Liver and Friends Flashcards
1
Q
What are the stages of alcoholic liver disease
A
- Alcoholic fatty liver - hepatic steatosis
- Alcoholic hepatitis
- Cirrhosis
2
Q
Which process of alcoholic liver disease is irreversible
A
Cirrhosis - functional liver tissue is replaced with scar tissue
3
Q
What is the alcoholic drinking recommendations
A
No more than 14 units per week
Across 3 days or more
No more than 5 units per day
4
Q
What questions (2) can be used to screen for harmful alcohol use
A
CAGE questions
AUDIT questionnaire
5
Q
Describe CAGE questions
A
Cut down?
Annoyed - commenting about drinking
Guilty
Eye opener - drink first thing in a morning
6
Q
Name 3 risk factors for alcoholic liver disease
A
Prolonged and heavy alcohol consumption
Hepatitis C
Female sex
7
Q
Name the clinical features of alcoholic liver disease
A
Ascites
Weight loss/gain
Malnutrition and wasting
Anorexia
Fatigue
Abdominal pain
Hepatomegaly
8
Q
Name the investigations for alcoholic liver disease
A
GS- liver biopsy
Blood tests
Liver ultrasound
Transient elastography
Endoscopy
CT and MRI scans
9
Q
What is the management of alcoholic liver disease
A
Stop drinking - alcohol withdrawal
Nutritional support - vitamins and high-protein diet
Treat complications of liver cirrhosis
Liver transplant
10
Q
Define non-alcoholic liver disease
A
Characterised by excessive fat in the liver cells (specifically triglycerides)
11
Q
Describe the pathophysiology of non-alcoholic fatty liver disease
A
Excessive fat interferes with normally functioning liver cells.
Can progress into hepatitis and cirrhosis
12
Q
What are the stages of non-alcoholic fatty liver disease
A
- Non-alcoholic fatty liver disease.
- Non-alcoholic steatohepatitis
- Fibrosis
- Cirrhosis
13
Q
What are the risk factors for non-alcoholic fatty liver disease the same as
A
CVD
14
Q
What is non-alcoholic fatty liver disease associated with
A
Metabolic syndrome = hypertension + obesity + diabetes
15
Q
Describe the clinical features of non-alcoholic fatty liver disease
A
Early - asymptomatic
Late -
Nausea
Vomiting
Jaundice
Pruritis
Ascites
Memory impairment
Easy bleeding
Loss of appetite
16
Q
Name 2 signs of non-alcoholic fatty liver disease
A
Jaundice
Spider angiograms
17
Q
What are the investigations of non-alcoholic fatty liver disease
A
Raised alanine aminotransferase (ALT)
Liver ultrasound
Enhanced liver fibrosis blood test
Transient elastography
Liver biopsy
18
Q
What tests can be used to score non-alcoholic fatty liver disease
A
NAFLD fibrosis score
Fibrosis 4
Both assess for liver fibrosis
19
Q
What is the gold standard test for non-alcoholic fatty liver disease
A
Liver biopsy
20
Q
What is the management for non-alcoholic fatty liver disease
A
Modifications
- Weight loss
- Healthy diet
- Avoid/limit alcohol intake
- stop smoking
- Control diabetes.
Refer patients for scoring
Specialist management
21
Q
Which hepatitis are RNA viruses
A
A, D, E
22
Q
Which hepatitis are DNA viruses
A
B, C
23
Q
Which hepatitis route of transmission is Faeco-oral
A
A, E
24
Q
Which hepatitis are blood/sexual transmission
A
B, C, D
25
What are the clinical features of hepatitis A infection
Cholestasis with:
- Pruritus
- Significant jaundice
- Dark urine
- Pale stools
26
Which hepatitis are a chronic infection
B, C, D
27
Describe the diagnosis of hepatitis A
IgM antibodies to hepatitis A
28
Describe the management of hepatitis A
Supportive - usually resolves without treatment
29
Describe the screening test for hepatitis B
Measure IgM and IgG versions of HBcAb
IgM - active infection
- high = acute
- low = chronic
IgG = past infection
HBsAg = active infection in acute phase (replicating)
29
Describe the management of hepatitis B
Supportive + antiviral (tenofovir, analogues)
30
Describe the serology of hepatitis C
HVC Ab = all patients
HCV RNA = chronic infection
31
Describe the investigations of hepatitis C
Hepatitis C antibody = screening test
Hepatitis C RNA testing - confirms diagnosis
32
What is the management of hepatitis C
Direct-acting antivirals
- Pegylated interferon weekly injections
+ Ribavirin tablets
33
When can someone have hepatitis D
With a hepatitis B infection
Increases complications and disease severity of hepatitis B
34
What is the management of hepatitis D
pegylated interferon alpha
35
Which hepatitis currently have a vaccine
A, B
36
What is the prevention for hepatitis A and B
Pre and post exposure immunisation
B as well - behaviour modification
37
How is hepatitis C prevented
Blood donor screening
Behaviour modification
38
How is hepatitis D prevented
HBV immunisation
Behaviour modification
39
How is hepatitis E prevented
Clean drinking water
40
What is the treatment for hepatitis E
Supportive
41
Define liver cirrhosis
Due to chronic inflammation and damage to liver cells. Functional cells are replaced with scar tissue (fibrosis) - nodules of scar tissue
42
What are the 4 most common causes of liver cirrhosis
Alcohol-related liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C
43
What are the risk factors of liver cirrhosis
Alcohol misuse
IVDU
Unprotected intercourse
Obesity
Birth country
44
Name a complication of liver cirrhosis
Portal hypertension
45
Name the clinical features of liver cirrhosis
Cachexia
Jaundice
Hepatomegaly
Small nodular liver
Splenomegaly
Spider naevi
Palmar erythema
46
Describe the investigations of liver cirrhosis
GS-Gastroscopy
Blood tests
- LFTs
- Albumin
- Prothrombin time
- FBC
Non-invasive liver screening
Imaging
47
Name 2 tests for clinical diagnosis of liver cirrhosis
MELD score - model for end-stage liver disease
Child-Pugh Score
48
Describe MELD Score
Score every 6 months in patients with compensated cirrhosis
49
Describe the Child-Pugh score for liver cirrhosis
Used 5 factors (score 1,2,3) to assess the severity of cirrhosis and the prognosis
Max score 15
ABCDE
Albumin
Bilirubin
Clotting (INR)
Dilation (ascites)
Encephalopathy
50
What are the 4 principles of the management of liver cirrhosis
1. Treat underlying condition
2. Monitor for complications
3. Manage complications
4. Live transplant
51
When is liver transplant considered in liver cirrhosis
When features of decompensated liver disease
Features
Ascites
Hepatic encephalopathy
Oesophageal varices bleeding
Yellow (jaundice).
52
Define jaundice
Yellow discolouration of the sclera and skin
53
Why does jaundice occur
Hyperbilirubinemia - occurs at > 51 micromol/L.
54
What is the normal range for total bilirubin
3.4-20 micromol/L
55
Describe the pathophysiology of jaundice
Bilirubin - conjugated within the liver = soluble.
Majority = ejested in the faeces as urobilinogen ad stercobilin
10% urobilinogen absorbed back into the blood stream and excreted by the kidneys
Jaundice occurs when this pathway is disrupted
56
Name the 3 types of jaundice
1. Pre-hepatic
2. Hepatocellular (intra-hepatic)
3. Post-hepatic
57
Describe pre-hepatic jaundice
Excessive red cell breakdown - overwhelms the liver's ability to make conjugated bilirubin
Causes - unconjugated hyperbilirubinemia
Unconjugated remains in the blood stream to cause the jaundice
58
Describe intra hepatic jaundice
Cirrhosis compresses the intra-hepatic proteins of the biliary tree to cause obstruction.
Leads to both conjugated and unconjugated bilirubin in the blood
59
Describe post hepatic jaundice
Obstruction of biliary drainage
Bilirubin is not excreted will have been conjugated by the liver
= conjugated hyperbilirubinemia
60
Name 3 causes pre-hepatic jaundice
Haemolytic anaemia
Gilbert's syndrome
Criggler-Najiar syndrome
61
Describe the potential causes of intra-hepatic jaundice
Alcoholic liver disease
Viral hepatitis
Iatrogenic
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Hepatocellular carcinoma
62
Describe the potential causes of post-hepatic jaundice
Intra-luminal causes - gallstones
Mural causes
Extra-mural causes
63
Name the risk factors of jaundice
Drugs and alcohol
Social history
Autoimmune
Sexual history
Inflammation of the bile duct
Haemolytic anaemia
Obstruction of the bile duct
64
Pre-hepatic jaundice
Name
Urine
Stools
Itching
Liver tests
Normal
Normal
No
Normal
65
Describe intra/post-hepatic jaundice
Urine
Stools
Itching
Liver tests
Dark
May be pale
Maybe
Abnormal
66
Describe the investigations of jaundice
Liver enzymes
Biliary obstruction
Imaging
67
Describe the management of jaundice
Dependent on underlying cause
Obstructive
- removal of gallstones
- cholangiopancreatography or stenting of common bile duct
Symptomatic treatment - itching
Identify and manage any complications
Treatment of confusion
68
What is the treatment of confusion due to decompensating chronic liver disease
Laxatives +/- neomycin
Rifaximin
Attempts to reduce the number of ammonia-producing bacteria in the bowel
69
Define autoimmune hepatitis
Chronic inflammatory disease of the liver with unknown aetiology.
Characterised by the presence of circulating auto-antibodies with a high serum globulin concentration, inflammatory response changes on liver histology and favourable responses to immunosuppressive treatment.
70
What are the causes of autoimmune hepatitis
Occur due to combination of genetic and environmental factors
71
Name the different types of autoimmune hepatitis
Type 1 and 2
72
Describe type 1 autoimmune hepatitis
Affects women
Late 40-50s
Presents around or after menopause with fatigue and features of liver disease on examination
Less acute than type 2
73
Describe type 2 autoimmune hepatitis
Children or young people
More commonly girls
Acute hepatitis
Transaminases and jaundice
74
Name the risk factors of autoimmune hepatitis
Female sex
Genetic pre-disposition
Immune dysregulation
75
Name the investigations of autoimmune hepatitis
High transaminases
Minimal changes in ALP levels
Raised IgG
Liver biopsy
76
Describe the management of autoimmune hepatitis
Prednisolone + azathioprine (90%)
Liver transplant - autoimmune hepatitis can reoccur
77
Define Wernicke's encephalopathy
Neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations
78
Define Korsakoff syndrome
Memory disorder that results from vitamin B1 deficency and is associated with alcoholism.
79
Describe the causes of Wernicke-Korsakoff syndrome
Acute or subacute deficiency of thiamine
Decreased intake - oral or parenteral
Increased demand, or malabsorption from the GI tract
Other causes:
- alcohol abuse
- dietary deficiency
- prolonged vomiting
- eating disorders
- effects of chemotherapy
80
Name the clinical features of Wernicke's encephalopathy
Damage to the brain's thalamus and hypothalamus
- Neuropsychiatric manifestations
- Confusion
- Oculomotor disturbances
- Ataxia
- Gait and balance disorders
81
Describe the clinical features of Korsakoff syndrome
Memory impairment - retrograde or anterograde
Behavioural changes
82
Describe the investigations of Wernicke-Korsakoff syndrome
Therapeutic trial of parenteral thiamine
Other tests
- Finger-prick glucose
- Bloods
83
Describe the management of Wernicke-Korsakoff syndrome
Treated in emergency with thiamine replacement
Wernicke's important to start thiamine replacement before beginning nutritional replenishment
84
What is the prevention of Wernicke-Korsakoff syndrome
Thiamine supplementation
Alcohol abstaining
85
Define hepatic encephalopathy
Brain dysfunction (neuropsychiatric syndrome) caused by acute or chronic advanced hepatic insufficiency and/or portosystemic shunt
86
Name the 3 pathophysiological mechanisms for hepatic encephalopathy
Ammonia absorbed into circulation through the portal venous system
Hyperammonaemia - affecting neurotransmitter synthesis
Increased activation of GABA
87
Describe the cause of hepatic encephalopathy
Combination of metabolic encephalopathy, brain atrophy and/or brain oedema
88
Name 4 symptoms of hepatic encephalopathy
Mood, sleep and motor disturbances
Advanced neurological deficits
89
Name 7 signs of hepatic encephalopathy
Asterixis
Palmar erythema
Spider angiomata
Peripheral oedema
Jaundice
Hepatomegaly
Ascites
90
Name the investigations for hepatic encephalopathy
Blood
Urine culture
Urine toxin screen
Ultrasonography
Head CT or MRI
91
Name the primary objectives of the management of hepatic encephalopathy
Provide supportive care
Exclude other causes of altered mental state
Identify and correct precipitating factors
Reduce the nitrogenous load from the gut
Assess the need for long-term therapy
92
Describe the pathophysiology of pancreatic cancer
Tumour in the head of the pancreas grows large enough to compress the bile duct
Spread metastasis early
93
Name the risk factors for pancreatic cancer
Smoking
Family history
94
Name the clinical features of pancreatic cancer
Key = painless obstructive jaundice
- yellow skin and sclera
- pale stools
- dark urine
- generalised itching
Other vague presenting features
95
Name the clinical signs of pancreatic cancer
Courvoisier's law
Trousseau's sign of malignancy
96
Describe Courvoisier's Law
Palpable gallbladder + jaundice = unlikely to be gallstones.
Usual cause - cholangiocarcinoma or pancreatic cancer
97
Describe Trousseau's sign of malignancy
Migratory thrombophlebitis = sign of malignancy
Blood vessels become inflamed with associated thrombus in multiple different locations over time.
98
Describe the investigations of pancreatic cancer
Imaging
CA19-9 (carbohydrate antigen) = tumour marker.
Biopsy
99
How is a diagnosis of pancreatic cancer made.
Imaging (usually CT scan) + histology from biopsy
100
What are the NICE referral guidelines for pancreatic cancer
> 40 + jaundice = 2 week wait
> 60 + weight loss + one additional symptom = referred for a direct access CT abdomen
101
Describe the management of pancreatic cancer
Options
Surgery
Palliative treatment (if no surgery).
102
Define hepatocellular carcinoma
Main type of primary liver cancer = originates in the liver
103
Name the risk factors for hepatocellular carcinoma
Liver cirrhosis = main
Diabetes
Obesity
Family history
104
Describe the clinical features of hepatocellular carcinoma
Asymptomatic originally
Present late = poor prognosis
Non-specific features
- weight loss
- abdominal pain
- anorexia
- nausea and vomiting
- jaundice
- pruritus
- upper abdominal mass on palpitation
105
Describe the investigations for hepatocellular carcinoma
Alpha-fetoprotein
Liver ultrasound
CT/MRI scans
Biopsy
106
Describe the screening for hepatocellular carcinoma
Patients with cirrhosis screened every 6 months
Ultrasound
Alpha-fetoprotein
107
Describe the management of hepatocellular carcinoma
Surgery
Radiofrequency ablation
TACE
Radiotherapy
Targeted drugs
108
Describe cholangiocarcinoma
Cancer that originates in the bile duct
Majority = adenocarcinomas
Common site = perihilar region
109
What are the key risk factors of cholangiocarcinoma
Primary sclerosing cholangitis
Liver flukes (a parasitic infection)
110
What are the clinical features of cholangiocarcinoma
Key - obstructive jaundice
- Pale stools
- Dark urine
- Generalised itching
Non-specific symptoms
Courvoisier's Law
111
Describe the investigations of cholangiocarcinoma
Imaging
CA19-9 tumour marker
112
What is the management of cholangiocarcinoma
Curative surgery
Palliative treatment
113
Name 6 types of hernias
1. Inguinal
2. Femoral
3. Umbilical
4. Incisional
5. Epigastric
6. Hiatal
114
Define the pathophysiology of a hernia
Occurs when there is a weak point in a cavity wall, usually affecting the muscle or fascia.
Weakness allows a body organ that would normally be contained within that cavity to pass through the cavity wall.
115
Describe an inguinal hernia
Soft lump in the inguinal region (in the groin)
116
What are the 2 types of inguinal hernia
1. Indirect inguinal hernia
- bowel herniates through the inguinal canal
2. Direct inguinal hernia
- Weakness in the abdominal wall at the Hesselbach's triangle
117
Define a femoral hernia
Involves herniation of the abdominal contents through the femoral canal
118
Describe the pathophysiology of a femoral hernia
Occurs below the inguinal ligament
Opening between the peritoneal cavity and the femoral canal = femoral ring
Femoral ring leaves only a narrow opening for femoral hernias
119
What risks are femoral hernias associated with
Incarceration
Obstruction
Strangulation
120
Describe umbilical hernias
Occur around the umbilicus due to a defect in the muscle around the umbilicus
121
Describe an incisional hernia
Occur at the site of an incision from a previous surgery
122
Describe the pathophysiology of an incisional hernia
Due to weakness where the muscle and tissues where closed after a surgical incision
Bigger incision = higher risk
Difficult to repair = high recurrence rate
123
Define an epigastric hernia
Hernias in the epigastric area (upper abdomen)
124
Describe a hiatal hernia
Herniation of the stomach up through the diaphragm
125
Describe the pathophysiology of an hiatal hernia
Diaphragm opening should be at the level of the lower oesophageal sphincter and should be fixed in place.
Narrow opening helps to maintain the sphincter and stop acid and stomach contents refluxing.
When opening is wider - stomach can enter through the diaphragm and contents can reflux
126
Name the types of hiatal hernia
1 - Sliding - stomach slides up through the diaphragm
2 - Rolling - separate portion of the stomach folds around the entry of the diaphragm alongside the oesophagus
3 - Combination of sliding and rolling.
4 - Large opening with additional organs entering the thorax
127
Name the risk factors of inguinal hernias
Male sex
Older age
Family history
Prematurity
AAA
128
Name the risk factors of femoral hernias
Women
Increased age
Low BMI
129
Name the risk factors for hiatus hernias
Increasing age
Obesity
Pregnancy
130
Name the risk factors of umbilical hernias
Women
Down's syndrome
Beckwith-Wiedemann syndrome
Raised intra-abdominal pressure
131
Name the risk factors of epigastric hernias
Men
Age 20-50
Central obesity
132
What are the clinical features of an abdominal hernia
A soft lump protruding from the abdominal wall
Lump may be reducible or protrude with coughing
Aching, pulling or dragging sensation
133
What are the clinical features of hiatus hernias
Present with dyspepsia
Heartburn
Acid reflux
Reflux of food
Burping
Bloating
Halitosis - bad breath
134
What is the general management of abdominal wall hernias
Conservative management
Tension-free repair (surgery)
Tension repair (surgery)
135
Define primary biliary cholangitis
Autoimmune condition which attacks the small bile ducts in the liver
Results in jaundice and liver disease
136
Describe the pathophysiology of primary biliary cholangitis
Affects intrahepatic ducts (bile ducts)
Inflammation and damage to cholangiocytes.
Overtime leads to obstruction through these ducts.
Reduced flow = cholestasis
Back pressure = liver fibrosis, cirrhosis and failure.
137
What is the typical presentation of primary biliary cholangitis
White woman
Aged 40-60
Presenting with itching
Positive AMA
Raised alkaline phosphate
138
What are the risk factors of primary biliary cholangitis
Women
Aged 40-60
139
What are the clinical features of primary biliary cholangitis
Often asymptomatic
Fatigue
Puritus - itching
GI symptoms - pale, greasy stools.
Jaundice
Dark urine
140
Describe the signs of primary biliary cholangitis
Xanthoma and xanthelasma
Excoriations
Hepatomegaly
Signs of liver cirrhosis and portal hypertension in end stage disease
141
Describe the investigations of primary biliary cholangitis
LFTS
Autoantibodies
Raised IgM
Ultrasound
Liver biopsy
142
Describe the management of primary biliary cholangitis
Ursodeoxycholic acid
Other treatments
- Obeticholic acid
- Cholestyramine
- Replacement of fat-soluble vitamins
- Immunosuppression
End stage - liver transplant
143
Define primary sclerosing cholangitis
Condition where the intrahepatic and extrahepatic bile ducts become inflamed and damaged, developing strictures that obstruct the flow of bile out of the liver and into the intestines.
144
Define sclerosis
Stiffening and hardening of the bile ducts
145
Define cholangitis
Inflammation of the bile ducts
146
What are the causes of primary sclerosing cholangitis
Unclear - genetics + environmental factors
Strong association with ulcerative colitis (70%).
147
What are the risk factors of developing primary sclerosing cholangitis
Male
Aged 30-40
Ulcerative colitis
Family history
148
Name the clinical features of primary sclerosing cholangitis
Pain and rigors
Jaundice
Abdominal pain in RUQ
Pruritus' - itching
Hepatomegaly
Splenomegaly
149
Describe the investigations of cholangitis
Liver function tests
Diagnosis - magnetic resonance cholangiopancreatography
Colonoscopy - for UC
Liver biopsy - used if diagnostic uncertainty
150
Describe the management of primary sclerosing cholangitis
No treatments proven to be effective
Endoscopic retrograde cholangio-pancreatography
Liver transplant
Other
- Cholestyramine
- Replacement fat soluble vitamins
- Monitoring for complications
151
What are some possible complications of primary sclerosing cholangitis
Biliary strictures
Acute bacterial cholangitis
Cholangiocarcinoma
Cirrhosis
Fat-soluble vitamin deficiency
Osteoporosis
152
Define spontaneous bacterial peritonitis
An infection of the ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory or surgical correctable condition
153
Describe the pathophysiology of spontaneous bacterial peritonitis
Bacterial translocation from the intestinal flora (sometimes not part of the intestinal flora) occurs by movement to the mesenteric lymph nodes from the bloodstream.
Cirrhosis predisposes to this colonisation and impairs the ability to resist infection.
After haematogenous spread of bacteria to the ascitic fluid, complement fluid cannot protect from infection due to many patients with cirrhosis have low ascites protein concentration.
154
Describe the causes of spontaneous bacterial peritonitis
Microbial
Gram negative bacteria
Most common pathogens:
- E. coli
- Staph. aureus
- Step. pneumoniae.
- Kleb. penumoniae.
- Pseudomonas aeruginosa
155
What are the risk factors of spontaneous bacterial peritonitis
Decompensated hepatic state (usually cirrhosis)
Low ascitic protein/complement.
GI bleeding.
Endoscopic sclerotherapy for oesophageal varices
156
Describe the investigations of spontaneous bacterial peritonitis
Bloods
- FBC
- Serum creatinine
- Culture
- LFT
- PN/INR
Ascitic laboratory tests
- cell count
- culture
- appearance
- absolute neutrophil count
Urine testing
156
Describe the clinical features of spontaneous bacterial peritonitis
Commonly minimally symptomatic, may be asymptomatic
Abdominal pain
Fever
Vomiting
Altered mental state
GI bleeding
157
Describe the clinical diagnosis of spontaneous bacterial peritonitis
Ascitic fluid absolute neutrophil count > 250 cells/mm^3
158
Describe the management of spontaneous bacterial peritonitis
Main = early administration of appropriate empirical antibiotics
Albumin
Continued antibiotics
- patients with ascitic fluid protein conc. < 15g/L
- Previous episode of SBP
159
Define cholangitis
Infection and inflammation in the bile ducts
160
What are the 2 main causes of cholangitis
1. Obstruction in the bile ducts stopping bile flow
2. Infection introduces in the common bile duct
161
What are the risk factors of cholangitis
Age > 50 years
Cholelithiasis
Benign stricture
Malignant stricture
Post-procedure injury to bile ducts
History of scleorsing cholangitis
162
Name the clinical features of cholangitis
Present with Charcot's Triad
- RUQ pain
- Fever
- Jaundice - raised bilirubin
163
Describe the investigations of cholangitis
Imaging - to diagnose bile duct stones and cholangitis
- Abdominal ultrasound scan
- CT scan
- ERCP
- Endoscopic ultrasound
164
Describe the acute management of sepsis and acute abdomen
Nil by mouth
IV fluids
Blood cultures
IV antibiotics
Involvement of senior and potentially HDU, ICU.
165
Describe the procedure options can be performed during an ERCP for cholangitis
Cholangio-pancreatography
Sphincterotomy
Stone removal
Balloon dilation
Biliary stenting
Biopsy
Percutaneous transhepatic cholangiogram
166
Name 5 differential diagnosis for cholangitis
Acute cholecystitis
Peptic ulcer disease
Acute pancreatitis
Hepatic abscess
Acute pyelonephritis
167
Define cholecystitis
Inflammation of the gallbladder
Causes blockage of the cystic duct preventing the gallbladder from emptying.
168
What are the causes of cholecystitis
Gallstones (95%) - calculous cholecystitis
Small number of cases = dysfunction in the gallbladder emptying. Acalculous cholecystitis
169
What are the risk factors of cholecystitis
Gallstones
Severe illness
Total parenteral nutrition
Diabetes
170
What are the clinical features of cholecystitis
Main = Pain in RUQ - may radiate to R. shoulder
Tenderness RUQ
Signs and symptoms of inflammation
Palpable mass
Presence of risk factors
Murphy's sign
171
Describe Murphy's sign
Place hand in RUQ and apply pressure.
Patient takes deep breath in.
Gallbladder will move downwards during
inspiration and encounter your hand.
Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration.
172
Describe the investigations of cholecystitis
Imaging
- Abdominal ultrasound
- MRCP
173
Describe the management of cholecystitis
Conservative management
- Nil by mouth
- IV fluids
- Antibiotics
- NG tube required if vomiting
ERCP
Cholecystectomy - removal of gallbladder
174
Define gallbladder empyema
Infected tissue and pus collecting in the gallbladder
175
Define acute pancreatitis
Presents with a rapid onset of inflammation and symptoms.
After an episode of acute pancreatitis, normally function usually returns.
176
Define chronic pancreatitis
Involves long-term inflammation and symptoms with a progressive and permanent deterioration in pancreatic function
177
What are the 3 main causes of pancreatitis
1. Gallstones
2. Alcohol (chronic)
3. Post-ERCP
178
What is the acronym to remember pancreatitis causes
I GET SMASHED
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs - furosemide, thiazide diuretics, azathioprine
179
Name the risk factors for acute pancreatitis
Middle-aged women
Gallstones
Alcohol
Hypertriglyceridemia
Use of causative drugs
180
Name the risk factors for chronic pancreatitis
Alcohol
Smoking
Family history
Coeliac disease
181
What are the general features of pancreatitis
Severe central pain going to the back
Nausea and vomiting
Fever
Oliguria
Cullens
Grey's turners sign
182
Describe the clinical features of acute pancreatitis
Severe epigastric pain
Radiating through to the back
Associated vomiting
Abdominal tenderness
Systemically unwell
- low grade fever
- tachycardia
183
Describe the investigation seen in pancreatitis
Amylase
- Raised > 3x upper limit
- May not rise in chronic
Lipase
C-reactive protein - level of inflammation
Ultrasound - initial investigation choice for gallstones
CT abdomen - assess for complications
184
What severity score is used in pancreatitis
MEWS
Good history
Response to resuscitation
Also - Glasgow Score
185
Describe the Glasgow Score
Assess the severity of pancreatitis
Numerical based on how many of the criteria are present
186
Describe the results of pancreatitis
PANCREAS
PaO2 < 8 kPa
Age > 55
Neutrophils (WBC > 15)
Calcium < 2
uRea > 16
Enzymes (LDH > 600 or AST/ALT > 200)
Albumin < 32
Sugar (glucose) > 10
187
What is the treatment for acute pancreatitis
Admission for supportive management
Involves:
ABCDE approach - initial resuscitation
IV fluids
Nil by mouth
Analgesia
Careful monitoring
Treatment of gallstones (if needed)
Treatment of complications
Most patients will improve within 3-7 days
188
Describe the management for chronic pancreatitis
Abstinence from alcohol and smoking
Analgesia
Replacement of pancreatic enzymes
Subcutaneous insulin regimes
ERCP with stenting
Surgery may be required
189
Name some diagnosis differentials for pancreatitis
Peptic ulcer disease
Intestinal obstruction
AAA
Cholangitis
Cholecystitis
190
Name some complications of acute pancreatitis
Necrosis of pancreas
Infection in a necrotic area
Abscess formation
Acute peripancreatic fluid collection
Pseudocysts
Chronic pancreatitis
191
Name some complications of chronic pancreatitis
Chronic epigastric pain
Loss of exocrine/endocrine function
Damage and strictures to the duct system
Formation of pseudocysts or abscesses
192
Define Gilbert's Syndrome
Inherited (usually autosomal recessive) metabolic disorder characterised by a mild and intermittent elevation of unconjugated (indirect) bilirubin levels, due to defective conjugating enzymes in the liver
193
Name the risk factors of Gilbert's syndrome
Post-pubertal age
Weak
- Family history
- Type 1 DM
194
Name the clinical features of Gilbert's syndrome
Generally - asymptomatic
Symptoms (alterative diagnosis should be considered)
Abdominal pain
Itch
Pale stools
Dark urine
195
Name the investigations for Gilbert's syndrome
Unconjugated bilirubin
Liver aminotransferases
Gamma-glutamyl transpeptidase
Lactate dehydrogenase
FBC
Peripheral blood smear
Direct Coomb's test
196
What would be the findings of Gilbert's syndrome
Mild unconjugated hyperbilirubinemia < 102 micromol/L
Liver function otherwise normal
197
When would Gilbert's syndrome suspected
Incidental finding of an increased serum bilirubin concentration + normal liver function test
Single episode (or intermittent) episode of mild jaundice with no clinical evidence of liver disease
198
Describe the management of Gilbert's syndrome
No treatment or regular monitoring required
Cannot progress or cause chronic liver disease
Any episodes of jaundice are self-limiting, should resolve within a few days
199
Name 3 metabolic liver disease's
Haemochromatosis
Wilson's disease
Alpha 1 antitrypsin deficiency
200
Define Wilson's disease
Autosomal recessive genetic condition resulting in the excessive accumulation of copper in the body tissues, particularly in the liver
201
Describe the pathophysiology of Wilson's disease
Lack of protein leads to decreased copper excretion from the liver.
Copper overload in hepatocytes.
When hepatic storage capacity is exceeded, copper is released into the circulation and deposited in other organs
202
What are the causes of Wilson's disease
Mutations of Wilson's protein on chromosome 13
Copper-transporting protein
Copper excreted into the bile
203
What are the risk factors for Wilson's disease
ATP7B gene mutation
Family history
204
Name the clinical features of Wilson's disease
1st - liver problems
Advanced stage
- Neurological symptoms
- Psychiatric symptoms
- Kayser-Fleischer in the cornea
- Haemolytic anaemia
205
Describe Kayser-Fleischer in the cornea
Deposition of copper in Descemet's membrane
Green-brown circles in surrounding iris of the eye
Usually seen with naked eye or silt lamp examination.
206
Describe the investigation of Wilson's disease
Initial screening = serum caeruloplasmin
24-hour urine copper assay
Liver biopsy
Scoring systems
207
Describe the management of Wilson's disease
Depends on clinical presentation and treatment phase
Copper chelation
Other treatments
- Zinc salts
- Liver transplantation
208
Describe the differential diagnosis for Wilson's disease
Hepatitis B/C
Haemochromatosis
Alpha-1 antitrypsin deficiency
Autoimmune cirrhosis
Parkinson's disease
209
Describe the prognosis of Wilson's disease
Neurological symptoms improve 5-6 months after start of treatment
Unless liver receives further insult should be normal life span
210
Define alpha-1 antitrypsin deficiency
Genetic condition caused by low levels of alpha-1 antitrypsin
211
What are the main 2 organs that alpha-1 antitrypsin deficiency affects
Lungs - COPD, bronchiectasis
Liver (depends on genotype) - dysfunction, fibrosis and cirrhosis
212
Describe the pathophysiology of Alpha-1 antitrypsin deficiency
Disease severity depends on copies of the gene.
Alpha-1 antitrypsin = protease inhibitor.
Normal conditions
Protease enzyme = neutrophil elastase
Enzyme is secreted by neutrophils
Digests elastin - protein in connective tissue that keeps tissue flexible
Alpha-1 antitrypsin offers protection by inhibiting this action
213
Describe alpha-1 antitrypsin deficiency pathophysiology in the liver
ATT produced in the liver.
Abnormal mutant version of protein gets trapped and builds up inside hepatocytes
Is toxic to them = inflammation
Overtime = fibrosis, cirrhosis and possible hepatocellular carcinoma
214
What is the cause of alpha-1 antitrypsin deficiency
Decreased circulating plasma levels of AAT, due to inheritance of variant alleles of SEPRINA1 gene
215
What are the clinical features of alpha-1 antitrypsin deficiency
Productive cough
SOB on exertion
Wheezing
216
Describe the investigations of alpha-1 antitrypsin deficiency
Assess lung damage
- chest x-ray
- high resolution CT thorax
- pulmonary function test
Liver biopsy
Plasma AAT level
LFTs
217
What is the clinical diagnosis of alpha-1 antitrypsin deficiency based upon
Low serum alpha-1 antitrypsin (screening test)
Genetic testing
218
Describe the management of alpha-1 antitrypsin deficiency
Stop smoking
Symptomatic management e.g. COPD
Organ transplantation
Monitor complications - hepatocellular carcinoma
Screening of family members
Infusion of alpha-1 antitrypsin
219
What are the differential diagnosis of alpha-1 antitrypsin deficiency
Asthma
COPD
Bronchiectasis
Viral hepatitis
Alcoholic liver disease
220
What are the complications of alpha-1 antitrypsin deficiency
Hepatocellular carcinoma
Necrotising panniculitis
Granulomatosis with polyangiitis
221
Describe the prognosis of alpha-1 antitrypsin deficiency
Non-smokers = normal
50-72% of deaths in AAT = respiratory failure
If people do not manifest pulmonary symptoms more likely to experience cirrhosis and liver failure
222
Define haemochromatosis
Autosomal recessive genetic condition resulting in iron overload.
= iron storage disorder.
223
Describe the pathophysiology of hemochromatosis
Majority of cases related to C282Y mutations in human hemochromatosis protein (chromosome 6).
Gene is important for regulating iron metabolism
224
Describe the causes of haemochromatosis
4 different types
C28Y and H63D = most common mutations of the HFE gene
225
Describe the clinical features of haemochromatosis
Chronic tiredness
Joint pain
Pigmentation - bronze skin
Testicular atrophy
Erectile dysfunction
Amenorrhoea
Cognitive symptoms
Hepatomegaly
226
Define amenorrhoea
Absence of period in women
227
Describe the investigations of haemochromatosis
Initial = serum ferritin
Other
- transferrin saturation
- genetic testing
- liver biopsy with Perl's stain
- MRI
228
Describe the management of haemochromatosis
Venesection - regularly removing blood to remove excess iron
Monitoring serum ferritin
Monitoring and treating complications
229
Name the differential diagnosis of haemochromatosis
Iron overload
Hepatitis B/C
NAFLD
Excessive iron supplementation
230
Name the complications of haemochromatosis
Secondary diabetes
Liver cirrhosis
Endocrine and sexual problems
Cardiomyopathy
Hepatocellular carcinoma
Hypothyroidism
Chondrocalcinosis
231
Describe chondrocalcinosis
Calcium pyrophosphate deposits in the joints
Causes arthritis
232
Define acute liver failure
Rare, life-threatening potentially reversible condition with rapid decline in hepatic function characterised by jaundice, coagulopathy (INR > 1.5) and hepatic encephalopathy in patients with no evidence of prior liver disease
233
What are the classifications of liver failure
Hyperacute
Acute
Subacute
234
Define chronic liver failure
Progressive deterioration of liver functions for more than 6 months, including synthesis of clotting factors, other proteins, detoxification of harmful products of metabolism and excretion of bile.
235
Name the causes of chronic liver disease/failure
Alcohol
Non-alcoholic steatohepatitis
Viral hepatitis B, C
Immune
Metabolic
Vascular
236
How is acute liver failure established by
History
Serological assays
Exclusion of alternative causes
237
What are the causes of acute liver disease/failure
Most common - paracetamol overdose
Idiosyncratic drug-induced liver injury
Acute hepatitis A
Autoimmune hepatitis
Ischaemia hepatitis
238
Name the risk factors of acute liver disease/failure
Chronic alcohol misuse
Poor nutritional status or feeding
Female sex
Pregnancy
Chronic hepatitis B
Chronic pain and narcotic use
Herbal and dietary supplement hepatotoxicity
Wilson's disease
239
Name 4 clinical features of acute liver disease/failure
Malaise
Nausea
Anorexia
Jaundice
240
Describe the clinical features of chronic liver failure/disease
Ascites
Oedema
Haematemesis (varices)
Malaise
Anorexia
Wasting
Easily bruising
Itching
Hepatomegaly
Abnormal LFTs
241
Describe the investigations of liver failure/disease
Liver function test
Viral serology
Immunology
Biochemistry
Radiological investigations
242
Describe the management of acute liver disease/failure
ALF grade 2 or higher hepatic encephalopathy - admitted to ITUS.
Neurological status monitored
Liver transplantation
243
Describe the general management of the complications of liver disease/failure
Malnutrition - naso-gastric feeding
Variceal bleeding - endoscopic banding, propranolol, terlipressin
Encephalopathy - lactulose
Ascites/oedema - salt/fluid restriction, diuretics, paracentesis
Infection - antibiotics
244
Name the differential diagnosis of liver disease/failure
Viral (A, B, C, CMV, EBV)
Drug-induced
Autoimmune
Alcoholic
245
What medications may be prescribed in liver disease/failure
Analgesia
Sedation - short acting benzodiazepines
Diuretics
Antihypertensives
AVOID
- aminoglycosides
- ACE inhibitors
246
What are the clinical features of a paracetamol overdose
Often asymptomatic
Mild GI symptoms
Untreated - vary liver injury 2-4 days after
Severe overdose
- coma
- severe metabolic acidosis
247
Describe the time course of drug-induced liver injury
Onset
- usually 1-12 weeks after starting
- earlier is unusual unless re-challenged
Resolution
- 3 months after stopping
- 5-10% prolonged
Inadvertent re-challenge
- Seen in 6% - 2% are fatal
248
Describe the investigations of drug induced liver injury
Serum paracetamol conc.
LFTs
Prothrombin time and INR
Blood glucose
U&E, creatinine
Venous or arterial blood gas
FBC
249
Describe the risk factors of drug induced liver-injury
History of:
- self harm
- frequent or repeated use of medications for pain relief
Glutathione deficiency
Drugs that induce liver enzymes
Low body weight < 50kg
250
What is the management of a paracetamol overdose
N acetyl cysteine
Supportive to correct
- coagulation defects
- fluid electrolyte and acid base balance
- renal failure
- hypoglycaemia
- encephalopathy
251
Describe the complications of poor prognosis of paracetamol overdose
80% mortality if below
Late presentation
Acidosis pH < 7.3
PT > 70 seconds
Serum creatinine > (or equal to) 300 umol/L
Consider emergency liver transplant
252
Define ascites
Pathological collection of fluid in the peritoneal cavity
253
Describe the pathophysiology of ascites in cirrhosis
Splanchnic arterial vasodilation leads to increased lymph formation = activation of RAAS system and SNS and release ADH
Causes renal sodium (major contributor) and water retention
Increased resistance to portal flow results in portal hypertension, collateral vein formation and shunting of blood in the systemic circulation
254
Describe the classification of ascites
Stage 1 - detectable only after careful examination/ultrasound scan
Stage 2 - easily detectable but of relatively small volume
Stage 3 - obvious, not tense ascites (moderate)
Stage 4 - tense ascites (large)
255
What are the causes of ascites
Most common = cirrhosis
Chronic liver disease
Neoplasia
Pancreatitis, cardiac causes
256
What are the risk factors of ascites
Liver disease
- heavy alcohol consumption
- Viral hepatitis
- IVDU
- blood transfusion pre 90s
- Tattoos
- Residence of birth
Non-alcoholic steatohepatitis
- DM type 2
- Obesity
- Hypercholesterolemia
Cancer
Cardiac
Renal-nephrotic syndrome
Malnutrition
257
Describe the clinical features of ascites
Abdominal distention
Shifting dullness
Nausea
Loss of appetite
Constipation
Cachexia
Weight loss
Pain/discomfort
- present - malignant
- absent - non malignant
258
What are the signs of ascites
Jaundice
Abdominal distention - up to 1.5-2L
Puddle sign 150mL
Shifting dullness 500mL
Flanks fullness 1500+ mL
Fluid thrill
259
Name the investigations of ascites
Imaging - confirms diagnosis
Blood test - LFTs
Abdominal diagnostic paracentesis
Microscopy and culture
Analysis of ascitic fluid
Biochemistry
260
Describe the management of ascites
Treat underlying cause
Hypertension
Shunts
261
What are the complications of ascites
Infections
Electrolyte imbalance
Bowel perforation
Bleeding
Leak of fluid through abdominal wall
Injury to the kidneys
262
Describe the management of ascites caused by hypertension
Fluid and salt restriction
Diuretics
- spironolactone
- +/- furosemide
- others - amiloride, metolazone, mannitol
Large-volume paracentesis + albumin
263
Name the causes of portal hypertension
Cirrhosis
Fibrosis
Portal vein thrombosis
264
Describe the pathology of portal hypertension
Increased hepatic resistance
Increased splanchnic blood flow
265
Define portal hypertension
Increased resistance and pressure in the portal system
266
Describe the pathophysiology of portal hypertension
Fibrosis affects the structure and blood flow through the liver
Increases the resistance in the vessel leading to the liver
267
Define oesophageal varices
Dilated collateral blood vessels that develops as a complication of portal hypertension, usually in the setting of cirrhosis
268
Describe the pathophysiology of oesophageal varices
Cirrhosis develops
Increases hepatic vein pressure gradient and deteriorating liver function may result in the formation of oesophageal varices
269
Name the cause of oesophageal varices
US + Europe - alcoholic liver disease
Worldwide - hepatitis B, C
270
Name the risk factors of oesophageal varices
Portal hypertension
Large varices
Red wale marks
Decompensated cirrhosis
271
Name the clinical features of oesophageal varices
Asymptomatic
Brisk haematemesis
272
Describe the investigations of oesophageal varices
Gastroscopy
Bloods
Coagulation profile
Blood typing/cross-matching
Hepatitis B surface antigen
Anti-hepatitis C virus IgG
273
Describe the management of oesophageal varices
Prevent development of variceal bleeding
- Non-selective beta-blockers
- endoscopic ligation
Additional management
- Prophylactic antibiotics
274
Define the differential diagnosis of oesophageal varices
Hiatal hernia
Gastric varices
Mallory-Weiss tear
Peptic ulcer disease
275
Define biliary colic
Crystalised bile causing sudden painful spasm of the gallbladder wall triggered by a gallstone
276
What are the types of biliary colic
Cholesterol
Pigment stones
- bile acid
- phosphate
- magnesium
Mixed stones
277
What are the risk factors of biliary colic
5 Fs
Forty
Fat
Female
Fertile
Fair
278
What are the clinical features of biliary colic
Post prandial colicky pain
Nausea and vomiting
Should not be that tender to touch
279
What are the investigations of biliary colic
1st - ultrasound
Other investigations
- Bloods
- MRCP vs ERCP
280
Describe MRCP
Image of the gallbladder and ducts
Similar to CT
Sees end of bile duct sits in the C with the 2nd part of the duodenum - lots of gas here so ultrasound will not be able to see
281
Why is CT not used as an image technique in gallstones
Some gallstones are opaque so will not show
282
Describe the management of biliary colic
Analgesia - NSAID with PPI cover
ERCP
Cholecystectomy
Bile duct exploration/reconstruction
283
Describe the blood results in alcoholic liver disease
Increase
- bilirubin
- PT
- GGT
Decrease
- albumin
AST:ALT > 2
FBC - macrocytic anaemia
284
What anaemia is seen in alcoholic liver disease
Macrocytic liver disease
285
Describe GGT marker
Increased in cholestasis - blockage of intra-/extrahepatic ducts
Increased in alcoholic liver disease
286
What is 1st pass metabolism completed by
Liver
287
What is the major blood supply to the liver
Portal vein
288
Describe AST and ALT
Enzyme made in hepatocytes
Marker for hepatic inflammation.
Injury of liver cells increases these
289
Describe AST
Low specificity for the liver
290
Describe ALT
High specificity for the liver
Think L
291
What type of injury will AST and ALT be raised in
Acute (recent injury)
Increase in all forms of liver injury does not tell about liver function
Think smoke with fire - there may be no smoke due to nothing left to burn (no hepatocytes) or the fire has been extinguished
292
What is a marker of long term injury of the liver
Albumin - has approx 20 day half life
293
Describe albumin
Protein made in the liver
Chronic hepatocellular damage
In acute it stays up
294
What is the key LFT for alcoholic liver disease
AST: ALT > 2
295
Describe PT/INR as a marker of liver disease
In acute and chronic liver damage
Measures clotting time - requires many enzymes made in the liver
Very sensitive
Shows how bad the liver is
296
What may affect PT/INR that is not liver damage
Warfarin
1972, or 1,5 factor deficiency
297
What are the key investigations in liver failure
LFTS
Increased - AST, ALT, PT
298
What are other investigations (than the main one) in alcoholic liver disease
Increased - bilirubin, PT, GGT
Decreased - albumin
299
What are the key investigations in non-alcoholic liver disease
LFTS
Increased - PT, INR, bilirubin
Decreased - albumin
300
Describe other investigations (than LFTs) in non-alcoholic liver disease
Ultrasound - hepatitic stenosis
Thrombocytopenia
Hyperglycaemia
301
What would a liver biopsy of primary biliary cholangitis show
Inflamed bile ducts with intraepithelial lymphocytes, epithelioid, granuloma + fibrosis
302
Describe LFTs and FBCs in primary biliary cholangitis
Increased - GGT, ALT, bilirubin
FBC - increased AMA
303
What is the GS investigation for primary sclerosing cholangitis
MRCP
304
What would be seen on blood tests of primary sclerosing cholangitis
Increased ALP
pANCA
305
What is the GS investigation for acute pancreatitis
Lipase and amylase
306
What is GS investigation for chronic pancreatitis
Abdominal USS + CT
307
How do you differentiate on tests between acute and chronic pancreatitis
Acute = raised lipase and amylase
Chronic = not raised
308
What would be raised in chronic pancreatitis
Faecal elastase
309
What is the mnemonic to remember the causes of acute pancreatitis
I GET SMASHED
310
Breakdown I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Scorpion stings
Mumps
Autoimmune
Steroids
Hypercalcaemia/hypertriglyceridemia
Endoscopic retrograde cholangiopancreatography
Drugs/medications
311
Define ERCP
Endoscopic retrograde cholangiopancreatography
Combines endoscopy + xray to examine and treat conditions of bile duct and pancreas ducts
312
Name some drugs that cause acute pancreatitis
Tetracyclines
Aminosalicylate e.g. sulfasalazine
Diuretics
313
What is the most common cause of acute pancreatitis
Gallstones
314
What is the most common cause of chronic pancreatitis
Ethanol (alcohol)
315
Name the 3 most common causes of acute pancreatitis
The GET in I GET SMASHED
Gallstones
Ethanol (alcohol)
Trauma
316
Name the symptoms of acute pancreatitis
Severe epigastric pain radiating to the back
Fever
N&V
Steatorrhea
317
Name the signs of acute pancreatitis
Grey tuners sign
Cullens sign
318
Define grey turners sign
For acute pancreatitis
Flank bleeding
319
Define cullen sign
For acute pancreatitis
Periumbilical bleeding
320
What scoring system is used in acute pancreatitis
Glasgow + Ranson's score
APPACHE II - severity in 24 hours
321
Describe the treatment of acute pancreatitis
Emergency hospital admission
IV fluids
Oxygen
Analgesia
IV antibiotics
Nil by mouth
NG tube for feeding
322
Describe systemic inflammatory response as a complication of acute pancreatitis
Tachycardia
Tachypnoea
Pyrexia
Increased WBC
323
Name the localised complications of acute pancreatitis
Pancreatic necrosis
Pseudocyst
Pancreatic abscess
324
Name the systemic complications of acute pancreatitis
Multi organ failure
Sepsis
AKI
ARDs
DIC
325
Define chronic pancreatitis
Chronic, irreversible inflammation and/or fibrosis of pancreas often characterised by severe pain + progressive endocrine and exocrine insufficiency for > 3 months.
326
What is the main symptom of chronic pancreatitis
Epigastric pain radiating to back - exacerbated by alcohol
327
Describe the management of chronic pancreatitis
Lifestyle modification – alcohol cessation
Pain management – NSAIDs
Pancreatic enzyme replacement therapy e.g. lipase, amylase, protease
