Liver and Biliary Tract Pathology Flashcards
1
Q
what is cirrhosis of the liver?
A
scarring of the liver after long term damage
2
Q
what are the 4 main consequences of liver cirrhosis?
A
reduced metabolic capacity
portal hypertension
ascites
shunting of blood by-passing liver
3
Q
why in liver cirrhosis does ascites occur mainly in the abdomen?
A
because of the low albumin and very higher pressure from portal system
(large hydrostatic pressure of capillaries [Pc], low osmatic drive of capillaries [pieC])
4
Q
what are the 4 main causes of liver damage?
A
obesity/diabetes
alcohol
viruses
drugs
5
Q
what happens to the size of the liver in cirrhosis?
A
becomes small shrunken and hard
6
Q
what is ‘caput medusae’?
A
when the umbilical vein (ligamentum hepes) becomes back in use because of portal hypertension
7
Q
what is the function of up-regulating of the umbilical vein?
A
to help with the diversion of blood from portal system to systemic system (shunting) in order to combat the high portal pressure
8
Q
what happens to highly metabolised drugs when there is portal-systemic shunting?
A
increased plasma levels
9
Q
why is there increased plasma levels of some drugs due to portal-systemic shunting?
A
due to lack of first pass metabolism
10
Q
what is meant by saturable kinetics of drugs?
A
metabolism increases until a certain point where it then remains at a constant rate- because liver has become saturated
11
Q
why in liver cirrhosis is the renin-angiotensin-aldosterone system up regulated?
A
because low albumin causes low plasma volume which activates renin production from the kidneys
12
Q
what can this up-regulation of the RAAS system cause in a patient with a cirrhotic liver?
A
secondary aldosteronism (liver is unable to break the aldosterone down anymore)
13
Q
why do both endothelin and oestrogen concentrations of the plasma increase in patients with cirrhotic livers?
A
because the liver become unable to metabolise endothelin and oestrogen leading to their accumulation
14
Q
what does the increased oestrogen due to liver cirrhosis cause to males?
A
gynaecomastia
feminisation of men and loss of secondary sexual characteristics
15
Q
what are the 3 main consequences of cirrhotic liver in respect to the kidneys?
A
water retention
sodium retention
potassium loss
16
Q
what is produced in response to hormone vasoconstrictors (such as endothelin, aldosterone, angiotensin II) that acts to maintain kidney function?
A
renal vasodilator prostaglandins
17
Q
why should NSAIDs be avoided if possible in patients in dehydrated states (such as alcoholism/cirrhotic livers)?
A
NSAIDs inhibit vasodilator prostaglandins so will worsen kidney impairment due to vasoconstriction
(due to the high concentration of vasoconstrictors produced because of the dehydration)
18
Q
if you are prescribing a NSAID for a patient with cirrhotic liver what must be co-prescibred?
A
a proton pump inhibitor
19
Q
what 2 phases occur in drug metabolism in the liver?
A
phase 1: biotransformation
phase 2: conjugation
20
Q
what drug metabolism phase is affected early in liver disease and what phase is affected late in liver disease?
A
phase 1 affected early
phase 2 affected late
21
Q
what is the highly reactive intermediate that knackers your liver and is formed from the metabolism of paracetamol?
A
N-acetyl-p-benzoquinonimine
22
Q
why are healthy patients unaffected by n-acetyl-p-benzoquinonimine?
(at advised doses of paracetmol)
A
n-acetyl-p-benzoquinonimine is removed quikly with glutathione
23
Q
what happens if the glutathione runs out and herefore not all the n-acetyl-p-benzoquinomine can be removed?
A
paracetamol overdose
-can lead to fulminant hepatitis
24
Q
why does being drunk reduce risk of overdosing when taking too many paracetamol tablets?
A
alcohol has used up all the enzyme paracetamol needs for metabolism, so paracetamol isn’t metabolised as quickly and acetyl-p-benzoquinomine is formed at a much slower rate
25
why does being a long term alcoholic increase risk of overdosing when taking too many paracetamol tablets?
(if not currently drunk)
as a long term alcoholic your body has more receptors and so the paracetamol will be metabolised much quicker and acetyl-p-benzoquinomine is formed at a much faster rate
26
why does liver failure increase risk of overdosing when taking normal doses of paracetamol?
liver failure reduces glutathione stores, so even though paracetamol is being metabolised at a normal rate, there isn't enough glutathione to remove the acetyl-p-benzoquinomine
27
what is Hy's Rule?
if ALT/AST > 5x Upper Limit Normal
and
Bilirubin > 3mg/dl
the drug is causing liver disease
28
which diuretic is best for people with liver cirrhosis to remove excess fluid?
spironolactone
| due to potassium-sparing effects
29
what type of excretion route do you want the drugs you are prescribing to a patient with liver cirrhosis to have?
renal excretion
30
what is acute liver disease?
rapid development of hepatic dysfunction without prior liver disease
(less than 6 months duration of symptoms)
31
in acute liver disease how do you get the liver to recover without scarring or ongoing damage?
remove stimulus
32
what do liver function tests measure?
ALT
AST
Alk Phos
GGT
33
what do true liver function tests measure?
bilirubin
albumin
prothrombin time
34
what happens to prothrombin time if there is liver disease?
increases
35
what does acute liver failure do on top of acute liver disease?
causes encephalopathy and prolonged coagulation
36
what must be abnormal for acute liver disease?
LFTs
37
where is pain most likely to be felt in acute liver disease?
right upper quadrant
38
what are the 8 clinical features you might expect with acute liver disease?
```
none
jaundice
lethargy
nausea
anorexia
pain
itch
arthralgia (although usually more chronic)
```
39
what are the 7 main causes of acute liver disease?
```
viral
drugs
shock liver
cholangitis
alcohol
malignancy
chronic liver disease
```
40
what are the most common viral causes of hepatitis?
```
hep A
hep B
hep C
hep D
hep E
cytomegalovirus
epstein-barr virus
toxoplasmosis
```
41
what drug is an important cause of acute liver disease?
paracetamol
42
how are hep B and C passed?
blood and some body fluids
| -mainly sex and passed through needles
43
how are hep A and E passed?
faecal-oral route
44
when can hep D cause infection?
only hepatitis B is also present
45
what is shock liver caused by?
sudden hypoperfusion leading to massive hepatocyte necrosis
46
what is Budd Chairi?
a rare cause of acute liver disease caused by obstruction of hepatic veins
47
who does Budd Chairi typically present in?
young women starting oral contraceptives
48
what are 2 rare causes of acute liver disease that are disease of pregnancy?
acute fatty liver of pregnancy
| cholestatsis of pregnancy
49
what are the 4 main factors for liver disease?
direct toxicity
nutrition
immunological
genetic predisposition
50
what is haemochromatosis?
a genetic condition where iron levels accumulate in the body
| patient absorbs more iron from their food than they should
51
what is non-alcoholic steatoic hepatitis caused by?
usually due to unhealthy lifestyle (high in fats) causing ongoing inflammation in the liver
52
what is the treatment of acute liver disease?
- rest (usually up to 3 months, may be 6)
- fluids
- no alcohol
- increase calories (but high fat food poorly tolerated)
- sodium bicarbonate bath, cholestryamine or uresodeoxycholic acid- for itch
53
why is hyoglycaemia a very serious clinical sign of acute liver disease?
because the liver usually makes glucose until the very end
54
what is fulminant hepatic failure?
jaundice and encephalopathy in a patient with previous normal liver
55
out of the hepatitis viruses which is the most likely to cause fulminant hepatic failure?
hepatitis B
56
what is the treatment of fulminant hepatic failure?
```
supportive
inotropes and fluids
renal replacement
management of raised ICP
possible transplantation
```
57
what is the main clinical manifestation of hepatitis viruses?
liver disease
58
how long does it take for patients with hep A to recover and rid their body of the virus?
usually within 3 months
59
how can all viral hepatitis infection be confirmed?
blood serology
60
which hepatitis' have a vaccine?
hep A
| hep B
61
when is chronic infection of hep B most likely to result?
if first exposure is in childhood
62
what 4 groups of people have a higher than average risk of hep B in the UK?
1. people born in areas of intermediate/high prevalence
2. people with multiple sexual partners
3. people who inject drugs
4. children of infected mothers
63
what antigen is present in the blood of all individuals infected with Hep B?
HBsAg
64
if HBsAg is in the blood of an individual for over 6 months what does this mean?
chronic Hep B infection
65
what 2 makers indicate an individual with hep B is highly infectious?
HBeAg (usually)
| high titre of HBV DNA
66
when does a patient have anti-HBs?
if a patient is immune to hep B- natural infection or vaccination
67
what marker does a patient who gained immunity through natural infection to hep B have that a patient who gained immunity through vaccination doesnt?
anti-HBc
| as well as the anti-HBs that vaccination also gives
68
what marker of Hep B is best at giving an indicator of prognosis?
HBV DNA
69
why do individuals with hep B need to be monitored regularly even if at first their viral load is very low?
relationship with infection is dynamic and so later on in disease progression they might have a very high HBV DNA load
70
what can be given a post-exposure prophylaxis for an individual who has come into contact with another individual with Hep B?
vaccine + HBIG
| HBIG = hyperimmune Hep B immunoglobulin
71
which is more easily transmitted by sex- hep B or C?
hep B
72
if patient has antibody to hep C virus what does this mean?
past or active infection
73
if a patient has hep C RNA what does this mean?
active infection
74
compare the nucleic acid present in hep B compared to hep C?
hep B= DNA
| hep C= RNA
75
once a patient with hep B has chronic infection can they have a spontaneous cure?
yes
76
once a patient with hep C has chronic infection can they have a spontaneous cure?
no
77
what is the progression of disease from chronic hepatitis?
chronic hepatitis
cirrhosis
hepatocellular carcinoma or chrnoic liver failure
death
78
compare the chances of hep B and hep C becoming a chronic infection?
hep C is more likely to become chronic than resolve
| hep B is more likely to resolve than become chronic (unless child is infected at birth)
79
if child is infected at birth with hep B what is the likely progression?
likely to become chronic rather than resolve
80
what is the management of acute viral hepatitis?
- supportive
- no antivirals given
- monitor for encephalopathy
- monitor for resolution
- notify public health
- immunisation of contacts
- test for other infections if at risk
- vaccinate against other infections if at risk
81
what is the management of chronic viral hepatitis?
- antivirals
- vaccination of other infections
- infection control
- reduced alcohol intake
- hepatocellular carcinoma awareness/screening
82
compare the number of antivirals on the market for hep C compared to hep B?
hep B= 6 antivirals
| hep C= 8 antivirals
83
what is a complete contraindication to the treatment of chronic hepatitis with antivirals?
hepatocellularcarcinoma
84
as HBV DNA load at initial infection increases what happens to the risk of hepatocellular carcinoma if infection becomes chronic?
greater risk of cancer
85
for chronic hepatitis, how is alpha interferon administered?
peginterferon injections
86
what are the common side effects of peginterferon?
flu-like symptoms
87
what are the less common, but more severe side effects of peginterferon?
thyroid disease
autoimmunde disease
psychiatric disease
88
what are the side effects of older HCV antivirals such as ribavirin, telaprevir and boceprevir?
anaemia
| telaprevir and boceprevircan also cause a sever rash
89
what are the 2 options for chronic hep B therapy?
1. peginterferon alone
| 2. suppressive antiviral drugs
90
what are the advantages of peginterferon treatment of chronic hep B?
sustained cure possible from a few months of therapy
91
what are the disadvantages of peginterferon treatment of chronic hep B?
only minority gain benefit
side effects
injections
92
what are the advantages of suppressive antiviral drug therapy for chronic hep B?
safer than peginterferone therapy
93
what are the diseadvantages of suppressive antiviral drug therapy for chronic hep B?
suppression not cure
| resistance can develop
94
what are the 3 virological aims in terms of chronic hep B therapy?
1. reduction in HBV DNA (suppression)
2. loss of HBeAg (further suppression)
3. loss of HBsAg (cure)
95
what are the 6 main aims of chronic hep B therapy?
1. virological aims
2. improved liver biochem
3. improved histopathology
4. reduced infectivity
5. reduced progression to cirrhosis and primary hepatocellular carcinoma
6. reduced mortality
96
what is a hepatitic C therapy response defined as?
SVR: sustained virological response (cure as relapse is rare)
97
what defines sustained virological response?
loss of HCV RNA in blood sustained to 6 months after end of therapy
98
even if patients have sustained virological response what must be continued if the patient already has cirrhosis?
6 monthly ultrasound screening for hepatocellular carcinoma
| even though risk has been reduced, because the liver is cirrhotic patient still has significant risk
99
what ribs protect the liver?
7-11
100
what ligament on the anterior surface of the liver separates the right and left lobe?
falciform ligament
101
in the acinar concept of the liver, what zone is closest to the central vein? what zone is furthest from the central vein?
zone 3 = closest to central vein
| zone 1 = furthest from central vein
102
what are the 3 main consequences of acute liver failure?
complete recovery
chronic liver disease
death from liver failure
103
what is the phrase that means jaundice within the sclera of the eyes?
icterus
104
what are the 3 classes of jaundice?
pre-hepatic
hepatic
post-hepatic
105
what type of bilirubin is excess in the blood in pre-hepatic jaundice?
unconjugated bilirubin
106
what type of bilirubin is excess in the blood in hepatic jaundice?
both unconjugated and conjugated bilirubin
107
what type of bilirubin is excess in the blood in post-hepatic jaundice?
conjugated bilirubin
108
what can cause pre-hepatic jaundice?
haemolysis of all causes
109
what can cause post-hepatic jaundice?
all obstructions of the biliary tree
| eg gallstones, strictures, tumours
110
what is cirrhosis of the liver defined by?
bands of fibrosis separating regenerative nodules of hepatocytes
-prevent regeneration
111
what are the 2 subgroups of cirrhosis?
macronodular or micronodular
112
which sub group of cirrhosis is caused by alcohol abuse?
micronodular
113
what are the differences between rectal varices and haemorrhoids?
anorectal varices= dilation of portal-systemic anastomosis due to portal hypertension
haemorrhoids = prolapse of rectal venous plexus (not due to portal hypertension)
114
what are the 3 main complications of cirrhosis?
portal hypertension (hepatic)
ascites
liver failure
115
what type of cause of portal hypertension is a portal vein thrombosis?
pre-hepatic portal hypertension
116
what type of cause of portal hypertension is hepatomegaly?
pre-hepatic portal hypertension
117
what type of cause of portal hypertension is right sided heart failure?
post-hepatic portal hypertension
118
what type of cause of portal hypertension is budd chairi (hepatic vein outflow obstruction)?
post-hepatic portal hypertension
119
why can chronic liver disease cause oedema?
reduced albumin synthesis resulting in hypoalbuminaemia
120
why can chronic liver disease causes ascites?
hypoalbinaemia
secondary hyperaldosteronism
portal hypertension
121
why can chronic liver disease cause haematemesis?
ruptured oeophageal varices due to portal hypertension
122
why can chronic liver disease cause spider naevi?
impaired ability to metabolise oestrogen causing hyperoestrogenism
123
why can chronic liver disease cause gynaecomastia?
impaired ability to metabolise oestrogen causing hyperoestrogenism
124
why can chronic liver failure cause purpura and bleeding?
reduced clotting factor synthesis
125
what is purpura?
bleeding of small blood vessels that cause purple spots on the skin
126
why can chronic liver failure cause a coma?
failure to eliminate toxic gut bacterial metbaolites
127
why can chronic live failure cause increased infection?
reduced kupffer cell number and function
128
what is the pathogenesis of alcoholic liver disease?
1. increased peripheral release of fatty acids and increased synthesis of fatty acids and triglyceride within hepatocytes
2. acetaldehyde (a product of alcohol metabolism) is responsible for liver cell injury
3. increased collagen synthesis by fibroblasts and stellate (ito) cells
129
when is alcoholic liver disease reversible?
fatty liver stage (2-3 days of drinking)
hepatitis stage (4-6 weeks of drinking)
ONLY IF CESSATION OF ALCOHOL
130
when is alcoholic liver disease irreversible?
```
fibrosis stage (months- years of drinking)
cirrhosis stage (years of drinking
```
131
why is liver disease irreversible after fibrosis stage?
because of collagen deposition around hepatocytes
132
what is NASH? (non-alcoholic steatoheaptitis)
pathologically identical to alcoholic liver disease but occurs in patient with diabetes, obesity or hyperlipidaemia insteaf of drinkers
133
why does hepatitis B cause liver damage?
due to antiviral host immune response
134
if you have HBsAg in your blood but are asymptomatic what are you known as?
a carrier
135
which is more likely to progress to hepatocelular carcinoma if it becomes chronic- hep B or hep C?
hep B
136
what autoantibodies is primary biliary cirrhosis associated with?
anti- mitochondria antibodies
| AMA
137
why do you use a biopsy within primary biliary cirrhosis?
to stage disease
138
what autoantibodies is autoimmune heaptitis associated with?
type 1: anti-nuclear antibodies (ANA)
anti-smooth-muscle antibodies (ASMA)
type 2: anti-liver-kidney-microsomal antibodies (anti-LKM-1)
anti-liver-cytosolic antibodies (anti-LC-1)
139
what is primary sclerosing cholangitis?
a chronic inflammatory process affecting intra and extra hepatic bile ducts which leads to periductal fibrosis, duct destruction and fibrosis
140
what is primary haemochromatosis?
an autosomal recessive condition which causes excess iron within the liver due increased absorption of iron from food
141
what is secondary haemochromatosis?
excess iron within the liver caused by iron overload from diet, transfusions or iron therapy
142
how is haemochromatosis treated?
venesection
143
what can haemochromatosis cause within the liver?
asymptomatic for years
| then stimulates fibrosis and cirrhosis if not treated
144
what does haemochromatosis predispose to?
hepatocellular carcinoma, diabetes, cardiac failure, impotence
145
what are the 2 major results of alpha-1-antitrypsin deficiency?
emphysema
| cirrhosis
146
what type of inheritance is alpha-1-antitrypsin deficiency?
autosomal recessive
147
what are the 2 types of primary cancers within the liver?
```
hepatocellular adenoma- benign
hepatocellular carcinoma (hepatoma)- malignant
```
148
who is more likely to get primary biliary cirrhosis- M or F?
females
149
who is more likely to get autoimmune hepatitis- M or F
females
150
who is more likely to get primary sclerosing cholangitis- M or F?
males
151
who is more likely to have haemochromatosis- M or F?
males
152
who is mre likely to get hepatocellular adenoma- M or F?
females
153
how long does liver disease has to be ongoing to be classed as chronic?
6 months
154
why do stellate cells start to produce collagen?
in response to cytokines produced from kupffer cells during times of inflammation
155
how do you diagose simple steatosis?
ultrasound
156
what is the treatment for simple steatosis?
weight loss and exercise
157
how do you diagnose NASH?
liver biopsy
158
what are the increased risks due to simple steatosis of the liver?
increased cardiovascular risks not liver risks
159
what are the main symptoms of PBC?
fatigue
itch without rash
xanthelasma
160
what is the treatment for PBC?
ureseodeoxycholic acid
161
what is the biomodal age distribution of type 1 autoimmune hepatitis?
10-20
| 45-70
162
compare the LFTs of AIH and PBC?
PBC- cholestatic picture
| AIH- hepatic picture
163
how do you confirm autoimmune hepatitis?
```
liver biopsy
(autoimmune antibodies don't confirm)
```
164
what is the treatment of AIH?
corticosteroids eg prednisolone
| azathioprine
165
for children with autoimmune hepatitis what treatment should you try first and why?
azathioprine monotherapy to try reduce effects of steroids (eg reduced bone growth)
166
what is the main feature of a patient with primary sclerosing cholangitis?
recurrent cholangitis
167
how do you diagnose primary scelrosing cholangitis?
imaging of the biliary tree
168
what is the treatment of alpha 1 anti-trypsin deficiency?
supportive
169
what is a serious adverse effect of methotrexate?
progressive fibrosis of liver and lungs
170
what is cardiac cirrhosis?
cirrhosis of the liver secondary to high right heart pressures
171
what are the 4 groups of collateral pathways from the portal system to systemic system?
esophageal plexus
umbilical vein
retroperitoneal collateral vessels
rectal venous plexus
172
what are the signs of decompensated liver failure?
```
all the signs of compensated liver failure plus:
jaundie
ascites
encephatlopathy
easy bruising
(ie problems with function)
```
173
when you press spider naevi how should the vessels refill?
from the middle to the edges
174
what is the treatment for ascited?
```
improve underlying liver disease
reduce salt intake, maintain nutrition
diuretics (spironolactone first)
paracentesis
TIPSS
transplantation
```
175
what is trans-jugular porto-systemic shunt?
a minimally invasive procedure which results in equalising pressures in portal and systemic systems
176
how does spontaneous bacterial peritonitis occur?
translocated bacterial infection caused by ascites
177
what is the treatment of spontaneous bacterial peritonitis?
antibiotics
terlipressin
maintain renal perfusion
178
in encephalopthy what should you use to clear gut?
lactulose
179
why should you use lactulose in encephalopathy?
to reduce time bacteria have to produce ammonia ie reduce transit time
180
what is the last resort for oesophageal varice bleeding? (ie if nothing else works)
balloon tamponade
181
why do cholesterol gallstones form?
imbalance between the ratio of cholesterol to bile salts
182
what are the 4 predisposing factors to cholesterol gallsontes?
female
obesity
diabetes
genetic
183
why do pigment gallstones form?
excess bilirubin present within stone due to exces haemolysis
184
what is cholecystitis?
inflammation of the gallbladder
185
what is cholecystitis usually associated with?
gallstones
186
why is the usual pathogenesis of acute cholecystitis?
gallstones obstructing outflow of bile
this becomes infected and may cause empyeme rupture and peritonitis
intense adhesions are formed
187
what is the wall of the gallbladder like in chronic cholecystitis?
thickened
| but not distended
188
what is the most common carcinoma of the gallbladder?
adenocarcinoma
| -still rare
189
what are carcinomas of the gallbladder generally associated with?
gallstones
190
what is the most common carcinoma of the bile ducts?
adenocarcinoma (cholangiocarcinoma)
| -still rare
191
what are carcinomas of the bile ducts (cholangiocarcinomas) generally associated with?
ulcerative cholitis and primary sclerosing cholangitis
192
in non-cirrhotic patients what is the most common solid liver tumour?
hemangioma (benign)
193
what are the 4 main benign focal nodules?
hemangioma
focal nodular hyperplasia
adenoma
liver cysts
194
what are the 6 primary liver cancer?
```
hepatocellular carcinoma
cholangiocarcinoma
fibrolamellar carcinoma
hepatoblastoma
angiosarcoma
haemangioendothelioma
```
195
what is the treamtent for a hemangioma?
none
196
what is a hemangioma?
a benign vascular tumour within a well demarcated capsule
197
what is a focal nodular hyperplasia?
a benign nodule formation of normal liver tissue
198
what do focal nodular hyperplasia lesions classically have in the centre?
a central scar containing an unusually large artery with radiating branches to the perphery
199
why do focal nodular hyperplasia lesions form?
as a response to a vascular abnormality
200
who are focal nodula hyperplasia lesions most common in?
young and middle aged women
201
what does hyperintense mean on MRI?
brighter than surrounding tissue
202
what does hypointense mean on MRI?
darker than surrounding tissue
203
what does isointense mean on MRI?
same colour as surrounding tissue
204
what is the treatment for focal nodular hyperplasia?
none
205
what is a hepatic adenoma?
a benign neoplasm composed of normal hepatocytes but with no portal tract, central ceins or bile ducts
206
who is hepatic adenomas more common in-M or F?
females
207
what are hepatic adenomas associated with?
contraceptive hormones especially high oestrogen pills
208
sometime hepatic adenomas can by symptomatic, what can they present as?
RUQ pain
209
what can be the complications of a hepatic adenoma?
rupture
haemorrhage
malignant transformation
210
what is adenomatosis?
a rare conditions with multiple adenomas
211
if a a hepatic adenoma is contraceptive pill driven what wilhappen if the pill is discontinued?
regression
212
what is the treatment of hepatic adenoma?
stop hormones
| observe every 6 months for 2 years and if no regression then surgical excision
213
what are the main differences between adenomas and focal nodular hyperplasia?
adenoma is purely a hepatocyte tumour which FNH contains all liver ultrastructure
adenomas can bleed and become malignant while FNH can't do either
214
which is a simple liver cyst?
liquid collection lined by an epithelium
215
what is a hydatid cyst?
a multilobular cyst
| ie contains many irregular cavities
216
what parasite can cause hydatid cysts in the liver?
echinococcous granulosus
217
what drug is given to patients with hydatid cysts to kill the echinococcus granulosus parasite?
albendazole
218
what is the main treatment of hyatid cysts?
surgical resection or marsupialization (surgical technique)
219
what are polycystic liver diseases?
a range of congenital conditions which results from embryonic ductal plate malformation of the intrahepatic biliary tree
(bile ducts never joined up to the rest of the biliary tree)
220
what are the 3 main types of polycystic liver disease?
Von Meyenburg Complexes (VMC
Polycystic Liver disease
Autosomal dominant polycystic kidney disease
221
rarely invasive procedures can be used in patients with PCLD or ADPKD, what are these procedures?
defenstration/aspiration
| liver transplantation
222
what is the presentation of a liver abscess?
high fever
leukocytosis
abdominal pain
223
what history usually proceeds liver abscesses?
abdominal or biliary infection
| dental procedure
224
what is the management of a liver abscess?
- initial empirical broad spectrum antibiotics
- aspiration/drainage percutaneously
- echocardiogram to make sure no infective endocarditis due to bacteraemia
- operation if no clinical improvement
- 4 weeks antibiotic therapy with repeat imaging
225
if theres no clinical improvement of a liver abscess what operations can be done?
open drainage
| resection
226
what is the most important risk factor for hepatocellular carcinoma?
cirrhosis
227
what protein is a hepatocellular carcinoma marker?
alfa feto protein
228
what treatment can be done for unresectable hepatocelluar carcinomas?
radiofrequency ablation
alcohol injection
chemoembolization
229
what is chemoembolization?
injecting chemotherapy selectively in hepatic artery and then injecting an embolic agent to block blood supply to tumour
230
what are the 2 main diseases of the biliary tract?
cholelithiasis
| cholangiocarcinoma
231
what are the 3 possible causes for gallstones?
abnormal bile composition (etither excess bilirubin or cholesterol)
bile stasis
infection
232
where do primary bile duct stones develop?
in the intrahepatic bile ducts or common bile ducts
233
where do secondary bile duct stones develop?
in the gall bladder
| much more common
234
what are the 5 risk factors for gall stones?
```
5 F's
Forty
Female
Fat
Fair (caucasians have a higher incidence)
Fertile (premenopause)
```
235
what is the main symptoms of bile stones?
biliary colic
236
where may the pain of biliary colic present?
build up pain in RUQ
| radiates to back shoulder
237
what is the pain of biliary colic associated with?
indigestion
| nausea
238
what are the 5 main reasons for severe acute epigastric pain?
```
biliary colic
peptic ulcer disease
oesophageal spasm
MI
acute pancreatitis
```
239
what is acute cholecystitis?
inflammation of the gallbladder
240
what is the usual cause of cholecystitis?
gall stones causing obstruction of the cystic duct, initially sterile then becomes infected
241
what are the 3 main ways to diagnose gallstones?
ultrasound
CT
MRCP/ERCP
242
what is the treatment of acute cholecystitis?
```
IV antibiotics
IV fluids
nil by mouth
US to confirm
urgent cholecystectomy
```
243
if a bile stone migrates into the common bile duct what are the 4 possible consequences?
jaundice
cholangitis
acute pancreatitis
gallstone ileus
244
what are the clinical symptoms of a gallstone within the common bile duct?
itch
nausea
anorexia
245
what are the clinical signs of af a gallstone within the common bile duct?
jaundice, abnormal LFTs
246
what is the only chance of cure of cholangioma?
surgical resection
247
what is the first line investigation for cholecystitis/biliary colic?
ultrasound
| then possible MRCP/ERCP
