ferritin

•Ferritin
-If > 400 ng/mL in men, or > 300 ng/mL in women, then need to check liver biopsy or genetic
testing

•Liver biopsy

•Homozygous hereditary hemochromatosis if iron index > 1.9
- If under age 40, and positive genetic testing, no biopsy needed.

•Genetic Testing

161
Q

what is autoimmune hepatitis?

A

Chronic, non-resolving liver disease leading to hepatocellular necrosis and cirrhosis. Sub-divided into types 1, 2 and 3
depending on associated autoantibodies & HLA type. Presentation varies – acute flares with jaundice Vs indolent disease

young to middle aged females`

162
Q

what would labs show in a patient with autoimmune hepatitis?

A

o Serum protein electrophoresis (SPEP) – if polyclonal increase in gamma globulin
o Anti-nuclear antibody (ANA)
o Anti-smooth-muscle antibody (SMA)
o Liver biopsy: should be performed if the above are negative, but autoimmune hepatitis still suspected.

163
Q

what is alpha-1-antitrypsin deficiency?

A

A failure of release from hepatocytes, rather than production
• Low serum levels of AAT
• No alveolar protection from elastases
• Build-up within hepatocytes results in damage
Emphysema and cirrhosis are the end result
• History: Family history, emphysema, young age

164
Q

what labs should be done to diagnose a patient with alpha 1 antitrypsin deficiency

A

alpha 1 antitrypsin level/phenotype

165
Q

what is the treatment for alpha 1 antitrypsin deficiency?

A

Intravenous alpha-1 antiprotease helps with lung disease, but liver transplant is ultimately only
treatment for liver disease.

166
Q

what is Wilson’s disease?

A

genetic disorder of biliary copper excretion

167
Q

what investigations would be performed in a patient with Wilson’s disease?

A

• History: Age (usually age 5 – 25, but up to age 40), family history of liver disease; neuropsychiatric disease
• Evaluation:
o Serum ceruloplasmin: Low
o Ophthalmologist: Exam for Kayser-Fleisher rings
o 24-hour urine copper
o Liver biopsy: Evaluate liver copper levels

168
Q

what is the treatment for Wilson’s disease?

A

o Copper chelating agents
o Zinc
o In some cases, ultimately liver transplant

169
Q

what is the aetiology of shock liver (ischaemic hepatits?

A

shock

severe hypotension

170
Q

what would lab results show in a patient with shock liver?

A

Severely elevated AST/ALT (50 times normal)

171
Q

what is the treatment for shock liver?

A

re-establish good blood pressure/perfusion

172
Q

what is the prognosis for shock liver?

A

Usually patients recover, but can progress to fulminant liver failure requiring transplant.

173
Q

what non-hepatic causes can cause mild increase in AST/ALT?

A 
• Muscle disorders
•Hypothyroidism/Hyperthyroidism
• Celiac Disease
• Adrenal Insufficiency
• Anorexia nervosa
• Drugs:
o Anabolic steroids, contraceptives, antibiotics
• Total parenteral nutrition (TPN)
• Cirrhosis:
o Viral hepatitis (Hepatitis B, C)
o Alcohol hepatitis
174
Q

what is jaundice?

A

yellow discolouration of the skin and mucous membranes caused by an increase in bilirubin
concentration in the body fluid

175
Q

what is the normal level of bilirubin?

A

3-17micromol/l

176
Q

what level does jaundice become detectable?

A

40micromol/l

177
Q

what tissues concentrate bilirubin best?

A

high content of elastic tissue – skin, sclera and blood vessels

178
Q

what causes raised bilirubin?

A

Obstructive liver disease – ALP and GGT usually raised too

Mechanical obstructive >50% of bilirubin is conjugated

Isolated levels: defect in conjugation – Gilberts disease, there is an increase in unconjugated bilirubin,
including haemolysis

179
Q

describe the physiology of bilirubin?

A

• Bile pigment produced by breakdown of haem and reduction of
biliverdin
o Unconjugated is insoluble > transported bound to albumin
o Normally 95% is unconjugated
• The hepatic sinusoids are large so that bilirubin-albumin complex can
diffuse to the plasma membrane of the hepatocyte. Made water
soluble in the liver cells by attaching sugar molecule to it =
conjugated. Passed into bile duct. Here, unconjugated bilirubin
dissociates from albumin and enters cytosol via facilitated transport
• In cytosol, conjugated by enzyme bilirubin UDP-glucuronyl
transferase > bilirubin diglucuronide
• Raised level of conjugated occurs in liver and bile duct conditions.
High if flow of bile is blocked. Gallstones or tumour in pancreas.
Also raised with hepatitis, liver injury or LT alcohol abuse.
• Enters gut via biliary tree, bilirubin glucoronides are degraded and
converted > urobilinogen and stercobilinogen. Urobilinogen
excreted into faeces > urobilin = brown

180
Q

what are the causes of jaundice?

A

• Pre-hepatic
• Hepatic
• Post-hepatic
Divided into unconjugated and conjugated bilirubin

181
Q

what are the prehepatic causes of jaundice?

A

haemolysis

182
Q

what are the intrahepatic causes of jaundice?

A 
viral hepatitis
drugs
alcoholic hepatitis 
cirrhosis 
pregnancy 
recurrent idiopathic cholestasis 
some congenital disorders
183
Q

what are the extrahepatic causes of jaundice?

A 
common duct stones
carcinoma
biliary stricture
sclerosing cholangitis 
pancreatic pseudocyst
184
Q

what do you ask for in a patient with jaundice?

A

• Age: younger = viral hepatitis, older = gallstones/malignancy
• Onset: slow with pruritus = cholestasis, rapid with nausea and anorexia = viral, episodic = gilberts
• Gender: F = AI disease, M = alcohol induced
• Other symptoms: pale stool/dark urine/itching = cholestasis. Pain = gallstones. Fever/rigors = cholangitis
(infection of common bile duct carriers bile from liver to GB and intestines)
• Drugs: prescribed, OTC, illicit/IV
• PMH: previous jaundice, ops, gallstones, carcinoma
• FH: jaundice, liver disease, haemolytic anaemia
• Social: high alcohol exposure, industrial exposure (vinyl chloride), food – shellfish, sexual contacts, travel
history/vaccinations.

185
Q

what do you check for on examination in a patient with jaundice?

A 
• Stigmata of LD
• Clubbing
• Palmer Erythema
• Dupuytren’s contracture
• Spider naevi
• Hepato-splenomegaly
• Ascites (fluid that accumulates in the abdominal (peritoneal) cavity. Complication of cirrhosis and appears as
an abdominal bulge)
186
Q

describe pre-hepatic jaundice?

A
  • Inability of liver to handle increase in bilirubin (haemolysis)
  • Limiting factor = enzyme glucuronyl transferase
  • Serum bilirubin increased, is unconjugated
  • NO urinary bilirubin as not water soluble
  • Other indicators are within normal range
187
Q

what is the aetiology of pre-hepatic jaundice?

A

• Physiological neonatal jaundice – most common
• Haemolysis (abnormality of RBC: sickle cell, spherocytosis),
-Leads to excessive breakdown of RBC with excessive bilirubin production> unconjugated
hyperbilirubinaemia (rare exceeds capacity of the liver to excrete bilirubin)
• Haematoma
• Ineffective erythropoiesis e.g. pernicious anaemia
• Severe rhabdomyolysis with release of myoglobin
• Bleeding into tissues e.g. in sports injuries

188
Q

describe hepatic causes of jaundice?

A
  • Inherited conditions of the liver which give a conjugated hyperbilirubinaemia
  • GILBERTs SYNDROME
  • AS dominant inherited.
  • Abnormality of glucuronidase activity
  • Jaundice is mild, worse with fasting and drinking alcohol or intercurrent illness
189
Q

what changes would you expect to see in a patient with hepatic jaundice?

A

Serum / blood:
• bilirubin (micormoles/l) 50-150; normal range 3-17
• Liver enzymes normal: AST, ALP, GGT, Albumin, PTT
• reticulocytes(%) 10-30; normal range <1
Urinary changes:
• bilirubin: absent
• urobilinogen: increased or normal
Faecal changes:
• stercobilinogen: normal

190
Q

descibe conjugated bilirubin?

A
  • Bilirubin taken up into hepatocytes from blood
  • Bound intracellularly
  • UDP glucuronic acid reacts with bilirubin to form mainly bilirubin diglucuronide
  • Glucuronide conjugated form of bilirubin is water soluble and excreted into bile
  • Disorders of bilirubin take up or conjugation can lead to hepatic jaundice
191
Q

describe hepatic jaundice?

A
  • Failure in function of hepatocytes to take up, metabolise or excrete bilirubin (secretion of bile)
  • Jaundice is rapid
  • Fatigue and malaise are common
  • Serum transaminases increased
  • Albumin reduced in chronic disease
  • PTT prolonged
192
Q

what are the most common aetiologies of hepatic jaundice?

A

• Hepato-cellular disease (viral hepatitis (hep A/B/C/E), alcoholic hepatitis, drugs, AI, cirrhosis)
• Cholestatic D (bile ducts – bile can’t flow from liver to the duodenum)
(Drugs, Mets, Cirrhosis, Sepsis, AI)

193
Q

what changes would you expect to see in hepatic jaundice?

A
  • serum / blood:
  • bilirubin (micromoles/l) 50-250; normal range 3-17
  • AST I.U. 300-3000; normal range <35
  • ALP I.U. <250-700; normal range <250
  • gamma GT I.U. 15-200; normal range 15-40
  • albumin g/l 20-50; normal range 40-50
  • reticulocytes (%) <1; normal range <1
  • prothrombin time (secs) 15-45; normal range 13-15
  • ( “ + parenteral vit. K) 15-45
  • urinary changes:
  • bilirubin: normal or increased
  • urobilinogen: normal or reduced
  • faecal changes:
  • stercobilinogen: normal or reduced
194
Q

describe post-hepatic jaundice?

A

• Converted to di- monoglucuronide before secretion into biliary canaliculi
• Degraded to urobilinogen
• Can be reabsorbed by gut and to the liver
• Converted to urobilin that colours faeces or reabsorbed and excreted by kidneys
• Or conjugated bilirubin can be acted upon by bacterial enzymes within the gut to form bile pigment
stercobilinogen
• Can be recycled in the liver or excreted by the kidney
• Or oxidised to stercobilin – is bile pigment, appears brown in faeces
• Failure of bilirubin to reach gut results in reduction in pigment within the stool = pale stools

195
Q

what are the causes of post hepatic jaundice?

A

• Biliary tract causes (CBD)

  • Gallstones
  • Stricture
  • Carcinoma
  • Extrinsic pressure

•Pancreatic Causes (head)

  • Carcinoma
  • Chronic pancreatitis

• Extrahepatic cholestasis results from mechanical obstruction to large bile ducts outside liver

  • Liver enlarged and intra hepatic bile ducts widely dilated
  • Bile ducts proliferate in portal zones
  • Infection of bile leads to cholangitis
  • Pale stool – no bilirubin reaching GI tract for conversion to stercobilin
  • Dark orange urine – conjugated bilirubin into blood, excreted in urine
  • Icterus
  • Pruritus
196
Q

what is courvoisiers law?

A
  • Jaundice and palpable gall bladder = unlikely to be due to gallstones more likely to be pancreatic cancer
  • Bastardisation: progressive painless jaundice = carcinoma
197
Q

what is Murphy’s sign used for and describe it?

A

• sign for gallstones/cholecystitis
•During abdo exam
• Breathe out and place hand below costal margin on the R side at the mid-clavicular line
• Patient then instructed to inspire (breathe in)
• During inspiration, abdo contents are pushed down as the diaphragm moves down. If patient stops breathing
in (as the GB is tender and moving down, comes in contact with examiners fingers)
• Winces with a catch in breath
• Test considered positive
• Same manoeuvre must not elicit pain when performed on the L side.
• Tender in RUQ on inspiration but not in LUQ

198
Q

what is charcot’s triad?

A

triad for ascending cholangitis-infection of common bile duct
• Fever
• Jaundice
• RUQ pain

199
Q

what is the aetiology of obstruction in the bile ducts?

A 
The cause of obstruction of any hollow organ may be divided into luminal, mural and extramural causes:
Obstruction of the lumen of the bile ducts:
• Gall stones – common
• Tumours
• Parasites:
o Hydatid disease
o Liver fluke
o Round worms
• Iatrogenic:
o Post-T-tube cholangiography
200
Q

what is mural obstruction?

A
  • congenital atresia
  • traumatic stricture e.g. ampullary stricture
  • sclerosing cholangitis
  • cholangiocarcinoma
201
Q

what is extramural obstruction?

A
  • carcinoma of the head of pancreas - common
  • carcinoma of the ampulla of Vater
  • pancreatitis
  • porta hepatis tumours (often secondary deposits)
  • chronic duodenal ulceration
202
Q

what changes occur when there is obstruction of bile ducts?

A
  • serum / blood:
  • bilirubin (micromoles/l) 100-500; normal range 3-17
  • AST I.U. 35-400; normal range <35
  • ALP I.U. >500; normal range <250
  • gamma GT I.U. 30-50; normal range 15-40
  • albumin g/l 30-50; normal range 40-50
  • reticulocytes(%) <1; normal range <1
  • prothrombin time (secs) 15-45; normal range 13-15
  • ( “ + parenteral vitamin K) falls
  • urinary changes:
  • bilirubin: increased
  • urobilinogen: reduced or absent
  • faecal changes:
  • stercobilinogen: reduced or absent
203
Q

What is cholestasis?

A

failure of normal amounts of bile to reach duodenum
o Source may reside in the main bile ducts = extrahepatic cholestasis 70% -
o Or in the liver = intrahepatic cholestasis 30%

204
Q

what is chronic cholestatic disease?

A

• Decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow through intra-or
extrahepatic bile ducts.
• Clinical definition of cholestasis is any condition in which substances normally excreted into bile are retained.

205
Q

what is primary biliary cirrhosis?

A

• AI disease of liver. Slow progressive destruction of the small bile ducts of the liver with the intralobular ducts
(canals of Hering) affected early on.
o Predominately in women, usually ages 35-65
o May have history of other autoimmune disease
• When these ducts are damaged, bile builds up in the liver = cholestasis and damages tissue. This can lead to
scarring, fibrosis and cirrhosis

206
Q

what are anti-mitochondrial antibodies?

A

autoantibodies formed against mitochondria in the cells of the liver.
Presence of AMAs in the blood or serum is indicative of AI diseases – present in 95% of cases of primary billiary cirrhosis

207
Q

what are the symptoms of primary billiary cirrhosis?

A

Prurutis, fatigue, hyperpigmentation, musculoskeletal complaints

208
Q

what investigations should be done in patients with primary biliary cirrhosis?

A

RUQ Ultrasound

Anti-mitochondrial antibody

Liver biopsy to verify diagnosis

209
Q

what is primary sclerosing cholangitis?

A

• Disease of the bile ducts that cause inflammation and
subsequent obstruction of bile ducts both at intrahepatic and
extrahepatic level. Impedes the flow of bile to the gut, lead to
cirrhosis of the liver, LF and Liver cancer.
• Chronic progressive disorder of unknown etiology that is
characterized by inflammation, fibrosis, and stricturing of
medium size and large ducts in the intrahepatic and
extrahepatic biliary tree.
• Underlying cause – AI
• More than 80% of those with PSC have UC
• Treat with liver transplant

210
Q

what are the clinical features of primary sclerosing cholangitis?

A

• Pruritus
• Icterus (jaundice)
• Xanthomas: palmar creases, below the breast, on the neck.
They indicate raised serum cholesterol of several months.
Xanthomas on the tendon sheaths are uncommonly
associated with cholestasis.
• Xanthelasma on the eyelids
• scratch marks: excoriation
• finger clubbing
• loose, pale, bulky, offensive stools – steatorrhoea leading to ADEK malabsorption
• bruising/bleeding (vitamin K deficiency)
• Vitamin D bone disease
• dark orange urine

211
Q

how does extrahepatic cholestasis present?

A
  • pain, due to gallbladder disease, malignancy, or stretching of the liver capsule
  • fever, due to ascending cholangitis
  • palpable and / or tender gallbladder
  • enlarged liver, usually smooth
212
Q

what are the initial investigations for jaundice?

A
  • Cause always sought as not a diagnosis itself
  • 2 most useful tests: viral markers for HAV, HBV, HCV with an US
  • liver biochemistry confirms
  • US for extrahepatic obstruction – dilated bile ducts, level of obstruction and cause
213
Q

describe liver biochemistry in jaundice?

A
  • In hepatitis, serum AST, ALT high early in disease
  • Extrahepatic obstruction, ALP high
  • PT prolonged in longstanding disease, serum albumin low
214
Q

what would haematological tests show in jaundice?

A
  • Bilirubin raised other is normal
  • Raised WCC indicate infection – cholangitis
  • Leucopenia in viral hepatitis
  • Mononuclear cells = infectious mononucleosis
215
Q

what are the common findings in a patient with cholestatic jaundice?

A
  • Dark urine (conjugated bilirubin)
  • Pale stools
  • Pruritus
  • Little in the way of pain
  • Oedema, ascites, bruising, spider naevi
  • Complications: GI bleeding (varices)
216
Q

what are the common findings in a patient with primary biliary cirrhosis?

A
  • AI condition intrahepatic biliary tree
  • Female:male 10:1
  • Antimitochondrial antibody
  • Liver biopsy
  • Supportive treatment, ursodeoxycholic acid, liver transplant
217
Q

what are the common clinical features of hepatomegaly?

A
  • Hepatomegaly: smooth generalised enlargement, with or without jaundice
  • Hepatomegaly: knobbly generalised enlargement with or without jaundice
  • HM: localised swellings
  • HM: mild, moderate, massive
218
Q

what causes massive hepatomegaly?

A
  • Secondary carcinoma
  • Alcoholic liver disease with fatty infiltration
  • RHF
  • Myeloproliferative disease
219
Q

what causes moderate hepatomegaly?

A
  • Haemochromatosis
  • Haematological disease
  • Fatty liver secondary to diabetes
220
Q

what causes mild hepatomegaly?

A
  • Hepatitis

* Biliary obstruction

221
Q

what causes smooth, generalised hepatomegaly with jaundice?

A
  • Infective causes: viral hepatitis, bacterial, protozoal, parasitic
  • Extra-hepatic biliary tract obstruction
  • Cholangitis
222
Q

what causes smooth generalised hepatomegaly without jaundice?

A
  • Congestive cardiac failure
  • Liver cirrhosis
  • Hepatic vein obstruction
  • Amyloidosis
223
Q

what causes knobbly hepatomegaly with jaundice?

A
  • Extensive secondary carcinoma

* Liver Cirrhosis

224
Q

what causes knobbly hepatomegaly without jaundice?

A

Secondary carcinoma
• Cirrhosis
• Polycystic disease

225
Q

what causes localised swelling on the liver?

A
  • Secondary carcinoma
  • Liver abscess
  • Cysts
226
Q

what investigations are done in a patient with hepatomegaly?

A
  • Bloods: FBC, U&Es, LFT, clotting, inflammatory markers
  • Full lover screen
  • US abdomen.
227
Q

describe chronic Al hepatitis (lupoid hepatitis), plasma cell hepatitis?

A
  • W more commonly than M
  • Associated with other AI disorders
  • Often presents with lethargy and rash/sub clinical and asymptomatic
  • Acute, fulminant onset
  • Chronic active hepatitis
  • Anti-antibody positive ANA/ASMA LKM1 antibodies
  • Aetiology screen and liver biopsy
  • Anti-nuclear AB associated with SLE, scleroderma, AI hepatitis
  • Liver kidney microsomal type 1 AB associated with AI hepatitis
228
Q

what is haemochromatosis?

A
  • AS Recessive – common
  • 75% present with abnormal LFTs
  • W present later than M
  • High ferritin
  • Multiple associations
229
Q

how does haemochromatosis present?

A

LFT – 75%
• Weakness and lethargy 74%
• Skin hyperpigmentation 70%
• Diabetes Mellitus – 48%

230
Q

what is the treatment of haemochromatosis?

A
  • Venesection – twice weekly until ferritin falls then infrequent
  • Cirrhosis can reverse
231
Q

describe alcoholic hepatitis?

A
  • Excess alcohol for a long time – without ill effect 40-70units/week
  • Suddenly become ill
  • Hepatomegaly, jaundice, pyrexia, anorexia
  • 50% die, 50% > cirrhosis
232
Q

Where is alkaline phosphatase found?

A

Found in liver, bone, intestine, first trimester placenta and kidney.

233
Q

When are alkaline phosphatase levels raised?

A

Raised in liver and bone disease.
If raised with GGT = liver.
Raised in cholestasis and biliary obstruction

Block 32 GI and surgery (12 decks)

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