5. Liver disease and intestinal failure

Question 1

Causes of Acute liver disease

Answer 1

acute insult:
viruses (Hep A, B, C, E, CMV, EBV)
drugs - termed DILI, paracetamol, herbal remedies, ecstasy
Immune - autoimmune hepatitis
Alcohol rarely

Question 2

Symptoms of acute liver disease

Answer 2

jaundice
increased serum bilirubin
dark urine
pale stools
bile duct obstruction or biliary obstruction
feeling unwell
nausea
occasionally fever
confusion due to hepatic encephalopathy and liver failure

Question 3

Cirrhosis and platelet count

Answer 3

Cirrhosis causes decrease in platelets

increased shear stress causing platelet aggregation

Thrombocytopenia:

Thrombopoietin is predominantly produced by the liver and is reduced when liver cell mass is severely damaged

Question 4

diagnose jaundice and severe itching

Answer 4

gall stone obstruction

Question 5

diagnose an increase in alkaline phosphotase and gamma GT

Answer 5

bile duct disease

Question 6

Bilirubin

Answer 6

breakdown product of heme proteins - hemoglobin&myoglobin
excreted in bile
conjugated with glucuronic acid
unconjugated fraction binds to serum albumin

unconjugated hyperbilirubinemia: haemolysis, gilberts (mild)
urinalysis is negatice for bilirubin

increased serum bilirubin indicates jaundice caused by hemolysis, liver disease (impairment of bilirubin handling) and biliary obstruction

Question 7

albumin

Answer 7

major circulating protein
synthesised in liver
half life 21 days, decreases during intercurrent infection

low serum albumin in infection eg pneumonia
low in renal loss - nephrotic syndrome
low in impaired synthesis - severe liver disease
low in severe malnutrition

Question 8

ALT or SGPT
alanine transaminase

Answer 8

cytosolic enzyme
liver enzyme&raquo_space;muscle
increases during liver injuries

Question 9

AST or SGOT
aspartate transaminase

Answer 9

muscle>liver
found in cytsols and mitochondria
alcohol is mitochondrial poison, so AST increases when alcohol increases

Question 10

transaminases

Answer 10

very high signifies liver cell injury with release of enzymes into circulation

very very very high = paracetamol overdose of ischemic hepatitis

moderately elevated = fatty liver, cholangitis

ALT > AST for liver injuries

AST>ALT w severe fibrosis or cirrhosis, alcohol excess or muscle injury

Question 11

alkaline phosphotase

Answer 11

in liver, bone, biliary, placenta and intestine
increased in pregnancy and bone disease (Pagets disease)

more cholestatic than hepatitic (involving bile duct/secretion)

increase in biliary obstruction or primary biliary cholangitis

Question 12

gamma glutamyl transpeptidase

Answer 12

Gamma GT is membrane-bound enzyme present in liver, kidney and pancreas
plays a role in the metabolism of glutathione (antioxygenase) and facilitates amino-acid transport.

Serum gamma-GT activity is induced by alcohol and certain drugs such as phenytoin and cholestasis or biliary obstruction.

Very sensitive: Modest increases common in most liver diseases

Very high levels suggest biliary obstruction or cholestasis or alcohol.

Question 13

FIB4 Score

Answer 13

An indirect biomarker of liver fibrosis
noninvasive test
Calculated from ALT, AST, Platelet count and age.
A score of <1.45 and >3.25 enables the correct identification of patients who have moderate or significant fibrosis, respectively

Question 14

chronic liver disease and causes

Answer 14

Chronic Liver disease
Repetitive liver injury
Finger prick analogy
Chronic inflammation leads to cell death and regeneration and fibrosis

Alcohol
Chronic viral hepatitis
Fatty liver disease
Autoimmune liver disease
Other causes – iron overload, biliary disease, inherited diseases

Question 15

alcoholic liver disease

Answer 15

Alcohol is metabolised to acetaldehyde and fat
Excess alcohol causes fatty liver
Need to drink >50-100 units alcohol per week for >10 years to developed alcohol related cirrhosis
Only 20% of patients who drink to excess develop alcohol related cirrhosis
The pathology is very similar to fatty liver disease – hence why sometimes called non-alcoholic fatty liver disease

Question 16

fatty liver disease
how its diagnosed

Answer 16

Diagnosed by ultrasound scan examination or other imaging
Of 100 patients with fatty liver disease only50% have abnormal liver function tests.
The critical determinate of fatty liver disease is whether or not a patient has NASH or simple steatosis.
85% have simple steatosis and 15% have NASH.
You can only tell by liver biopsy or if the patient has significant fibrosis on fibroscan.
Abnormal liver function tests do not predict whether a patient has NASH or simple steatosis.
FIB4 calculation enhances predictability.

Question 17

fibroscan

Answer 17

Determines liver stiffness and CAP score

Works by measuring the speed of ultrasound waves as they move through liver tissue. This measurement can tell us about the state of the liver. For example, ultrasound waves move faster through fibrotic/scarred livers.

Liver stiffness is measured in kPa and is an assessment of how wobbly the liver is. (Normal <6.0kPa)

CAP score measures fat content (normal <220dBM)

Question 18

chronic viral hepatitis

Answer 18

Only hepatitis B and C cause chronic liver disease.
300 million people worldwide have chronic hepatitis B – it is transmitted vertically, through sex, IVDU and IV products not screened.
60 million people worldwide have chronic hepatitis C – it is transmitted through IV drug use (IVDU) and IV products not screened.
Both can cause chronic inflammation of the liver and the development of cirrhosis.
Chronic hepatitis B and C both cause liver cancer with a risk of 2-4% per year in those with underlying cirrhosis.
Important to diagnose as current treatments are nearly 100% effective

Question 19

primary biliary cholangitis

Answer 19

Primary biliary cholangitis once a rare disease now affects neary 1: 1000 women over the age of 40 years in the UK. Men are less commonly affected (<10%).
Associated with anti-mitochondrial antibody and so is considered an autoimmune disease – but immunosuppression relatively ineffective.
It is treated with ursodeoxcholic acid.

Question 20

primary sclerosing cholangitis

Answer 20

Primary Sclerosing cholangitis (PSC) causes stricturing of the small and large bile ducts.
Associated with ulcerative colitis (80%) and yet only 5% of patients with ulcerative colitis develop PSC.
Some develop cirrhosis, and 10% develop cholangiocarcinoma over ten years.

Both may develop xanthalasma of the eyes or hands but most common is PBC and due to acumulatin of lipoprtien X

Question 21

Complications of cirrhosis

Answer 21

Portal Hypertension
Ascites
Varices
Hepatorenal syndrome
Hepatic encephalopathy
Immune paresis
Patients with cirrhosis are immunocompromised
20-40% develop infections when admitted to hospital

Question 22

diagnose severe abdominal pain and distension
and absolute constipation

Answer 22

bile obstruction

Question 23

vitamin D surgical sieve

Answer 23

vascular
infection/inflammation
trauma/toxic
autoimmune
metabolic
idiopathic
nutritional/neoplastic
degenerative

Question 24

how to assess someone’s nutritional status

Answer 24

bedside tests:
urine, blood glucose, ecg, rectal scan, history, temp, height/weight

blood tests:
cardiac screening, check for malnutrition, electrolyte abnormalities, inflammation, full blood test, haemoglobin

microbiology:
infection

plain xrays:
CT

specialist tests:
endoscopy

Question 25

small bowel obstruction investigation

Answer 25

CT to find mass lesion in mid/small bowel

laparotomy (opening of abdomen)
resection of mass (removal)

jejunostomy to see length of small bowel from duodeno-jejunal flexure

Question 26

MUST

Answer 26

malnutrition universal screening tool
0/1/2 risk
2 or more: treat

BMI, weight loss, acute disease effect score,

Question 27

jejunostomy length and support needed

Answer 27

0-50: parenteral (administered outside intestines), saline
51-100: parenteral, saline
101-150: oral/enteral, oral glucose solution
151-200: none, oral glucose solution

Question 28

short bowel syndrome
cause
consequences

Answer 28

cause: massive intestinal resection
resection <100cm: more bile salt malabsorption so diarrhoea
malabsorbed bile salts enter colon where they cause water secretion by activating cyclic adenosine monophosphate

> 100: more fatty acid loss in colon, more water secretion and diarrhoea
malabsorption of vitamin B12

loss of energy

malabsorption of fat, carbs and protein

Question 29

parts of the intestine
in order

Answer 29

oesophagus
stomach
duodenum
jejunum
ileum
large intestine

Question 30

stoma output
high

Answer 30

> 1500ml + dehydration = high output stoma

Question 31

rehydration solutions

Answer 31

hypertonic fluids
to keep sodium chloride levels up

dioralyte

Question 32

nutritional treatments

Answer 32

rehydration

encourage a hypercaloric diet:
high salt diet, more sodium content in lumen, decreases osmosis, keeps nutrients in body for it to be absorbed

increase gastric ph

slow GI transit:
loperamide
codeine

bile sale sequestrants

micronutrient replacement

Question 33

medical and dietary approach to managing short bowel syndrome
in order

Answer 33

determine location of intestine that was resected to estimate likelihood or diarrhoea, malabsorption and malnutrition

replace fluid losses and manage diarrhoea

select appropriate oral nutrition:
carbohydrate-electrolyte feeds
sodium chloride tablets

replace specific mineral and vitamin deficiencies
zinc
potassium
magnesium
vitamins A B12 D E K