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Final Year > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What is liver cirrhosis?

A

Chronic inflammation and damage
Cells replaced with scar tissue
Nodules of scar tissue form
Affects structure an blood flow through liver, increasing resistance- Portal HTN

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2
Q

What are the 4 most common causes of liver cirrhosis?

A

Alcoholic liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hep B
Hep C

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3
Q

What are the rarer causes of liver cirrhosis?

A

AI hep
PBC
Haemochromatosis
Wilson’s disease
Alpha-1 antitrypsin deficiency
CF
Amiodarone, methotrexate, sodium valproate

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4
Q

List examination findings of liver disease

A

Cachexia- Wasting of body and muscles
Jaundice- Raised bilirubin
Hepatomegaly
Small nodular liver
Splenomegaly- Due to portal HTN
Spider naevi- Telangiectasia with central arteriole and small vessels radiating away
Palmar erythema- Elevated oestrogen
Gynaecomastia and testicular atrophy- Endocrine dysfunction
Bruising- Abnormal clottingExcoriations
Ascites
Caput medusae- Distended paraumbilical veins due to portal HTN
Leukonychia (white fingernails)- associated with hypoalbuminaemia
Asterixis- Flapping tremor- Decompensated liver disease

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5
Q

Outline a non-invasive liver screen

A

Done following abnormal LFTs without a clear cause
US liver- Fatty liver
Hep B and C serology
Autoantibodies- AI hep, PBC and PSC
Immunoglobulins- AI hepatitis and PBC
Caeruloplasmin- Wilsons disease
Alpha-1 antitrypsin levels
Ferritin and transferrin (hereditary haemochromatosis)

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6
Q

Which autoantibodies are relevant to liver disease?

A

ANA
Smooth muscle antibodies
Antimitochondrial antibodies
Antibodies to liver kidney microsome type 1 (LKM-1)

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7
Q

What happens to LFTs in decompensated cirrhosis?

A

(Can be normal if not decompensated)
Deranged bilirubin, ALT, AST, and ALP

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8
Q

Which other bloods should be done for liver cirrhosis other than LFTs?

A

Low albumin- Due to reduced synthetic function of liver
Increased prothrombin time- Due to reduced synthetic function of liver (decreased production of clotting factors)
Thrombocytopenia (low platelets)- Indicates more advanced disease
Hyponatremia (low sodium)- Occurs with fluid retention in severe liver disease
Urea and creatinine- Deranged in hepatorenal syndrome
Alpha-fetoprotein- Tumour marker for hepatocellular carcinoma

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9
Q

What is the 1st line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

Enhanced liver fibrosis (ELF) blood test
Measures HA, PIIINP, TIMP-1
>10.51 - Advanced fibrosis
Recheck every 3y

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9
Q

How does liver cirrhosis present on US?

A

Nodularity on surface of liver
Corkscrew appearance to hepatic arteries with increased flow to compensate for reduced portal flow
Enlarged portal vein with reduced flow
Ascites
Splenomegaly

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10
Q

What are the screening tools used for hepatocellular carcinoma?

A

US
Alpha-fetoprotein

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10
Q

How does non-alcoholic fatty liver disease present on US?

A

Increased echogenicity

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11
Q

What is a transient elastography?

A

‘Fibroscan’
Assesses stiffness of liver using high-frequency sound waves
Determines degree of fibrosis to test for liver cirrhosis

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12
Q

What can happen to the oesophagus in portal HTN?

A

Oesophageal varices

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13
Q

When is the MELD score used?

A

Model for End-Stage Liver Disease
Used every 6 mths in compensated cirrhosis
Bilirubin, creatinine, INR, sodium, and whether they require dialysis
Gives an estimated 3mth mortality %

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14
Q

What is the Child-Pugh Score?

A

Assesses severity of liver disease and prognosis
Minimum score 5, maximum 15- Each scored 1-3
A- Albumin
B- Bilirubin
C- Clotting (INR)
D- Dilation (ascites)
E- Encephalopathy

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15
Q

Which underlying causes need to be addressed for liver cirrhosis?

A

Stop drinking alcohol
Lifestyle changes for non-alcoholic fatty liver disease
Antiviral drugs for Hep C
Endoscopy every 3y for oesophageal varices

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16
Q

How do you monitor for complications of liver cirrhosis?

A

MELD score every 6mths
US and AFP every 6mths for hepatocellular carcinoma
Endoscopy every 3y for oesophageal varices

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17
Q

When is a liver transplant considered in liver cirrhosis?

A

In decompensated liver disease
A- Ascites
H- Hepatic encephalopathy
O- Oesophageal varices bleeding
Y- Yellow (jaundice)

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18
Q

What is the prognosis of liver cirrhosis?

A

5y survival about 50% once cirrhosis developed

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19
Q

List complications of cirrhosis

A

Malnutrition and muscle wasting
Portal HTN, oesophageal varices, bleeding varices
Ascites and spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma

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20
Q

Why does cirrhosis lead to malnutrition?

A

Loss of appetite due to reduced intake
Cirrhosis affects protein metabolism in liver and reduces amount of protein liver produces
Disrupts ability of liver to store glucose as glycogen and release it when required

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21
Q

What is the management of malnutrition in cirrhosis?

A

Regular meals
High protein and calorie intake
Reduced sodium intake to minimise fluid retention
Avoid alcohol

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22
Q

Why does cirrhosis lead to portal HTN and varices?

A

Portal vein comes from Sup. mesenteric and splenic veins and delivers blood to liver
Liver cirrhosis increases resistance to blood flow in liver= Increased back pressure- Results in splenomegaly
Causes swollen and tortuous vessels at sites where collaterals form between portal and systemic venous systems- Distal oesophagus (oesophageal varices) and anterior abdo wall (caput medusae)

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23
Q

Outline management of varices in cirrhosis

A

Asymptomatic until start bleeding
High blood flow= Can exsanguinate quickly
Prophylaxis: Propanolol 1st line, variceal band ligation if BB CI

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24
Q

How are bleeding oesophageal varices managed?

A

Immediate senior help
Consider blood transfusion
Treat coagulopathy- FFP
Vasopressin analogues (terlipressin or somatostatin)- Cause vasoconstriction and slow bleeding
Prophylactic broad-spectrum ABs
Urgent endoscopy with variceal band ligation
Consider intubation and intensive care
Sengstaken-Blakemore tube (inflatable tube in oesophagus to tamponade bleeding varices)
Transjugular intrahepatic portosystemic shunt (TIPS)

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25
Q

What is a Sengstaken-Blakemore Tube?

A

Used to stop oesophageal variceal bleeds
Inflatable tube in oesophagus to tamponade bleeding varices

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26
Q

What is Transjugular Intrahepatic Portosystemic Shunt (TIPS)?

A

Used to stop bleeding oesophageal varices or refractory ascites
Interventional radiologist inserts wire via xray guidance into jugular vein, down vena cava into liver via hepatic vein
Connection made through liver between hepatic vein and portal vein and stent inserted
Allows blood to flow directly from portal vein to hepatic vein, relieving pressure in portal system

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27
Q

Why does cirrhosis lead to ascites?

A

Fluid in peritoneal cavity
Increased pressure in portal system causes fluid to leak out of capillaries in liver and other abdominal organs in peritoneal cavity
Drop in circulating volume caused by fluid loss into peritoneal cavity = Reduced BP in kidneys = Release renin = Increased aldosterone secretion via renin-angiotensin-aldosterone system = Reabsorption of fluid and sodium in kidneys = Fluid and sodium retention
Causes TRANSUDATIVE ascites (low protein)

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28
Q

Outline management of ascites in liver cirrhosis

A

Low sodium diet
Aldosterone antagonists (spironolactone)
Paracentesis (ascitic tap/drain)
Prophylactic ABs (ciprofloxacin) when <15g/l protein in ascitic fluid
TIPS considered in refractory ascites
Liver transplant considered in refractory ascites

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29
Q

Why can cirrhosis lead to spontaneous bacterial peritonitis?

A

Occurs in 10-20% patients with ascites
Mortality 10-20%
Infection in ascitic fluid and peritoneal lining w/o clear source of infection

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30
Q

What are the symptoms of spontaneous bacterial peritonitis?

A

Can be asymptomatic
Fever
Abdo pain
Deranged blood- Raised WBC, CRP, creatinine, or metabolic acidosis
Ileus (reduced movement in intestine)
Hypotension

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31
Q

What are the most common causative organisms of spontaneous bacterial peritonitis?

A

E. coli
Klebsiella pneumoniae

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32
Q

Outline management of spontaneous bacterial peritonitis

A

Sample ascitic fluid or culture before giving ABs
IV broad-spectrum ABs (piperacillin with tazobactam)

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33
Q

How can cirrhosis cause hepatorenal syndrome?

A

Impaired kidney function caused by changes in blood flow to kidneys relating to liver cirrhosis and portal HTN
Portal HTn causes portal vessels to release vasodilators = Significant vasodilation in splanchnic circulation = Reduced BP
Kidneys respond to low BP via RAAS = Vasoconstriction of renal vessels = Kidneys starved of blood

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34
Q

What is the prognosis and management of hepatorenal syndrome?

A

Poor prognosis unless liver transplant

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35
Q

How can liver cirrhosis cause hepatic encephalopathy?

A

Build up of neurotoxic substances that affect the brain
AMMONIA- Produced by intestinal bacteria when break down proteins - Absorbed in intestines and builds up
Ammonia build up due to liver cells functional impairment preventing them from metabolising ammonia into harmless waste products and collateral vessels between portal and systemic circulation means ammonia bypasses liver and enters systemic system directly

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36
Q

How does hepatic encephalopathy present?

A

Reduced consciousness
Confusion
Chronic- Changes to mood/personality and memory

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37
Q

List factors which can trigger or worsen hepatic encephalopathy

A

Constipation
Dehydration
Electrolyte disturbance
Infection
GI bleeding
High protein diet
Meds- Sedatives in particular

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38
Q

Outline management of hepatic encephalopathy

A

Lactulose (need 2-3 soft stools/day)
ABs (eg: Rifaximin)- Reduce number of intestinal bacteria producing producing ammonia
Nutritional support (NG tube)

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39
Q

Outline the step-wise progression of alcohol-related liver disease

A
  1. Alcoholic fatty liver- Reversible with abstinence
  2. Alcoholic hepatitis- Inflammation in liver cells- Binge drinking associated with same effect- Mild usually reversible with permanent abstinence
  3. Cirrhosis- Functional liver tissue replaced with scar tissue- Irreversible- Stop drinking to prevent further damage- Continued drinking has poor prognosis
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40
Q

What is the recommended alcohol consumption UK?

A

Do not regularly drink more than 14 units/wk spread evenly over 3+ days and not more than 5units in a single day
Binge drinking = 6+ units women, 8+ units men in single session

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41
Q

What can alcohol in pregnancy lead to?

A

Miscarriage
Small for dates
Preterm delivery
Fetal alcohol syndrome

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42
Q

List complications of alcohol

A

Alcohol-related liver disease
Cirrhosis and its complications (Hepatocellular carcinoma)
Alcohol dependence and withdrawal
Wernicke-Korsakoff syndrome
Pancreatitis
Alcoholic cardiomyopathy
Alcoholic myopathy, proximal muscle wasting
and weakness
Increased risk CVD
Increased risk cancer- Breast, mouth and throat

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43
Q

List examination signs suggestive of excessive alcohol consumption

A

Smelling of alcohol
Slurred speech
Bloodshot eyes
Dilated capillaries on face (telangiectasia)
Tremor

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44
Q

Outline potential blood test results of someone with alcoholic-related liver disease

A

Raised Mean cell volume (MCV)
Raised ALT and AST
AST:ALS ratio > 1.5
Raised gamma-GT
Raised ALP later in disease
Raised bilirubin in cirrhosis
Low albumin due to reduced synthetic function of liver
Increased PTT due to reduced synthetic function of liver (reduced production of clotting factors)
Deranged U&Es in hepatorenal syndrome

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45
Q

Outline investigations of alcoholic related liver disease other than bloods

A

Liver US- May show early fatty changes with increased echogenicity, then cirrhosis
Transient elastography (FibroScan)- Assess elasticity of liver using high frequency sound waves- Determines degree of fibrosis
Endoscopy- Assess and treat oesophageal varices when Portal HTN suspected
CT and MRI scans- Look for fatty infiltration of liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites
Liver biopsy- Confirms diagnosis (esp. if steroid treatment being considered for alcohol-related hep)

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46
Q

Outline the general management of alcohol-related LD

A

Stop drinking
CBT or motivational interviewing
Detoxication regime
Nutrition- Thiamine (B1) and high protein diet
Corticosteroids- Reduce inflammation in severe alcoholic hepatitis- Improves short-term outcomes
Treat complications
Liver transplant

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47
Q

When are corticosteroids considered in liver disease?

A

Severe alcoholic hepatitis- Improves short term outcomes by reducing inflammation

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48
Q

What is a requirement for a liver transplant?

A

6mths abstinence from alcohol

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49
Q

What is alcohol dependence?

A

Daily alcohol consumption
Strong urges and cravings
Difficulty controlling consumption
Tolerance to effects of alcohol
Withdrawal symptoms when stopping

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50
Q

Outline the CAGE questionnaire

A

C- Cut down? Do you ever think you should cut down?
A- Annoyed? Do you get annoyed at others commenting on your drinking?
G- Guilty? Do you ever feel guilty about drinking?
E- Eye opener? Do you ever drink in the morning to help your hangover or nerves?

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51
Q

Outline the timeline of alcohol withdrawal

A

6-12h: Tremor, sweating, headache, craving, anxiety
12-24h: Hallucinations
24-48h: Seizures
24-72h: Delirium tremens

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52
Q

What is the pathophysiology of delirium tremens?

A

Alcohol is a depressant
Alcohol stimulates GABA receptors in brain which relax brain
Alcohol inhibits glutamate receptors (NMDA receptors) which relaxes brain
Chronic use= GABA system down-regulated, Glutamate system up-regulated- When alcohol removed, GABA system under functions and glutamate system over functions= Extreme excitability of brain and excessive adrenergic activity (adrenaline)

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53
Q

Outline the presentation of delirium tremens

A

Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
HTN
Hyperthermia
Ataxia (difficulty coordinating movement)
Arrhythmias

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54
Q

How is alcohol withdrawal managed?

A

Chlordiazepoxide (benzo)- Give orally as reducing regime titrated to required dose- Reduce over 5-7d
High dose B vitamins (Pabrinex) given IM/IV followed by long term oral thiamine- Prevents Wernicke-Korsakoff syndrome

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55
Q

What causes Wernicke-Korsakoff Syndrome?

A

Alcohol excess leads to thiamine (B1) deficiency
Thiamine poorly absorbed in presence of alcohol

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56
Q

List features of Wernicke’s encephalopathy

A

Confusion
Occulomotor disturbances
Ataxia (difficulty coordinating movement)

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57
Q

Outline features of Korsakoff syndrome

A

Memory impairment (retro and anterograde)
Behavioural changes

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58
Q

What is the prognosis of delirium tremens w/o treatment?

A

35% mortality rate

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59
Q

What can non-alcoholic fatty liver disease progress to?

A

Hepatitis or cirrhosis

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60
Q

Outline the stages of NAFLD

A
  1. NAFLD
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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61
Q

What are the risk factors for NAFLD?

A

Middle age
Obesity
Poor diet and low activity levels
T2D
High cholesterol
High BP
Smoking

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62
Q

Which syndrome is NAFLD associated with?

A

Metabolic syndrome

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63
Q

What is metabolic syndrome?

A

Combination of HTN, obesity and diabetes

63
Q

What is often the first indication a patient has NAFLD?

A

Raised ALT

64
Q

Which markers does the enhanced liver fibrosis (ELF) blood test measure?

A

HA
PIIINP
TIMP-1

65
Q

What is the NAFLD fibrosis score (NFS) and what is it based on?

A

Assesses liver fibrosis in NAFLD
Age/BMI/AST and ALT/platelet count, albumin, diabetes

66
Q

What is the fibrosis-4 (FIB-4) score and what does it use?

A

Assesses liver fibrosis in NAFLD
Age/AST and ALT/platelet count

67
Q

When is transient elastography used in NAFLD?

A

When ELF test indicates advanced fibrosis
Determines degree of fibrosis and tests for cirrhosis

68
Q

Which ratio of AST:ALT indicates which liver diseases?

A

Normal ratio <1
> 0.8 in NAFLD = Advanced fibrosis
>1.5 (disproportionately high AST) = Alcohol-related LD

69
Q

How is NAFLD definitively diagnosed?

A

US findings of fatty liver
Risk factors
Exclude other causes- Alcohol history and full non-invasive liver screen
Liver biopsy- Gold standard

70
Q

Outline management of NAFLD

A

Weight loss
Mediterranean diet
Exercise
Avoid alcohol
Stop smoking
Control diabetes/BP/cholesterol
Refer if fibrosis
Specialist- Vit E, pioglitazone, bariatric surgery, liver transplant

71
Q

Which hepatitis’ are there vaccines for?

A

Hep A and Hep B

72
Q

Which hepatitis’ are RNA?

A

Hep A, Hep C, Hep D, Hep E

73
Q

Which hepatitis’ are DNA?

A

Hep B

74
Q

How is Hep A transmitted?

A

Faecal-oral route

75
Q

How is Hep B transmitted?

A

Body fluids

76
Q

How is Hep C transmitted?

A

Blood

77
Q

How is Hep D transmitted?

A

With Hep B

78
Q

How is Hep E transmitted?

A

Faecal-oral route

79
Q

How is Hep A treated?

A

Supportive

80
Q

How is Hep B treated?

A

Supportive/antivirals

81
Q

How is Hep C treated?

A

Direct-acting antivirals

82
Q

How is Hep D treated?

A

Pegylated interferon alpha- Over at least 48wks
Has significant SEs and not very effective

83
Q

How is Hep E treated?

A

Supportive

84
Q

What are the other causes of hepatitis?

A

Alcoholic hepatitis
Non-alcoholic steatohepatitis (NASH)
AI hepatitis
Drug-induced (eg: Paracetamol overdose)

85
Q

Outline presentation of hepatitis

A

Viral may be asymptomatic
Abdo pain
Fatigue
Flu-like illness
Pruritis (itching)
Muscle and joint aches
N+V
Jaundice

86
Q

Outline a ‘hepatic picture’ on LFTs

A

High transaminases (AST and ALT)
Proportionally less of a rise in ALP

87
Q

Why are transaminases released?

A

Liver enzymes released into blood due to inflammation of liver cells

88
Q

What other than transaminases also rises as a result of inflammation of liver cells?

A

Bilirubin

89
Q

How does Hep E present and how is it managed?

A

Usually produces mild illness
Virus cleared within a month
No treatment required
Rarely progresses to chronic hep and liver failure- Usually in immunocompromised

90
Q

Why does Hep D only survive in patients with Hep B?

A

Attaches to HBsAg and can’t survive w/o this protein

91
Q

What can Hep A lead to?

A

Cholestasis- Pruritis, significant jaundice, dark urine, pale stools

92
Q

What is cholestasis?

A

Slowing of bile through biliary system

93
Q

What are the symptoms of cholestasis?

A

Pruritis
Significant jaundice
Dark urine
Pale stools

94
Q

How is Hep A diagnosed?

A

IgM antibodies

95
Q

How is Hep A managed?

A

Usually resolves w/o treatment
Rarely leads to acute liver failure (fulminant hepatitis)
Management- Supportive, basic analgesia

96
Q

What is fulminant hepatitis?

A

Severe liver function impairment causing hepatic coma and decrease in synthesizing capacity of liver
Develops within 8wks onset of hepatitis

97
Q

Can Hep B be passed to the baby through pregnancy or breastfeeding?

A

Pregnancy and delivery- Yes (vertical transmission)
Breastfeeding- Low risk

98
Q

What is the progression of Hep B?

A

Most fully recover within 1-3mths
5-15% become chronic Hep B carriers

99
Q

What does Surface antigen (HBsAg) indicate?

A

Active Hep B infection

100
Q

What does E antigen (HBeAg) indicate?

A

Implies high infectivity

101
Q

What do core antibodies (HBcAb) indicate?

A

Past or current infection

102
Q

What does surface antibody (HBsAb) indicate?

A

Vaccination/past infection/current infection

103
Q

What is Hepatitis B virus DNA (HBV DNA) used for?

A

Direct count of viral load

104
Q

What are the initial screening tests for Hep B?

A

HBcAb (previous infection) and HBsAg (active infection)
If positive- Check HBeAg and HBV DNA

105
Q

What is the purpose of checking HBcAb?

A

Distinguishes acute/chronic/past infections
IgM- Active infection (high titre)
IgG- Indicates past infection where HBsAg negative

106
Q

Outline management of Hep B

A

Low threshold for screening
Screen for other viral infections
Refer to gastro/hepatology/infectious diseases
Avoid alcohol
Education about reducing transmission
Contact tracing
Test for cirrhosis and US for hepatocellular carcinoma
Antivirals to slow progression and reduce infectivity
Liver transplant if liver failure

107
Q

How is Hep C managed?

A

Antivirals- Sofosbuvir, daclatasvir

108
Q

What is the prognosis of Hep C w/o treatment?

A

25% full recovery
75% chronic Hep C

109
Q

What are the complications of Hep C?

A

Liver cirrhosis
Hepatocellular carcinoma

110
Q

How is Hep C diagnosed?

A

Screening- Hep C antibody
Hep C RNA testing- Confirms diagnosis- Calculate viral load and identify genotype

111
Q

Outline type 1 AI hepatitis

A

Type 1- Women in late 40s, presents after menopause with fatigue and features of liver disease, less acute than type 2

112
Q

Outline type 2 AI hepatitis

A

Type2- Affects children/young people, more common in girls, acute, high transaminases and jaundice

113
Q

List the autoantibodies in type 1 AI hepatitis

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

114
Q

List autoantibodies in type 2 AI hepatitis

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

115
Q

What are the findings on liver biopsy of AI hepatitis?

A

Interface hepatitis
Plasma cell infiltration

116
Q

What is shown on bloods in AI hepatitis?

A

High transaminases (AST and ALT)
Minimal change in ALP
Raised IgG

117
Q

Outline management of AI hepatitis

A

High-dose steroids (prednisolone)
Azathioprine (immunosuppressant)- To induce remission
Liver transplant- In end-stage LD- Can reoccur in new liver

118
Q

What is haemochromatosis?

A

Autosomal recessive condition resulting in iron overload
Excessive total body iron and deposition of iron in tissues

119
Q

Outline genetics of haemochromatosis

A

Autosomal recessive
Human haemochromatosis (HFE) gene on Chr 6
C282Y mutation

120
Q

Outline presentation of haemochromatosis

A

Chronic tiredness
Joint pain
Pigmentation (bronze skin)
Testicular atrophy
Erectile dysfunction
Amenorrhoea
Memory and mood disturbance
Hepatomegaly

121
Q

When does haemochromatosis present?

A

After age 40 when overload becomes symptomatic
Later in females due to menstruation eliminating iron from body regularly

122
Q

List causes of raised ferritin

A

Haemochromatosis
Infections
Chronic alcohol consumption
NAFLD
Hep C
Cancer

123
Q

How is haemochromatosis diagnosed?

A

Serum ferritin- Raised
Transferrin saturation- High (in other causes of raised serum ferritin= Normal level)
Genetic test- HFE gene
Liver biopsy- Perl’s stain establishes iron conc. in liver
MRI- Can quantify iron conc. in liver

124
Q

List complications of haemochromatosis

A

Secondary diabetes (iron affects pancreas)
Liver cirrhosis
Endocrine and sexual problems (hypogonadism, ED, amenorrhoea, reduced fertility)
Cardiomyopathy (iron deposits in heart)
Hepatocellular carcinoma
Hypothyroidism (iron deposits in thyroid)
Chondrocalcinosis (calcium pyrophosphate deposits in joints) causes arthritis

125
Q

What is the management of haemochromatosis?

A

Venesection (wkly removal blood to remove excess iron)
Monitor serum transferrin

126
Q

What is Wilson’s disease?

A

Autosomal recessive accumulation of copper, particularly in liver

127
Q

Outline the genetics of Wilson’s disease

A

Autosomal recessive
Mutation in Wilson disease protein gene on Chr 13 (ATP7B copper-binding protein)
This protein helps remove excess copper from body via liver
Copper excreted in bile

128
Q

When does Wilson’s disease present?

A

In teenagers or young adults
Rare for symptoms to start after 40y

129
Q

Outline initial presentation of Wilson’s disease

A

Liver issues arise first
Rarely can present initially with neuro or psychiatric problems

130
Q

Outline presentation of Wilson’s disease

A

Liver- Chronic hepatitis, cirrhosis
CNS- Tremor, dysarthria (speech difficulties), dystonia (abnormal muscle tone)
Copper deposition in basal ganglia- Parkinsonism (tremor, bradykinesia, rigidity
Kayser-Fleischer rings in cornea
Haemolytic anaemia
Osteopenia
Renal tubular damage

131
Q

Outline diagnosis of Wilson’s disease

A

Serum caeruloplasmin- Low (can be falsely elevated in cancer or inflammatory conditions)
24h urine copper assay- High urinary copper
Liver biopsy
Kayser-Fleischer rings
MRI brain- Double panda sign
Low Hb with haemolytic anaemia (negative Coombs test)
Genetic testing

132
Q

What is the characteristic sign on MRI of Wilson’s disease?

A

Double panda sign

133
Q

Outline management of Wilson’s disease

A

Copper chelation- Penicillamine or trientine
Zinc salts (inhibit copper absorption in GI tract)
Liver transplant

134
Q

What is the pathophysiology of Alpha-1 antitrypsin deficiency?

A

Alpha-1 antitrypsin is a protease inhibitor
A protease enzyme is neutrophil elastase which digests elastin (protein in CT that keeps tissue flexible)- Alpha-1 Antitrypsin (AAT) offers protection by inhibiting neutrophil elastase
In lungs lack of functioning AAT leads to excess protease attacking CT

135
Q

Outline the inheritance of alpha-1 antitrypsin deficiency

A

Autosomal co-dominant inheritance (both gene copies expressed and contribute to outcome- Neither is dominant or recessive)

136
Q

Outline effect of alpha-1 antitrypsin deficiency on the lungs

A

Destruction of elastic tissue in lungs = Bronchiectasis and emphysema (smoking accelerates process)

137
Q

Outline effect of alpha-1 antitrypsin deficiency on the liver

A

AAT is produced in liver
Abnormal mutant version made in certain AAT deficiency and gets trapped/builds up inside liver cells- Toxic to hepatocytes causing inflammation- Progresses to fibrosis/cirrhosis/hepatocellular carcinoma

138
Q

What are the less common associations of AAT deficiency?

A

Panniculitis- Tender skin nodules caused by inflammation of subcutaneous fat
Granulomatosis with polyangiitis- Small and medium vessel vasculitis

139
Q

How is AAT deficiency diagnosed?

A

Low serum AAT- Screening test
Genetic testing

140
Q

How is lung damage assessed in AAT deficiency?

A

Chest xray
High resolution CT thorax
Pulmonary function tests

141
Q

What can a liver biopsy show in AAT deficiency?

A

Periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment

142
Q

Outline the management of AAT deficiency

A

Stop smoking
Symptomatic management- Standard treatment of COPD
Organ transplant for end-stage liver/lung disease
Monitor for hepatocellular carcinoma
Screen family members

143
Q

What is primary biliary cholangitis?

A

AI condition
Immune system attacks small bile ducts in liver
Results in obstructive jaundice and liver disease

144
Q

Outline pathophysiology of primary biliary cholangitis

A

Affects small bile ducts (intrahepatic ducts)- Inflammation and damage to epithelial cells of bile ducts (cholangiocytes)
Over time leads to obstruction of bile flow through these ducts= Cholestasis
Back pressure of bile and disease process leads to liver fibrosis/cirrhosis/failure

145
Q

How does primary biliary cholangitis affect bile?

A

Bile acid/bilirubin/cholesterol excreted through bile ducts into intestines
Obstruction means build up in blood
Raised bile acids in blood- Itching, raised bilirubin, jaundice
Decreased bile acids in GI tract- Abdo symptoms, malabsorption of fat, greasy stools

146
Q

How does primary biliary cholangitis affect cholesterol?

A

Raised cholesterol
Xanthelasma- Cholesterol deposits in skin
Xanthomas- Larger deposits of cholesterol in skin or tendons
Increased risk atherosclerosis and CVD

147
Q

What colour is stool in cholestasis and why?

A

Pale
Bilirubin makes stool dark- Lack of bilirubin = Pale stools
Excretion of bilirubin via urine= Dark urine

148
Q

Who is more at risk of getting primary biliary cholangitis?

A

White women
40-60y

149
Q

How does primary biliary cholangitis present?

A

Fatigue
Pruritis
GI symptoms and abdo pain
Jaundice
Pale, greasy stools
Dark urine

150
Q

Outline presentation of primary biliary cholangitis on examination

A

Xanthoma and xanthelasma
Excoriations
Hepatomegaly
Signs of liver cirrhosis and portal HTN in end stage disease- Splenomegaly and ascites

151
Q

What are the key investigation findings of primary biliary cholangitis?

A

Antimitochondrial antibodies (AMA)
Alkaline phosphatase

152
Q

Middle aged white woman- Itching, positive AMA, raised ALP

A

Primary biliary cholangitis

153
Q

How is primary biliary cholangitis diagnosed?

A

LFT- Raised ALP (obstructive pathology), other liver enzymes and bilirubin raised later in disease
Autoantibodies- AMA (most specific), ANA (present in 35%)
Raised IgM (non-specific)
US- Helps exclude other pathology
Liver biopsy- Diagnose and stage disease

154
Q

Outline treatment of primary biliary cholangitis

A

Ursodeoxycholic acid- Non-toxic, hydrophilic bile acid that protects cholangiocytes from inflammation and damage- Makes bile less harmful to epithelial cells of bile ducts, slows disease progression
Colestyramine for pruritis
Replace fat soluble vitamins
Immunosuppression (steroids)
Liver transplant in end-stage liver disease

155
Q

What is a key complication of primary biliary cholangitis?

A

Liver cirrhosis

156
Q

What are the other complications of primary biliary cholangitis?

A

Fat-soluble vit deficiency (A, D, E, K)
Osteoporosis
Hyperlipidaemia (raised cholesterol)
Sjogren’s syndrome (dry eyes, dry mouth, vaginal dryness)
Connective tissue disease (systemic sclerosis)
Thyroid disease

157
Q
A

Final Year (14 decks)

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