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medicine phase 2 a > liver > Flashcards

liver Flashcards

1
Q

What is the most common cause of acute liver disease?

A

paracetamol overdose

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2
Q

What are the key presentations of acute liver disease?

A

jaundice
hepatic encephalopathy
coagulopathy
renal failure

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3
Q

What are the 1st line and gold standard investigations for acute liver disease?

A

LFTs - hyperbilirubinaemia + raised liver enzymes
INR >1.5

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4
Q

What is the 1st line care for all patients with acute liver disease?

A

ICU monitoring + liver transplant assessment

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5
Q

What is the treatment for paracetamol overdose?

A

acetyl cysteine

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6
Q

what is the treatment for herpes simplex hepatitis?

A

aciclovir

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7
Q

What is the treatment for hep b?

A

oral nucleoside (adefovir/telbivudine)

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8
Q

What is the treatment for autoimmune hepatitis?

A

methylprednisolone

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9
Q

What are the two ways in which alcohol is broken down by the liver?

A

alcohol dehydrogenase (leads to NADH production which increases fatty acid oxidation)
cytochrome P450 ( generates free radicals through oxidation of NADPH)

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10
Q

What are the key presentations of alcoholic liver disease?

A

abdo pain
hepatomegaly

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11
Q

What are the first line investigations for alcoholic liver disease?

A

aspartate aminotransferase (AST)
alanine aminotransferase (ALT)
AST:ALT
FBC

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12
Q

What is the gold standard investigation for alcoholic liver disease?

A

liver biopsy

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13
Q

What is the 1st line treatment for alcoholic liver disease?

A

alcohol abstinence
liverstyle factors
ADJUNCT - corticosteroids + sodium restriction (diuretics)

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14
Q

What is the key mechanism for hepatic steatosis?

A

insulin resistance - triglyceride accumulation in the liver

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15
Q

What are the key presentations of non alcoholic fatty liver disease?

A

absence of alcohol misuse
fatigue + malaise
hepatosplenomegaly
truncal obesity
jaundice

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16
Q

What is fetor hepaticus?

A

The characteristic breath of patients with liver disease - garlic/rotten eggs

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17
Q

What are the first line investigations for hepatic steatosis?

A

aspartate aminotransferase AST, alanine aminotransferase ALT, AST:ALT
FBC

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18
Q

What is the gold standard test for hepatic steatosis?

A

diagnosed by exclusion + histology (biopsy)

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19
Q

What is the 1st line management for hepatic steatosis?

A

lifestyle modification + insulin sensitiser (thiazolidinediones) in DM

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20
Q

What is the 2nd line treatment for hepatic steatosis?

A

transjugular intrahepatic portosystemic shunt (TIPS)

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21
Q

What are the key presentations of hepatitis?

A

abdo pain (RUQ)
fatigue
pruritis
jaundice
nausea/vomiting
anorexia
fever

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22
Q

How is hep a transmitted?

A

faecal-oral route - contaminated water/food

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23
Q

What are the 1st line investigations for hepatitis?

A

serum transaminases (AST/ALT) (high)
INR
bilirubin (high)

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24
Q

What is the treatment for a patient with recent exposure to hep A?

A

hep a vaccination and/or immunoglobulin

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25
Q

What is the treatment for confirmed hep A infection?

A

supportive care, often goes away on its own
w/ worsening jaundice and encephalopathy-> liver transplant

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26
Q

How is hep b transmitted?

A

blood products, sexually
vertical transmission (mother to baby)

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27
Q

What proportion of people infected with hep b become carriers? (HBV DNA integrates with patients)

A

10%

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28
Q

What is the gold standard investigation for hep b?

A

serum HBV DNA

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29
Q

What is the 1st line treatment for an acute hep b infection?

A

supportive care
ADJUNCT - antiviral therapy + assess for liver transplant

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30
Q

What is the 1st line treatment for a chronic hep b infection?

A

antiviral therapy - tenofovir

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31
Q

What antiviral treatments are used for hep b?

A

tenofovir, pegylated interferon alpha

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32
Q

What is the 1st line and gold standard investigation for hep c?

A

hepatitis C virus (HCV) - RNA PCR

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33
Q

What are the complications of hep C?

A

cirrhosis
hepatocellular carcinoma

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34
Q

What is the treatment for hep C?

A

direct acting antiviral (DAAs) - ribavirin
+ protease inhibitors - ritonavir

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35
Q

What must patients be infected with to have Hep D?

A

HBV infection

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36
Q

What is the gold standard investigation for Hep D?

A

PCR of hep D RNA

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37
Q

What are the treatments for hep D?

A

same as hep B
antiviral therapy pegylated interferon alfa, tenofovir)
(liver transplant in liver failure)

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38
Q

How is hep E transmitted?

A

faecal-oral route

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39
Q

What is the gold standard investigation for Hep E?

A

PCR of hep E RNA

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40
Q

What is autoimmune hepatitis?

A

T cells of the immune system attack the liver - cause necrosis and fibrosis

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41
Q

What is the gold standard test for autoimmune hepatitis?

A

liver biopsy

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42
Q

What is the first line treatment for immune hepatitis?

A

high dose prednisolone + immunosuppressants (azathioprine)
(liver transplant with advanced liver disease)

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43
Q

Give an example of a drug that can cause liver cirrhosis

A

amiodarone/methotrexate/methyldopa

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44
Q

What are the four most common causes of cirrhosis

A

alcoholic liver disease
NAFLD
hep B and C

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45
Q

What are the key presentations of liver cirrhosis?

A

abdominal distension - ascites
jaundice and pruritus
haematemesis and malena
hand and nail features

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46
Q

What will blood tests show in cirrhosis?

A

can often be normal
in decompensated cirrhosis:
Liver enzymes and bilirubin raised

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47
Q

What are the best serum indicators of liver function?

A

prothrombin time and albumin

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48
Q

What scan tests liver elasticity and can diagnose cirrhosis?

A

Fibroscan

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49
Q

What score is used to assess the severity of cirrhosis?

A

Child-Pugh score

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50
Q

What is the gold standard investigation for liver cirrhosis?

A

liver biopsy

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51
Q

What is the first line treatment for liver cirrhosis?

A

Treat underlying condition, prevent further hepatic damage
ADJUNCT
sodium restriction

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52
Q

What is the 2nd line treatment for liver cirrhosis?

A

liver transplantation OR transjugular portosytemic shunt (TIPSS)

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53
Q

What is a transudative ascites?

A

low protein content ascites

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54
Q

What is exudative ascites?

A

high protein content ascites

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55
Q

How would you treat ascites?

A

diuretics - spironolactone + restrict sodium

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56
Q

How would you treat cerebral oedema?

A

mannitol - decreases ICP

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57
Q

How would you treat bleeding in liver cirrhosis?

A

vitamin K or fresh frozen plasma (FFP)

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58
Q

How does cirrhosis cause encephalopathy?

A

ammonia is not detoxified or bypasses the liver

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59
Q

How would you treat encephalopathy?

A

laxatives - lactulose (decreases ammonia), abx (rifamaxin) and enemas

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60
Q

What would you give for hypoglycaemia in liver cirrhosis?

A

dextrose

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61
Q

What are varices?

A

a result of portal hypertension that results in swelling of the anastomoses between the portal system and systemic venous system

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62
Q

what medication can be used to help stable varices?

A

propanolol

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63
Q

What surgical technique can relieve pressure on varices?

A

TIPS (transjugular intra-hepatic portosystemic shunt)

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64
Q

How would you treat bleeding oesophageal varices?

A

vasopressin analogues - terlipressin
Vit K or fresh frozen plasma
prophylactic borad spectrum antibiotics

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65
Q

What complication can occur in patients with ascites secondary to liver cirrhosis?

A

spontaneous bacterial peritonitis

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66
Q

How is spontaneous bacterial peritonitis treated?

A

IV cephalosporin - cefotaxime

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67
Q

What are the most common organisms to to cause spontaneous bacterial peritonitis?

A

e. coli
gram postive cocci (staphylococci/enterococcus)

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68
Q

What is a pre-hepatic cause of portal hypertension?

A

thrombosis (portal or splenic vein)

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69
Q

What is an intrahepatic cause of portal hypertension?

A

cirrhosis mainly
schistosomiasis (common worldwide)

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70
Q

What is hepatorenal syndrome?

A

loss of blood supply to the kidney because of pooling in the portal vessels

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71
Q

What is a post-hepatic cause of portal hypertension?

A

Budd-chiari syndrome, right heart failure, veno-occlusive disease

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72
Q

What are the signs of portal hypertension?

A

depends on underlying cause
ascites
splenomegaly
signs of hepatic encephalopathy
jaundice

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73
Q

What are the gold standard investigations for portal hypertension?

A

wedged hepatic venous pressure (reflects sinusoidal pressure)
free hepatic venous pressure (reflects systemic venous pressure
pressure gradient

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74
Q

What are some of the treatments for portal hypertension?

A

treat underlying cause
surgical decompressive shunts
beta blockers
liver transplant

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75
Q

What is the most common cause of ascites?

A

cirrhosis

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76
Q

What are the key presentations of ascites?

A

abdominal distension
flank bulging
signs of underlying cause

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77
Q

What are the gold standard tests for ascites?

A

abdominal ultrasound
SAAG (serum-ascites albumin gradient) >11g/L (indicates portal hypertension)

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78
Q

What drug can be given to control ascites?

A

spironolactone (aldosterone antagonist)
furosemide if response is poor

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79
Q

What else can be done to treat ascites?

A

fluid restriction + low salt diet

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80
Q

explain a pre-hepatic cause of jaundice

A

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

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81
Q

explain an intra-hepatic cause of jaundice

A

dysfunction of hepatic cells - stops livers ability to transport conjugated bilirubin into the biliary system
conjugated hyperbilirubinaemia

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82
Q

explain a post-hepatic cause of jaundice

A

obstruction of the biliary drainage
conjugated hyperbilirubinaemia

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83
Q

What would LFTs show in cholestatic jaundice?

A

raised ALP/GGT

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84
Q

What would LFTs shoe in hepatocellular jaundice?

A

raised ALT/AST

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85
Q

What are the risk factors for biliary colic?

A

5fs
Fat
Female
Fertile
Forty
fair

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86
Q

What causes the formation of gallstones?

A

an increase in cholesterol and decrease in bile salts and biliary stasis

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87
Q

What are the key presentations of biliary colic?

A

RUQ pain - intermittent and crampy
worse after fatty foods
nausea and vomiting

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88
Q

What are the first line investigations for biliary colic?

A

LFTS
CRP
ESR
will all be normal

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89
Q

What is the gold standard test for biliary colic?

A

abdominal ultrasound

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90
Q

What invasive procedure is used to treat gallstones?

A

laparoscopic cholecystectomy

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91
Q

What is an alternative to surgery with gallstones?

A

manage with diet - this is tricky so most will have surgery

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92
Q

What is acalculous cholecystitis?

A

multiple pathopysiologies - gallbladder stasis, hyperperfusion, infection

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93
Q

What is acute cholecystitis?

A

fixed obstruction in cystic duct
irritation due to build up of bile
prostaglandin secretion mediates inflammatory respone

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94
Q

What test can differentiate cholecystitis from biliary colic?

A

FBCs (WBCs)
CRP
ESR
all will be raised, sign of inflammation

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95
Q

What is the first line treatment for cholecystitis?

A

analgesia, early cholecystectomy
Consider - fluid resus + abx therapy

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96
Q

What is primary biliary cirrhosis?

A

immune system attack the bile ducts and causes cholestasis

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97
Q

What physical manifestation can raised cholesterol cause?

A

xanthelasma and xanthomas (cholesterol deposits in skin

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98
Q

What antibodies are tested for an are tested for in primary biliary cirrhosis?

A

anti-mitochondrial antibodies (most specific)
anti-nuclear antibodies

99
Q

what medication is used to reduce intestinal absorption of cholesterol to treat PBC?

A

ursodeoxycholic acid

100
Q

What medication prevents absorption of bile in the gut to help pruritus in PBC?

A

colestyramine

101
Q

What are the 3 defects that cause cholelithiasis?

A

bile supersaturated with cholesterol
accelerated nucleation
gallbladder hypermobility

102
Q

What is accelerated nucleation in regards to the gallbladder?

A

its the precipitation of cholesterol microcrystals in the gallbladder by the presence of nucleating agents (e.g. mucin)

103
Q

What is gallbladder hypermobility?

A

retention fo abnormal bile-
microcrystals agglomerate in a mucin scaffold and grow into gallstones

104
Q

What is the main treatment for all gallbladder symptoms?

A

laparoscopic cholecystectomy

105
Q

What is ascending cholangitis?

A

infection of the biliary tree due to obstruction of the common bile duct and bacteria seeding in the biliary tree - growth of bacteria can cause extravasation of bacteria into the blood

106
Q

What is charcots triad (the key presentations for cholangitis)?

A

fever
jaundice
RUQ pain

107
Q

What is the gold standard investigation for ascending cholangitis?

A

ERCP - endoscopic retrograde cholangiopancreatography

108
Q

What is the first line treatment for ascending cholangitis?

A

IV abx, intensive medical management, biliary decompression

109
Q

What antibiotics are normally used for ascending cholitis?

A

penicillins and aminoglycosides

110
Q

What is the second line treatment for ascending cholangitis?

A

biliary decompression - surgery + IV abx
consider lithotripsy opioid analgesic+ paracetamol

111
Q

What is primary sclerosing cholangitis?

A

intra/extrahepatic ducts become strictured and fibrotic causing cholestasis

112
Q

What is the gold standard diagnostic tool for primary sclerosing cholangitis?

A

Magnetic resonance cholangiopancreatography (MRCP)

113
Q

What medication can be used to treat primary sclerosing cholangitis?

A

colestyramine

114
Q

What intervention can be used to treat primary sclerosing cholangitis?

115
Q

What is primary biliary cholangitis?

A

a chronic disease of the small intrahepatic bile ducts by progressive damage and eventual loss

116
Q

describe the pathophysiology of primary biliary cholangitis

A

portal inflammation -> bile duct damage -> loss of bile duct area -> cholestasis -> bile duct damage -> secondary liver damage

117
Q

What are the key presentations of primary biliary cholangitis?

A

pruritus
fatigue
female sex + 45-60yrs

118
Q

What are the gold standard tests for primary biliary cholangitis?

A

LFTs - ALP raised
anit-mitochondrial antibodies (AMA)
liver biopsy

119
Q

What is the treatment for early stage primary biliary cholangitis?

A

bile acid analogue + immunomodulatory therapy + antipruritic + lifestyle modification

120
Q

What are the key presentations of primary sclerosing cholangitis

A

male sex and history of IBD

121
Q

What is the gold standard investigation for primary sclerosing cholangitis?

A

ERCP - endoscopic retrograde cholangiopancreatography

122
Q

What are some of the treatments for early stage primary sclerosing cholangitis?

A

1st line - lifestyle changes
calcium and vit D supplementation
bisphosphonate +/- HRT
pruritus relief
no effective medication available (liver transplant in end stage liver disease)

123
Q

What are the most common causes of acute pancreatitis?

A

gallstones and excessive alcohol consumption

124
Q

What are the key presentations of acute pancreatitis?

A

sudden onset of mid epigastric/LUQ abdo pain that radiates to the back
nausea and vomiting
signs fo hypokalaemia - hypotension/oliguria
anorexia

125
Q

What is the 1st line blood test for acute pancreatitis?

A

serum lipase (more sensitive and specific) or amylase

126
Q

What is the first line care for acute pancreatitis?

A

fluid resus + analgesia + nutritional support

127
Q

What imaging can be done to assess for complication in pancreatitis?

A

ultrasound (gallstones)
CT abdomen

128
Q

What score is used to assess the severity of pancreatitis?

A

Glasgow score

129
Q

What mnemonic can be used to remember the criteria for the Glasgow score?

A

PANCREAS
PaO2 <8
Age >55
Neutrophils (WBC >15)
Calcium >2
uRea >16
Enzymes (LDH, ALT/AST)
Albumin <32
Sugar glucose >10

130
Q

if acute pancreatitis fails to improve, what treatments should be used?

A

1st line - CECT (contrast enhanced computed tomography) + supportive care and nutritional support

131
Q

What is the most common cause of chronic pancreatitis?

A

chronic alcohol ingestion

132
Q

What are the key presentations of chronic pancreatitis?

A

abdominal pain
steatorrhea (excessive fat in faeces)
jaundice
(similar to acute but less severe and longer lasting)

133
Q

What is the first line investigation for chronic pancreatitis?

A

CT/MRI of abdomen (gold standard)

134
Q

What is the first line treatment for chronic pancreatitis?

A

lifetsyle mods - alcohol + smoking cessation

135
Q

What can be given to replace pancreatic enzyme?

A

pancrelipase

136
Q

What invasive procedure can help pancreatitis?

A

ERCP with stenting

137
Q

What is the most common cause of peritonitis?

A

bacterial infection (E.coli, strep, staph aureus etc)

138
Q

Describe and intestinal cause of peritonitis

A

bacterial translocation from intestinal flora into mesenteric lymph nodes, into the bloodstream -> leads to colonisation of ascitic fluid

139
Q

Give and example of a non-intestinal cause of peritonitis

A

resp infection/UTI/invasive procedure

140
Q

What are the key presentations of peritonitis?

A

abdo pain
fever
nausea
signs of ascites
diarrhoea

141
Q

What are the gold standard investigations for peritonitis?

A

ascitic fluid absolute neutrophil count (ANC)
periscreen - rules out spontaneous bacterial peritonitis

142
Q

What is the 1st line treatment for spontaneous bacterial peritonitis (SBP)?

A

empirical IV antibiotics (initital abx regimen)

143
Q

What is the 1st line treatment for non SBP?

144
Q

What is hepatic encephalopathy?

A

a brain dysfunction caused by liver dysfunction and/or portosystemic shunt

145
Q

What is the pathophysiology of hepatic encephalopathy?

A

ammonia is not detoxed by the liver and travels to the brain where it alters the amino acid conc, effects neurotransmitter synthesis

146
Q

What are the key presentations of hepatic encephalopathy?

A

mood/sleep/motor disturbances
neurological defecits

147
Q

What is the gold standard investigation for hepatic encephalopathy?

A

PHES - psychometric hepatic encephalopathy score

148
Q

What is the first line care of hepatic encephalopathy?

A

supportive care+reversal of precipitating factors + lactulose

149
Q

What other drugs can be given in hepatic encephalopathy?

A

2nd line - rifamixin +/- lactulose
3rd line L-ornithine-L-aspartate or branched amino acids

150
Q

What is wernickes encephalopathy?

A

a neurological emergency resulting from thiamine deficiency

151
Q

What is thiamine used for?

A

its a water soluble vitamin used to make pyruvate dehydrogenase + alpha ketoglutarate in the krebs cycle

152
Q

What are the key presentations of wernickes encephalopathy?

A

mental slowing
oculomotor dysfunction
mental status changes
gait dysfunction

153
Q

What is the 1st line and gold standard test for wernickes encephalopathy?

A

therapeutic trial of parenteral thiamine

154
Q

What is the first line management of wernickes encephalopathy?

A

stabilisation + thiamine + magnesium + multivitamins

155
Q

What is haemochromatosis?

A

an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation

156
Q

What does hepcidin do?

A

its an iron regulation hormone - decreases duodenal absorption, decreases macrophage iron release

157
Q

What are the key presentations of haemochromatosis?

A

fatigue, weakness, arthralgias, impotence in males, skin pigmentation (bronze/slate grey skin)

158
Q

What is the 1st line investigation for haemochromatosis?

A

serum ferritin
serum transferrin

159
Q

Why is transferrin checked as well as ferritin in haemochromatosis?

A

ferritin can increase with inflammation, a high transferrin will show the increase is due to iron overload

160
Q

What is the gold standard investigation for haemochormatosis?

A

liver biopsy

161
Q

What is the 1st line treatment for haemochromatosis (stage 1 and 0)

A

observation - yearly follow up, lifestyle modification, hep A and B vaccine

162
Q

What is the treatment for stages 2,3, and 4 haemochromatosis?

A

phlebotomy or iron chelation therapy

163
Q

How can haemochromatosis effect the heart?

A

Can cause cardiomyopathy due to iron build up

164
Q

How can haemochromatosis effect the thyroid?

A

can cause hypothyroidism by depositing iron in the thyroid

165
Q

What other complications can haemochromatosis cause?

A

hepatocellular carcinoma
chrondocalcinosis/pseudogout (calcium build up in joints)

166
Q

What is Wilsons disease?

A

an autosomal recessive disease of copper accumulation and toxicity

167
Q

What parts of the body does excessive copper damage?

A

liver (copper is stored in the liver)
basal ganglia (most sensitive)

168
Q

What are the neurological symptoms of Wilsons disease?

A

dysarthria
dystonia

169
Q

What does deposition of copper in the basal ganglia lead to?

A

parkinsonism - tremor, bradykinesia and rigidity

170
Q

What is a feature of motor symptoms in Wilsons disease?

A

they are often asymmetrical

171
Q

What may be visible in the corneas of patients with Wilsons disease?

A

Kayser-fleischer rings

172
Q

What is the first line investigation for Wilsons disease?

A

serum caeruloplasmin - elevated (suggestive but not specific of Wilsons disease)

173
Q

What is the treatment for acute copper toxicity (in Wilsons disease)?

A

trientine + zinc + dietary restriction
if nazer score is >9 - liver transplant

174
Q

What supplementation reduces copper accumulation?

175
Q

What drug is used as an alternative to trientine?

A

penicillamine

176
Q

What does alpha-1-antitripsin do?

A

protects the body - especially the lungs - from harmful enzymes

177
Q

What is elastase secreted by?

A

neutrophils

178
Q

What does elastase do?

A

is breaks down connective tissue

179
Q

What does alpha-1-antitripsin do?

A

inhibits the action of elastase

180
Q

What two main organs are effected by alpah-1-antitripsin deficiency?

A

the lungs and liver

181
Q

How does A1AT deficiency effect the liver?

A

causes cirrhosis

182
Q

How does A1AT deficiency effect the lungs?

A

causes bronchiectasis and emphysema

183
Q

What are the key presentations of alpha-1-antitripsin?

A

productive cough
SOB
hepatomegaly
ascites
confusion
(hepatic syms due to accumulation in liver)

184
Q

What is the first line and gold standard investigation for A1ATD?

A

serum A1AT level - low

185
Q

What would a liver biopsy show in A1ATD?

A

cirrhosis and acid-schiff-positive staining globules

186
Q

What is the first line treatment for A1ATD?

A

smoking cessation, polluting avoidance, hep A vacc (NICE recommend AGAINST A1AT replacement)

187
Q

What may de done for end stage lung or liver disease as a result of A1ATD?

A

liver/lung transplant

188
Q

hat are the two main types of liver cancer?

A

hepatocellular carcinoma, cholangiocarcinoma

189
Q

What mutation can cause hepatocellular carcinoma?

A

a mutation resulting in ineffective AAT

190
Q

What are the main risk factors for hepatocellular carinoma?

A

liver cirrhosis due to:
viral hep B and C
alcohol
NAFLD
chronic liver disease

191
Q

How does liver cancer typically present?

A

weight loss
abdo pain
anorexia
nausea/vomiting
jaundice
pruritus

192
Q

What is the main tumour marker for hepatocellular carcinoma?

A

alpha-fetoprotein

193
Q

What is the main tumour marker for cholangiocarcinoma?

194
Q

What is the gold standard investigation for liver cancer?

A

liver biopsy (not done frequently)

195
Q

What treatments are there for hepatocellular carcinoma?

A

resection, liver transplant
kinase inhibitors

196
Q

How do kinase inhibitors treat HCC?

A

they prevent proliferation of cancer cells

197
Q

Give an example of a kinase inhibitor

A

sorafenib, regorafenib, lenvatinib

198
Q

What are the treatment options for cholangiocarcinoma?

A

surgical resection
endoscopic retrograde cholangiopancreatography (ERCP) with stenting

199
Q

Which area of the pancreas is more likely to be affected by cancer?

A

the head (65% of pancreatic cancers)

200
Q

Name a precursor lesion to pancreatic cancer

A

pancreatic intraepithelial neoplasia
intraductal papillary mucinous neoplasm
mucinous cystic neoplasm

201
Q

What are the key presentations of pancreatic cancer?

A

painless obstructive jaundice
weight loss
jaundice
upper abdo pain
pale stools
dark urine
pruritus

202
Q

What genetic mutation is associated with pancreatic cancer?

203
Q

What does a new diagnosis of diabetes or poor glycaemic control with diabetes sometimes indicate?

A

pancreatic cancer

204
Q

What is Courvoisiers law?

A

a palpable gallbladder with jaundice is unlikely gallstones - its more likely cholangiocarcinoma or pancreatic cancer

205
Q

What is trousseau’s sign of malignancy?

A

migrating thrombophlebitis - inflammtion and blood clotting occuring in different locations over time

206
Q

What are the gold standard investigations for pancreatic cancer?

A

biopsy and CT thorax, abdo, pelvis

207
Q

What blood marker may be raised in cholangiocarcinoma and pancreatic caner?

208
Q

What are some of the treatments for pancreatic cancer?

A

surgical recision
enzyme replacement
radio/chemotherapy
biliary stenting

209
Q

What surgical options are there for pancreatic cancer?

A

total pancreatectomy
distal pancreatectomy
(modified) Whipple procedure

210
Q

What is removed in a Whipple procedure?

A

head of the pancreas
pylorus of stomach
duodenum
gall bladder
bile duct
relevant lymph nodes

211
Q

What is an inguinal hernia?

A

a protrusion of abdominal contents through a dilated internal inguinal ring or attenuated inguinal floor into the inguinal canal

212
Q

What is an indirect cause of an inguinal hernia?

A

congenital - processus vaginalis fails to undergo regression

213
Q

What is a direct cause of an inguinal hernia?

A

weakness in abdominal wall at Hesselbach’s triangle

214
Q

What is the 1st line treatment for a large/symptomatic hernia?

A

open mesh or laparoscopic repair
prophylactic abx

215
Q

What is the treatment for an incarcerated or strangulated hernia?

A

surgical repair
prophylactic abx

216
Q

What is a femoral hernia?

A

a protrusion of abdominal contents through a dilated femoral ring into the femoral canal

217
Q

What are the key presentations of a femoral hernia?

A

small lump in groin

218
Q

What is the treatment for femoral hernia?

A

herniotomy - ligation and excision of sac
herniorrhaphy - hernia pushed back and tissue repaired

219
Q

What is the treatment for small/symptomatic umbilical hernias?

A

observation - most umbilical hernias will close by 4-5 yrs of age
(option for elective surgical repair)

220
Q

What is the treatment for incarcerated umbilical hernia?

A

surgical repair following attempted reduction

221
Q

What are the 4 surgical options for treatment of incision hernia?

A

laparoscopic mesh repair
abdo wall reconstruciton
open mesh repair
suture repair

222
Q

What is an epigastric hernia?

A

a protrusion through the linea alba above the umbilicus

223
Q

What is the gold standard investigation for epigastric hernias?

A

upper Gi series

224
Q

surgical treatment of epigastric hernias is the same as incision hernias, what are the treatment options?

A

laparoscopic mesh repair
abdo wall reconstruction
open mesh repair
suture repair

225
Q

What is hiatal hernia?

A

a hernia through an enlarged oesophageal hiatus of the diaphragm

226
Q

What does hiatal hernia dispose patients to and why?

A

GORD due to decrease in lower oesophageal sphincter pressure

227
Q

What are the key presentations of hiatal hernia?

A

can be asymptomatic
heartburn
regurgitation
bowel sound in chest

228
Q

What is the gold standard investigation for hiatal hernia?

A

upper GI series

229
Q

What is the first line treatment for hiatal hernia?

A

surgical repair w/ anti-reflux procedure (PPI- lanzoprazole (-zole))

230
Q

What two steps does the liver use to metabolise paracetamol?

A

glucuronidation
sulfonation

231
Q

What is the name of paracetamols toxic intermiediate?

A

NAPQI (N-acetyl-p-benzoquinone imine)

232
Q

What detoxifies NAPQI?

A

glutathione

233
Q

What are the key presentations of paracetamol overdose?

A

GI symptoms
nausea and vomiting

234
Q

What is the gold standard test for paracetamol overdose?

A

serum paracetamol concentration

235
Q

What drug, when used at least 8 hours after overdose, is used for a paracetamol OD?

A

acetylcysteine

236
Q

What is Gilbert syndrome?

A

an inherited disorder - decreased levels of UDPGT=impaired conjugation of bilirubin
results in unconjugated hyperbilirubinaemia

237
Q

What are the key presentations of Gilberts syndrome?

A

sometimes asymptomatic
jaundice
absence of hepatosplenomegaly
no chronic liver disease

238
Q

What are the gold standard investigations for gilberts syndrome?

A

elevated unconjugated bilirubin
normal LFTs and FBCs

239
Q

What is the 1st line treatment for gilberts syndrome?

A

patient education + avoidance/reversal of inciting factors

240
Q

How is hep E transmitted?

A

faecal-oral route

241
Q

What scan tests liver elasticity and can diagnose cirrhosis?

242
Q

How would you treat encephalopathy?

A

lactulose (decreases ammonia), abx and enemas

243
Q

What are the main risk factors for hepatocellular carinoma?

A

liver cirrhosis due to:
viral hep B and C
alcohol
NAFLD
chronic liver disease

244
Q

What is primary schelerosing cholangitis?

A

intra/extrahepatic ducts become strictured and fibrotic causing cholestasis

medicine phase 2 a (10 decks)

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