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FINALS > Liver + Friends > Flashcards

Liver + Friends Flashcards

1
Q

What kind of virus is hepatitis A?

A

An RNA virus

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2
Q

How is hepatitis A transmitted?

A

Feco-orally

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3
Q

What is a presentation of viral hepatitis in different age groups?

A

Asymptomatic in children

symptomatic in adults

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4
Q

What is the treatment of viral hepatitis?

A

A) supportive +/- IVIG or vaccine –> transplant

B) entecavir —-> transplant

C) glecaprevir/pibrentavir —-> transplant

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5
Q

Who is most at risk of getting a severe infection of Hepatitis A?

A

Anyone with the coinfection of hepatitis B or C

anyone with any other underlying liver disease

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6
Q

What kind of virus is hepatitis B?

A

DNA virus

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7
Q

Does hepatitis B always progress to chronic liver disease?

A

No it is often self-limiting requiring no treatment

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8
Q

Who is most at risk of developing chronic liver disease from hepatitis B?

A

If the virus is acquired parenterally or if infection occurred in childhood

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9
Q

What is the treatment of hepatitis B?

A

B ET

Antivirals – entecavir
if pregnant - tenofovir

+ supportive

liver transplant if decompensated

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10
Q

How is hepatitis B transmitted?

A

percutaneous, per mucosal, sexually

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11
Q

What type of virus is hepatitis C?

A

RNA virus

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12
Q

What is the most common method of spread of hepatitis C?

A

IV drug users

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13
Q

What proportion of patients develop symptoms of hepatitis C in the acute phase?

A

1/3

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14
Q

What is management of hepatitis C?

A

Antivirals - glencaprevir

+ supportive

liver transplant

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15
Q

What are symptoms of viral hepatitis?

A

Fever and malaise - acute phase
jaundice
ascieties
signs of encephalopathy

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16
Q

If you suspect someone has viral hepatitis what investigations should you perform?

A

LFT - ALT(especially) and ALP raised, bilirubin,

Coagulation profile - PT raised

U+E - hepatorenal disease, and monitor kidneys if on diuretics

FBC - anaemia of chronic disease, WCC raised in acute infection

Viral PCR or

Hep A IGM
Hep B surface antigen test or core antigen test or serum antibody test
Hep C antibody immunoassay

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17
Q

What specific diagnostic test can you perform for hepatitis A (apart from viral PCR)?

A

Hep A IGM

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18
Q

What specific diagnostic test can you perform for hepatitis B (apart from viral PCR)?

A

Hep B surface antigen test or core antigen test or serum antibody test

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19
Q

What specific diagnostic test can you perform for hepatitis C (apart from viral PCR)?

A

Hep C antibody immunoassay

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20
Q

What are the three stages of alcoholic liver disease?

A

Fatty liver – steatosis
alcoholic hepatitis – inflammation and necrosis
cirrhosis

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21
Q

Describe the pathophysiology of alcoholic liver disease?

A

The breakdown of alcohol inhibits gluconeogenesis and increases fatty acid oxidation

promoting fatty in filtration and producing free radicals

ree radicals and the deficiency of antioxidants (vitamins E- usually from malnutrition) causes oxidative stress

promotes necrosis and apoptosis

free radicals also cause lipid oxidation causing further inflammation and fibrosis

acetyl-aldehyde a metabolite from alcohol breakdown induces inflammation

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22
Q

How does alcoholic liver disease usually present?

A 
Right upper quadrant pain – acute hepatitis
hepatomegaly
weight loss or weight gain
malnutrition and wasting
jaundice 
ascites (in cirrhosis)
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23
Q

What bloods do you need to perform in alcoholic liver disease?

A

LFTs

  • AST ALC serum bilirubin GGT (all +)
  • serum alk phosphate usually normal but can be +
  • serum albumin/protein (-)

PT/INR (+)

FBC (+ WCC thrombocytopenia, microcytic anaemia)
serum electrolytes especially magnesium and phosphate (–)
U+E (hepatorenal)

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24
Q

Apart from blood what other investigations should you perform in alcoholic liver disease?

A 
Hepatic ultrasound scan:
hepatomegaly 
fatty liver
Chirossis
ascites 
portal hypertension 
splenomegaly
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25
Q

What is the management of alcoholic liver disease?

A

Alcohol abstinence
corticosteroids – high bilirubin or hepatic encephalopathy
diuretics and sodium restriction – ascites

Lifestyle factors:
weight loss, smoking cessation, nutritional supplements, immunisation of hepatitis influenza and pneumococcal

liver transplant

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26
Q

What is non-alcoholic fatty liver disease?

A

Includes a spectrum of conditions characterised by hepatic steatosis/cirrhosis who do not consume excess alcohol

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27
Q

what is the thought pathophysiology Of non-alcoholic fatty liver disease?

A

Insulin resistance

causes an accumulation of triglycerides

develops into hepatic steatosis

causes inflammation and oxidative injury

necrosis occurs

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28
Q

what are risk factors associated with non-alcoholic fatty liver disease?

A 
Obesity
type II diabetes
hyperlipidaemia
hypertension
rapid weight loss
hepatotoxic medications
TPN
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29
Q

What medications are hepatotoxic?

A 
Tamoxifen
corticosteroids
diltiazem
nifedipine
methotrexate
valproate
amiodarone
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30
Q

What is the presentation of non-alcoholic fatty liver disease?

A

Fatigue and malaise - most common initial presenting Sx

hepatosplenomegaly
right upper quadrant pain

if more severe jaundice and ascites

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31
Q

How would you investigate non-alcoholic fatty liver disease?

A

LFTs

  • AST ALC serum bilirubin GGT (all +)
  • serum alk phosphate usually normal but can be +
  • serum albumin/protein (-)

PT/INR (+)

FBC (+ WCC thrombocytopenia, microcytic anaemia)
serum electrolytes especially magnesium, phosphate, sodium (–)
U+E (hepatorenal)

same pathophysiology as FLD so bloods the same

+ Hepatic USS

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32
Q

What is the management of non-alcoholic fatty liver disease?

A

Diet and exercise with weight loss intention
pharmacology or surgery for weight loss

supplemental vitamins E

good diabetic control of type II diabetic new in starting if hyperlipidaemia

liver transplant

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33
Q

what is cirrhosis?

A

A diffuse pathological process characterised by fibrosis and conversion of normal liver architecture to abnormal nodules

it is the final stage of liver disease

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34
Q

What are consequences of cirrhosis?

A

Portal hypertension
liver failure
hepatocell carcinoma

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35
Q

What is the presentation of Cirrhosis?

A 
Ascites and peripheral oedema
jaundice and pruritus
haematemesis or melena
right upper quadrant pain
muscle wasting and constitutional symptoms
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36
Q

on examination what features may you see of cirrhosis?

A

Hand and nail features:
leukinochia, spider nevi palmar erythema

facial features:
telangactasia, spider nevi

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37
Q

What is the management of cirrhosis?

A

Managing the underlying liver disease
monitoring for any complications

corticosteroids – high bilirubin or hepatic encephalopathy
diuretics and sodium restriction – ascites

transplant

life style factors

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38
Q

what is portal hypertension?

A

An increase of pressure within the portal vein due to impeding flow through the liver

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39
Q

What is a common consequence of portal hypertension?

A

Abdominal/oesophageal varices

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40
Q

What is the presentation of portal hypertension?

A 
haematemesis
ascites
encephalopathy
thrombocytopenia
microcytic anaemia - any bleeds
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41
Q

How do you diagnose portal hypertension?

A

based on the presence of ascites or of dilated veins or varices

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42
Q

What is ascites?

A

A pathological collection of fluid in the peritoneal cavity most commonly because of cirrhosis

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43
Q

Why does cirrhosis cause ascites?

A

There is renal dysfunction and abnormal hepatic circulation (splanchnic arterial vasodilation) due to hepatic fibrosis

this leads to increased lymph node formation and activation of the RAAS system stimulating the release of antidiuretic hormone

this along with increased resistance to portal flow due to cirrhosis causes portal hypertension also causes

collateral rain formation and the shunting of blood to systemic circulation

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44
Q

How do you diagnose ascites?

A

Clinical (O/E shifting dullness)

can also be aided by ultrasound scan if unsure

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45
Q

How do you manage ascites?

A

Diuretics and sodium restriction

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46
Q

What is acute pancreatitis?

A

A disorder of the exocrine pancreas caused by acing cell injury with local and systemic inflammatory responses

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47
Q

what commonly causes pancreatitis?

A

I GET SMASHED

idiopathic
gallstones
ethanol
trauma
steroids
mumps
autoimmune
scorpion venom (??)
hyperlipideamia / calcaemia / hypothermia
ERCP + emboli
Drugs inc/ HRT
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48
Q

What risk factors are associated with acute pancreatitis?

A

Alcohol use
history of gallstones
azathioprine and other similar medications

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49
Q

What is the presentation of acute pancreatitis?

A

Nausea and vomiting, – most common
made epigastric/LUQ pain radiating to back, constant and severe, sudden onset, exacerbated by movement

symptoms of hypovolaemia can be present due to vomiting (oliguria dry mucous membrane decreased skin turgor UTC)

can have weight loss due to N+V and decrease intake

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50
Q

What complication is common in acute pancreatitis and what would you find on examination?

A

Pleural effusion

reduced air entry, dullness on percussion

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51
Q

How do you diagnose acute pancreatitis?

A

Check serum lipase or amylase

imaging not required unless the diagnostic doubt or failure to improve within 48 to 72 hours of treatment

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52
Q

Apart from checking pancreatic enzymes what other investigations are useful in acute pancreatitis?

A

ALT indicates gallstones

U+E is elevated in severe cases and shows at risk patients electrolytes should also be checked for imbalances caused by vomiting which can lead to arrhythmias

FBC - WCC (+)

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53
Q

How do you manage acute pancreatitis?

A

Fluid recess analgesia and nutritional support (replacing calcium and magnesium)
empirical IV antibiotics if infection is suspected
plus treating underlying cause

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54
Q

How do you manage gallstones with cholangitis (as a cause of acute pancreatitis)?

A

ERCP within 24 hours plus normal pancreatitis Mx

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55
Q

How do you manage gallstones with bile duct obstruction (as a cause of acute pancreatitis)?

A

ERCP With sphincterotomy normal pancreatitis Mx

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56
Q

How do you manage acute pancreatitis which is alcohol related?

A

normal pancreatitis Mx Plus vitamin replacement and alcohol withdrawal programs

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57
Q

What you do if acute pancreatitis is not improving within five – seven days?

A 
Perform contrast enhanced CT
give ongoing supportive and nutrition treatment
do a fine needle aspirate and culture
IV antibiotics if suspecting infection
catheter draining or debridement
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58
Q

What is chronic pancreatitis?

A

progressive pancreatic injury to the pancreas and surrounded structures causing scarring and loss of function

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59
Q

What are the four types of chronic pancreatitis ?

A

Recurrent acute pancreatitis
idiopathic pancreatitis
chronic relapsing pancreatitis
established chronic pancreatitis

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60
Q

What is recurrent acute pancreatitis?

A

There is an identifiable cause of acute pancreatitis which keeps on repairing but does not lead to chronic pancreatitis
examples are:
gallstones, drugs, hypercalcaemia

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61
Q

What is idiopathic pancreatitis?

A

No cause has ever been found Usually encompasses chronic relapsing and established chronic pancreatitis

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62
Q

What is chronic relapsing pancreatitis?

A

Relapsing pain no other relapsing clinical features of pancreatitis
there are pathological changes in tissue specimens

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63
Q

What is established chronic pancreatitis?

A 
All the hallmark clinical features of pancreatitis are present:
reduced exocrine functions
malabsorption
diabetes
pancreatic calcifications
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64
Q

What are risk factors associated with chronic pancreatitis?

A

Alcohol
smoking
family history
coeliac disease

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65
Q

What is the presentation of chronic pancreatitis?

A

Abdominal pain – epigastric, dull, radiating to back, occurring 30 minutes post-prandial,
SWAB A DECK

steatorrhoea
weight loss inc. N+V
abdo pain
bloating
ADECK deficiency
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66
Q

What investigations are required to diagnose chronic pancreatitis?

A

Raised serum amylase
raised blood glucose (occurring import X crying function)
CT
CT unavailable then ultrasound

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67
Q

What findings would you see on a CT scan of chronic pancreatitis?

A

Pancreatic calcifications
local or diffuse enlargement pancreas
ductal dilatations
can have vascular complications

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68
Q

What is the management of chronic pancreatitis?

A

Analgesia for acute pain
+ ocreotide is a somatostatin analogue which may help relieve pain

pancreatic enzymes
PPI
dietary modifications including possible enteric feeding for malnutrition

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69
Q

What are some complications of chronic pancreatitis?

A

Pseudo-cysts
Biliary complications
pancreatic stone
intractable pain and pancreatic duct dilatation

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70
Q

how would you manage a Pseudo-cysts in chronic pancreatitis?

A

Decompression

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71
Q

How would you manage any Biliary complications?

A

If bilirubin has been raised for one month or more usually surgery will be required

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72
Q

How would you manage pancreatic stones?

A

Shockwave therapy ESWL

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73
Q

How would you manage pancreatic duct dilatations?

A

Decompression

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74
Q

What is biliary colic?

A

A clinical symptom of pain in the right upper quadrant or epigastric region
a constant pain lasting over 30 minutes
pain increases with intensity in this time
usually has a post-prandial onset

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75
Q

What is biliary colic commonly associated with?

A

Gallstones a.k.a. cholelithiasis

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76
Q

What is the presentation of gallstones?

A 
Biliary colic
dyspepsia
heartburn
flatulence
bloating
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77
Q

what sign can indicate cholecystitis?

A

RUQ tenderness/epigastric tenderness

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78
Q

What are risk factors associated with gallstones?

A 
pregnancy
exogenous oestrogen
Obesity and diabetes
NAFLD
prolonged fasting and rapid weight loss
TPN
terminal highly disease or resection
drugs: ocreotide and ceftriaxone
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79
Q

How do you diagnose gallstones?

A

Abdominal ultrasound scan

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80
Q

What should you check for in a patient with gallstones?

A 
Acute pancreatitis (lipase and amylase)
liver impact (LFTs)
cholangitis, cholecystitis (WCC)
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81
Q

How do stones in gallbladder (cholelithiasis) affects LFTs?

A

normal LFT

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82
Q

How do stones in bile duct (choledocholithasis) affects LFTs?

A

+ ALP

+ bilirubin

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83
Q

What is the management of gallstones in gallbladder?

A

cholecystectomy if symptomatic

otherwise observation

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84
Q

What is the management of gallstones in the bile duct?

A

ERCP with stenting or balloon dilatation

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85
Q

What is ascending cholangitis?

A

An infection of the biliary tree most commonly caused by obstruction

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86
Q

What is the pathophysiology of ascending cholangitis?

A

Impeded biliary flow allows for bacterial seeding and growth in the biliary tree it can lead to mild inflammation or even sepsis

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87
Q

What is the presentation of ascending cholangitis?

A

RUQ/epigastric pain and tenderness
jaundice and fever
pale stools and pruritus
signs of sepsis such as fever tachycardia

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88
Q

What are risk factors for ascending cholangitis?

A 
Over 50
history of bile duct stones
history of primary/secondary sclerosing cholangitis
the structures of the biliary tree
trauma to the bile duct
89
Q

What investigations should be performed in ascending cholangitis?

What are the results?

A

FBC - + WCC

U+E (+cr) - raised in severe disease/may indicate sepsis, Mg and K may be reduced

LFT - + Bilirubin, ALT,AST,ALP

Blood cultures - positive

Abdominal USS - stones and dilated ducts

ERCP - diagnostic

Sepsis screen

90
Q

What is the management of ascending cholangitis?

A

IV antibiotics – metronidazole and cefamine

supportive care including O2 magnesium potassium and coagulation factors

biliary decompression and drainage

opioid analgesia

91
Q

What is primary biliary cholangitis?

A

A chronic disease of the small intrahepatic bile ducts characterised by progressive bile duct damage and eventual loss

92
Q

What is the pathophysiology of primary biliary cholangitis?

A

Insult to the portal tract caused by inflammation which then becomes chronic causing fibrosis and can lead to cirrhosis

93
Q

What risk factors are associated with primary biliary cholangitis?

A 
Female
aged 45 – 60
history of autoimmune diseases
history of high cholesterol
family history of autoimmune diseases
94
Q

What is the presentation of primary biliary cholangitis?

A 
itch
fatigue
dry eyes and mouth (Sjogren's syndrome)
postural dizziness
the hepatomegaly
95
Q

How do you diagnose primary biliary cholangitis?

A

has ONLY increased ALP

is ANA positive!

USS to exclude obstruction like stone

96
Q

How do you manage primary biliary cholangitis?

A

urdeoxycholic acid

Corticosteroid/immuno modulation (prednisolone) – if there is significant information or overlapped autoimmune hepatitis
cholestiramine if itchy
liver transplant in end-stage disease

97
Q

A patient presents with right upper quadrant pain pruritus
fatigue
weight loss
and jaundice
they say they have an on and off low-grade fever

blood tests revealed that they have elevated a LP GGT AST and ALC as well as slightly raised bilirubin

what is the diagnosis?

A

Primary sclerosing cholangitis

98
Q

What is primary sclerosing Cholangitis?

A

A chronic progressive cholestatic liver disease
it is characterised by inflammation and fibrosis of the intra/extra hepatic bile ducts

this results in diffuse multifocal structures forming damaging both bile ducts and the liver

99
Q

What disease is primary sclerosing cholangitis is commonly associated with?

A

Inflammatory bowel disease

100
Q

Summarise the key present team points of primary sclerosing cholangitis?

A 
Pruritus
right upper quadrant pain
fatigue
weight loss
fever
jaundice
101
Q

What serum markers/antibodies may be present in primary sclerosing cholangitis?

A

AN CA

AMA – anti-mitochondrial antibody

102
Q

what blood tests should you run for primary sclerosing cholangitis and what are their results?

A

ALP +
GGT +
AST/ALT +
Billirubin can be +
albumin normal unless advanced disease then -
Coagulation screen deranged in advanced liver disease

ANCA/AMA

103
Q

what test is diagnostic for Primary sclerosing cholangitis?

and what would it show?

A

MRCP

dilatations and strictures

104
Q

What drug is used to provide pruritus relief?

A

colestyramine

105
Q

What complications can occur due to primary sclerosing cholangitis?

A

Liver disease/ cirrhosis
hepatic osteopenia/ osteoporosis
strictures

106
Q

How would you treat hepatic osteoporosis?

A

alendronic acid and HRT can be used

107
Q

how would you treat hepatic osteopenia?

A

Ergocalciferol and calcium carbonate

108
Q

When would you use immunosuppressant in the treatment of primary sclerosing cholangitis?

A

Overlapping autoimmune hepatitis

109
Q

what is the treatment of Primary sclerosing cholangitis?

A

observation and lifestyle changes – healthy weight diets and limiting alcohol
observation of bone mineral density every 2 – 4 years
if they have IBD check that with colonoscopy

then symptomatic relief

end stage disease = transplant

110
Q

What cells does liver cancer derive from?

A

Hepatocytes

111
Q

What risk factors are associated with liver cancer?

A 
Cirrhosis
hepatitis B+C
chronic heavy alcohol abuse
diabetes
obesity
family history of liver cancer
increasing age
112
Q

How is liver cancer usually diagnosed?

A

On routine screening as patient almost always have underlying liver conditions

113
Q

What are the symptoms of liver failure which can develop in liver cancer?

A 
Abdominal distension
right quadrant pain
early satiety and weight loss
leg oedema and ascites
hepatic encephalopathy
the splenomegaly
jaundice
Asterix's
spider naevi
Palmar erythema
peri-umbilical collateral veins
fetur hepaticus
114
Q

What blood results are expected in liver failure caused by hepatic cancer?

A

LFT will be derranged (AST ALT ALP bilirubin - high, albumin - low
PT time - prolonged
FBC - microcytic anaemia and thrombocytopenia from chronic disease and also variceal bleeding
hepatitis screen may be positive
alpha-fetoprotein will be elevated in advanced disease

115
Q

Apart from blood tests what further investigations should be performed in liver cancer?

A

CT (or USS if ct not possible)

liver biopsy is not required because of seeding

116
Q

A patient presents with :
jaundice
non-specific upper abdominal pain which can radiate to the back
weight loss

what is a possible diagnosis?

A

Pancreatic cancer

117
Q

What type of cancer is pancreatic cancer usually?

A

adenocarcinoma

118
Q

what test is diagnostic of pancreatic cancer?

A

Pancreatic CT

119
Q

What would liver function tests show in pancreatic cancer

A

they will be abnormal because Of obstructive jaundice

120
Q

What is a management plan for pancreatic cancer?

A

Because it is a late stage diagnosis usually surgery is no longer possible for palliative care is needed

121
Q

A patient comes in with painless jaundice what should you immediately think of?

A

cholangiocarcinoma

but pancreatic cancer can also be a cause

122
Q

What are the risk factors associated with cholangiocarcinoma?

A 
Over 50
biliary or bile tract disease
ulcerative colitis
liver disease
HIV
123
Q

What test is diagnostic for cholangiocarcinoma?

A

Ultrasound scan

124
Q

What tumour markers are usually present in cholangiocarcinoma?

A

Ca 19-9
Ca- 125
CEA

125
Q

What is a liver abscess?

A

Purulent collections in the liver parenchyma resulting from bacterial fungal or parasitic infections

126
Q

What pathogens usually cause liver abscesses?

A

E. coli
klebisella
Streptococcus

but is usually polymicrobial

127
Q

What is the presentation of liver abscesses?

A

Constitutional symptoms of infection

right upper quadrant tenderness and hepatomegaly

128
Q

What is a fairly common complication of liver abscesses?

A

diaphragmatic irritation causing cough shortness of breath or chest pain

129
Q

what investigations should you perform for a liver abscess?

A

Blood cultures
aspirated abscess fluid
liver ultrasound or CT

FBC LFT coag screens

130
Q

What is the management of liver abscesses?

A

Empirical antibiotics such as the family with metronidazole
if haemodynamically unstable consider adding a coverage for MRSA such as vancomycin

drainage of abscess

131
Q

What can cause recurrent liver abscesses?

A

biliary abnormalities

132
Q

What does elevation in serum ALP mean?

A

ALP elevated in injury to in bile ducts, liver and bones. However is mainly an indication for cholestasis

It is raised in liver injury usually secondary to cholestasis

but elevation of ALP can indicate injury to any of these structures, usually finding out which one requires looking at other bloods.

133
Q

what does ALP stand for?

A

Alkaline phosphatase

134
Q

what does ALT stand for?

A

Alanine transaminase

135
Q

when is ALT raised

A

hepatic injury

136
Q

what does raised ALT and slightly raised ALP mean

A

hepatic injury

137
Q

what does raised ALP but slightly raised ALT mean

A

biliary injury / cholestasis

138
Q

what does elevated GGT mean ?

A

suggestive of biliary epithelial damage and bile flow obstruction

also raised in alcohol and drugs like phenytoin

139
Q

what does ALP raised only (No ALT or GGT)?

A

Bony metastases or primary bone tumours (e.g. sarcoma)
Vitamin D deficiency
Recent bone fractures
Renal osteodystrophy

140
Q

Raised ALP and raised GGT meaning?

A

ALP with a raised GGT is highly suggestive of cholestasis/ biliary causes

141
Q

what are causes of unconjugated hyperbillirubinaemia

A

Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (e.g. Gilbert’s syndrome)

142
Q

what are causes of conjugated hyperbillirubinaemia?

A

Hepatocellular injury

Cholestasis

143
Q

what do the symptoms of

Normal urine + normal stools

indicate about the cause of jaundice?

A

pre hepatic

144
Q

what do the symptoms of

dark urine + normal stools

indicate about the cause of jaundice?

A

hepatic

145
Q

what do the symptoms of

dark urine + dark stools

indicate about the cause of jaundice?

A

post hepatic

146
Q

why does pre hepatic jaundice not change stools/urine?

A

Unconjugated bilirubin is water-insoluble and, therefore, doesn’t affect the colour of the patient’s urine

147
Q

what is the function of albumin?

A

synthesised in the liver and helps to bind water, cations, fatty acids and bilirubin. It also plays a key role in maintaining the oncotic pressure of blood.

148
Q

when would you get low serum albumin?

A

Liver disease in later stages (e.g. cirrhosis).

Inflammation triggering an acute phase response which temporarily decreases the liver’s production of albumin

Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome.

149
Q

when would PT time be deranged in liver disease?

A

specifically assessing the extrinsic pathway.

In the absence of other secondary causes such as anticoagulant drug use and vitamin K deficiency

an increased PT can indicate liver disease and dysfunction - more severe stage

150
Q

what does ALT > AST ratio mean?

A

chronic liver disease

151
Q

what does AST > ALT ratio mean?

A

associated with cirrhosis and acute alcoholic hepatitis

152
Q

what does low glucose mean in terms of liver disease

A

very advanced liver disease

Gluconeogenesis tends to be one of the last functions to become impaired in the context of liver failure.

153
Q 
a patient presents (20y/o) with:
tremor
dysarthria 
dystonia 
incoordination 
jaundice

what diagnosis do you suspect?

A

Wilson’s disease

154
Q

What investigations would you perform for ?Wilsons disease - what would the results be?

A

LFT - abnormal
blood ceruloplasm - low

24h urine copper measurements - high >100

Opthalmological slit lamp - Keyser flesher rings

DIAGNOSTIC - liver biopsy - increased copper

155
Q

what is Wilsons disease?

A

an autosomal recessive disease of copper accumulation
leading to copper toxicity
caused by mutations in ATP 7B gene (that is part of the biliary excretion pathway)

156
Q

what gene is responsible for Wilsons disease ?

A

ATP 7B gene

157
Q

what are all the movement disorders associated with Wilsons disease?

A 
tremour
dysarthria
dystonia
incoordination
sloppy/small handwriting
dysdidokinesia
158
Q

what neurological Sx are NOT present in Wilsons disease?

A

normal sensation
normal muscular strength
normal reflexes

159
Q

what are the key features of a history of Wilsons disease

A

young (10-40y)

evidence of hepatic disease PLUS movement disorders of psychiatric disorder

160
Q

what is the management of Wilsons disease?

A

zink or trientine (chelating agent)

161
Q

who is Trientine contraindicated in?

A

those with neurological Sx as it can worsen symptoms however if Zinc is not tolerated it can be tried

transplantation

162
Q

what is a complication of Wilsons?

A

hepatic failure
ascites
fulminant liver failure

163
Q

are neurological sx reversible in wilsons?

A

yes

164
Q

what is fulminant liver failure?

A

sudden massive liver necrosis

165
Q

what is the presentation of fulminant liver failure?

A

encephalopathy
astirixus
jaundice
septic like symptoms

166
Q

what is the management of fulminant liver failure?

A

lactulose for encephalopathy - decreases ammonia absorption, ICU, liver transplant

167
Q

what is haemochromatosis?

A

a multisystem disorder of dysregulated dietary iron absorption and increased iron release from macrophages

168
Q

what risk factors are associated with haemochromatosis?

A 
Middle-aged
Male
White ancestry
family history
supplemental iron intake
169
Q

What is the presentation of haemochromatosis?

A 
Fatigue and weakness
arthralgia
hypogonadism and loss of libido
bronzing skin pigmentation
jaundice and other features associated with cirrhosis
170
Q

What conditions are Caused by haemochromatosis?

A

Diabetes mellitus

cirrhosis

171
Q

How do you diagnose haemochromatosis?

A

Fasting transferrin saturation and serum ferritin will be raised

final diagnosis is through genetic testing

172
Q

How do you manage haemochromatosis?

A

Observation and follow-ups every three years in stable
disease or yearly in stage I disease

low iron diet

hepatitis A and B vaccinations

phlebotomy
iron chelation therapy therapy using desferrioxamine

173
Q

What are cholechondyl cysts?

A

Congenitalconditions involving cystic die notations of the bile ducts

174
Q

What is the presentation of a chocholedocal cysts?

A

Symptomatic within the first year of life
abdominal pain
jaundice
right upper quadrant abdominal mass is sometimes present

175
Q

What causes symptoms in choledochal cysts?

A

Obstructions of bile ducts caused by the cyst

176
Q

How do you diagnose choledochall cysts?

A

Can be diagnosed in the antenatal period

otherwise ultrasound scan

177
Q

What is the management of Choledochal cysts ?

A

Surgery

178
Q

What are paediatric causes of liver failure?

A

Excess paracetamol
viral hepatitis
Wilson’s disease and other metabolic conditions

179
Q

How do you manage liver failure in paediatrics?

A

IV dextrose
empirical broad-spectrum antibiotics and antifungals
IV vitamin K and FFP

180
Q

What are complications of paediatric liver failure?

A 
Cerebral oedema
haemorrhage
gastritis
coagulopathy
sepsis
pancreatitis
181
Q

What is biliary atresia?

A

A progressive idiopathic necro inflammatory process that may involve a segment or the entire extrahepatic biliary tree

182
Q

What is the pathophysiology of biliary atresia?

A

The the necro inflammation causes fibro of alliterative obstruction of the extrahepatic biliary tree then progresses to the intrahepatic ducts which are developing and utero or during the neonatal period

183
Q

what will the blood tests be like for biliary atresia

A

Liver function tests- initially normal but v high GGT
coagulation initially normal
Billirubin may be ++

184
Q

What is the diagnostic investigation for biliary atresia?

A

cholangiogram showing decreased patency

liver biopsy can be used to differentiate from differential diagnoses

abdominal USS

185
Q

how do you manage biliary atresia?

A

surgery + urseodeoxycholic acid
if severe enough liver transplant may be needed

nutritional support

trimethoprim/sulfemathozole prophylactic antibiotics for the 1st year of life

186
Q

What is a Wilms’ tumour?

A

nephroblastoma the most common cause of renal malignancy in children

187
Q

What is the presentation of a Wilms’ tumour?

A

Abdominal/flank mass/swelling
abdominal distension
abdominal pain - in less than 30% of patients
pallor

188
Q

What investigations are required for a Wilms’ tumour?

A

Ultrasound scan will show mass CT shows extents of disease (10% of patients have mets)
biopsy

189
Q

What will urinalysis and renal function tests reveal in Wilms’ tumour?

A

Urinalysis= haematuria

renal function will be normal unless there are bilateral tumours

190
Q

What is a hepatoblastoma?

A

An uncommon malignant liver cancer originating from immature liver precursor cells

191
Q

Who is at risk of hepatblastoma?

A

Children with familial adenomatous polyposis

192
Q

What is the presentation of hepatoblastoma?

A

Abdominal mass

193
Q

what blood test is required in hepatoblastoma?

A

Alpha-fetoprotein (raised)

194
Q

What conjenital infections cause neonatal hepatitis?

A

Cytomegalovirus
rubella
measles
hepatitis ABC

195
Q

What are the causes of neonatal hepatitis?

A

Congenital infections
inborn metabolic errors
cystic fibrosis

rarer causes:
intestinal failure
progressive familial intrahepatic cholestasis
galactosaemia

196
Q

What is familial intrahepatic cholestasis?

A

Inherited recessive mutation causing decreased bile production

197
Q

What is the presentation of familial intrahepatic cholestasis?

A

prolonged new natal jaundice

pruritus

198
Q

What are the consequences of familial intrahepatic cholestasis if untreated?

A

Failure to thrive

Ricketts

199
Q

What is the GGT level in familial intrahepatic cholestasis?

A

Low

200
Q

What is the management of familial intrahepatic cholestasis?

A

uredeoxycholic acide
vitamins ADEK

if v severe : transplant

201
Q

What is galactosaemia?

A

High levels of galactose from inability to metabolise sugars causing eventual liver failure

202
Q

What is a presentation of galactosaemia?

A

Neonatal jaundice
vomiting
poor feeding
hepatomegaly

203
Q

What are the consequences of galactosaemia if not treated?

A

DIC
developmental delayed
cataracts
recurrent bacterial infections

204
Q

How do you diagnose galactosaemia?

A

Urine dipstick And your analysis shows increased sugars (galactose)

205
Q

How do you manage galactosaemia?

A

Sugar/galactose/ lactose free diet

206
Q

What are inborn errors of metabolism?

A

cause faulty biosynthesis causing cholestasis

207
Q

What with the GGT and liver enzyme levels be like in inborn errors of metabolism?

A

Normal GGT

abnormal liver enzymes (ALP very high ALT slightly high)

208
Q

How do you manage inborn errors of metabolism caused hepatitis?

A

uredeoxycholic acid

209
Q

Splenomegaly appear in neonatal hepatitis and if so what would be the consequences of it?

A

yes

if untreated can cause portal hypertension and Aids the process of cirrhosis

210
Q

What are common causes of neonatal jaundice- conjugated?

A

Neonatal hepatitis

bile duct obstruction

211
Q

What are common causes of neonatal jaundice – unconjugated?

A

Breastmilk jaundice
rubella
measles
hepatitis ABC

212
Q

when is neonatal jaundice physiological?

A

Up to 14 days

213
Q

Why does physiological neonatal jaundice occur?

A

fetal haemoglobin and red blood cells are replaced

214
Q

What are treatments of neonatal jaundice?

A

phototherapy

Exchange transfusion: if bilirubin levels are very high/unstable

215
Q

What is kernictus?

A

Occurs when jaundice is left untreated or Billy Rubin is very high
bilirubin deposits in the brain causing brain damage

216
Q

What are the potential consequences of kernictus?

A

Cerebral palsy
developmental delay
hearing loss

217
Q

What are symptoms of kernictus?

A 
Irritable baby
lethargic
high-pitched cry
floppy baby
seizures as it progresses
218
Q

What is the management of kernictus?

A

Exchange transfusion, supportive care and phototherapy

FINALS (24 decks)

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