LIVER & FRIENDS Flashcards
1
Q
Give 4 functions of the liver
A
- Glucose and fat metabolism
- Detoxification and excretion
- Protein synthesis (e.g. albumin, clotting factos)
- Bile production
2
Q
Name 3 things that liver function tests measure
A
- Serum bilirubin
- Serum albumin
- Pro-thrombin time
3
Q
Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease)
A
Alkaline phosphate (ALP)
4
Q
What enzymes increase in the serum in hepatocellular liver disease?
A
Transaminases - e.g. AST and ALT
5
Q
What tests give no index of liver function and why?
A
Liver enzymes - alkaline phosphate, GGT, AST, ALT Released by damaged cells
6
Q
Define jaundice
A
Raised serum bilirubin
7
Q
Name the 3 broad categories of jaundice
A
- Pre-hepatic (unconjugated)
- Hepatic (conjugated)
- Post-hepatic (conjugated)
8
Q
Give 2 causes of pre-hepatic jaundice
A
Excess bilirubin production
- Haemolytic anaemia
- Gilberts disease
9
Q
Give 4 causes of hepatic jaundice
A
- Liver disease
- Hepatitis - viral, drug, immune, alcohol
- Ischaemia
- Neoplasm - HCC, mets
- Congestions - CCF
10
Q
Give 3 causes of post-hepatic jaundice
A
Duct obstruction
- Gallstones
- Stricture - Malignancy, ischaemia, inflammatory
- Blocked stent
11
Q
What colour is the urine and stools in pre-hepatic jaundice?
A
Both are normal
No itching and the LFTs are normal
12
Q
What colour is the urine and stools in someone with cholestatic jaundice (hepatic and post hepatic)?
A
Dark urine
Pale stools
Itching
LFTs are abnormal
13
Q
What can cause raised unconjugated bilirubin?
A
A pre-hepatic problem (haemolysis, hypersplenism)
14
Q
What can cause raised conjugated bilirubin?
A
Indicated cholestatic problem
[liver disease (hepatic) or bile duct obstruction (post hepatic)]
15
Q
Give 3 symptoms of jaundice
A
- Biliary pain
- Rigors - indicate an obstructive cause
- Abdomen swelling
- Weight loss
16
Q
Why are liver patients vulnerable to infection?
A
- Impaired reticuloendothelial function
- Reduced opsonic activity
- Leucocyte function
- Permeable gut wall
17
Q
Give 3 causes of Gallstones
A
- Obesity and rapid weight loss
- DM
- Contraceptive pill
- Liver cirrhosis
18
Q
what are the risk factors for gallstones
A
- Female
- Fat
- Fertile
- Forty
- Family history
19
Q
Name 2 types of gallstones
A
- Cholesterol (70%)
2. Pigment (30%)
20
Q
Describe the pathophysiology of cholesterol gallstones
A
Excess cholesterol/lack of bile salts –> cholesterol crystals –> gallstone formation, precipitated by reduced gallbladder motility
21
Q
Describe the pathophysiology of pigment gallstones
A
Excess bilirubin –> polymers and calcium bilirubinate –> stones
seen in haemolytic anaemia
22
Q
Give 4 symptoms of gallstones
A
Most are asymptomatic
- Biliary colic (sudden RUQ pain radiating to the back and epigastrium +/- nausea/vomiting) - AFTER EATING FATTY MEALS
- Acute cholecystitis (gallbladder distension –> inflammation, necrosis, ischaemia)
- Obstructive jaundice
- Cholangitis
- Pancreatitis
23
Q
How can gallstones be removed from the gallbladder?
A
Laparoscopic cholecystectomy
ERCP with removal or destruction (mechanical lithotripsy) or stent placement
Bile acid dissolution therapy (for people not suitable for surgery)
24
Q
What is liver failure?
A
When the liver has lost the ability to regenerate to repair, so that decompensation occurs
25
Name 3 types of liver failure
1. Acute = sudden failure in previously healthy liver
2. Chronic = liver failure on the background cirrhosis
3. Fulminant = massive necrosis of liver cells --> severe liver function impairment
26
Give 5 causes of acute liver disease
1. Viral hepatitis
2. Drug induced hepatitis
3. Alcohol induced hepatitis
4. Vascular - Budd-Chiari
5. Obstruction
27
Give 2 possible outcomes of acute liver disease
1. Recovery
| 2. Liver failure
28
Give 5 causes of chronic liver disease
1. Alcohol
2. NAFLD
3. Viral hepatitis (B,C,E)
4. Autoimmune diseases
5. Metabolic
6. Vascular - Budd-Chairi
29
Give 2 possible outcomes of chronic liver disease
1. Cirrhosis
| 2. Liver failure
30
Give 5 signs of acute liver failure
1. Jaundice
2. Fetor hepaticus (smells like pears)
3. Coagulopathy
4. Asterixis - liver flap
5. Malaise
6. Lethargy
7. Encephalopathy
31
Give 5 signs of chronic liver disease
1. Ascites
2. Oedema
3. Bruising
4. Clubbing
5. Depuytren's contracture
6. Palmar erythema
7. Spider naevi
32
What investigations are conducted on someone on with liver failure?
Blood tests - FBCs, U+Es, LFTs, clotting factors, glucose
Imaging - EEG, USS, CXR, doppler USS
Microbiology - blood and urine culture and ascitic tap
33
What do the blood tests show in someone with liver failure?
```
Raised bilirubin
Low glucose
High AST and ALT
Low levels of coagulation factors
Raised prothrombin time
High ammonia levels
```
34
Describe the treatment for liver failure
1. Nutrition
2. Supplements
3. Treat complications
- Raised intracranial pressure = mannitol
- PPI = reduce GI bleeds
- bleeding = vitamin K
- encephalopathy = lactulose
- ascites = diuretics
- sepsis = sepsis 6, antibiotics
4. Liver transplant
35
Give 4 complications of of liver failure
1. Hepatic encephalopathy
2. Abnormal bleeding
3. Jaundice
4. Ascites
36
What drugs should be avoided in liver failure?
Constipators
Oral hypoglycaemics
Warfarin has enhanced effects
Opiates
37
What is cirrhosis?
Loss of normal hepatic architecture with fibrosis - liver injury causes necrosis and apoptosis- irreversible
38
Give 3 causes of cirrhosis
common:
- chronic alcohol abuse
- non-alcoholic fatty liver disease
- hepatitis
others
- haemochromatosis
- Wilson's disease
- alpha-antitrypsin deficiency
39
Give 4 signs of cirrhosis
- ascites
- clubbing
- palmar erythema
- xanthelasma
- spider naevi
- hepatomegaly
- peripheral oedema
40
What investigations are done in someone with cirrhosis?
- Bloods = low platelets, high INR, low albumin
- US and CT - hepatomegaly
- liver biopsy - diagnostic
41
What is the treatment for liver cirrhosis?
1. Good nutrition and alcohol abstinence
2. Treat underlying cause
3. Fluid and salt restriction for ascites --> spironolactone, furosemide, prophylactic ciprofloxacin
4. liver transplant = definitive
5. Screen for HCC - increased AFP
42
Give 4 complications of cirrhosis
Ascites
portal hypertension
1. Decompensation
2. SBP
3. Increased risk of HCC
43
Approximately what percentage of blood flow to the liver is provided by the portal vein?
75%
44
Give 3 causes of portal hypertension
1. Pre-hepatic = blockage of hepatic portal vein before the liver (portal vein thrombosis)
2. Hepatic = distortion of liver architecture (cirrhosis, schistosomiasis, Budd Chiari syndrome)
3. Post-hepatic = venous blockage outside the liver (RHF, IVC obstruction)
45
what is the clinical presentation of portal hypertension?
- often asymptomatic
- splenomegaly
- spider naevi
- GI bleeding
- ascites
- hepatic encephalopathy
46
Why can portal hypertension lead to varices?
Obstruction to portal blood flow
| Blood is diverted into collaterals and so causes varices
47
What are the potential consequences of varices?
If they rupture --> haemorrhage
| blood is then digested -> melaena
48
What is the primary treatment for varices?
Variceal banding – band put around varices using endoscope – after few days the banded varix degenerates and drops off leaving a scar
49
Describe the pathophysiology of hepatic encephalopathy
Ammonia accumulates and crosses the BBB causing cerebral oedema
50
Name 4 conditions that can develop as a result of having hepatic encephalopathy
SAVE
1. Splenomegaly
2. Ascites
3. Varices
4. Encephalopathy
51
What is ascites?
Chronic accumulation of fluid in the peritoneal cavity that leads to abdominal distension
52
Give 4 causes of ascites and an example for each
1. Local inflammation - peritonitis
2. Leaky vessels - imbalance between hydrostatic and oncotic pressures
3. Low flow - cirrhosis, thrombosis, cardiac failure
4. Low protein - hypoalbuminaemia
53
Describe the pathophysiology of ascites
1. Increased intra-hepatic resistance leads to portal hypertension --> ascites
2. Systemic vasodilation leads to secretion of RAAS, NAd and ADH --> fluid retention
3. Low serum albumin also leads to ascites
Transudate = blockage of venous drainage
Exudate = inflammation
54
Give 3 signs of ascites
1. Distension
2. Dyspnoea
3. Shifting dullness on percussion
4. Signs of liver failure
55
What investigations might you do in someone who you suspect has ascites?
1. USS
| 2. Ascitic tap
56
Describe the treatment for ascites
1. Restrict sodium and fluids
2. Diuretics - spirolactone
3. Paracentesis
4. Albumin replacement
57
Describe the effects of alcoholic liver disease
1. Fatty liver --> hepatitis --> cirrhosis and fibrosis
2. GIT --> gastritis, varices, peptic ulcers, pancreatitis , carcinoma
3. CNS --> Degreased memory and cognition, wernicke's encephalopathy
4. Folate deficiency --> anaemia
5. Reproduction --> testicular atrophy, reduced testosterone/progesterone
6. Heart --> dilated cardiomyoapthy, arrhythmias
58
What might be seen histologically that indicates a diagnosis of alcoholic liver disease?
Neutrophils and fat accumulation within hepatocytes
59
What type of anaemia do you associate with alcoholic liver disease?
Macrocytic anaemia
60
What blood test might show that someone has alcoholic liver disease?
Serum GGT will be elevated
61
What distinctive feature is often seen on biopsy in people suffering form alcoholic liver disease?
Mallory bodies
62
What are the CAGE questions?
1. Cut down?
2. Annoyed at criticism?
3. Guilty about drinking?
4. Eyeopener?
63
How do you treat alcoholic liver disease?
● Stop alcohol – treat delirium tremens with diazepam
● IV thiamine to prevent Wernicke-Korsakoff encephalopathy
● High vitamin and protein diet
● Fatty liver – if alcohol stopped fat disappears
● Hepatitis
o Nutrition maintained with enteral feeding and vitamin supplements
o Steroids show short term benefit – reduce inflammation
o Infections treated and prevented
● Cirrhosis
o Reduce salt intake, stop drinking for life
o Avoid aspirin and NSAIDS
o Liver transplant
64
How does alcoholic hepatitis present?
```
Jaundice
Anorexia
Nausea and vomiting
Fever
Encephalopathy
Cirrhosis
Hepatomegaly
Ascites, bruising, clubbing
```
65
How long does hepatitis persist for to be deemed chronic?
6 months
66
Give 4 types of hepatitis?
1. Viral - A,B,C,D,E
2. Drug induced
3. Alcohol induced
4. Autoimmune
67
Give 3 infective causes of acute hepatitis
1. Hepatitis A-E infections
2. EBV
3. CMV
68
Give 3 non-infective causes of acute and chronic hepatitis
1. Alcohol
2. Drugs
3. Toxins
4. Autoimmune
69
Give 3 symptoms of acute hepatitis
1. General malaise
2. Myalgia
3. GI upset
4. Abdominal pain
5. Raised AST, ALT
6. +/- jaundice
70
What are the potential complications of chronic hepatitis?
Uncontrolled inflammation --> fibrosis --> cirrhosis --> HCC
71
If HAV a RNA or DNA virus?
RNA virus - PicoRNAvirus
72
How is HAV transmitted?
Faeco-oral transmission - contaminated food/water, shellfish
73
Who could be at risk of HAV infection?
Travellers and food handlers
74
Is HAV acute or chronic?
Acute 100% immunity after infection
75
How might you diagnose someone with HAV infection?
bloods - ALT/AST raised
raised IgG and IgM
76
Describe the management of HAV infection
1. Supportive
2. Monitor liver function to ensure no fulminant hepatic failure
3. Manage close contacts
77
What is the primary prevention of HAV?
Vaccination
78
Is HBV a RNA or DNA virus?
DNA virus Replicates in hepatocytes
79
How is HBV transmitted?
Blood borne transmission - blood products and bodily fluids
IVDU, needle-stick, sexual, vertical
Highly infectious
Vertical transmission from mother to child during parturition is most common method of transmission
80
Describe the natural history of HBV in 4 phases
1. Immune tolerance phase: unimpeded viral replication --> high HBV DNA levels.
2. Immune clearance phase: the immune system ‘wakes up’ = liver inflammation and high ALT
3. Inactive HBV carrier phase: HBV DNA levels are low = ALT levels are normal, no liver inflammation
4. Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver --> fibrosis
81
What HBV protein triggers the initial immune response?
The core proteins
82
How might you diagnose someone with HBV?
HBV assay- HBs-Ag - present 1-6 months after exposure. Presence for >6 months implies carrier status- anti-HBs
83
Describe the management of HBV infection
```
vaccination
pegylated interferon alpha 2a
nucleotide analogue (tenofovir) - inhibits viral replications
```
84
How would you know if someone had acute or chronic HBV infection?
Follow up appointment at 6 months to see if HBsAg still present
still present = chronic hepatitis
85
What are the potential consequences of chronic HBV infection?
1. Cirrhosis
2. HCC
3. Decompensated cirrhosis
86
How can HBV infection be prevented?
Vaccination - injecting a small amount of inactivated HbsAg
87
Give 3 side effects of alpha interferon treatment for HBV
1. Myalgia
2. Malaise
3. Lethargy
4. Thyroiditis
5. Mental health problems
88
Give 2 HBV specific symptoms
Arthralgia
| Urticaria (hives)
89
If HCV a RNA or DNA virus?
RNA virus - flavivirus
90
How is HCV transmitted?
Blood borne
91
Give 4 risk factors for developing HBV/HCV infection
1. IVDU
2. People who have required blood products - blood transfusion
3. Needle stick injuries
4. Unprotected sex
5. Vertical transmission
92
How might you diagnose someone with current HCV infection?
HCV RNA - indicates current infection
| Anti-HCV serology
93
Describe the treatment for HCV
Direct acting antivirals
NS5A inhibitor - Ritonavir
NS5B inhibitor - Sofosbuvir
94
What percentage of people with acute HCV infection will progress onto chronic infection?
Approximately 70%
95
What percentage of people with acute HBV infection will progress onto chronic infection?
Approximately 5%
96
How can HCV infection be prevented?
1. Screen blood products
2. Lifestyle modification
3. Needle exchange
No vaccination, and previous infection doesn't confer immunity
97
Is HDV a RNA or DNA virus?
Incomplete RNA virus Needs Hep B for assembly
98
How is HDV transmitted?
Blood borne transmission - particularly IVDUit is transmitted in the same way as HBV
99
Is HEV a RNA or DNA virus?
Small RNA virus
100
How is HEV transmitted?
Faeco-oral transmission
101
Is HEV acute or chronic?
Usually acute but there is a risk of chronic disease in the immunocompromised
102
How might you diagnose someone with HEV infection?
HEV RNA - HEV IgM, IgGanti-HEV
103
Describe the primary prevention of HEV
Good food hygiene
| Vaccine is in development
104
What types of viral hepatitis are capable of causing choric infection?
Hepatitis B (+/- D), C and E in the immunosuppressed
105
What is non alcoholic steatoheptitis (NASH)?
An advanced form of non-alcoholic fatty liver disease
106
Give 3 causes of non-alcoholic fatty liver disease
1. T2DM
2. Obesity
3. Hypertension
4. Hyperlipidaemia
107
How do you manage NAFLD?
Lose weight
Control HTN,
DM and lipids
108
What is Budd-Chiari syndrome?
Hepatic vein occlusion --> ischaemia and hepatocyte damage --> liver failure or insidious cirrhosis
109
Name 3 metabolic disorders that can cause liver disease
1. Haemochromatosis - iron overload
2. Alpha 1 anti-trypsin deficiency
3. Wilson's disease - disorder of copper metabolism
110
90% of people with haemochromatosis have a mutation in which gene?
HFE - chromosome 6
111
Haemochromatosis is a genetic disorder, how is it inherited?
Autosomal recessive inheritance
112
Describe the pathophysiology of haemochromatosis
Uncontrolled intestinal iron absorption --> deposition of iron in liver, heart, pancreas, joins, skin --> fibrosis and functional organ failure
113
Give 4 signs of haemochromatosis
* Fatigue, arthralgia, weakness
* Hypogonadism – eg erectile dysfunction
* SLATE-GREY SKIN (brownish/bronze)
* Chronic liver disease, heart failure, arrythmias
114
How might you diagnose someone with haemochromatosis?
1. bloods - Raised ferritin, LFTs
2. HFE genotyping - C282Y
3. Liver biopsy - gold standard
115
What is the treatment for haemochromatosis?
1. Iron removal - venesection
2. Monitor DM
3. Low iron diet
4. Screening for HFE
5. iron-chelating drugs
116
Give 2 complications of haemochromatosis?
Liver cirrhosis --> failure/cancer
| DM due to pancreatic depositions
117
How is alpha 1 anti-trypsin deficiency inherited?
Autosomal recessive mutation in serine protease inhibitor gene
118
How does Alpha 1 anti-trypsin deficiency present?
Liver disease in the young - cirrhosis, jaundice Lung disease in the old (smokers) - emphysema
119
What is the treatment for Alpha 1 anti-trypsin deficiency?
Smoking cessation
| Liver/lung transplant
120
What is Wilson's disease?
An autosomal recessive disorder of copper metabolism
| Excess deposition of copper in the liver
121
Describe the pathophysiology of Wilson's disease
Impaired incorporation of Cu into caeruloplasmin --> Cu accumulation in liver
122
How does Wilson's disease present?
Children = liver disease - hepatitis, cirrhosis, fulminant liver failure
Adults = CNS problems, mood changes, and Kayser-Fleischer rings
123
What are Kayser-Fleischer rings?
Cu in iris and cornea --> bronze ring
124
What CNS changes are seen in a patient with Wilson's disease?
```
Tremor
Dysarthria
Dyskinesia
Ataxia
Parkinsonism
Dementia
Depression
```
125
What is the treatment for Wilson's disease?
Lifetime treatment with penicillamine (chelating agent)
Low Cu diet - no liver, nuts, chocolate, mushrooms, shellfish
Liver transplant
126
Describe the pathophysiology of autoimmune hepatitis
Abnormal T cell function and autoantibodies vs hepatocyte surface antigens
127
What people are more likely to present with autoimmune hepatitis?
Young (10-30) and middle aged (>40) women
128
How does autoimmune hepatitis present?
```
Fatigue, fever, malaise
Hepatitis
Hepatosplenomegaly
Amenorrhoea
Polyarthritis
Pleurisy
Lung infiltrates
Glomuleronephritis
```
129
What diseases are associated with autoimmune hepatitis?
Autoimmune thyroiditis
DM
Pernicious anaemia
PSCUC
130
What results would you see from the investigations of someone who you suspect has autoimmune hepatitis?
Raised LFTs - increased bilirubin, AST, ALT, ALP
Hypersplenism = low WCC and platelets
Autoantibodies = +ve anti-nuclear antibody
Liver biopsy = mononuclear infiltrate
131
How is autoimmune hepatitis treated?
Prednisolone - immunosuppression
| Liver transplant
132
What is primary biliary cirrhosis?
An autoimmune disease where intra-hepatic bile ducts are destructed by chronic granulomatous inflammation --> cholestatis (bile in liver) --> cirrhosis, fibrosis, portal hypertension
133
Describe 2 features of the epidemiology of primary biliary cirrhosis
1. Females > males
| 2. Familial - 10 fold risk increase
134
Give 3 disease associated with primary biliary cirrhosis
1. Thyroiditis
2. RA
3. Coeliac disease
4. Lung disease
Other autoimmune diseases
135
Give 3 symptoms of primary biliary cirrhosis
1. Pruritis
2. Fatigue
3. Hepatosplenomegaly
4. Obstructive jaundice
5. Cirrhosis and coagulopathy
136
What would investigations show in someone with biliary cirrhosis?
Bloods = AMA antibody, LFT - GGT and ALP raised
Positive anti-mitochondrial antibody = diagnostic
low albumin
Liver biopsy = epithelial disruption and lymphocyte infiltration
137
What is the treatment for primary biliary cirrhosis?
early stage = Ursodeoxycholic acid + steroids + Cholestyramine
ADEK vitamins
severe = Liver transplant
138
What is Primary sclerosing cholangitis?
Autoimmune inflammation and narrowing of intra and extra hepatic bile ducts
139
Describe the pathophysiology of primary sclerosing cholangitis
Inflammation of the bile duct --> stricture and hardening --> progressive obliterating fibrosis of bile duct branches --> cirrhosis --> liver failure
140
Give 3 causes of primary sclerosing cholangitis
1. Primary = unknown causes
2. Infection
3. Thrombosis
4. Iatrogenic trauma
141
Give 3 symptoms of primary sclerosing cholangitis
1. Pruritus
2. Charcot's triad = fever with chills, RUQ pain, obstructive jaundice
3. Cirrhosis
4. Liver failure
5. Fatigue
142
What would the investigations show in someone with primary sclerosing cholangitis?
Bloods = increased Alk phos, elevated ALP, bilirubin and Ig, AMA negative
Imaging = ERCP and MRCP
Liver biopsy = fibrous and obliterative cholangitis
143
What is the treatment for primary sclerosing cholangitis?
- Cholestyramine for pruritus
- Ursodeoxycholic acid - may protect against colon cancer and improve LFT
- ADEK vitamins
- Liver transplant
144
What complications might occur due to primary sclerosing cholangitis?
Increased risk of bile duct, gallbladder, liver and colon cancer
145
What is ascending cholangitis?
- Obstruction of biliary tract causing bacterial infection
- usually caused by bacteria ascending from its junction with the duodenum
- Regarded as a medical emergency
146
Give 3 causes of ascending cholangitis?
Gallstone
Primary infection (Klebsiella, E. coli)
Strictures following surgery
Pancreases head malignancy
147
Name the triad that describes the 3 common symptoms of ascending cholangitis
Charcot's triad
1. Fever
2. RUQ pain
3. Jaundice
148
What other symptoms can present with Charcot's triad with ascending cholangitis?
Reynolds pentad
- Charcot's triad (fever, RUQ pain, jaundice)
- Hypotension
- Confusion/altered mental state
149
What investigations might you do in someone who you suspect might have ascending cholangitis?
1. USS
2. Blood tests - LFTS
3. CT - excludes carcinoma
4. ERCP - definitive investigation
150
Describe the management of ascending cholangitis
```
Fluid resuscitation
Treat infection with broad spectrum antibiotics (cefotaxime, metronidazole)
ERCP to clear obstruction
Stenting
Laparoscopic cholecystectomy
```
151
What is the difference between the clinical presentation of ascending cholangitis and acute cholecystitis?
A patient with acute cholecystitis would not have signs of jaundice
152
What is the main difference between biliary colic and acute cholecystitis?
Acute cholecystitis has an inflammatory component
153
What complications can occur due to acute ascending cholangitis?
```
Sepsis
Biliary colic
Acute cholecystitis
Empyema
Carcinoma
Pancreatitis
```
154
What is peritonitis?
Inflammation of the peritoneal lining
155
what are the different types of peritonitis?
1. Primary = spontaneous bacterial peritonitis, ascites, immunocompromised
2. Secondary = Bowel perforation, abdomen organ inflammation, TB, bowel ischaemia
156
Give 3 symptoms of peritonitis
1. Abdominal pain and tenderness
2. Nausea and vomiting
3. Chills
4. Rigors
5. Fever
157
Give 3 signs of peritonitis on an abdomen examination
1. Guarding
2. Rebound tenderness
3. Rigidity
4. Silent abdomen
5. lying still
158
What investigations might you do in someone who you suspect could have peritonitis?
1. Blood tests: raised WCC, platelets, CRP, amylase, reduced blood count
2. CXR: look for air under the diaphragm
3. Abdominal x-ray: look for bowel obstruction
4. CT: can show inflammation, ischaemia or cancer
5. ECG: epigastric pain could be related to the heart
6. B-HCG: a hormone secreted by pregnant ladies
159
What is the management for peritonitis?
1. ABCDE
2. Treat the underlying cause - might be surgery if perforated bowel
3. IV fluids
4. IV antibiotics - first broad spectrum then specific
5. peritoneal lavage (clean the cavity surgically)
160
Give 5 potential complications of peritonitis
1. Hypovolaemia
2. Kidney failure
3. Systemic sepsis
4. Paralytic ileus
5. Pulmonary atelectasis (lung collapse)
6. Portal pyaemia (pus in portal vein)
161
What is the commonest serious infection in those with cirrhosis?
Spontaneous bacterial peritonitis
162
Name a bacteria that can cause spontaneous bacterial peritonitis
1. E. coli
| 2. S. pneumoniae
163
How can spontaneous bacterial peritonitis be diagnosed
By looking for the presence of neutrophils in ascitic fluid
164
Describe the treatment for spontaneous bacterial peritonitis
Cefotaxime and metronidazole
165
What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important
Ascitic tap to rule out spontaneous bacterial peritonitis
166
You do an ascitic in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?
Spontaneous bacterial peritonitis
167
What is acute pancreatitis?
An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase)
the pancreas returns to functionally and structurallynormal after the episode
Occurs as isolated or recurrent attacks
168
Describe the pathophysiology of acute pancreatitis
Main two causes are alcohol and gallstones:–
Gallstones:
Blockage of bile duct = backup of pancreatic juices. This change in luminal concentration causes Ca2+ release inside pancreatic cells and cause them to activate trypsinogen early which digests the pancreas.
Alcohol:
Contracts the Ampulla of Vater obstructing the bile clearance and also messes with Ca2+homeostasis causing the same as above.
• Leaky and damaged pancreas an auto digest nearby structures causing haemorrhage and Grey
Turner’s sign abdominal skin discolouration from retroperitoneal bleeding.
• Deranges pancreatic function so can cause hyperglycemia from reduction of insulin production
169
What are the causes of acute pancreatitis?
```
I GET SMASHED – remember
I = Idiopathic
G = Gallstones (60%)
E = Ethanol = alcohol (30%)
T = Trauma
S = Steroids
M = Mumps
A = Autoimmune
S = Scorpion venom
H = Hyperlipidaemia/ hypothermia/ high Ca
E = ERCP (endoscopic retrograde cholangiopancreatography)
D = Drugs (furosemide, corticosteroid, NSAIDs, ACEi)
```
170
Give 4 symptoms of acute pancreatitis
1. Severe epigastric pain that radiates to the back
2. Anorexia
3. Nausea, vomiting
4. Signs of septic shock - fever, dehydration, hypotension, tachycardia
5. Necrotising - umbilical (Cullens sign) vs flank (Grey Turners sign)
171
What investigations are done on someone you think has acute pancreatitis?
Raised serum amylase and lipase urinalysis - raised urinary amylase
Erect CXR
Contrast CT
MRI
172
Describe the treatment for acute pancreatitis
- analgesia
- nil by mouth
- IV fluids
- prophylactic antibiotics
173
Give 2 potential complications of acute pancreatitis
1. Systemic inflammatory response syndrome
2. Multiple organ dysfunction
3. Pancreatic necrosis- hyperglycaemia- hypocalcaemia- renal failure- shock
174
Why is morphine contraindicated in acute pancreatitis?
Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis
175
What is chronic pancreatitis?
Chronic inflammation of the pancreas leads to irreversible damage
- Progressive loss of exocrine pancreatic tissue which is replaced by fibrosis
176
Describe the pathogenesis of chronic pancreatitis
Pancreatic duct obstruction leads to activation of pancreatic enzymes --> necrosis --> fibrosis
177
Name 3 causes of chronic pancreatitis
1. Excess alcohol - most common
2. CKD
3. Idiopathic
4. Recurrent acute pancreatitis
5. hereditary
6. CF - all have it from birth
7. autoimmune
8. tropical
178
Describe how alcohol can cause chronic pancreatitis
Alcohol --> proteins precipitate in the ductal structure of the pancreas (obstruction) --> pancreatic fibrosis
179
what is the clinical presentation of chronic pancreatitis?
1. Severe epigastric pain that radiate through to the back - worse after alcohol/meal and better on leaning forward
2. Weight loss, malabsorption
3. Nausea, vomiting
4. Steatorrhea (lack of lipase)
5. Exocrine/endocrine dysfunction (DM)
6. jaundice
180
A sign of chronic pancreatitis is exocrine dysfunction, what can be consequence of this?
1. Malabsorption
2. Weight loss
3. Diarrhoea
4. Steatorrhoea
181
A sign of chronic pancreatitis is endocrine dysfunction, what can be consequence of this?
DM
182
What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?
IgG4
183
How is autoimmune chronic pancreatitis treated?
Steroids
184
What is the treatment for chronic pancreatitis?
Alcohol cessation
Analgesia (NSAIDs, tramadol)
Pancreatic enzyme (creon) and vitamin replacement
pancreatin + omeprazole
If DM = insulin
Surgery - local resection, for unremitting pain and duct draining
185
Why can pancreatitis cause malabsorption?
Pancreatitis result in pancreatic insufficiency and so lack of pancreatic digestive enzymes
Defective intra-luminal digestion leads to malabsorption
186
What 2 enzymes, if raised, suggest pancreatitis?
LDH (lactate dehydrogenase) and AST
187
Give 3 complications of chronic pancreatitis
1. Diabetes
2. Pseudocyst
3. Biliary obstruction --> obstructive jaundice, cancer
188
Name a drug that can cause drug induced liver injury
1. Co-amoxiclav
2. Flucloxacillin
3. Erythromycin
4. TB drugs
189
Give 5 causes of diarrhoea infection
1. Traveller's diarrhoea
2. Viral - (rotavirus/norovirus)
3. Bacterial (E. coli)
4. parasites (helminths, protozoa)
5. Nosocomial (C. diff)
190
Give 5 causes of non-diarrhoeal infection
1. Gastritis/peptic ulcer disease (H. pylori)
2. Acute cholecystitis
3. Peritonitis
4. Thyphois/paratyphoid
5. Amoebic liver abscess
191
Give 3 ways in which diarrhoea can be prevented
1. Access to clean water
2. Good sanitation
3. Hand hygiene
192
What is the diagnostic criteria for travellers diarrhoea?
> 3 unformed stools per day and a least one of:
- abdominal pain
- cramps
- nausea
- vomiting
Occurs within 2 weeks (usually 3 days) of arrival in a new country
193
give 3 causes of travellers diarrhoea
1. Enterotoxigenic E. coli
2. Norovirus
3. Giardia
194
Describe the pathophysiology of traveller's diarrhoea
Heat labile ETEC modifies Gs and it is in a permanent 'locked on' state
Adenylate cyclase is activated and there is increased production of cAMP
Leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient --> diarrhoea
195
Which type of E. coli can cause bloody diarrhoea and has a shiga like toxin?
Enterohaemorrhagic E.coli (EHEC)
196
What does EIEC stand for?
Enteroinvasive E. coli
197
What type of E. coli is responsible for causing large volumes of watery diarrhoea?
Enteropathogenic E.coli (EPEC)
198
What does EAEC stand for?
Enteroaggregative E. coli --> infantile diarrhoea
199
What does DAEC stand for?
Diffusely adherent E. coli
200
What is the leading cause of diarrhoea illness in young children?
Rotavirus
| There is a vaccine = rotary
201
Name a helminth responsible for diarrhoea infection?
Schistosomiasis
| Strongyloides
202
Give 5 symptoms of helminth infection
1. Fever
2. Eosinophilia
3. Diarrhoea
4. Cough
5. Wheeze
203
Why is c. diff infectious?
Spore forming bacteria (gram positive)
204
Give 5 risk factors for c.diff infection
1. Increasing age
2. Comordities
3. Antibiotic use
4. PPI
5. Long hospital admission
6. NG tube feeding and GI surgery
7. Immunocompromised - HIV, anti-caner drugs
205
Name 5 antibiotics that can cause c. diff infection
1. Ciprofloxacin (quinolones)
2. Co-amoxiclav (penicillins)
3. Clindamycin
4. Cephlosporins
5. Carbapenems
RULE OF C's
206
Describe the treatment for c. diff infection
Metronidazole and vancomycin (PO)
Rifampicin/rifaximin
Stool transplant
207
What can helicobacter pylori infections cause?
H. pylori produces urease --> ammonia --> damage to gastric mucosa --> neutrophil recruitment and inflammation
Causing gastritis, peptic ulcer disease, gastric cancer
208
Describe H. pylori
A gram negative bacilli with a flagellum
209
Describe the treatment for H. pylori infection
Triple therapy = 2 antibiotics and 1 PPI
Omeprazole, clarithomyocin and amoxicillin
210
Define biliary colic
Pain associated with the temporary obstruction of the cystic or common bile duct by a stone
211
what investigations should be undertaken for jaundice?
- liver enzymes - very high ALT/AST- MRCP or ERCP
- urine - bilirubin absent in pre-hepatic, in obstructive urobilinogen absent
- FBC
- ultrasound
212
what is the treatment for jaundice?
treat the underlying cause
213
what is the clinical presentation of biliary colic?
● Recurrent episodes of severe and persistent pain in the upper abdomen which subsides after several hours
● Pain may radiate to right shoulder and suprascapular region
● Vomiting
● Normal examination
214
what investigations should be undertaken for biliary colic?
● History and US showing gallstones
● Increases of serum alkaline phosphatase and bilirubin during an attack support the diagnosis of biliary pain
● Absence of inflammatory features differentiates this from acute cholecystitis
215
what is the management of biliary colic?
● Analgesics and elective cholecystectomy
● Abnormal liver biochemistry or a dilated CBD on US is an indication for preoperative MRCP
● CBD stone removed at ERCP
216
what is cholecystitis?
inflammation of the gallbladder
● Follows the impaction of a stone in the cystic duct or neck of the gallbladder
● Can occasionally occur without stones
217
what is the clinical presentation of cholecystitis?
* Generalised epigastric pain migrating to severe RUQ pain.
* Signs of inflammation like a fever or fatigue.
* Pain associated with tenderness and guarding from inflamed gallbladder and local peritonitis.
Tenderness worse on inspiration (Murphy's sign)
218
what are the investigations for cholecystitis?
* Positive Murphy’s Sign = Severe pain on deep inhalation with examiners hand pressed into the RUQ.
* Inflammatory markers - FBCs, CRP
* Ultrasound: Thick gallstone walls from inflammation
219
what is the management of cholecystitis?
• Antibiotics IV,
heavy analgesia,
IV fluids
an eventual Cholecystectomy if needed.
220
what is the pathophysiology of cholecystitis?
• Stone is blocking the ducts. Bile builds up, distending the gallbladder. Vascular supply may be reduced from this distension.
Inflammation follows these events secondary to the retained bile, inflaming the gall bladder.
221
what are the complications of cholecystitis?
● Empyema (pus)
| ● Perforation with peritonitis
222
what is the pathophysiology of primary biliary cholangitis?
* Due to prolonged bile duct blockage, bile isn’t ‘flushing’ out the tubes so bacteria can climb up from the GI tract and cause biliary tree infection and consolidation.
* This prevents bile entering the GI tract and causes jaundice.
* 5-10% mortality and infection can affect the pancreas too since it shares ducts with the gallbladder.
223
what is the clinical presentation of primary biliary cholangitis?
* Severe RUQ pain, with fever (rigors) AND jaundice.
| * Patient may present as septic and/or have developed some level of pancreatitis.
224
what are the investigations for primary biliary cholangitis?
* FBCs, LFTs, CRP - Leukocytosis, Raised ALP and Bilirubin, raised CRP
* Blood cultures/MC&S: work out what the pathogen is so you can use the trust’s advised ABs
* Ultrasound +/- ERCP (Endoscopic Retrograde Cholangiopancreatography) (basically a biliary treecontrast x-ray)
225
what is the treatment for primary biliary cholangitis?
• Treat sepsis, ERCP and stenting to mechanically clear the blockage, surgery/cholecystectomy possible
226
what is primary biliary cholangitis?
● Infection of the biliary tree
| ● Most often occurs secondary to CBD obstruction
227
what are the causes of primary biliary cholangitis?
● CBD obstruction
● Benign biliary strictures
● Pancreatic or bile duct carcinoma
228
what is ascending cholangitis?
bile duct infection, usually caused by bacteria ascending from its junction with the duodenum
229
what is the clinical presentation of ascending cholangitis?
RUQ pain, jaundice, & rigors (Charcot’s triad’)
230
what is the treatment for ascending cholangitis?
Cefuroxime IV & Metronidazole IV/PR.
231
what is primary sclerosing cholangitis?
a disease of the bile ducts that causes inflammation and obliterative fibrosis of bile ducts inside and/or outside of the liver.
- This pathological process impedes the flow of bile to the intestines and can ultimately lead to cirrhosis of the liver, liver failure, and bile duct and liver cancer
232
what is the epidemiology of alcoholic liver disease?
● Most common cause of liver disease in the Western World
● Men > women
● Usually presents in 4th and 5th decades
233
what are the causes of alcoholic liver disease?
Alcohol abuse, genetic predisposition, immunological mechanisms
234
what happens to fatty liver on cessation of alcohol intake?
the fat disappears
235
what are the pre-hepatic causes of portal hypertension?
portal vein thrombosis
236
what are the intrahepatic causes of portal hypertension?
- schistosomiasis
- cirrhosis
- budd-chiari syndrome
237
what are the post-hepatic causes of portal hypertension?
- RH failure
| - IVC obstruction
238
what is the pathophysiology of portal hypertension?
- Increased resistance to blood flow leads to portal hypertension causes splanchnic vasodilation
- This results in a drop in BP
- CO increases to compensate for BP resulting in salt and water retention
- Hyperdynamic circulation/increased portal flow leads to the formation of collaterals between portal and systemic systems
239
what is the treatment of GI varices?
● fluid resuscitation until haemodynamically stable
● If anaemic – blood transfusion
● Correct clotting abnormalities – vitamin K and platelet transfusion
● Vasopressin – IV terlipressin or octreotide
● Prophylactic antibiotics
● Variceal banding
● Balloon tamponade
● TIPS
240
what is the clinical presentation of varices?
```
o Haematemesis
o Abdominal pain
o Shock
o Fresh rectal bleeding
o Hypotension and tachycardia
o Pallor
o Suspect varices as cause of GI bleeding if alcohol abuse or cirrhosis
Splenomegaly and hyponatraemia
```
241
what investigations should be done for varices?
endoscopy - find source
242
what is the prevention of varices?
o Nonselective B blockade – propranolol – reduced resting pulse and decrease portal pressure
o Variceal banding repeated to obliterate varices
o TIPSS
o Liver transplant
243
what is ascites?
accumulation of fluid in peritoneal cavity
| common complication of cirrhosis and common post op
244
what are the risk factors for developing ascites?
- high sodium diet
- HCC
- splanchnic vein thrombosis causing portal hypertension
245
what are the causes of ascites?
```
● liver failure - cirrhosis
● Portal hypertension e.g. cirrhosis
● Hepatic outflow obstruction
● Budd-Chiari syndrome
● Peritonitis
● Pancreatitis
● Cardiac failure
● Constrictive pericarditis
```
246
what are the clinical features of ascites?
- large distended abdomen
- mild pain and discomfort
- shifting dullness - classic sign, percuss abdomen and observe dullness over fluid versus resonance over air. Ask the patient to roll on to one side, wait a good few seconds for fluid to settle at a new level then percuss on the side and observe the dullness has shifted.
247
what investigations should be done for ascites?
● Diagnostic aspiration of 10-20ml of ascitic fluid
o Raised white cell count indicates bacterial peritonitis
o Gram stain and culture
o Cytology for malignant cells
o Amylase to exclude pancreatic ascites
● Protein measurement of ascitic fluid
o Transudate (low protein) - Portal hypertension, constrictive pericarditis, cardiac failure, Budd-Chiari syndrome
o Exudate (high protein) BAD!! - Malignancy, peritonitis, pancreatitis, peritoneal tuberculosis, nephrotic syndrome
248
what is the management of ascites?
- treat underlying cause
- low sodium diet
- spironolactone and furosemide
- drain fluid - paracentesis
249
what can be a complication of ascites?
spontaneous bacterial peritonitis
250
what investigations are undertaken for chronic pancreatitis?
- serum amylase and lipase - may be raised
| - abdominal US, CT and MRI
251
what is alpha 1 antitrypsin deficiency?
- rare cause of cirrhosis
- autosomal recessive condition
- mutation of alpha-1-antitrypsin gene on chromosome 14
252
what is the pathophysiology of alpha-1-antitrypsin deficiency?
● A mutation in the alpha-1-antitrypsin gene on chromosome 14 leads to reduced hepatic production of alpha-1-antitrypsin which normally inhibits the proteolytic enzyme, neutrophil elastase
● Deficiency results in emphysema, liver cirrhosis and hepatocellular carcinoma
253
what are the investigations for alpha-1-antitrypsin deficiency?
Serum alpha-1-antitrypsin levels are low
254
what is the treatment for alpha-1-antitrypsin deficiency?
● No treatment
● Treat complications such as liver disease
● Stop smoking
● Those with hepatic decompensation should be assessed for liver transplant
● Manage emphysema
255
what is the treatment for gallstones?
● Analgesics and elective cholecystectomy
| ● CBD stone removed at ERCP
256
what investigations are undertaken for gallstones?
FBC and CRP: Looking for signs of an inflammatory response - suggestive of cholecystitis
• LFTs: Raised ALP - Bilirubin and ALT usually normal.
• Amylase: Check for pancreatitis
• Ultrasound = diagnostic:
1.Stones
2.Gallbladder wall thickness (inflammation)
3.Duct dilation (suggests distal blockage)
257
what are the side-effects of chelating agents?
skin rash,
fall in WCC, HB and platelets,
haematuria,
renal damage
258
what are the investigations for wilsons disease?
* Serum copper and ceruloplasmin reduced (but can be normal)
* 24hr urinary copper excretion high
* Liver biopsy – diagnostic
259
what are the causes of peritonitis?
bacterial = most common
- gram -ve coliforms - e.coli
- gram +ve staphylococcus
chemical - bile, old clotted blood
260
what is the clinical presentation of HAV?
nausea,
anorexia,
distaste for cigarettes
some become jaundiced - dark urine and pale stool
261
what is the epidemiology of HEV?
● Common in Indochina
● More common in older men
● Commoner than Hep A in UK
● High mortality rate in pregnancy
262
what is the management of HEV?
● Prevention via good sanitation and hygiene, vaccine also available
● Once you’ve had it once you cannot become infected again
263
what are the test results for HBV?
● HBsAg is present 1-6 months after exposure
● HBsAg presence for more than 6 months implies carrier status
● Anti-HBs – antibodies
264
what are the clinical features of HDV?
similar to HBV
265
what are the investigations for HDV?
similar to HBV
HDV-RNA
anti-HDV
266
what is the treatment for HDV?
treat HBV
SC pegylated interferon-alpha-2a
267
what is the epidemiology of HCV?
● High incidence in Egypt due to failed public health initiative
● Transmitted by blood and blood products
● Very high incidence in IV drug users
● Limited sexual transmission
● Vertical transmission is rare
268
how do you remember the viral hepatitis information?
● A is Acquired by mouth from Anus, is Always cleared Acutely and only ever Appears once
● E is Even in England and can be Eaten (found in pigs), if not always beaten
● B is Blood-Borne and if not Beaten can be Bad
● B and D is DastarDly
● C is usually Chronic but Can be Cured at Cost
269
what are the risk factors for non-alcoholic fatty liver disease?
```
Obesity,
diabetes,
hyperlipidaemia,
parental feeding,
jejuno-ileal bypass,
wilsons disease,
drugs - Amiodarone, Tetracycline ,Methotrexate, Tetracycline
```
270
which drugs increase the risk of developing non-alcoholic fatty liver disease?
Amiodarone, Tetracycline ,Methotrexate
271
what are the clinical features of non-alcoholic fatty liver disease?
Usually no symptoms; liver ache in 10%
| Fat, sometimes with inflammation & fibrosis
272
what are the investigations for non-alcoholic fatty liver disease?
Fat, sometimes with inflammation & fibrosis
| Need biopsy to distinguish NAFL from NASH
273
what is the treatment for non-alcoholic fatty liver disease?
control risk factors, bariatric surgery - to treat obesity
274
what is the pathophysiology of fatty changes of the liver?
o Most common biopsy finding in alcoholic individuals
o Symptoms usually absent and on examination there may be hepatomegaly
o Lab tests often normal although elevated MCV indicates heavy drinking
o GGT level usually elevated
o Fat disappears on cessation of alcohol
275
what is the pathophysiology of alcoholic hepatitis?
o Generally, occurs years after heavy drinking
o Ballooned hepatocytes often contain amorphous eosinophilic material
o Rapid onset of jaundice
276
what is the pathophysiology of alcoholic cirrhosis?
o Classically of the micronodular type but mixed pattern is also seen accompanying fatty change, and evidence of pre existing alcoholic hepatitis may be present
277
what are the clinical features of fatty liver?
o No symptoms or signs
| o Vague abdominal symptoms are due to general effects of alcohol on the GI tract
278
what are the clinical features of alcoholic hepatitis?
o May only be apparent on liver biopsy
o Occasionally mild jaundice and signs of chronic liver disease (ascites, bruising, clubbing)
o If severe the patient will have jaundice and ascites, abdominal pain, high fever
279
what are the clinical features of alcoholic cirrhosis?
o Final stage of liver disease from alcohol
o Patients can be well with very few symptoms
o Usually signs of chronic liver disease
o Diagnosis confirmed by liver biopsy
o Features of alcohol dependency
280
what are the investigations for fatty liver?
o Elevated MCV indicates heavy drinking
o Raised ALT and AST
o Ultrasound or CT/liver histology will demonstrate fatty infiltration
281
what are the investigations for alcoholic hepatitis?
o FBC – leucocytosis, elevated MCV, thrombocytopenia
o Serum electrolytes abnormal – elevated serum creatinine
o Elevated AST, ALT, bilirubin, prothrombin time
o Microscopy and culture of blood, urine and ascites to search for infection
o Liver and biliary US used to identify obstruction
282
what is the management for fatty liver?
if alcohol is stopped fat disappears
283
what is the management for alcoholic hepatitis?
o Nutrition maintained with enteral feeding and vitamin supplements
o Steroids show short term benefit – reduce inflammation
o Infections treated and prevented
284
what is the management for alcoholic cirrhosis?
o Reduce salt intake, stop drinking for life
o Avoid aspirin and NSAIDS
o Liver transplant
285
what is the epidemiology of alcoholic liver disease?
● Most common cause of liver disease in the Western World
● Men > women
● Usually presents in 4th and 5th decades
● Only 10-20% of people who drink alcohol develop cirrhosis
286
what are the causes of alcoholic liver disease?
Alcohol abuse, genetic predisposition, immunological mechanisms
287
which condition is associated with primary sclerosing cholangitis?
IBD - especially ulcerative colitis
288
what do the following serological markers indicate in HBV infection?
- HBsAg
- HBeAg
- HBV-DNA
- anti-HBs
- anti-HBc IgM
- anti HBc IgG
- anti HBe
- HBsAg = acute infection (persistence after >6months implies chronic infection)
- HBeAg = acute infection (persistence implies active viral replication) - can distinguish between active and inactive chronic infection
- HBV-DNA = implies viral replication (present in acute and chronic)
- anti-HBs = immunity to HBV from immunisation or previous cleared infection
- anti-HBc = implies previous or current infection
- anti-HBc IgM = recent infection within last 6 months
- anti-HBc IgG = persists long term
- anti-HBe = seroconversion and is present for life
289
what do the following liver function tests indicate?
| ALT, ALP, AST, GGT
```
ALT = liver specific
ALP = bile duct specific
AST = alcohol specific
GGT = differentiate between bone and liver
```
290
what are the primary bile salts?
colic acid and chenodeoxycholic acid`
291
what are the secondary bile salts?
deoxycholic acid and lithocholic acid
292
how are primary bile salts turned into secondary bile salts?
Primary bile salts turn into secondary bile salts by dehydroxylation by bacteria in the gut
293
where is bile synthesised?
in the liver and stored in the gallbladder
294
what is the role of bile?
emulsification of lipids to aid absorption
295
where is the primary site of lipid digestion and absorption?
small intestine
296
what is the process of lipid absorption?
Bile salts emulsify fats and pancreatic lipase hydrolyses fats into monoglycerides and fatty acids
Pancreatic lipase makes fatty acids form micelles which diffuse through epithelial cells
This forms chylomicrons which are absorbed into lymphatic system
297
what structures make up the portal triad?
portal vein
hepatic artery
hepatic bile duct
298
what are the investigations for NAFLD?
1st line
- enhanced liver fibrosis test (<7.7 = non-mild, >7.7-9.8 = moderate, >9.8 = severe)
- LFTs - increased AST and ALT (AST:ALT ratio close to 1)
- FBC - anaemia or thrombocytopenia
gold standard
- liver US (diffuse fatty infiltration and abnormal echotexture)
- liver biopsy (required for diagnosis)
299
how can you tell the difference between NAFLD and alcoholic liver disease?
AST:ALT ratio
ratio close to 1 = NAFLD
2:1 ratio = alcoholic liver disease
300
what are the symptoms of pre-hepatic jaundice?
pallor
fatigue
exertional dyspnoea
301
what are the symptoms of intra-hepatic jaundice?
anorexia
fatigue
nausea
abdominal pain
302
what are the symptoms of post-hepatic jaundice?
```
pale stools
dark urine
pruritus
steatorrhea
RUQ pain
hepatomegaly
```
303
what conditions are associated with primary biliary cholangitis?
IBD
304
which vitamins are people with chronic pancreatitis at risk of becoming deficient in?
fat soluble vitamins
| ADEK
305
what are the investigations for chronic pancreatitis?
CT or MRI - pancreatic duct dilation, calcification, atrophy or pseudocysts
endoscopic ultrasound
fecal elastase test - decreased elastase
306
what cancer marker is present in hepatocellular carcinoma?
alpha-fetoprotein
