GI and Liver Flashcards
1
Q
How long does hepatitis persist for to be deemed chronic?
A
6 months.
2
Q
Give 3 infective causes of acute hepatitis.
A
- Hepatitis A to E infection.
- EBV.
- human herpes virus
3
Q
Give 5 (6) non-infective causes of acute and chronic hepatitis.
A
- Alcohol
- Drugs.
- Toxins.
- Autoimmune.
- non alcoholic fatty liver disease
- pregnancy (acute)
4
Q
Give 3 symptoms of acute hepatitis.
A
- General malaise.
- Myalgia.
- GI upset.
- Abdominal pain.
- Raised AST, ALT.
- +/- jaundice.
5
Q
Give 3 infective causes of chronic hepatitis.
A
- Hepatitis B (+/-D).
- Hepatits C.
- Hepatitis E.
6
Q
What are the potential complications of chronic hepatitis?
A
Uncontrolled inflammation -> fibrosis -> cirrhosis -> HCC.
7
Q
Is HAV a RNA or DNA virus?
A
HAV is a RNA virus.
8
Q
How is HAV transmitted?
A
Faeco-oral transmission. E.g. contaminated food/water; shellfish.
9
Q
Who could be at risk of HAV infection?
A
Travellers and food handlers.
10
Q
Is HAV acute or chronic?
A
Acute! There is 100% immunity after infection.
11
Q
How might you diagnose someone with HAV infection?
A
Viral serology: initially anti-HAV IgM and then anti-HAV IgG.
also
- serum transaminases: raised
- serum bilirubin: raised
- prothrombin time: prolonged
- serum creatinine: raised
12
Q
Describe the management of HAV infection.
A
- Supportive.
- Monitor liver function to ensure no fulminant hepatic failure.
- Manage close contacts.
13
Q
Describe the primary prevention of HAV.
A
Vaccination.
14
Q
Is HEV a RNA or DNA virus?
A
HEV is a small RNA virus.
15
Q
How is HEV transmitted?
A
Faeco-oral transmission.
16
Q
Is HEV acute or chronic?
A
Usually acute but there is a risk of chronic disease in the immunocompromised.
17
Q
How might you diagnose someone with HEV infection?
A
Viral serology: Initially anti-HEV IgM and then anti-HEV IgG.
18
Q
Describe the primary prevention of HEV.
A
- Good food hygiene.
2. A vaccine is in development.
19
Q
Is HBV a RNA or DNA virus?
A
HBV is a DNA virus! It replicates in hepatocytes.
20
Q
How is HBV transmitted?
A
Blood-borne transmission e.g. IVDU, needle-stick, sexual, MTCT (vertical transmission).
HBV is highly infectious!
21
Q
Describe the natural history of HBV in 4 phases.
A
- Immune tolerance phase: unimpeded viral replication -> high HBV DNA levels.
- Immune clearance phase: the immune system ‘wakes up’. There is liver inflammation and high ALT.
- Inactive HBV carrier phase: HBV DNA levels are low. ALT levels are normal. There is no liver inflammation.
- Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver -> fibrosis.
22
Q
What HBV protein triggers the initial immune response?
A
The core proteins.
23
Q
what do the different immunoglobulin levels and antigens mean in hepatitis?
IgG, IgM, antigens present
A
- IgM (means currently ongoing acute infection)
- IgG (chronic current or Previous infection)
- Any antigens present => current infection (chronic or acute)
24
Q
Describe the management of HBV infection.
A
- Screen at risk patients for hep B/C + HIV, notify public health, stop smoking + alcohol
- Antiviral med (entecavir), slows progression and decrease infectivity
- test for complications: fibroscan (cirrhosis), ultrasound (HCC)
- Follow up at 6 months to see if HBV surface Ag has cleared. if present -> chronic hepatitis
25
How would you know if someone had acute or chronic HBV infection?
You would do a follow up appointment at 6 months to see if HBV surface Ag had cleared. If it was still present then the person would have chronic hepatitis.
26
What are the potential consequences of chronic HBV infection?
1. Cirrhosis.
2. HCC.
3. Decompensated cirrhosis.
27
How can HBV infection be prevented?
Vaccination - injecting a small amount of inactivated HbsAg.
28
Describe treatment options for HBV infection.
Antivirals e.g. entecovir. They inhibit viral replications.
29
What is HBV treatment
- screen at risk patients for hep b/c + HIV
- notify public health
- stop smoking and drinking
- antivirals (entecavir)
- test for complications (fibroscan, ultrasound)
30
Is HDV a RNA or DNA virus?
It is a defective RNA virus. It required HBsAG to protect it.
31
Infection with what virus is needed for HDV to survive?
HDV can't exist without HBV infection! It needs HBsAg to protect it.
32
How is HDV transmitted?
Blood-borne transmission, particularly IVDU.
33
Is HCV a RNA or DNA virus?
HCV is a RNA virus.
34
How is HCV transmitted?
Blood borne.
35
Give 4 risk factors for developing HBV/HCV infection.
1. IVDU.
2. People who have required blood products e.g. blood transfusion.
3. Needle-stick injuries.
4. Unprotected sexual intercourse.
5. Materno-foetal transmission.
36
How might you diagnose someone with current HCV infection?
Viral serology - HCV RNA tells you if the infection is still present.
37
You want to find out if someone has previously been infected with HCV. How could you do this?
Viral serology - anti-HCV IgM/IgG indicates that someone has either a current infection or a previous infection.
38
Describe the treatment for HCV.
- Screen at risk patients for Hep B/C + HIV, notify public health, stop drinking and smoking
- antiviral med (glecaprevir) slows progression and decrease infectivity
- test for complications: fibroscan (cirrhosis), ultrasound (HCC)
39
What percentage of people with acute HCV infection will progress onto chronic infection?
Approximately 70%.
40
What percentage of people with acute HBV infection will progress onto chronic infection?
Approximately 5-10%.
41
How can HCV infection be prevented.
1. Screen blood products.
2. Lifestyle modification.
3. Needle exchange.
There is currently no vaccination and previous infection does not confer immunity.
42
What types of viral hepatitis are capable of causing chronic infection?
Hepatitis B (+/-D); C and E in the immunosuppressed.
43
What is acute pancreatitis?
An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase).
44
What are the 3 different types of acute pancreatitis?
1. 70% are oedematous; acute fluid collection.
2. 25% are necrotising.
3. 5% are hemorrhagic.
45
Give 5 causes of acute pancreatitis.
IGETSMASHED
- Idiopathic
- Gallstones
- Ethanol/ alcohol
- Trauma
- Steroids
- Mumps
- Autoimmune
- Scorpion venom
- Hyperlipidaemia
- ERCP
- Drugs (methotrexate)
46
Give 4 symptoms of acute pancreatitis.
1. Severe epigastric pain that radiates to the back, worse with movement.
2. Anorexia.
3. Nausea, vomiting.
4. Signs of septic shock e.g. fever, dehydration, hypotension, tachycardia.
47
How can acute pancreatitis be diagnosed?
Pancreatitis is diagnosed on the basis of 2 out of 3 of the following:
1. Characteristic severe epigastric pain radiating to the back.
2. Raised serum amylase.
3. Abdominal CT scan pathology (necrosis, abscesses + fluid collection)
48
Name a scoring system that can be used a prognostic tool in acute pancreatitis.
The abbreviated glasgow scoring system.
49
What 8 points make up the glasgow scoring system?
```
PaO2 < 8kPa.
Age > 55 years.
Neutrophils > 15x10^9.
Calcium < 2mmol/L.
Raised urea > 15mmol/L.
Elevated enzymes.
Albumin < 32g/L.
Sugar - serum glucose > 15mmol/L.
```
50
Describe the treatment for acute pancreatitis.
1. ANALGESIA! (ibuprofen, opioids)
2. IV fluids, nil by mouth
3. Drainage of oedematous fluid collections.
4. treat underlying cause (IGETSMASHED)
51
Give 2 potential complications of acute pancreatitis.
1. Systemic inflammatory response syndrome.
2. Multiple organ dysfunction.
3. necrosis of pancreas
4. chronic pancreatitis
52
What is chronic pancreatitis?
Chronic inflammation of the pancreas leads to irreversible damage.
53
Describe the pathogenesis of chronic pancreatitis.
The pathogenesis is not fully understood but the current theory is that pancreatic duct obstruction leads to activation of pancreatic enzymes -> necrosis -> fibrosis.
54
Describe how alcohol can cause chronic pancreatitis.
Alcohol -> proteins precipitate in the ductal structure of the pancreas (obstruction) -> pancreatic fibrosis.
55
What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?
IgG4.
56
How is autoimmune chronic pancreatitis treated?
- stop drinking and smoking
| It is very steroid responsive.
57
Give 5 symptoms of chronic pancreatitis.
1. Severe abdominal pain.
2. Epigastric pain radiating to the back.
3. Nausea, vomiting.
4. Decreased appetite.
5. Exocrine/endocrine dysfunction (diabetes, steatorrhoea, malnutrition).
58
A sign of chronic pancreatitis is exocrine dysfunction. What can be a consequence of this?
1. Malabsorption.
2. Weight loss.
3. Diarrhoea.
4. Steatorrhoea.
59
A sign of chronic pancreatitis is endocrine dysfunction. What can be a consequence of this?
Diabetes mellitus.
60
What is the treatment for chronic pancreatitis?
1. analgesia - Opiates in a controlled environment for severe pain.
2. stop smoking and alcohol
3. replacement of pancreatic enzymes, sub cut insulin, ERCp with stunting (biliary obstruction), surgery
61
Give 4 functions of the liver.
1. Bile production and excretion
2. Excretion of bilirubin, cholesterol and drugs
3. Metabolism of fat, proteins + carbs
4. Enzymes activation
5. Storage of glycogen, vitamins + minerals
6. Synthesis of plasma proteins (albumin) + clotting factors
62
Name 4 things that liver function tests measure.
1. Serum bilirubin.
2. Serum albumin.
3. Pro-thrombin time
4. liver enzymes (ALT, ALP, AST)
63
Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease).
Alkaline phosphatase.
64
What enzymes increase in the serum in hepatocellular liver disease?
Transaminases e.g. AST and ALT.
65
Name two hepatocellular enzymes.
Transaminases e.g. AST and ALT.
66
Name a cholestatic enzyme.
Alkaline phosphatase.
67
Give 4 causes of hepatitis.
1. Viral e.g. A, B, C, D, E.
2. Drug induced.
3. Alcohol induced.
4. Autoimmune
5. metabolic - haemochromatosis
68
Give 2 possible outcomes of acute liver disease.
1. Recovery.
| 2. Liver failure.
69
Give 5 causes of acute liver disease.
1. Viral hepatitis.
2. Drug induced hepatitis.
3. Alcohol induced hepatitis.
4. Vascular.
5. Obstruction.
70
Give 3 symptoms of acute liver disease.
1. Malaise.
2. Lethargy.
3. Anorexia.
4. Jaundice may develop later on.
71
Give 2 possible outcomes of chronic liver disease.
1. Cirrhosis.
| 2. Liver failure.
72
Give 5 causes of chronic liver disease.
1. Alcohol.
2. NAFLD.
3. Viral hepatitis (B, C, E).
4. Autoimmune diseases.
5. Metabolic e.g. haemochromatosis.
6. Vascular e.g. Budd-Chiari.
73
What is Budd-Chiari syndrome?
A vascular disease associated with occlusion of hepatic veins that drain the liver.
74
Give 5 signs of chronic liver disease.
1. Ascites.
2. Oedema.
3. Malaise.
4. Anorexia.
5. Bruising.
6. Itching.
7. Clubbing.
8. Palmar erythema.
9. Spider naevi.
75
Drug induced liver injury is common. What question should you remember to ask in a patient history?
Have you started taking any new medication recently?
76
Name a drug that can cause drug induced liver injury.
1. Co-amoxiclav.
2. Flucloxacillin.
3. Erythromyocin.
4. TB drugs.
77
Name 3 drugs that are not known to cause drug induced liver injury.
1. Low dose aspirin.
2. Beta blockers.
3. HRT.
4. CCB.
5. paracetamol
78
What enzyme is responsible for 'mopping up' reactive intermediates of paracetamol and so prevents toxicity and liver failure?
Glutathione transferase.
79
What are the potential consequences of hepatocyte regeneration in someone with liver cirrhosis?
Neoplasia and therefore HCC. Hepatocyte regeneration is liable to errors.
80
Give 3 causes of iron overload.
1. Genetic disorders e.g. haemochromatosis.
2. Multiple blood transfusions.
3. Haemolysis.
4. Alcoholic liver disease.
81
90% of people with haemochromatosis have a mutation in which gene?
HFE - human haemochromatosis gene
82
Haemochromatosis is a genetic disorder. How is it inherited?
Autosomal recessive inheritance.
83
Describe the pathophysiology of haemochromatosis.
which organs it affects ?
Uncontrolled intestinal iron absorption leads to deposition in the liver, heart and pancreas -> fibrosis -> organ failure.
84
What protein is responsible for controlling iron absorption?
Hepcidin.
| Levels of this protein are decreased in haemochromatosis => loss of control
85
How might you diagnose someone with haemochromatosis?
1. Raised ferritin and raised transferratin.
- ferritin can be raised in inflamm so if both high then distinguishes iron overload from inflammation)
2. HFE genotyping.
3. Liver biopsy.
86
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.
87
Describe the mechanism by which alpha 1 anti-trypsin deficiency can lead to chronic liver disease.
Alpha 1 anti-trypsin deficiency results in protein retention in the liver -> eventually cirrhosis.
88
What is Wilson's disease?
An autosomal recessive disorder of copper metabolism; there is excessive deposition of copper in the liver. This can lead to fulminant hepatic failure and cirrhosis.
89
What can cause raised unconjugated bilirubin?
A pre-hepatic problem e.g. haemolysis due to sickle cell disease, spherocytosis, hypersplenism etc.
90
Describe the urine and stools in someone with pre-hepatic jaundice?
Urine and stools are normal. There is no itching and the LFT's are normal.
91
What can cause raised conjugated bilirubin?
Raised conjugated bilirubin indicates a cholestatic problem e.g. liver disease (hepatic) or bile-duct obstruction (post-hepatic).
92
Describe the urine and stools in someone with cholestatic jaundice?
Dark urine and pale stools. There may be itching (pruritus due to bile salts) and LFT's are abnormal.
93
Give 3 causes of duct obstruction.
1. Gallstones (cholelithiasis)
2. Stricture (narrowing) e.g. malignant, inflammatory.
3. Carcinoma.
4. Blocked stent.
94
Give 4 causes of hepatic jaundice.
1. Viral hepatitis.
2. Alcoholic hepatitis.
3. Drugs.
4. Cirrhosis.
5. autoimmune hepatitis
95
Give 3 symptoms of jaundice.
1. Biliary pain.
2. Rigors - indicate an obstructive cause.
3. Abdomen swelling.
4. Weight loss.
96
What is ascites?
An accumulation of fluid in the peritoneal cavity that leads to abdominal distension.
97
Give 4 pathophysiological causes of ascites and an example for each.
1. Portal hypertension (cirrhosis)
2. hypoalbuminaemia (nephrotic syndrome)
3. malignant ascites (peritoneal mesothelioma)
4. infectious peritonitis (TB)
98
Describe the pathogenesis 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.
4. Low serum albumin also leads to ascites.
99
What are the 3 phases of alcoholic liver disease.
1. Fatty change: hepatocytes contain triglycerides.
2. Alcohol hepatitis.
3. Alcoholic cirrhosis: destruction of liver architecture and fibrosis.
100
What might be seen histologically that indicates a diagnosis of alcoholic liver disease?
Neutrophils and fat accumulation within hepatocytes.
101
What is non alcoholic steato-hepatitis (NASH)?
An advanced form of non-alcoholic fatty liver disease.
102
Give 3 causes of non-alcoholic fatty liver disease.
the usual stuff
1. Type 2 diabetes mellitus.
2. Hypertension.
3. Obesity.
4. Hyperlipidaemia.
103
What is cirrhosis?
A chronic disease of the liver resulting from necrosis of liver cells followed by fibrosis. The end result is impairment of hepatocyte function and distortion of liver architecture.
104
Give 3 causes of cirrhosis.
1. Alcohol!
2. Hepatitis B and C.
3. Autoimmune hepatitis
4. Metabolic (haemachromotosis)
any chronic liver disease
105
What is the treatment of liver cirrhosis?
1. Treat underlying cause (stop drinking alcohol, hep b) and manage complications (portal hypertension, hepatic encephalopathy, ascites)
2. Screening for HCC (alphafetoprotein and ultrasound)
3. High protein, low salt diet
3. Consider transplant (MELD score)
106
Approximately what percentage of blood flow to the liver is provided by the portal vein?
75%.
107
Portal hypertension can lead to varices. Explain why.
Obstruction to portal blood flow e.g. cirrhosis leads to portal hypertension. Blood is diverted into collaterals e.g. the gastro-oesophageal junction and so causes varices.
108
Give 3 causes of portal hypertension.
1. Cirrhosis and fibrosis (intra-hepatic causes).
2. Portal vein thrombosis (pre-hepatic).
3. Budd-Chiari (post-hepatic cause).
109
What are the potential consequences of varices?
If they rupture -> haemorrhage.
110
What is the primary treatment for varices?
Endoscopic therapy - elastic band ligation
111
What is peritonitis?
Inflammation of the peritoneum often due to infection.
112
What can cause peritonitis?
1. Bacterial infection due to a perforated organ; spontaneous bacterial peritonitis; infection secondary to peritoneal dialysis.
2. Non-infective causes e.g. bile leak; blood from ruptured ectopic pregnancy.
113
What is the commonest serious infection in those with cirrhosis?
Spontaneous bacterial peritonitis.
It can also affect immunocompromised people and those undergoing peritoneal dialysis.
114
Name a bacteria that can cause spontaneous bacterial peritonitis.
1. E.coli.
2. klebsiella .pneumoniae.
3. s.aureus
115
How can spontaneous bacterial peritonitis be diagnosed?
Is there ascites?
| By looking for the presence of neutrophils in ascitic fluid.
116
Give 3 symptoms of peritonitis.
1. Pain.
2. Tenderness.
3. Systemic symptoms e.g. nausea, chills, rigor.
117
Name a cause of pelvic inflammatory disease.
A complication of chlamydial infection.
118
Give 4 reasons why liver patients are vulnerable to infection.
1. They have impaired reticulo-endothelial function.
2. Reduced opsonic activity.
3. Leukocyte function is reduced.
4. Permeable gut wall.
119
What is primary biliary cirrhosis?
An autoimmune disease where there is progressive lymphocyte mediated destruction of intra-hepatic bile ducts -> cholestasis -> cirrhosis.
120
Describe 2 features of the epidemiology of primary biliary cirrhosis.
1. Females affected more than men.
| 2. Familial - 10 fold risk increase.
121
Describe the pathophysiology of primary biliary cirrhosis.
Lymphocyte mediated attack on bile duct epithelia -> destruction of bile ducts -> cholestasis -> cirrhosis.
122
Give 3 diseases associated with primary biliary cirrhosis.
1. Thyroiditis.
2. RA.
3. Coeliac disease.
4. UC
5. Crohns
(Other autoimmune diseases).
123
Give 5 symptoms of primary biliary cirrhosis.
1. Itching.
2. Jaundice
3. Fatigue
4. Joint pains.
5. Variceal bleeding.
6. Xanthelasma (cholesterol deposits in skin)
124
What is the treatment for primary biliary cirrhosis?
- Bile acid analogue (ursodeoxycholic acid)
- immunosuppression steroids (prednisolone)
- Anti pruritus (cholestyramine)
- If end stage liver failure => Liver transplant
125
Give 5 risk factors for gallstone development.
1. Female.
2. Obese (fat).
3. Fertile.
4. Forties
5. Flatulent
126
How can gallstones be removed from the gall bladder?
Laproscopic cholecystectomy.
127
Give 4 potential complications of gallstones in the bile duct.
1. Biliary pain.
2. Obstructive jaundice.
3. Cholangitis (infection of the biliary tract).
4. Pancreatitis.
128
What is ascending cholangitis?
Obstruction of biliary tract causing bacterial infection. Regarded as a medical emergency.
129
Name the triad that describes 3 common symptoms of ascending cholangitis.
Charcot's triad:
1. Fever.
2. RUQ pain.
3. JAUNDICE (cholestatic)!
130
What is charcot's triad?
It describes 3 common symptoms of ascending cholangitis:
1. Fever.
2. RUQ pain.
3. Jaundice (cholestatic)!
131
What investigations might you do in someone who you suspect might have ascending cholangitis?
1. abdominal Ultrasound.
2. Blood tests - LFT's (raised transaminases)
3. ERCP - definitive investigation.
132
Describe the management of ascending (acute) cholangitis.
- Nil by mouth
- IV fluid.
- take blood cultures
- IV antibiotics e.g. cefotaxime and metronidazole.
- ERCP to remove stone blocking the bile duct
133
What is the difference between ascending cholangitis and acute cholecystitis?
A patient with acute cholecystitis would not have signs of jaundice!
134
What is acute cholecystitis?
Inflammation of the gall bladder caused by blockage of the bile duct -> obstruction to bile emptying.
135
Give 3 symptoms of acute cholecystitis.
1. RUQ pain (+ guarding)
2. Fever.
3. Nausea, vomiting
4. Raised inflammatory markers.
5. NO JAUNDICE! (less common)
136
Give 3 risk factors for acute cholecystitis.
1. History or gallstones
2. Diabetes.
3. prolonged episodes of fasting
137
Describe the pathophysiology of primary sclerosing cholangitis.
Inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure.
138
Give 3 symptoms of primary sclerorsing cholangitis.
1. Pruritus
2. Fatigue
3. Chronic RUQ pain
4. Jaundice.
75% also have IBD.
139
What is biliary colic?
Gallbladder attack - RUQ pain due to a gall stone blocking the bile duct.
140
What can trigger biliary colic?
Eating a heavy meal especially one that is high in fat.
141
Give 5 causes of diarrhoeal infection.
1. Traveller's diarrhoea.
2. Viral e.g. rotavirus, norovirus.
3. Bacterial e.g. E.coli.
4. Parasites e.g. helminths.
5. Nosocomial e.g. c.diff.
142
Give 5 causes of non-diarrhoeal infection.
1. Gastritis/peptic ulcer disease e.g. h.pylori.
2. Acute cholecystitis.
3. Peritonitis.
4. Typhoid/paratyphoid.
5. Amoebic liver disease.
143
Give 3 ways in which diarrhoea can be prevented.
1. Access to clean water.
2. Good sanitation.
3. Hand hygiene.
144
What is the diagnostic criteria for traveller's diarrhoea?
>3 unformed stools per day and at least one of:
- Abdominal pain.
- Cramps.
- Nausea.
- Vomiting.
It occurs within 3 days of arrival in a new country.
145
Give 3 causes of traveller's diarrhoea.
1. Enterotoxigenic e.coli (ETEC).
2. Campylobacter.
3. Norovirus.
146
Describe the pathophysiology of traveller's diarrhoea.
ETEC => increased production of cAMP => increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient -> diarrhoea.
147
Which type of e.coli can cause bloody diarrhoea and has a shiga like toxin?
Enterohaemorrhagic e.coli (EHEC) aka e.coli 0157.
148
What does EIEC stand for?
Enteroinvasive e.coli.
149
Which type of e.coli is responsible for causing large volumes of watery diarrhoea?
Enteropathogenic e.coli (EPEC).
150
What does EAEC stand for?
Enteroaggregative e.coli.
151
What does DAEC stand for?
Diffusely adherent e.coli.
152
What is the leading cause of diarrhoeal illness in young children?
Rotavirus.
There is a vaccine - rotarix.
153
Name a helminth responsible for causing diarrhoeal infection.
Schistosomiasis.
154
Give 5 symptoms of helminth infection.
1. Fever.
2. Eosinophilia.
3. Diarrhoea.
4. Cough.
5. Wheeze.
155
Briefly describe the reproductive cycle of schistosomiasis.
1. Fluke matures in blood vessels and reproduces sexually in human host.
2. Eggs expelled in faeces and enter water source.
3. Asexual reproduction in an intermediate host.
4. Larvae expelled and penetrate back into human host.
156
Why is c.diff highly infectious?
It is a spore forming bacteria.
| Gram positive
157
Give 5 risk factors for c.diff infection.
1. Increasing age.
2. Co-morbidities.
3. Antibiotic use.
4. PPI.
5. Long hospital stays.
158
Describe the treatment for c.diff infection.
Metronidazole or vancomyocin (PO).
159
Name 5 antibiotics prone to causing c.diff infection.
1. Ciprofloxacin.
2. Co-amoxiclav.
3. Clindamycin.
4. Cephlasporins.
5. Carbapenems.
RULE OF C's!
160
What can helicobacter pylori infection cause?
H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.
161
Describe h.pylori.
gram stain
A gram negative bacilli with a flagellum.
162
Describe the treatment for H.pylori infection.
Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromyocin and amoxicillin.
163
Who is most likely to be affected by diverticular disease?
Older patients and those with low fibre diets.
164
Describe the pathophysiology of diverticulitis.
Out-pouching of bowel mucosa -> faeces can get trapped here and obstruct the diverticula -> abscess and inflammation -> diverticulitis.
can rupture => peritonitis
165
What part of the bowel is most likely to be affected by diverticulitis?
The descending colon.
166
What is acute diverticulitis?
A sudden attack of swelling and inflammation in the diverticula. Can be due to surgical causes or infection
167
Describe the signs of acute diverticulitis.
Similar to the signs of appendicitis but on the left side e.g. pain in the left iliac fossa region, fever, tachycardia.
- fever, diarrhoea, nausea + vomiting, rectal bleeding
168
Name the 3 broad categories that describe the causes of intestinal obstruction.
1. Blockage.
2. Contraction.
3. Pressure.
169
Intestinal obstruction: give 3 causes of blockage.
1. Tumour.
2. Diaphragm disease.
3. Gallstones in ileum (rare).
170
Intestinal obstruction: what is thought to cause diaphragm disease?
NSAIDS.
171
Intestinal obstruction: give 2 causes of contraction.
1. Inflammation.
| 2. Intramural tumours.
172
Describe how Crohn's disease can cause intestinal obstruction.
Crohn's disease -> fibrosis -> contraction -> obstruction.
173
Describe how Diverticular disease can cause intestinal obstruction.
Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.
174
Intestinal obstruction: give 3 causes of pressure.
1. Adhesions.
2. Volvulus.
3. Peritoneal tumour.
175
Intestinal obstruction: what are adhesions?
Adhesions often form secondary to abdominal surgery. Loops of bowel stick together and the bowel is pulled and distorted. 40% of intestinal obstructions are due to adhesions.
176
Intestinal obstruction: what causes adhesions?
| aetiology
Adhesions often form secondary to abdominal surgery.
177
Intestinal obstruction: what is volvulus?
Volvulus is a twist/rotation in the bowel; closed loop obstruction. There is a risk of necrosis.
178
Intestinal obstruction: which areas of the bowel are most likely to be affected by volvulus?
Volvulus occurs in free floating areas of the bowel e.g. bowel with mesentery. The sigmoid colon has a long mesentery and so can twist on itself.
179
Give 4 common causes of small bowel obstruction in adults.
1. Adhesions (surgery)
2. Hernias.
3. Crohn's disease (gum to bum)
4. Malignancy.
180
Which is more common: small bowel obstruction or large bowel obstruction?
Small bowel obstruction is more common; it makes up 75% of intestinal obstruction.
181
Give 3 common causes of small bowel obstruction in children.
1. Appendicitis.
2. Volvulus.
3. Intussusception.
182
Intestinal obstruction: what is intussusception?
Intussusception is when part of the intestine invaginates into another section of the intestine -> telescoping. It is caused by force in-balances.
183
Define hernia.
The abnormal protrusion of an organ into a body cavity it doesn't normally belong.
184
What are the risks of hernia's if left untreated?
incarceration: can't go back from herniated position
obstruction
strangulation: base of hernia becomes so tight => cuts of blood supply => ischaemia
185
Give 2 symptoms of hernia.
1. Pain.
| 2. Palpable lump.
186
Give 5 symptoms of small bowel obstruction.
1. Vomiting.
2. Pain.
3. Constipation.
4. Distension.
5. Tenderness.
187
Would dilatation, distension and increased secretions be seen proximal or distal to an intestinal obstruction?
Proximal.
188
Give 4 signs of small bowel obstruction.
1. Vital signs e.g. increased HR, hypotension, raised temperature.
2. Tenderness and swelling.
3. dehydration
4. Bowel sounds (early => hyperactive, late => hypoactive)
189
What investigations might you do in someone who you suspect to have a small bowel obstruction?
Take good history (prep surgery => adhesions)
1. CT
2. ABG (raised lactate => poor tissue perfusion
3. FBC (raised WBC)
4. elevated inflammatory markers
190
What is the management/treatment for small bowel obstruction?
1. Fluid resuscitation
2. Analgesia (morphine)
3. Nasogastric decompression
4. treat underlying cause
5. Surgery e.g. laparotomy, bypass segment, resection.
191
Give 2 common causes of large bowel obstruction.
1. Colorectal malignancy.
| 2. Volvulus (especially in the developing world).
192
Give 5 symptoms of large bowel obstruction.
1. Tenesmus.
2. Constipation.
3. Abdominal discomfort.
4. Bloating.
5. Vomiting.
6. Weight loss.
193
What investigations might you do in someone who you suspect to have a large bowel obstruction?
```
lifethreatening surgical emergency
1. CT scan (urgent)
2 .Lower gastrointestinal endoscopy or flexible sigmoidoscopy (confirm diagnosis)
3. FBC (raised WBC)
4. CRP: raised
```
194
Describe the management for a large bowel obstruction.
1. Nil by mouth
2. Supplement O2.
3. IV fluids to replace losses and correct electrolyte imbalance.
4. Urinary catheterisation to monitor urine output.
5. emergency surgery
195
Give 2 consequences of untreated intestinal obstructions.
1. Ischaemia => necrosis
| 2. Perforation.
196
Describe the progression from normal epithelium to colorectal cancer.
1. Normal epithelium.
2. Adenoma.
3. Colorectal adenocarcinoma.
4. Metastatic colorectal adenocarcinoma.
197
Define adenocarcinoma.
A malignant tumour of glandular epithelium.
198
How can adenoma formation be prevented?
NSAIDS are believed to prevent adenoma formation.
199
What is the treatment for adenoma?
removal - Endoscopic resection.
200
What is the treatment for colorectal adenocarcinoma?
Surgical resection can be done when there is no spread. Remember to balance risks v benefits. The patient has a pre-op assessment.
201
What is the treatment for metastatic colorectal adenocarcinoma?
Chemotherapy and palliative care.
202
Give 3 reasons why bowel cancer survival has increased over recent years.
1. Introduction of the bowel cancer screening programme.
2. Colonoscopic techniques.
3. Improvements in treatment options.
203
Give 5 risk factors for colorectal cancer.
1. Low fibre diet.
2. Increasing age
3. Alcohol.
4. Smoking.
5. A PMH of adenoma or ulcerative colitis.
6. A family history of colorectal cancer; FAP or HNPCC.
204
What can affect the clinical presentation of a colorectal cancer?
How close the cancer is to the rectum affects its clinical presentation.
205
Give 3 signs of rectal cancer.
1. PR bleeding.
2. Mucus.
3. Thin stools.
4. Tenesmus.
206
Give 2 signs of a left sided/sigmoid cancer.
1. Change of bowel habit e.g. diarrhoea, constipation.
| 2. PR bleeding.
207
Give 3 signs of a right sided cancer.
1. Anaemia.
2. Mass.
3. Diarrhoea that doesn't settle.
208
Describe the emergency presentation of a left sided colon cancer.
The LHS of the colon is narrow and so the patient is likely to present with signs of obstruction e.g. constipation; colicky abdominal pain; abdominal distension; vomiting.
209
Describe the emergency presentation of a right sided colon cancer.
The RHS of the colon is wide and so the patient is likely to present with signs of perforation.
210
What investigations might you do in someone who you suspect might have colorectal cancer?
Colonoscopy = gold standard!
It permits biopsy and removal of small polyps.
- Staging CT scan (thorax + abdo + pelvis to look for metastases)
- Faecal occult blood is used in screening but not diagnosis.
211
Give 5 non-infective causes of diarrhoea.
1. Neoplasm.
2. Inflammatory.
3. Irritable bowel.
4. Radiation.
212
Give 3 infective causes of dysentery.
1. Shigella.
2. Salmonella.
3. Campylobacter.
4. E.coli 0157.
213
Give 2 infective causes of non-bloody diarrhoea.
1. Rotavirus.
| 2. Norovirus.
214
Describe the chain of infection.
Reservoir -> agent -> transmission -> host -> person to person spread.
215
Give 3 ways in which infection can be transmitted.
1. Direct e.g. faeco-oral.
2. Indirect e.g. vectorborne (malaria).
3. Airborne e.g. respiratory route.
216
What is the treatment for vibrio cholerae infection?
HYDRATE e.g. ORS. What goes out must be replaced.
217
Describe the management of c.diff infection.
1. Control antibiotic use.
2. Infection control measures.
3. Isolate the case.
4. Case finding.
5. Test stool samples for toxin.
218
Give 4 groups at risk of diarrhoeal infection.
1. Food handlers.
2. Health care workers.
3. Children who attend nursery.
4. Persons of doubtful personal hygiene.
219
Give 3 causes of peptic ulcers.
1. Prolonged NSAID or steroid use -> decreased mucin production.
2. H.pylori infection.
3. Hyper-acidity (stress, alcohol, smoking, excess caffeine)
220
Give 3 symptoms of peptic ulcers.
1. epigastric discomfort, tenderness on palpation
2. nausea and vomiting
3. dyspepsia (indigestion)
4. haematemesis + coffee ground vomit
5. Iron deficiency anaemia (if prolonged bleeding)
221
What investigations might you do in someone who you suspect to have peptic ulcers?
1. H.pylori test e.g. urease breath test and faecal antigen test.
2. Gastroscopy.
3. Barium meal.
222
Give 3 treatments for peptic ulcers.
1. Stop NSAIDS.
2. PPI's e.g. omeprazole.
3. H.pylori eradication.
223
Give 2 potential complications of oesophago-gastroduodenoscopy (OGD).
1. Cardiopulmonary.
| 2. Small risk of bleeding or perforation.
224
Give 3 indications for OGD.
1. Dyspepsia.
2. Dysphagia.
3. Anaemia.
4. Suspected coeliac disease.
225
Give 3 indications for colonoscopy.
1. Altered bowel habit.
2. Diarrhoea +/- dysentery.
3. Anaemia.
226
Give 3 symptoms of GORD.
1. Heart burn.
2. Acid reflux.
3. Dysphagia.
227
Describe the pathophysiology of coeliac disease.
autoimmune antibodies made in response to gluten exposure => target epithelial cells of small intestine => inflammation (jejunum) => crypt hypertrophy + villous atrophy => malabsorption
228
Give 5 symptoms of coeliac disease.
1. Diarrhoea.
2. Weight loss.
3. Irritable bowel.
4. Iron deficiency anaemia.
5. Mouth ulcers.
6. Abnormal liver function.
229
What investigations might you do in someone who you suspect to have coeliac disease?
1. Serology - look for auto-antibodies - TTG and EMA.
2. Gastroscopy - duodenal biopsies.
3. HLA-DQ2/HLA-DQ8 Genetic typing (good to rule out coeliac (if -ve))
230
What part of the bowel is commonly affected by Crohn's disease?
Can affect anywhere from the mouth to anus (gum to bum)
but often terminal ileum
231
What part of the bowel is commonly affected by ulcerative colitis?
It only affects the rectum. It spreads proximally but only affects the colon.
232
Give 5 complications of Crohn's disease.
1. Malabsorption.
2. abscess formation
3. Obstruction.
4. Perforation.
5. Anal fissures.
6. Neoplasia.
233
Give 3 complications of ulcerative colitis.
1. Colon: blood loss and colorectal cancer.
2. Arthritis.
3. primary sclerosing cholangitis.
234
Give an example of a functional bowel disorder.
IBS.
235
Describe the multi-factorial pathophysiology of IBS.
The following factors can all contribute to IBS:
- Psychological morbidity e.g. trauma in early life.
- Abnormal gut motility.
- Genetics.
- Altered gut signalling (visceral hypersensitivity).
236
Give 3 symptoms of IBS.
1. ABDOMINAL PAIN!
2. Pain is relieved on defecation.
3. Bloating.
4. Change in bowel habit.
5. Mucus.
6. Fatigue.
237
Give an example of a differential diagnosis for IBS.
1. Coeliac disease.
2. Lactose intolerance.
3. Bile acid malabsorption.
4. IBD.
5. Colorectal cancer.
238
What investigations might you do in someone who you suspect has IBS?
1. Bloods - FBC, U+E, LFT.
2. CRP.
3. Coeliac serology.
239
Describe the treatment for mild IBS.
Education, reassurance, dietary modification e.g. FODMAP.
240
Describe the treatment for moderate IBS.
Pharmacotherapy and psychological treatments:
- Antispasmodics for pain.
- Laxatives for constipation.
- Anti-motility agents for diarrhoea.
- CBT and hypnotherapy.
241
Describe the treatment for severe IBS.
MDT approach, referral to specialist pain treatment centres.
- Tri-cyclic anti-depressants.
242
Why are all gastric ulcers re-scoped 6-8 weeks after treatment?
All peptic ulcers are re-scoped to ensure they've healed. If they haven't healed it could be a sign of malignancy.
243
What is the criteria for dyspepsia?
>1 of the following:
- Postprandial fullness.
- Early satiation.
- Epigastric pain/burning.
244
Give 5 causes of dyspepsia.
1. Excess acid.
2. Prolonged NSAIDS.
3. Large volume meals.
4. Obesity.
5. Smoking/alcohol.
6. Pregnancy.
245
Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.
1. Unexplained weight loss.
2. Anaemia.
3. Dysphagia.
4. Upper abdominal mass.
5. Persistent vomiting.
246
What investigations might you do in someone with dyspepsia?
1. Endoscopy.
2. Gastroscopy.
3. Barium swallow.
4. Capsule endoscopy.
247
What is the management for dyspepsia if the red flag criteria has been met?
1. Suspend NSAID use and review medication.
2. Endoscopy.
3. Refer malignancy to specialist.
248
What is the management for dyspepsia without red flag symptoms?
1. Review medication.
2. Lifestyle advice.
3. Full dose PPI for 1 month.
4. Test and treat h.pylori infection.
249
What kind of lifestyle advice might you give to someone with dyspepsia?
1. Lose weight.
2. Stop smoking.
3. Cut down alcohol.
4. Dietary modification.
250
Describe the treatment for GORD.
1. PPI.
2. Lifestyle modification.
3. Anti-reflux surgery.
251
Give a potential consequence of anterior ulcer haemorrhage.
Acute peritonitis.
252
Give a potential consequence of posterior ulcer haemorrhage.
Pancreatitis.
253
Name 5 things that can break down the mucin layer in the stomach and cause gastritis.
1. Not enough blood - mucosal ischaemia.
2. H.pylori.
3. Aspirin, NSAIDS.
4. Increased acid - stress.
5. Bile reflux - direct irritant.
6. Alcohol.
254
Describe the treatment for gastritis.
1. Reduced mucosal ischaemia.
2. PPI.
3. H2RA.
4. Enteric coated aspirin.
255
Give 5 broad causes of malabsorption.
1. Defective intra-luminal digestion.
2. Insufficient absorptive area.
3. Lack of digestive enzymes.
4. Defective epithelial transport.
5. Lymphatic obstruction.
256
Malabsorption: what can cause defective intra-luminal digestion?
1. Pancreatic insufficiency due to pancreatitis, CF. There is a lack of digestive enzymes.
2. Defective bile secretion due to biliary obstruction or ileal resection.
3. Bacterial overgrowth.
257
Why can pancreatitis cause malabsorption?
Pancreatitis results in pancreatic insufficiency and so a lack of pancreatic digestive enzymes. There is defective intra-luminal digestion which leads to malabsorption.
258
Malabsorption: what can cause insufficient absorptive area?
1. Coeliac disease.
2. Crohn's disease.
3. Extensive parasitisation.
4. Small intestine resection.
259
Malabsorption: give an example of when there is a lack of digestive enzymes.
Lactose intolerance - disaccharide enzyme deficiency.
260
Malabsorption: what can cause lymphatic obstruction?
1. Lymphoma.
| 2. TB.
261
Describe the distribution of inflammation seen in Crohn's disease.
Patchy, granulomatous, transmural inflammation (can affect just the mucosa or go through the bowel wall).
```
No blood or mucus
Entire GI tract offended (gum to bum)
Smoking - risk factor
Terminal ileum most affected
Skip lesions
```
262
Describe the distribution of inflammation seen in ulcerative colitis.
Continuous inflammation affecting only the mucosa, from rectum proximally
263
Histologically, what part of the bowel wall is affected in ulcerative colitis?
Just the mucosa.
264
Histologically, what part of the bowel wall is affected in crohn's disease?
Can affect just the mucosa or can go all the way through to the bowel wall -> transmural inflammation.
265
What is the treatment for crohn's disease and ulcerative colitis?
crohns: steroids
UC: aminosalicylate
266
Name the break down product of gluten that can trigger coeliac disease.
Gliadin.
267
What part of the small intestine is mainly affected by coeliac disease?
Duodenum.
268
What disorders might be associated with coeliac disease?
Other autoimmune disorders:
1. T1 diabetes.
2. Thyroxoicosis.
3. Hypothyroidism.
4. Addisons disease.
Osteoporosis is also commonly seen in people with coeliac disease.
269
What is the prevalence of coeliac disease?
1%.
270
What cells normally line the oesophagus?
Stratified squamous non-keratinising cells.
271
What is Barrett's oesophagus?
When squamous cells undergo metaplastic changes and become columnar cells.
272
What can cause Barrett's oesophagus?
1. GORD.
| 2. Obesity.
273
Give a potential consequence of Barrett's oesophagus.
Adenocarcinoma.
274
Describe how Barrett's oesophagus can lead to oesophageal adenocarcinoma.
1. GORD damages normal oesophageal squamous cells.
2. Glandular columnar epithelial cells replace squamous cells (metaplasia).
3. Continuing reflux leads to dysplastic oesophageal glandular epithelium.
4. Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
275
Give 5 symptoms of oesophageal carcinoma.
1. Dysphagia.
2. Odynophagia (painful swallowing).
People often present very late.
3. Vomiting.
4. Weight loss.
5. Anaemia.
6. GI bleed.
7. Reflux.
276
Give 3 causes of squamous cell carcinoma (oesophageal)
1. Smoking.
2. Alcohol.
3. Poor diet.
277
What can cause oesophageal adenocarcinoma?
Barrett's oesophagus.
278
Give 3 causes of gastric cancer.
1. Smoked foods.
2. Pickles.
3. H.pylori infection.
4. Pernicious anaemia.
279
Describe how gastric cancer can develop from normal gastric mucosa.
Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.
280
Give 3 causes of oesophageal carcinoma.
1. GORD -> Barrett's.
2. Smoking.
3. Alcohol.
281
What investigations might you do in someone who you suspect to have oesophageal carcinoma?
1. Barium swallow.
| 2. Endoscopy.
282
Describe the 2 treatment options for oesophageal cancer.
1. Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
2. Medically unfit and metastases = palliative care. Stents can help with dysphagia.
283
Give 3 signs of gastric cancer.
1. Weight loss.
2. Anaemia.
3. Vomiting blood.
4. Melaena.
5. Dyspepsia.
284
A mutation in what gene can cause familial diffuse gastric cancer?
CDH1 - 80% chance of gastric cancer.
| Prophylactic gastrectomy is done in these patients.
285
What investigations might you do in someone who you suspect has gastric cancer?
1. Endoscopy.
2. CT.
3. Laparoscopy.
286
What is the advantage of doing a laparoscopy in someone with gastric cancer?
It can detect metastatic disease that may not be detected on ultrasound/endoscopy.
287
What is the treatment for proximal gastric cancers that have no spread?
3 cycles of chemo and then a full gastrectomy. Lymph node removal too.
288
What is the treatment for distal gastric cancers that have no spread?
3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.
289
What vitamin supplement will a patient need following gastrectomy?
They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.
290
Give 3 symptoms of spontaneous bacterial peritonitis.
1. Dull to percussion.
2. Temperature.
3. Abdominal pain
4. signs of ascites
291
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. diagnostic paracentesis
292
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 the portal vein).
293
Explain how paralytic ileus can lead to respiratory problems.
Peristaltic waves stop -> dilation of bowel -> distended abdomen therefore increased pressure -> pushes on diaphragm -> respiration affected.
294
What is the management for peritonitis?
1. ABC.
2. Treat the underlying cause!
3. antibiotic therapy
4. Analgesia
5. Call a surgeon.
295
What can cause exudative ascites?
Increased vascular permeability secondary to infection; inflammation (peritonitis) or malignancy.
296
What can cause transudative ascites?
Increased venous pressure due to cirrhosis, cardiac failure or hypoalbuminaemia.
297
Give 2 signs of ascites.
1. Flank swelling.
2. Dull to percuss and shifting dullness
3. abdo distension
4. jaundice
298
What investigations might you do in someone who you suspect has ascites?
1. Ultrasound, CT or MRI
| 2. Ascitic tap.
299
Describe the treatment for ascites.
1. Restrict sodium.
2. anti aldosterone Diuretics (spironolactone)
3. Drainage.
4. prophylactic Abx
300
Where in the colon do the majority of colon cancers occur?
In the descending/sigmoid colon and rectum.
301
Why do proximal colon cancers have a worse prognosis?
They have fewer signs and so people often present with them at a very advanced and late stage.
302
What 3 histological features are needed in order to make a diagnosis of coeliac disease?
1. Raised intraepithelial lymphocytes.
2. Crypt hyperplasia.
3. Villous atrophy.
303
What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important.
It is important to do an ascitic tap so you can rule out spontaneous bacterial peritonitis as soon as possible.
304
What would be raised in the blood tests taken from someone with primary biliary cirrhosis?
1. Raised IgM.
2. Raised ALP.
3. Positive AMA.
305
What 4 features would you expect to see in the blood test results taken from someone who has overdosed on paracetamol.
1. Metabolic acidosis.
2. Prolonged pro-thrombin time (due to coagulability).
3. Raised creatinine (renal failure).
4. Raised ALT.
306
What 3 symptoms make up the triad of Wernicke's encephalopathy?
1. Ataxia.
2. Opthalmoplegia (extraocular muscle palsy)
3. Confusion.
307
How can Wernicke's encephalopathy be reversed?
Give IV thiamine.
308
What histological stain can be used for haemochromatosis?
Perl's stain.
309
Name 4 fat soluble vitamins.
A, D, E and K.
310
What is the main difference between biliary colic and acute cholecystitis?
Acute cholecystitis has an inflammatory component!
311
What is the treatment for acute cholecystitis?
- Bill by mouth (rest gall bladder)
- IV fluids
- IV Abx
- IRCP (remove stones trapped in CBD)
- Laparoscopic cholecystectomy (GB removal)
312
Why might someone with primary biliary cirrhosis experience itching as a symptom?
Because there is a build up of bilirubin.
313
Give 3 components of gallstones.
1. Cholesterol.
2. Bile pigment.
3. Phospholipid.
314
What investigations might you do in someone who you suspect has gallstones?
Ultrasound!
| ERCP.
315
Are most liver cancers primary or secondary?
Secondary - they have metastasised to the liver from the GI tract, breast and bronchus.
316
Where have most secondary liver cancers arisen from?
1. The Gi tract.
2. Breast.
3. Bronchus.
317
Describe the aetiology of HCC.
Most HCC is in patients with cirrhosis. This is often due to HBV/HCV and alcohol.
318
Give 5 symptoms of HCC.
1. Weight loss.
2. Anorexia.
3. Fever.
4. Malaise.
5. Ascites.
319
What investigations might you do on someone who you suspect has HCC?
1. Bloods: serum AFP may be raised.
2. US or CT to identify lesions.
3. MRI.
4. Biopsy if diagnostic doubt.
320
Describe the treatment for HCC.
1. Surgical resection of solitary tumours.
2. Liver transplant.
3. Percutaneous ablation.
321
How long after infection with hepatitis B virus is HBsAg present in the serum for?
HBsAg will be present in the serum from 6 weeks - 3 months after infection.
322
How long after infection with hepatitis B virus is anti-HBV core (IgM) present in the serum for?
Anti-HBV core (IgM) slowly rises from 6 weeks after infection and its serum level peaks at about 4 months.
323
Give 3 symptoms of haemochromatosis.
1. Hepatomegaly.
2. Cardiomegaly.
3. Diabetes mellitus.
4. Hyperpigmentation of skin.
5. Lethargy.
324
Name 3 diseases that lead to heamolytic anaemia and so a raised unconjugated bilirubin and pre-hepatic jaundice.
Causes of haemolytic anaemia:
1. Sickle cell disease.
2. Hereditary spherocytosis/elliptocytosis.
3. GP6D deficiency.
4. Hypersplenism.
325
Give 3 causes of liver failure.
1. Infection e.g. viral hepatitis B, C.
2. Induced e.g. alcohol, drug toxicity.
3. Inherited e.g. autoimmune.
326
Hepatic encephalopathy is a complication of liver failure. Describe the pathophysiological mechanism behind this.
The liver can't get rid of ammonia and so ammonia crosses the BBB -> cerebral oedema.
327
Give 4 complications of liver failure.
1. Hepatic encephalopathy.
2. Abnormal bleeding.
3. Jaundice.
4. Ascites.
328
Describe the treatment for liver failure.
1. Nutrition.
2. Supplements.
3. Treat complications.
4. Liver transplant.
329
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.
330
Describe the treatment for spontaneous bacterial peritonitis.
Cefotaxime and metronidazole.
331
Give 5 symptoms of ruptured varices.
1. Haematemesis.
2. Melaena.
3. Abdominal pain.
4. Dysphagia.
5. Anaemia.
332
How would you know if an individual had been vaccinated against hepatitis B?
They would have anti-HBVs IgG in their serum.
333
What type of anaemia do you associate with alcoholic liver disease?
Macrocytic anaemia.
334
Name a protozoa that can cause amoebic liver abscess?
Entemoeba histolytica.
335
What are the symptoms of entemoeba histolytica?
- RUQ pain.
- Bloody diarrhoea.
- Fever and malaise.
Often the patient has a history of foreign/rural travel.
336
What is the treatment for entemoeba histolytica?
Metronidazole.
337
What is the treatment for mild/moderate UC?
Mesalazine.
338
A 4-year-old girl presents with diarrhoea and is hypotensive. What is the physiological reason that fluid moves from the interstitium to the vascular compartment in this case?
Reduced hydrostatic pressure.
Fluid will move from the interstitium into the plasma if there is an increase in osmotic pressure or a decrease in hydrostatic pressure. As this patient is hypotensive it is more likely to be the latter.
339
What drug would you give to someone that has overdosed on paracetamol?
IV N-Acetyl-Cysteine.
340
With which disease would you associate Reynold's pentad?
Ascending cholangitis.
341
Describe Reynold's pentad.
- Charcot's triad (fever, RUQ pain and jaundice).
- + hypotension.
- + altered mental state.
342
What is a potential consequence of h.pylori infection in a person with decreased gastric acid?
Gastric cancer.
343
What is a potential consequence of h.pylori infection in a person with increased gastric acid?
Duodenal ulcer.
344
What might pain radiating to the back be a sign of?
Pancreatitis or AAA.
345
What blood test might show that someone has alcoholic liver disease?
Serum GGT (gamma-glutamyl transferase) will be elevated.
346
What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?
Mallory bodies.
347
What feature seen on liver biopsy is diagnostic of cirrhosis?
Nodular regeneration.
348
A man has his ascites drained and is advised to restrict his diet. Which non-hormonal substance will promote re-accumulation of the ascites?
Salt.
349
What is the treatment for Wilson's disease.
Lifetime treatment with penicillamine.
350
Name the 2 main pathophysiological factors that contribute to the formation of ascites.
1. High portal venous pressure.
| 2. Low serum albumin.
351
Give 2 indications for the need of immediate surgical intervention in someone with a small bowel obstruction.
1. Signs of perforation (peritonitis).
| 2. Signs of strangulation.
352
Why is morphine contraindicated in acute pancreatitis?
Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis.
353
What two enzymes, if raised, suggest pancreatitis?
LDH and AST.
354
Where is folate absorbed?
In the jejunum.
355
Where is vitamin B12 absorbed?
In the terminal ileum.
356
Where is iron absorbed?
In the duodenum.
357
In someone with coeliac disease, what are they most likely to be deficient in - iron, folate, or B12?
Iron.
Coeliac disease mainly affects the duodenum and iron is absorbed in the duodenum. Folate is absorbed in the jejunum and B12 in the terminal ileum.
358
Give 5 histological features of a malignant neoplasm.
1. High mitotic activity.
2. Rapid growth.
3. Border irregularity.
4. Necrosis.
5. Poor resemblance to normal tissues.
359
What lymph nodes can oesophageal carcinoma commonly metastasise to?
Para-oesophageal lymph nodes.
360
What hormone is responsible for the production of gastric acid?
Gastrin.
361
State two pathological changes that occur in the liver with continued consumption of excessive amounts of alcohol.
1. Fatty liver.
2. Alcoholic hepatitis.
3. Cirrhosis.
362
A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.
Hypoalbuminaemia.
363
List 5 important questions a GP should ask when taking a history to establish a cause of diarrhoea.
1. Blood or mucus in the stools.
2. Family history of bowel problems?
3. Abdominal pain.
4. Recent foreign travel history.
5. Bloating.
6. Weight loss.
364
List two blood tests a GP might perform to help differentiate between the different causes of diarrhoea.
1. FBC.
| 2. ESR/CRP.
365
List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.
1. Stool culture.
| 2. Faecal calprotectin.
366
State one histological feature that will be seen in ulcerative colitis.
1. Crypt abscess.
| 2. Increase in plasma cells in the lamina propria.
367
What investigations might you do in someone with inflammatory bowel disease?
1. Bloods - FBC, ESR, CRP.
2. Faecal calprotectin - shows inflammation but is not specific for IBD.
3. Flexible sigmoidoscopy.
4. Colonoscopy.
368
Name 3 drugs or classes of drugs that can cause acute pancreatitis.
1. NSAIDs.
2. Diuretics.
3. Steroids.
369
What 2 products does haem break down in to?
Haem -> Fe2+ and biliverdin.
370
What enzyme converts biliverdin to unconjugated bilirubin?
Biliverdin reductase.
371
What is the function of glucuronosyltransferase?
It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.
372
What protein does unconjugated bilirubin bind to and why?
Albumin.
It isn't H2O soluble therefore it binds to albumin so it can travel in the blood to the liver.
373
What does conjugated bilirubin form?
Urobilinogen.
374
What is responsible for the conversion of conjugated bilirubin into urobilinogen?
Intestinal bacteria.
375
What can urobilinogen form?
1. It can go back to the liver via the enterohepatic system.
2. It can go to the kidneys forming urinary urobilin.
3. It can form stercobilin which is excreted in the faeces.
376
What disease could be caused by a non-functioning mutation in NOD2?
Crohn's.
