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Gastroenterology > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What is haemochromatosis?

A

excessive iron absorption- treat by venesection

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2
Q

What is haemosiderosis?

A

an iron overload disorder resulting from transfusion

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3
Q

What is Wilson’s Disease?

A

Copper accumulation

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4
Q

What are the causes of hepatic injury?

A 
accumulation of toxins
infection
immune mediated
bile retention
amyloid
sarcoidosis
diabetes
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5
Q

What is cirrhosis of the liver?

A

nodules of hepatocytes separated by bands of fibrous tissue

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6
Q

Explain the development of chronic liver injury

A

injury–>fibrous expansion–>bridging (fibrotic areas start to join)–>cirrhosis–>liver failure–>death/cancer–>death/transplant

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7
Q

What are the features of decompensated cirrhosis?

A 
Jaundice (pre-hepatic, intra-hepatic and post-hepatic)
Ascites
Encephalopathy
Palmar erythema
Spider naevi
Caput medusa
Gynaecomastia
GI bleeding
Sepsis
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8
Q

What is steatosis?

A

Fatty liver disease

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9
Q

Explain the progression from steatosis to liver cancer

A

steatosis–>fatty hepatitis–>fibrosis–>cirrhosis (irreversible)–>liver cancer

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10
Q

What are some causes of fatty liver disease (steatosis)?

A

Alcohol
Obesity
Hep C
T2DM

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11
Q

What are the complications of liver cirrhosis?

A

Liver failure- poor exchange between hepatocytes and blood (decreased plasma protein conc reduces oncotic pressure leading to ascites)
Portal hypertension- from the increase vascular resistance
Nodule formation leading to hepatocellular carcinoma (liver cancer)

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12
Q

Explain the role of albumin

A

Albumin in produced by the liver so in liver disease it is reduced. it transports fatty acts and is important in maintaining oncotic pressure

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13
Q

What are the biomarkers for liver damage?

A 
decreased clotting and platelets
increased ammonia and amino acids
decreased albumin
increased bilirubin-->jaundice
hypoglycaemia due to decreased gluconeogenesis
increased ALT, AST and ALP
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14
Q

What are the causes of liver failure?

A 
Viral infections e.g. Hep B, C, CMV, yellow fever, leptospirosis
Paracetamol OD
Alcohol
fatty liver disease
primary biliary cholangitis
primary sclerosing cholangitis
hamochromatosis
autoimmune hepatitis
wilsons disease
alpha 1 antitrypsin deficiency
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15
Q

What would you expect in liver failure?

A

coagulopathy (INR>1.5)
Encephalopathy
jaundice
asterixis/flap

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16
Q

What tests would you order if you suspected liver failure?

A 
Bloods- FBCs, U&Es, LFTs, Clotting (increase PT/INR), glucose, paracetamol levels, ferritin, alpha 1 antitrypsin
Blood culture, urine culture
Ascitic tap- are there neutrophils
CXR
abdo US
EEG
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17
Q

Explain the management of liver failure

A 
ABCDE 
monitor bloods and abs
10% glucose IV 1L/12hrs- to avoid hypoglycaemia
treat cause if known
treat malnutrition 
treat seizures with phenytoin
about drugs metabolised by the liver
liaise with transplant team
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18
Q

What are the signs of liver cirrhosis?

A

leuconychia, dupytrens contracture, clubbing, spidernaevi, xanthelasma, gynaecomastia, loss of body hair, hepatomegaly, ascites, splenomegaly, atrophic testes

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19
Q

How would you manage liver cirrhosis?

A

Stop drinking alcohol
avoid NSAIDs, sedatives and opiates
if ascites- fluid restriction, spironolactone (100mg/24hr)- can add furosemide if needed
Liver transplant

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20
Q

what marker in the blood can be used to monitor hepatocellular carcinoma recurrence?

A

AFP

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21
Q

What is SAAG used for?

A

used to determine if ascites is due to portal HTN or not.(if raised, the ascites is caused by portal HTN.

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22
Q

does budd chiari cause portal hypertension?

A

Yes

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23
Q

does liver cirrhosis cause portal hypertension?

A

Yes

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24
Q

What is the most common cause of acute liver failure in the UK?

A

paracetamol OD

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25
Q

What is the most common cause of liver failure worldwide?

A

Viral hepatitis

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26
Q

what are some clinical features of liver failure?

A

ascites, hepatomegaly, infections (decreased immunoglobulins), hepatic encephalopathy, jaundice, hypoglycaemia, bruising and haemorrhage, fetor hepaticus

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27
Q

why is it important to check U+Es in liver failure?

A

to assess for the presence of hepatorenal syndrome

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28
Q

why do you give lactulose in liver failure?

A

to minimise nitrogenous substance absorption by the gastrointestinal tract.

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29
Q

what drugs can you give in liver failure if encephalopathy is present?

A

lactulose

rifaximin (abx)

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30
Q

list 5 hepatotoxic drugs

A

methotrexate, paracetamol, isoniazid, tetracyclines, salicylates

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31
Q

what are some prognostic factors in liver failure?

A 
grade 3/4 hepatic encephalopathy
age >40
albumin <30g/L
increased INR
drug induced liver failure
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32
Q

it is 8 hrs after a patient has taken a large paracetamol OD what is the most appropriate management?

A

Start NAC

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33
Q

it has been 4-6hrs since a patient has taken a large paracetamol OD- what is the appropriate management?

A

Take bloods ASAP- paracetamol level, U and Es, LFTs, INR and PT, BM, ABG

34
Q

a patient presents within 1hr of taking a large paracetamol overdose what is the most appropriate management?

A

give activated charcoal

35
Q

a patient presents within 1hr of taking a <75mg/kg paracetamol overdose what is the most appropriate management?

A

delay bloods until 4hrs after ingestion

36
Q

a patient presents within 8hr of taking a <75mg/kg paracetamol overdose what is the most appropriate management?

A

Do bloods ASAP- paracetamol level, U and Es, LFTs, INR and PT, BM, ABG

37
Q

what are some complications of liver cirrhosis?

A

compensated liver failure–>ascites, coagulopathy etc
portal HTN–>splenomegaly, ascites, varices, encephalopathy
Spontaneous bacterial peritonitis
increased risk of HCC
hepatorenal syndrome

38
Q

What specific treatment would you give in hep C virus liver cirrhosis?

A

interferon alpha

39
Q

What specific treatment would you give in primary biliary cirrhosis liver cirrhosis?

A

ursodeoxycholic acid

40
Q

What specific treatment would you give in wilson’s disease liver cirrhosis?

A

Penicillamine

41
Q

how should patients with liver cirrhosis be followed up?

A

regularly with imaging and AFP testing- due to high risk of HCC

42
Q

what grading tool do you use in liver cirrhosis?

A

Child-Pugh Grading- it predicts the risk of bleeding, mortality and the need for treatment
A- albumin
B- Bilirubin
C- clotting
D- distension ascites
E- encephalopathy
a score >8 indicates a significant bleeding risk

43
Q

What is hepatorenal syndrome?

A

renal failure in a patient with chronic liver disease

44
Q

what is the underfill theory of how chronic liver failure leads to hepatorenal syndrome?

A

cirrhosis causes splanchnic arterial vasodilation leading to RAAS activation and renal artery vasoconstriction. persistence underselling of the renal circulation leads to renal failure

45
Q

how would you manage hepatorenal syndrome?

A

colloids and vasopressor analogues
IV albumin+Splanchnic vasoconstriction (terlipressin)
haemodyalysis (if severe metabolic acidosis and hyperkalaemia)
liver transplant is treatment of choice

46
Q

What is the most common cause of portal HTN in the UK?

A

Cirrhosis

47
Q

what is the most common cause of portal HTN worldwide?

A

Schistosomiasis

48
Q

What are some possible presentations of portal HTN?

A

oesophageal varices
anorectal varices
Caput medusae

49
Q

why do you get encephalopathy in hepatic problems?

A

the liver’s metabolic function is impaired therefore toxins from the liver are diverted into the systemic circulation. ammonia accumulates and passes into the brain. as a result glutamate is converted to glutamine which when it increases causes an osmotic imbalance and cerebral oedema

50
Q

what features make up hepatic encephalopathy?

A

asterixis, ataxia, confusion, instructional apraxia and seizures

51
Q

how do you manage hepatic encephalopathy?

A

nurse with head at 20 degrees
lactulose +/- phosphate enema to remove nitrogen forming bacteria from the bowel
consider rifaximin
correct any precipitants

52
Q

what is a useful investigation in hepatic encephalopathy?

A

plasma NH4 levels

53
Q

what is the mechanism of ascites formation?

A

activation of RAAS (increased renin release and therefore salt and water retention), increased vascular resistance due to portal HTN and decreased albumin leading to less oncotic pressure

54
Q

what are the conservative management options for ascites?

A

bed rest which reduced RAAS activation
daily wt aiming for <0.5kg/day reduction
fluid restriction <1.5L/d and a low sodium diet

55
Q

what are some medical management options for ascites?

A

Spironolactone (1st line)
Frusomide (if poor response)
therapeutic paracentesis with albumin infusion (give 100ml of 20% albumin per litre drained)- the colloid maintains intravascular volume

56
Q

what are the surgical management options for ascites?

A

refractory ascites: TIPSS- producing a shunt with the liver from portal vein to hepatic vein.
consider for liver transplant.

57
Q

what are 3 complications of ascites?

A

Intractable ascites (ie ascites that doesn’t respond to retractable diuretic use)
Spontaneous bacterial peritonitis (SBP) (treat with Tazocin or cefotaxime until sensitivities known)
Splenomegaly due to splenic congestion

58
Q

what is Wernickes encephalopathy?

A

neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics.

59
Q

what are the features of wernicke’s encephalopathy?

A 
Features
nystagmus (the most common ocular sign)
ophthalmoplegia
ataxia
confusion, altered GCS
peripheral sensory neuropathy
60
Q

how do you treat wernicke’s encephalopathy?

A

urgent thiamine replacement

61
Q

what would happen if wernicke’s encephalopathy is not treated?

A

If not treated Korsakoff’s syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the above symptoms.

62
Q

what is the management of alcohol withdrawal?

A

chlordiazepoxide (a BDZ) helps with the withdrawal symptoms

pabrinex (replace thiamine)

63
Q

describe the mechanism behind alcohol withdrawal

A

Mechanism
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

64
Q

how does alcoholic hepatitis present?

A 
anorexia
Diarrhoea and vomiting
tender hepatomegaly
ascites
if severe: jaundice, bleeding, encephalopathy
65
Q

what is the maangement of alcoholic hepatitis?

A 
stop drinking alcohol
treat withdrawal (chlordiazepoxide)
give pabrinex
optimise nutrition
daily wt, LFTs, U+Es and INR
manage and complications of liver failure
66
Q

what score predicts mortality in alcoholic hepatitis?

A

The maddrey score

67
Q

painless jaundice in an elderly patient is what until proven otherwise?

A

obstructive malignancy e.g. cholangiocarcinoma, cancer of the head of the pancreas

68
Q

dark urine, pale stools- what sort of jaundice have they got?

A

intrahepatic jaundice e.g. due to hepatitis

69
Q

what does leukonychia indicate?

A

hypoalbuminaemia

  • not enough in - malabsorption and malnutrition
  • not enough produced in the liver- chronic liver disease
  • increased excretion- nephrotic syndrome (kidneys), protein losing enteropathy
70
Q

what causes koilonychia? (spoon shaped nails)

A

iron deficiency anaemia

71
Q

what are some GI causes of clubbing?

A

alcoholic chronic liver disease
IBD
GI malignancy (upper GI from hepatic and pancreatic to stomach and oesophageal etc)

72
Q

4 causes of palmar erythema?

A

thyrotoxicosis
pregnancy
chronic liver disease
hyper dynamic circulation (Pagets and high output cardiac states)

73
Q

What are some causes of dupytrens contracture?

A 
idiopathic (familial)
alcoholic liver disease
?DM
phenytoin/epilepsy
vibrating tools e.g pneumatic jack hammer
trauma
74
Q

3 causes for asterixis

A

hepatic flap (encephalopathy )
CO2 retention
uraemia

75
Q

what are some risk factors for primary liver tumours?

A

HBV, HCV, smoking, alcohol, obesity, DM

76
Q

true of false

90% of liver tumours are secondary metastases

A

true

77
Q

what is tehmost common type of primary liver tumour?

A

hepatocellular carcinoma

78
Q

name 3 types of benign liver tumours

A

haemangioma, hepatocellular adenomas and cysts

79
Q

what investigation must you never do if you suspect a patient has liver haemangiomas?

A

never biopsy due you risk of bleeding (NB risk blood supply)

80
Q

what is the most common organism to be found in the peritoneal fluid in spontaneous bacterial peritonitis ?

A

Spontaneous bacterial peritonitis: most common organism found on ascitic fluid culture is E. coli

81
Q

what does Courvoisier’s sign state?

A

states that in a patient with a painless, enlarged gallbladder and mild jaundice the cause is unlikely to be gallstones. Furthermore, it is more likely to be a malignancy of the pancreas or biliary tree.

Gastroenterology (10 decks)

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