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.
- CMV.
- Toxoplasmosis.
3
Q
Give 3 non-infective causes of acute and chronic hepatitis.
A
- Alcohol.
- Drugs.
- Toxins.
- Autoimmune.
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.
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.
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
How might you diagnose someone with HBV?
A
Viral serology: HBV surface antigen can be detected from 6w - 3m or anti-HBV core IgM after 3 months.
24
Q
Describe the management of HBV infection.
A
- Supportive.
- Monitor liver function.
- Manage contacts.
- 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 two treatment options for HBV infection.
1. Alpha interferon - boosts immune system.
| 2. Antivirals e.g. tenofovir. They inhibit viral replications.
29
HBV treatment: give 3 side effects of alpha interferon treatment.
1. Myalgia.
2. Malaise.
3. Lethargy.
4. Thyroiditis.
5. Mental health problems.
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.
Lots of new drugs have been developed recently for HCV infection. Direct acting antivirals (DAA) are currently in use e.g. NS5A and NS5B.
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%.
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.
1. Gallstones.
2. Alcohol.
3. Hyperlipidaemia.
4. Direct damage e.g. trauma.
5. Idiopathic.
6. Toxic e.g. drugs, infection, venom.
46
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 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.
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!
2. Catheterise and ABC approach for shock patients.
3. Drainage of oedematous fluid collections.
4. Antibiotics.
5. Nutrition.
6. Bowel rest.
51
Give 2 potential complications of acute pancreatitis.
1. Systemic inflammatory response syndrome.
| 2. Multiple organ dysfunction.
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?
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.
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?
Opiates in a controlled environment for severe pain.
61
Give 4 functions of the liver.
1. Glucose and fat metabolism.
2. Detoxification and excretion.
3. Protein synthesis e.g. albumin, clotting factors.
4. Defence against infection.
62
Name 3 things that liver function tests measure.
1. Serum bilirubin.
2. Serum albumin.
3. Pro-thrombin time.
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.
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. NSAIDS.
3. Beta blockers.
4. HRT.
5. CCB.
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.
82
Haemochromatosis is a genetic disorder. How is it inherited?
Autosomal recessive inheritance.
83
Describe the pathophysiology of haemochromatosis.
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.
85
How might you diagnose someone with haemochromatosis?
1. Raised ferritin.
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 and LFT's are abnormal.
93
Give 3 causes of duct obstruction.
1. Gallstones.
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.
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. Local inflammation e.g. peritonitis.
2. Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures.
3. Low flow e.g. cirrhosis, thrombosis, cardiac failure.
4. Low protein e.g. hypoalbuminaemia.
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.
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. Any chronic liver disease e.g. autoimmune, metabolic, vascular etc.
105
What is the treatment of liver cirrhosis?
1. Deal with the underlying cause e.g. stop drinking alcohol.
2. Screening for HCC.
3. Consider transplant.
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 - banding.
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. S.pneumoniae.
115
How can spontaneous bacterial peritonitis be diagnosed?
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. Lung disease.
(Other autoimmune diseases).
123
Give 5 symptoms of primary biliary cirrhosis.
1. Itching.
2. Fatigue.
3. Dry eyes,
4. Joint pains.
5. Variceal bleeding.
124
What is the treatment for primary biliary cirrhosis?
Ursodeoxycholic acid; improves liver enzymes; reduces inflammation and portal pressure and therefore the rate of variceal development.
125
Give 3 risk factors for gallstone development.
1. Female.
2. Obese (fat).
3. Fertile.
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. Ultrasound.
2. Blood tests - LFT's.
3. ERCP - definitive investigation.
132
Describe the management of ascending cholangitis.
- IV fluid.
- IV antibiotics e.g. cefotaxime and metronidazole.
- ERCP to remove stone.
- Stenting.
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.
2. Fever.
3. Raised inflammatory markers.
- NO JAUNDICE!
136
Give 2 risk factors for acute cholecystitis.
1. Obesity.
| 2. Diabetes.
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. Itching.
2. Rigor.
3. 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.
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. This leads to 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 and 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.
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.
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 in the diverticula. Can be due to surgical causes.
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.
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 3 causes of contraction.
1. Inflammation.
2. Intramural tumours.
3. Hirschprung's disease.
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
What is Hirschprung's disease?
A congenital condition where there is a lack of nerves in the bowel and so motility is affected. This leads to obstruction and gross dilatation of the bowel.
175
Intestinal obstruction: give 3 causes of pressure.
1. Adhesions.
2. Volvulus.
3. Peritoneal tumour.
176
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.
177
Intestinal obstruction: what causes adhesions?
Adhesions often form secondary to abdominal surgery.
178
Intestinal obstruction: what is volvulus?
Volvulus is a twist/rotation in the bowel; closed loop obstruction. There is a risk of necrosis.
179
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.
180
Give 4 common causes of small bowel obstruction in adults.
1. Adhesions.
2. Hernias.
3. Crohn's disease.
4. Malignancy.
181
Which is more common: small bowel obstruction or large bowel obstruction?
Small bowel obstruction is more common; it makes up 75% of intestinal obstruction.
182
Give 3 common causes of small bowel obstruction in children.
1. Appendicitis.
2. Volvulus.
3. Intussusception.
183
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.
184
Define hernia.
The abnormal protrusion of an organ into a body cavity it doesn't normally belong.
185
What are the risks of hernia's if left untreated?
They can become strangulated and you may not be able to return them into their correct body cavity - irreducible.
186
Give 2 symptoms of hernia.
1. Pain.
| 2. Palpable lump.
187
Give 5 symptoms of small bowel obstruction.
1. Vomiting.
2. Pain.
3. Constipation.
4. Distension.
5. Tenderness.
188
Would dilatation, distension and increased secretions be seen proximal or distal to an intestinal obstruction?
Proximal.
189
Give 4 signs of small bowel obstruction.
1. Vital signs e.g. increased HR, hypotension, raised temperature.
2. Tenderness and swelling.
3. Resonance.
4. Bowel sounds.
190
What investigations might you do in someone who you suspect to have a small bowel obstruction?
1. Take a good history - ask about previous surgery (adhesions)!
2. FBC, U+E, lactate.
3. X-ray.
4. CT, ultrasound, MRI.
191
What is the management/treatment for small bowel obstruction?
1. Fluid resuscitation.
2. Bowel decompression.
3. Analgesia and anti-emetics.
4. Antibiotics.
5. Surgery e.g. laparotomy, bypass segment, resection.
192
Give 2 common causes of large bowel obstruction.
1. Colorectal malignancy.
| 2. Volvulus (especially in the developing world).
193
Give 5 symptoms of large bowel obstruction.
1. Tenesmus.
2. Constipation.
3. Abdominal discomfort.
4. Bloating.
5. Vomiting.
6. Weight loss.
194
What investigations might you do in someone who you suspect to have a large bowel obstruction?
1. Digital rectal examination.
2. Sigmoidoscopy.
3. Plain X-ray.
4. CT scan.
195
Describe the management for a large bowel obstruction.
1. Fast the patient.
2. Supplement O2.
3. IV fluids to replace losses and correct electrolyte imbalance.
4. Urinary catheterisation to monitor urine output.
196
Give 3 consequences of untreated intestinal obstructions.
1. Ischaemia.
2. Necrosis.
3. Perforation.
197
Describe the progression from normal epithelium to colorectal cancer.
1. Normal epithelium.
2. Adenoma.
3. Colorectal adenocarcinoma.
4. Metastatic colorectal adenocarcinoma.
198
Define adenocarcinoma.
A malignant tumour of glandular epithelium.
199
What is familial adenomatous polyposis?
Familial adenomatous polyposis is a genetic condition where you develop thousands of polyps in your teens.
200
Describe the pathophysiology of familial adenomatous polyposis.
There is a mutation in apc protein and so the apc/GSK complex isn't formed -> beta catenin levels increase -> up-regulation of adenomatous gene transcription.
201
Describe the pathophysiology of HNPCC.
There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.
202
How can adenoma formation be prevented?
NSAIDS are believed to prevent adenoma formation.
203
What is the treatment for adenoma?
Endoscopic resection.
204
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.
205
What is the treatment for metastatic colorectal adenocarcinoma?
Chemotherapy and palliative care.
206
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.
207
Give 5 risk factors for colorectal cancer.
1. Low fibre diet.
2. Diet high in red meat.
3. Alcohol.
4. Smoking.
5. A PMH of adenoma or ulcerative colitis.
6. A family history of colorectal cancer; FAP or HNPCC.
208
What can affect the clinical presentation of a colorectal cancer?
How close the cancer is to the rectum affects its clinical presentation.
209
Give 3 signs of rectal cancer.
1. PR bleeding.
2. Mucus.
3. Thin stools.
4. Tenesmus.
210
Give 2 signs of a left sided/sigmoid cancer.
1. Change of bowel habit e.g. diarrhoea, constipation.
| 2. PR bleeding.
211
Give 3 signs of a right sided cancer.
1. Anaemia.
2. Mass.
3. Diarrhoea that doesn't settle.
212
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.
213
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.
214
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.
- Tumour markers are good for monitoring progress.
- Faecal occult blood is used in screening but not diagnosis.
215
Give 5 non-infective causes of diarrhoea.
1. Neoplasm.
2. Inflammatory.
3. Irritable bowel.
4. Anatomical.
5. Chemical.
6. Hormonal.
7. Radiation.
216
Give 3 infective causes of dysentery.
1. Shigella.
2. Salmonella.
3. Campylobacter.
4. E.coli 0157.
217
Give 2 infective causes of non-bloody diarrhoea.
1. Rotavirus.
| 2. Norovirus.
218
Describe the chain of infection.
Reservoir -> agent -> transmission -> host -> person to person spread.
219
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.
220
What is the treatment for vibrio cholerae infection?
HYDRATE e.g. ORS. What goes out must be replaced.
221
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.
222
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.
223
Give 3 causes of peptic ulcers.
1. Prolonged NSAID use -> decreased mucin production.
2. H.pylori infection.
3. Hyper-acidity.
224
Give 3 symptoms of peptic ulcers.
Often acute onset of symptoms:
1. Pain.
2. Bleeding.
3. Perforation.
225
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.
226
Give 3 treatments for peptic ulcers.
1. Stop NSAIDS.
2. PPI's e.g. omeprazole.
3. H.pylori eradication.
227
Give 2 potential complications of oesophago-gastroduodenoscopy (OGD).
1. Cardiopulmonary.
| 2. Small risk of bleeding or perforation.
228
Give 3 indications for OGD.
1. Dyspepsia.
2. Dysphagia.
3. Anaemia.
4. Suspected coeliac disease.
229
Give 3 indications for colonoscopy.
1. Altered bowel habit.
2. Diarrhoea +/- dysentery.
3. Anaemia.
230
Give 3 symptoms of GORD.
1. Heart burn.
2. Acid reflux.
3. Dysphagia.
231
Describe the pathophysiology of coeliac disease.
Gliadin (product of gluten digestion) = immunogenic. It can have direct toxic effects by up-regulating the innate immune system or HLADQ2 can present it to T helper cells in the lamina propria -> inflammation -> villi atrophy -> malabsorption.
232
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.
233
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.
234
What part of the bowel is commonly affected by Crohn's disease?
Can affect anywhere from the mouth to anus.
235
What part of the bowel is commonly affected by ulcerative colitis?
It only affects the rectum. It spreads proximally but only affects the colon.
236
Give 5 complications of Crohn's disease.
1. Malabsorption.
2. Fistula.
3. Obstruction.
4. Perforation.
5. Anal fissures.
6. Neoplasia.
7. Amyloidosis (rare).
237
Give 5 complications of ulcerative colitis.
1. Colon: blood loss and colorectal cancer.
2. Arthritis.
3. Iritis and episcleritis.
4. Fatty liver and primary sclerosing cholangitis.
5. Erythema nodosum.
238
Give an example of a functional bowel disorder.
IBS.
239
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).
240
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.
241
Give an example of a differential diagnosis for IBS.
1. Coeliac disease.
2. Lactose intolerance.
3. Bile acid malabsorption.
4. IBD.
5. Colorectal cancer.
242
What investigations might you do in someone who you suspect has IBS?
1. Bloods - FBC, U+E, LFT.
2. CRP.
3. Coeliac serology.
243
Describe the treatment for mild IBS.
Education, reassurance, dietary modification e.g. FODMAP.
244
Describe the treatment for moderate IBS.
Pharmacotherapy and psychological treatments:
- Antispasmodics for pain.
- Laxatives for constipation.
- Anti-motility agents for diarrhoea.
- CBT and hypnotherapy.
245
Describe the treatment for severe IBS.
MDT approach, referral to specialist pain treatment centres.
- Tri-cyclic anti-depressants.
246
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.
247
What is the criteria for dyspepsia?
>1 of the following:
- Postprandial fullness.
- Early satiation.
- Epigastric pain/burning.
248
Give 5 causes of dyspepsia.
1. Excess acid.
2. Prolonged NSAIDS.
3. Large volume meals.
4. Obesity.
5. Smoking/alcohol.
6. Pregnancy.
249
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.
250
What investigations might you do in someone with dyspepsia?
1. Endoscopy.
2. Gastroscopy.
3. Barium swallow.
4. Capsule endoscopy.
251
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.
252
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.
253
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.
254
Describe the treatment for GORD.
1. PPI.
2. Lifestyle modification.
3. Anti-reflux surgery.
255
Give a potential consequence of anterior ulcer haemorrhage.
Acute peritonitis.
256
Give a potential consequence of posterior ulcer haemorrhage.
Pancreatitis.
257
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.
258
Describe the treatment for gastritis.
1. Reduced mucosal ischaemia.
2. PPI.
3. H2RA.
4. Enteric coated aspirin.
259
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.
260
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.
261
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.
262
Malabsorption: what can cause insufficient absorptive area?
1. Coeliac disease.
2. Crohn's disease.
3. Extensive parasitisation.
4. Small intestine resection.
263
Malabsorption: give an example of when there is a lack of digestive enzymes.
Lactose intolerance - disaccharide enzyme deficiency.
264
Malabsorption: what can cause lymphatic obstruction?
1. Lymphoma.
| 2. TB.
265
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).
266
Describe the distribution of inflammation seen in ulcerative colitis.
Continuous inflammation affecting only the mucosa.
267
Histologically, what part of the bowel wall is affected in ulcerative colitis?
Just the mucosa.
268
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.
269
What is the treatment for crohn's disease and ulcerative colitis?
Anti-inflammatories.
270
Name the break down product of gluten that can trigger coeliac disease.
Gliadin.
271
What part of the small intestine is mainly affected by coeliac disease?
Duodenum.
272
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.
273
What is the prevalence of coeliac disease?
1%.
274
What cells normally line the oesophagus?
Stratified squamous non-keratinising cells.
275
What is Barrett's oesophagus?
When squamous cells undergo metaplastic changes and become columnar cells.
276
What can cause Barrett's oesophagus?
1. GORD.
| 2. Obesity.
277
Give a potential consequence of Barrett's oesophagus.
Adenocarcinoma.
278
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.
279
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.
280
Give 3 causes of squamous cell carcinoma.
1. Smoking.
2. Alcohol.
3. Poor diet.
281
What can cause oesophageal adenocarcinoma?
Barrett's oesophagus.
282
Give 3 causes of gastric cancer.
1. Smoked foods.
2. Pickles.
3. H.pylori infection.
4. Pernicious anaemia.
283
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.
284
Give 3 causes of oesophageal carcinoma.
1. GORD -> Barrett's.
2. Smoking.
3. Alcohol.
285
What investigations might you do in someone who you suspect to have oesophageal carcinoma?
1. Barium swallow.
| 2. Endoscopy.
286
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.
287
Give 3 signs of gastric cancer.
1. Weight loss.
2. Anaemia.
3. Vomiting blood.
4. Melaena.
5. Dyspepsia.
288
A mutation in what gene can cause familial diffuse gastric cancer?
CDH1 - 80% chance of gastric cancer.
| Prophylactic gastrectomy is done in these patients.
289
What investigations might you do in someone who you suspect has gastric cancer?
1. Endoscopy.
2. CT.
3. Laparoscopy.
290
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.
291
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.
292
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.
293
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.
294
Give 3 symptoms of spontaneous bacterial peritonitis.
1. Dull to percussion.
2. Temperature.
3. Abdominal pain.
295
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.
296
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).
297
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.
298
What is the management for peritonitis?
1. ABC.
2. Treat the underlying cause!
3. Call a surgeon.
4. Set up post-management support.
299
What can cause exudative ascites?
Increased vascular permeability secondary to infection; inflammation (peritonitis) or malignancy.
300
What can cause transudative ascites?
Increased venous pressure due to cirrhosis, cardiac failure or hypoalbuminaemia.
301
Give 2 signs of ascites.
1. Flank swelling.
| 2. Dull to percuss and shifting dullness.
302
What investigations might you do in someone who you suspect has ascites?
1. Ultrasound.
| 2. Ascitic tap.
303
Describe the treatment for ascites.
1. Restrict sodium.
2. Diuretics.
3. Drainage.
304
Where in the colon do the majority of colon cancers occur?
In the descending/sigmoid colon and rectum.
305
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.
306
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.
307
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.
308
What would be raised in the blood tests taken from someone with primary biliary cirrhosis?
1. Raised IgM.
2. Raised ALP.
3. Positive AMA.
309
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.
310
What 3 symptoms make up the triad of Wernicke's encephalopathy?
1. Ataxia.
2. Opthalmoplegia.
3. Confusion.
311
How can Wernicke's encephalopathy be reversed?
Give IV thiamine.
312
What histological stain can be used for haemochromatosis?
Perl's stain.
313
Name 4 fat soluble vitamins.
A, D, E and K.
314
What is the main difference between biliary colic and acute cholecystitis?
Acute cholecystitis has an inflammatory component!
315
What is the treatment for acute cholecystitis?
Laparoscopic cholecystectomy.
316
Why might someone with primary biliary cirrhosis experience itching as a symptom?
Because there is a build up of bilirubin.
317
Give 3 components of gallstones.
1. Cholesterol.
2. Bile pigment.
3. Phospholipid.
318
What investigations might you do in someone who you suspect has gallstones?
Ultrasound!
| ERCP.
319
Are most liver cancers primary or secondary?
Secondary - they have metastasised to the liver from the GI tract, breast and bronchus.
320
Where have most secondary liver cancers arisen from?
1. The Gi tract.
2. Breast.
3. Bronchus.
321
Describe the aetiology of HCC.
Most HCC is in patients with cirrhosis. This is often due to HBV/HCV and alcohol.
322
Give 5 symptoms of HCC.
1. Weight loss.
2. Anorexia.
3. Fever.
4. Malaise.
5. Ascites.
323
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.
324
Describe the treatment for HCC.
1. Surgical resection of solitary tumours.
2. Liver transplant.
3. Percutaneous ablation.
325
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.
326
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.
327
Give 3 symptoms of haemochromatosis.
1. Hepatomegaly.
2. Cardiomegaly.
3. Diabetes mellitus.
4. Hyperpigmentation of skin.
5. Lethargy.
328
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.
329
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.
330
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.
331
Give 4 complications of liver failure.
1. Hepatic encephalopathy.
2. Abnormal bleeding.
3. Jaundice.
4. Ascites.
332
Describe the treatment for liver failure.
1. Nutrition.
2. Supplements.
3. Treat complications.
4. Liver transplant.
333
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.
334
Describe the treatment for spontaneous bacterial peritonitis.
Cefotaxime and metronidazole.
335
Give 5 symptoms of ruptured varices.
1. Haematemesis.
2. Melaena.
3. Abdominal pain.
4. Dysphagia.
5. Anaemia.
336
How would you know if an individual had been vaccinated against hepatitis B?
They would have anti-HBVs IgG in their serum.
337
What type of anaemia do you associate with alcoholic liver disease?
Macrocytic anaemia.
338
Name a protozoa that can cause amoebic liver abscess?
Entemoeba histolytica.
339
What are the symptoms of entemoeba histolytica?
- RUQ pain.
- Bloody diarrhoea.
- Fever and malaise.
Often the patient has a history of foreign/rural travel.
340
What is the treatment for entemoeba histolytica?
Metronidazole.
341
What is the treatment for mild/moderate UC?
Mesalazine.
342
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.
343
What drug would you give to someone that has overdosed on paracetamol?
IV N-Acetyl-Cysteine.
344
With which disease would you associate Reynold's pentad?
Ascending cholangitis.
345
Describe Reynold's pentad.
- Charcot's triad (fever, RUQ pain and jaundice).
- + hypotension.
- + altered mental state.
346
What is a potential consequence of h.pylori infection in a person with decreased gastric acid?
Gastric cancer.
347
What is a potential consequence of h.pylori infection in a person with increased gastric acid?
Duodenal ulcer.
348
What might pain radiating to the back be a sign of?
Pancreatitis or AAA.
349
What blood test might show that someone has alcoholic liver disease?
Serum GGT (gamma-glutamyl transferase) will be elevated.
350
What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?
Mallory bodies.
351
What feature seen on liver biopsy is diagnostic of cirrhosis?
Nodular regeneration.
352
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.
353
What is the treatment for Wilson's disease.
Lifetime treatment with penicillamine.
354
Name the 2 main pathophysiological factors that contribute to the formation of ascites.
1. High portal venous pressure.
| 2. Low serum albumin.
355
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.
356
Why is morphine contraindicated in acute pancreatitis?
Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis.
357
What two enzymes, if raised, suggest pancreatitis?
LDH and AST.
358
Where is folate absorbed?
In the jejunum.
359
Where is vitamin B12 absorbed?
In the terminal ileum.
360
Where is iron absorbed?
In the duodenum.
361
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.
362
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.
363
What lymph nodes can oesophageal carcinoma commonly metastasise to?
Para-oesophageal lymph nodes.
364
What hormone is responsible for the production of gastric acid?
Gastrin.
365
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.
366
A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.
Hypoalbuminaemia.
367
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.
368
List two blood tests a GP might perform to help differentiate between the different causes of diarrhoea.
1. FBC.
| 2. ESR/CRP.
369
List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.
1. Stool culture.
| 2. Faecal calprotectin.
370
State one histological feature that will be seen in ulcerative colitis.
1. Crypt abscess.
| 2. Increase in plasma cells in the lamina propria.
371
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.
372
Name 3 drugs or classes of drugs that can cause acute pancreatitis.
1. NSAIDs.
2. Diuretics.
3. Steroids.
373
What 2 products does haem break down in to?
Haem -> Fe2+ and biliverdin.
374
What enzyme converts biliverdin to unconjugated bilirubin?
Biliverdin reductase.
375
What is the function of glucuronosyltransferase?
It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.
376
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.
377
What does conjugated bilirubin form?
Urobilinogen.
378
What is responsible for the conversion of conjugated bilirubin into urobilinogen?
Intestinal bacteria.
379
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.
380
What disease could be caused by a non-functioning mutation in NOD2?
Crohn's.
