Liver, Biliary Tract and Pancreatic Diseases Flashcards
(242 cards)
1
Q
What causes pre-hepatic jaundice?
A
Too much haem to break down- unconjugated bilirubin enters small intestine
2
Q
What will pre-hepatic jaundice show with regards to urine and stool colours?
A
Normal
3
Q
What causes hepatic jaundice?
A
Hepatocyte damage means not enough bile is produced
4
Q
What will hepatic jaundice show with regards to urine and stool colours?
A
Dark urine and may or may not cause pale stools
5
Q
What causes post-hepatic jaundice?
A
Some kind of obstruction
6
Q
What will post-hepatic jaundice show with regards to urine and stool colours?
A
Dark urine and pale stools
7
Q
What can alcoholic liver disease cause?
A
Portal hypertension, malnutrition and increased risk of hepatocellular carcinoma
8
Q
Which enzymes break down alcohol?
A
Alcohol dehydrogenase and aldehyde dehydrogenase
9
Q
What is alcohol broken down to form?
A
Catalase and ketone bodies
10
Q
What is an effective short term treatment for alcoholic liver disease?
A
Prednisolone
11
Q
What class of LFTs will alcoholic liver disease show?
A
Mixed hepatic and cholestatic
12
Q
What effect will alcohol have on the liver after 2-3 days and is this reversible?
A
Fatty liver- yes
13
Q
What effect will alcohol have on the liver after 4-6 weeks and is this reversible?
A
Inflammation (hepatitis)- yes
14
Q
What effect will alcohol have on the liver after months-years and is this reversible?
A
Fibrosis- no
15
Q
What effect will alcohol have on the liver after many years and is this reversible?
A
Cirrhosis- no
16
Q
How do fat vacuoles appear on histology?
A
White blobs in hepatocytes
17
Q
What are essential features of alcoholic hepatitis?
A
Excess alcohol, bilirubin > 80, exclusion of other causes, AST < 500
18
Q
What is laid down around cells in alcoholic fibrosis? What colour will this be when dyed?
A
Collagen- blue
19
Q
What LFTs will NAFLD show?
A
Hepatitic- increased ALT and AST
20
Q
What is significant about an ALT of above 300?
A
Unlikely to be NAFLD
21
Q
What does steatosis (the first stage of NAFLD) mean?
A
Fat depositions in the liver
22
Q
What does steatohepatitis (the second stage of NAFLD) mean?
A
Fat deposits have resulted in inflammation
23
Q
What is NAFLD very closely associated with?
A
Metabolic syndrome
24
Q
How is simple steatosis diagnosed?
A
Ultrasound
25
How is steato-hepatitis diagnosed?
Liver biopsy
26
What are the outcomes of steatosis?
If it doesn't progress then there are no liver outcomes, however there is an increased CV risk
27
What are the outcomes of steato-hepatitis?
Risk of progression to fibrosis and cirrhosis
28
What is the main treatment for NAFLD?
Weight loss and exercise
29
What will any type of hepatitis show in terms of LFTs?
A predominant rise in aminotransferases (AST, ALT)
30
How is Hep A spread?
Faecal-oral spread
31
What is the incubation time of Hep A?
Short
32
Is hepatitis A directly cytopathic or is the damage caused by an inflammatory response?
Directly cytopathic
33
Is there a carrier state of Hep A?
No
34
What is the outcome of Hep A usually?
Mild illness with full recovery
35
How is Hep B spread?
Blood, blood products, sexually or vertically
36
What is the incubation time of Hep B?
Long (4-6 months)
37
Is hepatitis B directly cytopathic or is the damage caused by an inflammatory response?
Inflammatory response
38
Do carriers of Hep B exist?
Yes, but fairly infrequent
39
What is the outcome of Hep B?
Fulminant acute infection and death, chronic hepatitis, hepatocellular carcinoma
40
Is Hep B infectious?
Very
41
How is Hep C spread?
Blood, blood products, sexually
42
Is Hep C infectious?
Yes- but less so than hep B
43
What is the incubation time of Hep C?
Shorter (4-6 weeks)
44
What is the outcome of hep C?
It is commonly asymptomatic and becomes chronic hepatitis which can lead to cirrhosis and hepatocellular carcinoma
45
What is the most common hepatitis in the UK?
Hep C
46
Who are at risk groups for Hep C?
PWID, vast sexual history, tattoos, Pakistani/Indian ethnicity
47
What gives a fairly solid diagnosis of Hep C and what should be done if this is found?
Positive Hep C antibodies- find out the genotype and refer to hepatology for treatment
48
Who is autoimmune hepatitis most common in?
Females (peaks at 30-40 and 55-65) and people with other autoimmune disease
49
Autoimmune hepatitis is strongly associated with what?
Anti-smooth muscle antibodies
50
What is shown in terms of LFTs for autoimmune hepatitis?
Increased ALT and AST, increased PT
51
An increase in what antibody is also associated with autoimmune hepatitis?
IgG
52
What are common presentations of autoimmune hepatitis?
Hepatomegaly, splenomegaly, jaundice, stigmata of chronic liver disease
53
What treatment is used short and long term for autoimmune hepatitis?
Short- prednisolone
| Long- azathioprine
54
What complications can develop from autoimmune hepatitis?
Cirrhosis or oesophageal varices
55
What are indicators of a poor prognosis in autoimmune hepatitis?
Ascites and encephalopathy
56
Who does primary biliary cholangitis occur most commonly in?
Women aged 50-65
57
What is primary biliary cholangitis strongly associated with?
Anti-mitochondrial antibodies
58
What antibody will potentially be raised in primary biliary cholangitis?
IgM
59
What is the mediator of primary biliary cholangitis?
T lymphocytes (CD4+ reacts to M2 target)
60
Primary biliary cholangitis is an inflammatory process of where?
Microscopic bile ducts
61
What may be seen on histology of primary biliary cholangitis?
Granulomas and bile duct loss
62
What disease is associated with numerous plasma cells?
Autoimmune hepatitis
63
What are common symptoms of primary biliary cholangitis?
Fatigue, itch, increased cholesterol and jaundice
64
What will primary biliary cholangitis show in terms of LFTs?
Cholestatic- increased ALP and slight increase of ALT and bilirubin
65
What is treatment for primary biliary cholangitis?
Ursodeoxcholic acid and treatment for itch
66
Who does primary sclerosing cholangitis occur more commonly in?
Males and people with ulcerative colitis
67
What is strongly associated with primary sclerosing cholangitis?
Anti-nuclear cytoplasmic antibodies
68
Which bile ducts does primary sclerosing cholangitis affect?
Intra and extra hepatic- large and small
69
How is a diagnosis of primary sclerosing cholangitis made?
Imaging of biliary tree (ERCP)
70
What is the outcome of primary sclerosing cholangitis?
Jaundice, periductal fibrosis and duct destruction
71
What is haemochromatosis?
Genetic condition causing excess iron in liver
72
What are secondary causes of haemochromatosis?
Excess iron in diet, blood transfusions and certain therapies
73
What other conditions can primary haemochromatosis predispose to?
Diabetes, cardiac failure, impotence and arthritis
74
What is a treatment option for haemochromatosis?
Venesection
75
What tests should always be done for haemochromatosis?
Serum iron and ferritin/transferrin saturations
76
What is the stain for iron known as?
Perl's stain
77
What is Wilson's disease?
Autosomal recessive disorder of copper metabolism which causes copper to accumulate in the liver and brain
78
Wilson's disease is a loss of function of what?
Caeruloplasmin
79
What are characteristics of Wilson's disease?
Low caeruloplasmin and Kayser-Fleisher rings
80
When does Wilson's disease typically present?
Young age
81
What can Wilson's disease result in?
Chronic hepatitis and neurological symptoms
82
What should you always test for in Wilson's disease?
Serum and urine copper/serum caeruloplasmin
83
How can you treat Wilson's disease?
Copper-chelation drugs
84
What can occur as a result of alpha 1 anti-trypsin deficieny?
Lung emphysema, liver deposition of mutant protein
85
What is the treatment for alpha 1 anti-trypsin deficiency?
Supportive
86
What is Budd-Chiari?
Thrombosis of hepatic veins
87
What deficiencies are common in Budd Chiari?
Protein S or C
88
What are acute presentations of Budd Chiari?
Jaundice and tender hepatomegaly
89
What can chronic Budd Chiari cause?
Ascites
90
How is Budd Chiari diagnosed?
Ultrasound of hepatic veins
91
What is treatment of Budd Chiari?
Recanalisation or stent
92
What is methotrexate and what does it cause?
Drug used to treat rheumatoid arthritis and psoriasis which can cause progressive fibrosis
93
What is the treatment for liver disease secondary to methotrexate?
Stop the drug
94
What is the cause of cardiac cirrhosis?
High right sided pressure (incompetent tricuspid valve, congenital, rheumatic fever, constrictive pericarditis)
95
What does cardiac cirrhosis cause clinically?
Ascites and liver impairment from CCF
96
How do you treat cardiac cirrhosis?
By treating the cardiac condition
97
What is the common final end point for any chronic liver disease?
Cirrhosis
98
Cirrhosis is scarring of the liver which causes what?
Obstruction
99
Cirrhosis is a vascular disease, associated with what?
Hyperdynamic circulation and portal hypertension
100
What is portal hypertension?
Portal pressure >5mmHg
101
What causes pre-hepatic portal hypertension?
Blockage of portal vein before the liver (e.g. portal vein thrombosis)
102
What causes intra-hepatic portal hypertension?
Distortion of liver architecture (e.g. Budd Chiari)
103
What is compensated cirrhosis?
Usually clinically normal and often an incidental finding
104
What can patients with compensated cirrhosis present with?
Haematemesis
105
What is decompensated cirrhosis?
Liver failure as a result of end stage liver disease
106
What are 5 signs of compensated cirrhosis?
Spider naevi, palmar erythema, clubbing, gynecomastia, hepato/splenomegaly
107
What are 4 signs of decompensated cirrhosis?
Jaundice, ascites, encephalopathy, bruising
108
What are treatment options for decompensated cirrhosis?
Treat underlying cause, prevent NaCl retention, small frequent meals, vitamin B supplements
109
Patients with a UKELD score of what can be listed for transplant?
49 or more
110
What are the major complications of cirrhosis?
Ascites, encephalopathy and oesophageal varices
111
How does ascites occur?
Vasodilation results in driving the action of vasoconstrictors which causes increased fluid retention
112
How is ascites diagnosed?
Shifting dullness and darkness on ultrasound
113
What are treatment options for ascites?
Treat underlying disease, decrease salt intake, prevent NaCl reabsorption, spironolactone, paracentesis, shunt, transplant
114
What is a complication of ascites and what should you do to test for it?
Spontaneous bacterial peritonitis- WCC
115
What does encephalopathy cause?
Confusion, hepatic flap, neurological symptoms
116
When is a common time to see encephalopathy?
Alcohol withdrawal
117
How does encephalopathy occur?
Ammonia is taken to the brain without being metabolised which causes disturbances in neurotransmitters of the brain
118
What is treatment for encephalopathy?
Treat underlying cause, give lactulose and maintain nutritional status
119
What should be done if encephalopathy occurs spontaneously?
Transplant
120
What can varices lead to?
Decompensation, liver failure and death
121
What is primary prophylaxis for varices?
Beta blockers (propranolol) and endoscopic ligation
122
What is the emergency treatment for varices? What are the risks?
Balloon tamponade- aspiration and perforation which is usually fatal
123
What are primary liver tumours?
Hepatocellular carcinoma/adenocarcinoma
124
Where is metastases to the liver commonly from?
Colon, pancreas, stomach, breast and lung
125
What is a liver tumour in an old patient most likely to be?
Malignant metastases
126
What is a liver tumour in an CLD patient most likely to be?
Primary liver cancer
127
What is a liver tumour in a non-cirrhotic patient most likely to be?
Haemangioma
128
What is a haemangioma?
Commonest liver tumour, mostly found in women
129
Are there symptoms of haemangioma?
No
130
How can a diagnosis of haemangioma be made?
MRI, CT, ultrasound
131
Is there treatment for haemangioma?
No treatment needed
132
What is focal nodular hyperplasia?
Benign nodule formation in normal tissue
133
Who is focal nodular hyperplasia most common in?
Women but has no relation to sex hormones
134
Does focal nodular hyperplasia have symptoms?
Usually not but may cause slight RUQ pain
135
How is focal nodular hyperplasia diagnosed and does it need treatment?
US, CT, MRI, FNA- no treatment
136
Who are adenomas most common in?
Woman
137
What are a common cause of adenomas?
Sex hormones and other steroidal therapies
138
Are there symptoms of adenomas?
Usually not, but could cause some pain, or rupture/bleed
139
Where are adenomas most often found?
Right lobe
140
What is associated with multiple adenomas?
Glycogen storage disease
141
How are adenomas diagnosed?
CT, US, MRI, FNA
142
What is 1st line treatment for adenomas?
Stop taking hormones and lose weight
143
When do adenomas need to be removed?
Always in males and if they are >5cm in women (regular reviews)
144
What is a cyst?
Liquid collection lined by epithelium
145
Do cysts have symptoms?
Mostly asymptomatic but can cause haemorrhage, infection, rupture or compression
146
What are treatment options for cysts?
No treatment, follow ups or surgery
147
What is a hyatid cyst? How does it present?
Caused by a tapeworm- may present with spread disease or erosion into other structures
148
What is treatment for hyatid cysts?
Surgery, percutaneous drainage, albendazole (anti-helminth)
149
What are some signs are symptoms of a liver abscess?
High fever, leucocytosis, abdominal pain, complex liver lesions
150
When are liver abscesses common?
After abdominal or biliary infection or a dental procedure
151
What is treatment for a liver abscess?
Broad spectrum antibiotics, drainage and operate if no improvement
152
What is hepatocellular carcinoma associated with?
Any form of chronic hepatitis
153
Hepatocellular carcinoma can be asymptomatic, but how can it present?
Mass, RUQ pain, weight loss or obstruction
154
Where is hepatocellular carcinoma likely to metastasise to?
Other parts of liver, portal vein, lymph nodes, lung, bone and brain
155
Alfa Ferroprotein levels above what is highly suggestive of hepatocellular carcinoma?
> 100
156
How can a diagnosis of hepatocellular carcinoma be made?
History, ultrasound, triphasic CT, MRI, biopsy
157
What does the prognosis of hepatocellular carcinoma depend on?
Tumour size, spread, underlying disease and patient performance
158
What is the best treatment for hepatocellular carcinoma?
Liver transplant
159
What requirements must be met for a liver transplant?
Single tumour < 5cm, less than 3 tumours < 3cm
160
Apart from liver transplant, what other treatment options are available for hepatocellular carcinoma?
Resection, local ablation
161
Who is fibrolaminar carcinoma most common in?
Young patients, mostly children
162
What is fibrolaminar carcinoma NOT to do with?
Alcohol or cirrhosis
163
What is the AFP value in fibrolaminar carcinoma?
Normal
164
What is the treatment for fibrolaminar carcinoma?
Surgical resection or transplant
165
What does normal bile contain?
Bile salts, cholesterol, bilirubin and phospholipids
166
Where is bile released?
2nd part of the duodenum through common bile duct and Ampulla of Vater
167
What causes cholesterol stones?
Imbalance between the ratio of cholesterol to bile salts during micelle formation
168
Who are cholesterol stones more common in?
Women, obesity and diabetes
169
What causes pigment stones?
Excess bilirubin cannot be solubilised into bile salts
170
In reality, what are gallstones most commonly?
A mix of cholesterol and pigment cells
171
How does gallstones present?
Pain, jaundice, anorexia, nausea, abnormal cholestatic LFTs
172
How do you confirm a diagnosis of gallstones?
ERCP
173
What increases the risk of gallstones?
Fat, female, forty, fertile, fair
174
What are complications of gallstones?
Biliary colic, acute pancreatitis and gallstone ileus
175
What causes biliary colic?
Stone impacts the cystic duct
176
How does biliary colic present?
Gradual build up of pain in RUQ which radiates to the back and shoulders and may be associated with indigestion and nausea
177
How is biliary colic diagnosed?
Bloods (LFTs), ultrasound, ERCP
178
What is the treatment for uncomplicated biliary colic?
Painkillers, weight loss, low fat diet
179
If symptoms of biliary colic are persisting, what is the treatment?
Refer for cholecystectomy or if this isn't possible use ursodeoxycholic acid
180
What is acute cholecystitis?
Inflammation of the gallbladder which causes obstruction
181
How do you diagnose cholcystitis?
Ultrasound
182
What is the treatment for cholecystitis?
IV antibiotics and fluids and urgent cholecystectomy (within a week)- if not possible do interval cholecystectomy after 3 months
183
What is gallstone ileus?
Fistula has occurred between the gallbladder and duodenum which causes a gallstone to enter the small bowel and cause obstruction
184
How does gallstone ileus present?
Intermittent colic followed by full blown pain and a swollen tummy
185
What is the treatment for gallstone ileus?
Urgent laparotomy
186
When should you do a follow up cholecystectomy following a gallstone ileus?
Only if there are more stones present- check with ultrasound first
187
What type of carcinoma is found in the gallbladder?
Adenocarcinoma
188
What is gallbladder carcinoma most likely to be?
Metastases
189
What is cholangiocarcinoma?
Adenocarcinoma of large or small bile ducts
190
What is cholangiocarcinoma associated with?
UC and primary sclerosing cholangitis
191
How does cholangiocarcinoma present?
Obstructive jaundice
192
What are the main causes of acute pancreatitis?
Alcohol and gallstones
193
What are all the causes of acute pancreatitis?
Idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion bites, hypercalcaemia/parathyroidism/lipidaemia, ERCP, drugs
194
Where does the gallstone blockage occur which causes pancreatitis?
Sphincter of Oddi
195
How does acute pancreatitis present?
Sudden onset severe abdominal pain, nausea, vomiting, jaundice
196
What tests should be done for acute pancreatitis?
ABG, FBC, coagulation, U and E, LFT, Ca++, glucose, amylase/lipase, CRP
197
What is important about serum amylase in pancreatitis?
3xULN is diagnostic
198
What will pancreatitis sometimes show on imaging?
Pleural effusion of sentinel loop
199
What test should all patients with pancreatitis receive?
Ultrasound
200
What test can be used to assess severity of pancreatitis?
CT
201
If pancreatitis was caused by gallstones, should a cholecystectomy be performed?
Yes, within 2 weeks to prevent recurrence
202
What are complications of pancreatitis?
Death, shock, pseudocysts, necrosis, haemorrhage, abscess, hypocalcaemia, hyperglycaemia
203
How are 80% of cases of pancreatitis managed?
Analgesia and fluids
204
A score of what on the Glasgow criteria for pancreatitis is indicative of severe pancreatitis?
3 or more
205
What causes pseudocysts?
Leakage of pancreatic juices
206
What do pseudocysts present with?
Nausea, vomiting, jaundice, weight loss
207
What is the treatment for pseudocysts?
None, or drainage
208
What are causes of chronic pancreatitis?
Alcohol, gallstones, cystic fibrosis, hyperparathyroidism, familial
209
What is treatment for chronic pancreatitis?
Treat acute cases and Creon can be given as enzyme replacement
210
What are complications of chonic pancreatitis?
Splenic vein thrombosis, pseudocysts, pleural effusion, ascites, pancreatic cancer, obstruction
211
What does a calcified pancreatic duct suggest?
Tropical pancreatitis
212
What type of cancer is in the pancreas?
Adenocarcinoma
213
What does pancreatic cancer commonly present as?
Jaundice with no pain
214
What are investigations for pancreatic cancer?
US, triple phase CT, MRI, MRCP
215
What are treatment options for pancreatic cancer?
Resect if possible, if not then maybe stent
216
What type of LFTs does pancreatic cancer cause?
Mixed
217
What does treatment of acute viral hepatitis include?
No antivirals, monitoring for encephalopathy and resolution
218
What are precautions that should take place when a case of acute viral hepatitis is diagnosed?
Notify public health and immunise contacts
219
What vaccinations should be given to chronic viral hepatitis patients?
Other hepatitis vaccines and if they are cirrhotic then also influenza and pneumococcal
220
What are the most commonly used antivirals?
Adefovir and entecavir
221
What environmental factors are often associated with Hep A?
Poor hygiene and overcrowding
222
When is the peak incidence of SYPTOMATIC Hep A?
Older children and young adults
223
What is the main laboratory test for Hep A?
Bloods for serology to looks for hep A IgM
224
When is chronic infection of Hep B more likely?
When the first exposure is in childhood
225
When is HBsAg present?
In the blood of all infectious individuals?
226
When is HBeAg present?
Usually present in highly infectious individuals
227
When is hep B viral DNA present?
Always in highly infectious individuals
228
When is hepatitis B IgM most likely to be present?
Recently infected cases
229
When is Anti-HBs present?
Immunity
230
Is there a vaccine for Hep B?
Yes
231
Is there a vaccine for Hep C?
No
232
If the test for Hep C antibody is positive, what test should you do?
Hep C virus RNA by PCR
233
When is the only time Hep D will be found?
alongside hepatitis B virus
234
What does Hepatitis D do?
Exacerbates hep B
235
When can hep D infect?
At the same time as hep B or after
236
Where is Hep E more common?
Tropics
237
Where can Hep E be contracted?
Food, commonly found in pigs
238
How is Hep E spread?
Faecal-oral
239
Hep E is clinically similar to what?
Hep A
240
Tropical genotypes of Hep E are associated with what?
Severe disease in pregnant women
241
Is there a vaccine for Hep E?
No
242
Who can develop a chronic infection from Hep E?
Immunocompromised
