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GI and General Surgery > Liver > Flashcards

Liver Flashcards

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1
Q

Why does jaundice occur?

A

Due to increased levels of bilirubin in the blood

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2
Q

What is bilirubin?

A

A normal breakdown product of RBCs

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3
Q

What are the classifications of jaundice?

A

pre-hepatic
hepatocellular
post-hepatic

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4
Q

What causes pre-hepatic jaundice? Examples?

A

excessive RBC breakdown - overwhelms to livers ability to conjugate bilirubin
causes a unconjugated hyperbilirubinaemia

haemolytic anaemia
Gilbert’s syndrome

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5
Q

What causes hepatocellular jaundice? Examples?

A

dysfunction or injury to hepatic cells - liver loses ability to conjugate bilirubin (unconjugated hyperbilirubinaemia)

alcoholic liver disease 
viral hepatitis 
medication 
PBC, PSC
hepatocellular carcinoma
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6
Q

What causes post-hepatic jaundice? Examples?

A

obstruction to biliary drainage
conjugated hyperbilirubinaemia

gall stones
cholangiocarcinoma, strictures
pancreatic cancer

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7
Q

When does dark urine occur in jaundice?

A

in conjugated hyperbilirubinaemia - as conjugated bilirubin can be excreted via the urine (unconjugated can’t)

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8
Q

Why might you get pale stools in obstructive jaundice?

A

decreased stercobilin entering GI tract (colours stool)

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9
Q

What does a raised ALT/AST suggest?

A

intrahepatic damage

is specific to the liver

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10
Q

What does a raised ALP suggest?

A

post hepatic obstruction of bile flow

is also raised in bone disease, pregnancy, some cancers - not specific

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11
Q

What is gamma GT used for?

A

to confirm raised ALP is hepatic in nature

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12
Q

How is hepatitis A spread?

A

faecal oral spread (ask about foreign travel)

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13
Q

How does hepatitis A usually present?

A 
acute - not associated with chronic liver disease/cirrhosis 
prodromal phase (flu like illness)
jaundice 
hepatosplenomegaly 
lymphadenopathy
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14
Q

How is hep A investigated?

A

LFTs - raised ALT/AST, raised bilirubin

serology - hep A IgM

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15
Q

How is hep A managed?

A

supportive management

vaccine prophylaxis

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16
Q

How is hep B transmitted?

A

vertical
UPSI
blood contact

high risk populations: PWID, MSM

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17
Q

How does hep B present?

A

acute: similar to hep A but ++, extrahepatic features (arthralgia, urticaria), deranged LFTs
chronic: that of chronic liver disease

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18
Q

When is hepatitis B deemed chronic?

A

When HBsAg has been +ve for more than 6 months

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19
Q

What serology is positive in all ongoing infections of hep B?

A

HBsAg

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20
Q

What does the presence of anti-HBs in a patient’s blood indicate?

A

immunity to hep B (either vaccine or infection)

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21
Q

When is Hep B IgM positive?

A

acute or recent infection (present about 6 months)

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22
Q

How is Hep B managed?

A

acute: supportive
minimise exposure to high risk groups
vaccination

chronic:
peg interferon
antivirals e.g. tenevir, entecavir

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23
Q

How is Hep C transmitted?

A

blood
sex
vertical

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24
Q

What is the natural history of hep C?

A

acute infection - mild, asymptomatic

majority progress to chronic infection

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25
How does hep C present?
acute - as per hep A (usually mild) | chronic - as per chronic liver disease
26
How is hep C investigated?
patient at risk or signs of chronic disease test for hep C antibody if positive: (past or active infection) - test for Hep C RNA (PCR) - positive in active infection
27
How is hep C managed?
peg interferon + ribavirin
28
When does hep D occur?
only alongside hep B | exacerbates hep B
29
What is the route of transmission for hep E?
faecal oral
30
How does hep E present?
similar to hep A | severe disease in pregnant women
31
What is acute liver disease?
any insult to the liver causing damage - previously normal liver <6mths
32
What can cause acute liver disease?
``` viral hep drugs: NSAIDS, fluclox, coamox alcohol cholangitis malignancy ask about paracetemol ```
33
What are clinical features of acute liver disease?
``` abnormal LFTs itch pain arthralgia anorexia, nausea, malaise, lethargy jaundice ```
34
How is acute liver disease managed?
rest - up to 3 to 6 months no alcohol itch - sodium bicarb bath, urseodeoxycholic acid observe for failure
35
How would acute liver failure present?
prolonged coagulation encephalopathy in a patient with a previously healthy liver
36
How does chronic liver disease present?
``` stigmata of cirrhosis jaundice deranged LFTs clubbing, palmar erythema, Dupuytren's gynaecomastia spider naevia, caput medusa ```
37
What is the pathophysiology of chronic liver disease?
insult/injury recurrent inflammation and process of fibrosis cirrhosis (compensated) cirrhosis (decompensated) - chronic liver failure
38
What is cirrhosis?
formation of fibrotic bands that seperate nodules of functional liver tissue common end point for chronic liver disease
39
What is portal hypertension?
complication of cirrhosis | increased pressure within low pressure portal system
40
What does portal hypertension cause?
splenomegaly - as splenic vein drains into portal vein varices - portal vein collaterals form at anastomoses with systemic circulation (oesophagus, umbilical, haemorrhoidal, retroperitoneal)
41
What are caput medusa?
portal vein collaterals around umbilicus
42
How is chronic liver disease investigated?
``` LFTs liver screen imaging - fibroscan (transient elastography) - MRCP - USS (ascites, splenomegaly, irregular liver contour) US guided biopsy - gold standard but risky (pain and bleeding) ```
43
What is the management of chronic liver disease?
weight loss no alcohol ascites: drain, spironolactone, fluid and salt restriction routine monitoring: OGD, bloods, fibroscan itch: urseodeoxycholic acid transplant is only curative management
44
What are complications of chronic liver disease?
``` encephalopathy portal hypertension hepatocellular carcinoma decreased synthetic function: coagulopathy, hypoalbuminaemia, hypoglycaemia spontaneous bacterial peritonitis ```
45
What bacteria is most commonly found in SBP in patients with chronic liver failure?
E. coli
46
When should you suspect SBP?
sudden detioration of a patient with ascites
47
What is SBP?
peritonitis without an obvious source | almost exclusively a patient with portal htn
48
What is non alcoholic fatty liver disease?
fatty liver
49
What does NAFLD progress to?
NASH - non alcoholic steatohepatitis (inflammation of liver due to fat deposition)
50
How are NAFLD/NASH diagnosed? management?
USS +/- biopsy weight loss and exercise
51
What are the autoimmune liver disease?
PBC - primary biliary cholangitis/cirrhosis PSC - primary sclerosis cholangitis Autoimmune hepatitis
52
What is PBC?
destruction of interlobar bile ducts chronic, progressive, granulomatous inflammatory disorder
53
What does PBC cause?
cholestasis
54
How does PBC present?
``` itch fatigue obstructive jaundice ?asymptomatic middle aged women association with other AI conditions ```
55
How is PBC investigated?
positive AMA cholestatic LFTs liver biopsy
56
How is PBC managed?
urseodeoxycholic acid (itch)
57
What is PSC?
autoimmune destruction, fibrosis and stricturing of large and medium bile ducts
58
What liver disease is associated with UC?
PSC
59
How does PSC present?
recurrent cholangitis RUQ pain fatigue
60
How is PSC investigated?
cholestatic LFTs MRCP - multiple biliary strictures (beaded appearence) positive pANCA biopsy - onion skinning fibrosis
61
How is PSC managed?
maintain bile flow | monitor for cholangiocarcinoma, colorectal carcinoma
62
Who commonly gets autoimmune hepatitis?
young to middle aged women
63
What are the types of autoimmune hepatits?
type 1 - affects children and adults, ANA, antismooth muscle type 2 - only children, anti LKM
64
What is the hallmark of autoimmune hepatitis?
interface hepatitis piecemeal necrosis
65
How is AI hep managed?
steroids azathioprine transplant
66
What is Wilson's disease?
autosomal recessive disorder | failure to adequately excrete copper
67
Where does copper accumulate in Wilson's?
liver | CNS - basal ganglia
68
How does Wilson's disease present?
neurological signs, psych and behavioural problems children cirrhosis or liver failure on exam - Keyser Fischer rings
69
How is Wilson's diagnosed?
24 hour copper increased | serum copper and caeruloplasmin reduced
70
How is Wilson's managed?
copper chelation drugs - penicillamine
71
What is a1-anti-trypsin deficiency?
autosomal recessive | loss of a1 antitrypsin enzyme
72
What are the clinical features of a1 anti trypsin deficiency?
lung emphysema | liver deposition of mutant protein --> cirrhosis and hepatocellular carcinoma
73
How is A1AT deficiency diagnosed? managed?
serum A1AT levels | supportive
74
What is haemachromatosis?
autosomal recessive | defect in iron regulating hormone - increased intestinal absorption
75
What are the clinical features of haemachromotosis?
'the bronzed diabetic' cirrhosis cardiomyopathy pancreatic failure
76
How is haemachromatosis managed?
venesection
77
What is liver failure?
failure of the liver to maintain synthetic and metabolic functions end stage liver disease or an acute event on top of chronic liver disease
78
How does liver failure present?
reduced synthetic function - coagulopathy - ascites (reduced albumin and protein) - variceal bleeds (portal htn) reduced metabolic function - encephalopathy (accumulation of toxins produced by gut - ammonia) - jaundice
79
What are the signs of liver failure?
``` ascites jaundice confusion, altered behaviour, slurred speech, drowsy hepatosplenomegaly liver flap stigmata of cirrhosis ```
80
How is hepatic encephalopathy managed?
lactulose - promotes excretion of ammonia
81
How is the synthetic function of the liver best assessed?
prothrombin time | albumin level
82
What are risk factors for hepatocellular carcinoma?
``` chronic inflammatory processes - viral hep - haemachromatosis - chronic alcholism - PBC >70 family history ```
83
What are clinical features of hepatocellcular carcinoma?
features of cirrhosis non specific malignancy symptoms dull ache RUQ advanced - liver failure O/E - irregular, enlarged, craggy and tender liver
84
What are investigations of suspected hepatocellular carcinoma?
deranged LFTs prolonged clotting, reduced platelets tumour marker - AFP (alpha fetoprotein) imaging - USS (mass + raised AFP virtually diagnostic) - MRI liver scanning - biopsy - risks of biopsy and tumour seeding
85
What are the surgical options for hepatocellular carcinoma?
resection (early disease) | transplant
86
What are non surgical options for hepatocellular carcinoma?
``` ablation transarterial chemoembolisation (TACE) ```
87
Where metastasises to the liver?
``` bowel breast pancreas stomach lung ```
88
What are clinical features of a liver abscess?
fever rigors abdo pain on exam - hepatomegaly, RUQ tenderness

GI and General Surgery (10 decks)

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