1
Q
Causes of Acute liver failure(4)
A
- paracetamol overdose
- alcohol
- viral hepatitis (usually A or B)
- acute fatty liver of pregnancy
2
Q
the ratio ofAST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of
A
Acute alcoholic hepatitis
3
Q
liver function tests’ do not always accurately reflect the synthetic function of the liver. This is best assessed by looking at
A
- the prothrombin time
- albumin level.
4
Q
Treatment of Pseudocysts
A
Treatment is either with
- endoscopic or
- surgical cystogastrostomy or
- aspiration
5
Q
Treatment of Pancreatic abscess
A
- Transgastric drainage is one method of treatment,
- endoscopic drainage is an alternative
6
Q
Drugs causing Acute pancreatitis (8)
A
- azathioprine
- mesalazine
- steroids
- furosemide
- bendroflumethiazide
- pentamidine
- didanosine
- sodium valproate
*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
7
Q
7 factors indicating severe pancreatitis include:
A
- age > 55 years
- hypocalcaemia
- hyperglycaemia
- hypoxia
- neutrophilia
- elevated LDH and AST
8
Q
Which test may be used to assess exocrine function of pancreas if imaging inconclusive
A
faecal elastase
9
Q
Treatment of chronic pancreatitis
A
- pancreatic enzyme supplements
- analgesia
- antioxidants: limited evidence base - one study suggests benefit in early disease
10
Q
Treatment of Alcoholic ketoacidosis
A
The most appropriate treatment is aninfusion of saline & thiamine.
Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.
11
Q
management notes for alcoholic hepatitis:
A
- glucocorticoids( prednisolone) are often used during acute episodes of alcoholic hepatitis
- pentoxyphylline is also sometimes used
Maddrey’s discriminant function (DF)is often used during acute episodes to determine who would benefit from glucocorticoid therapy
12
Q
Maddrey’s discriminant function (DF)is often used during acute episodes to determine who would benefit from
A
glucocorticoid therapy in alcoholic hepatitis
13
Q
SAAG <11g/L
A
- Hypoalbuminaemia
- nephrotic syndrome
- severe malnutrition (e.g. Kwashiorkor)
- Malignancy
- peritoneal carcinomatosis
- Infections
- tuberculous peritonitis
- Other causes
- pancreatitis
- bowel obstruction
- biliary ascites
- postoperative lymphatic leak
- serositis in connective tissue diseases
14
Q
SAAG > 11g/L
(indicates portal hypertension)
A
- Liver disorders are the most common cause
- cirrhosis/alcoholic liver disease
- acute liver failure
- liver metastases
- Cardiac
1. right heart failure
2. constrictive pericarditis - Other causes
1. Budd-Chiari syndrome
2. portal vein thrombosis
3. veno-occlusive disease
4. myxoedema
15
Q
Management of ascites
A
- reducing dietary sodium
- fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
- Aldactone & lasix
- drainage if tense ascites
- TIPS
- prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. ‘ oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved
16
Q
hepatic encephalopathy on EEG
A
triphasic slow waves on EEG
17
Q
8 Precipitating factors Of Hepatic encephalopathy
A
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
18
Q
Diagnosis of SBP
A
paracentesis:neutrophil count > 250 cells/ul
19
Q
the most common organism found on ascitic fluid culture is
A
E. coli
20
Q
Management of SBP
A
Iv cefotaxime
21
Q
a marker of poor prognosis in SBP
A
Alcoholic liver disease
22
Q
Antibiotic prophylaxis should be given to patients with ascites if:
A
- patients who have had an episode of SBP
- patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
23
Q
TIPSS connects …….to ……
A
connects the hepatic vein to the portal vein
24
Q
Screening for hepatocellular cancer
A
liver ultrasound every 6 months (+/- alpha-feto protein)
25
screening for cirrhosis NICE made a specific recommendation, suggesting to offer transient elastography
1. people with HCV infection
2. people diagnosed with alcohol liver disease
3. men who drink alcohol over 50 units per week
4. women who drink alcohol over 35 units per week
26
pathophysiology of HRS
vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance.
This results in 'underfilling' of the kidneys.
27
Type 1 HRS
- Rapidly progressive Doubling of serum creatinine to > 221 µmol/L or a having of the creatinine clearance to < 20 ml/min over a period of less than 2 weeks
- Very poor prognosis
28
Autoimmune hepatitis associated with
hypergammaglobulinaemia and
HLA B8, DR3
29
Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present
Tpye 1 : "Affects both adults and children"
- ANA
- ASMA
Type 2: " Affects children only"
- LKM1
Type 3: " Affects adults in middle-age"
- Soluble liver-kidney antigen
30
Management of autoimmune hepatitis
steroids, other immunosuppressants e.g. azathioprine
liver transplantation
31
Haemochromatosis is an autosomal ...... disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome ......
1. autosomal recessive
2. chromosome 6
32
Reversible complications of haemochromatosis
1. Cardiomyopathy
2. Skin pigmentation
33
Typical iron study profile in patient with haemochromatosis
1. transferrin saturation > 55% in men or > 50% in women
2. raised ferritin (e.g. > 500 ug/l) and iron
3. low TIBC
34
Screening for iron overload
1. transferrin saturation
2. genetic testing for HFE mutation
35
Liver biopsy in haemochromatosis indicated if
only used if suspected hepatic cirrhosis
36
Management of haemochromatosis
1. venesection is the first-line treatment
- monitoring adequacy of venesection: transferrin saturation should be kept < 50% and the serum ferritin concentration < 50 ug/l
2. desferrioxamine may be used second-line
37
Wilson's disease is ............. disorder
an autosomal recessive
38
Wilson's disease is caused by a defect in the ........... gene located on chromosome ........
in the ATP7B gene located on chromosome 13.
39
Investigations of Wilson disease
1. slit lamp examination for Kayser-Fleischer rings
2. reduced serum caeruloplasmin
3. reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
- free (non-ceruloplasmin-bound) serum copper is increased
4. increased 24hr urinary copper excretion
5. the diagnosis is confirmed by genetic analysis of the ATP7B gene
40
Management of Wilson's disease
1. penicillamine (chelates copper) has been the traditional first-line treatment
2. trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
3. tetrathiomolybdate is a newer agent that is currently under investigation
41
4 Risks of ERCP
1. Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
2. Duodenal perforation 0.4%
3. Cholangitis 1.1%
4. Pancreatitis 1.5%
42
Management of Acute cholecystitis
Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation)
43
Management of Gallbladder abscess
Imaging with USS +/- CT Scanning
Ideally, surgery although subtotal cholecystectomy may be needed if Calot's triangle is hostile
In unfit patients, percutaneous drainage may be considered
44
Management of Cholangitis (4)
1. Fluid resuscitation
2. Broad-spectrum intravenous antibiotics
3. Correct any coagulopathy
4. Early ERCP
45
Management of Gallstone ileus
Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.
46
Management of Acalculous cholecystitis
If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy
47
Causes of hepatosplenomegaly
1. chronic liver disease* with portal hypertension
2. infections: glandular fever, malaria, hepatitis
3. lymphoproliferative disorders
4. myeloproliferative disorders e.g. CML
5. amyloidosis
48
Contraindications to percutaneous liver biopsy
1. INR > 1.4
2. low platelets (e.g. < 60 * 109/l)
3. anaemia
4. extrahepatic biliary obstruction
5. hydatid cyst
6. haemoangioma
7. uncooperative patient
8. ascites
49
The most common organisms found in pyogenic liver abscesses are ............. in children and ....... in adults.
Staphylococcus aureus in children
Escherichia coli in adults.
50
Management of pyogenic liver abscesses
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
51
Budd Chiari syndrome
classically a triad of:
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly
52
studies is very sensitive and should be the initial radiological investigation in Budd-Chiari syndrome
ultrasound with Doppler flow
53
In liver failure all clotting factors are .... 1....., except .....2. Because....3..
1. Low
2. factor VIII which is paradoxically supra-normal.
3. because factor VIII is synthesised in endothelial cells throughout the body, unlike the other clotting factors which are synthesised purely in hepatic endothelial cells.
54
Pathogenesis of Primary biliary cholangitis
Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis
55
Primary biliary cholangitis
Association with
Sjogren's syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease
56
Diagnosis of Primary biliary cholangitis
anti-mitochondrial antibodies
smooth muscle antibodies in 30% of patients
raised serum IgM
57
In Primary biliary cholangitis
required before diagnosis to exclude an extrahepatic biliary obstruction by
Ultrasound or MRCP
58
Management of PBC
1. first-line: ursodeoxycholic acid
slows disease progression and improves symptoms
2. pruritus: cholestyramine
3. fat-soluble vitamin supplementation
4. liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem
59
Complications of PBC
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
60
Primary sclerosing cholangitis is characterised by ...?
inflammation and fibrosis of intra and extra-hepatic bile ducts.
61
Primary sclerosing cholangitis
Association with
1. ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
2. Crohn's (much less common association than UC)
3. HIV
62
Primary sclerosing cholangitis
Investigations
- raised bilirubin + ALP
- ERCP or MRCP are the standard diagnostic investigations, showing multiple biliary strictures giving a 'beaded' appearance.
- P-ANCA
- there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as 'onion skin'
-
63
Complications of Primary sclerosing cholangitis
- cholangiocarcinoma (in 10%)
- increased risk of colorectal cancer
64
Ascending cholangitis
1. Which is the most common organism?
2. What is the most common predisposing factor ?
1. E.coli
2. Gallstones
65
Charcot's triad
1. right upper quadrant (RUQ) pain,
2. fever
3. jaundice
66
Investigations of Ascending cholangitis
ultrasound is generally used first-line in suspected cases to look for bile duct dilation and bile duct stones
67
Management of Ascending cholangitis
1. Iv antibiotics
2. ERCP after 24-48 hours to relieve any obstruction
68
Hydatid cysts are caused by
caused by the tapeworm parasite Echinococcus granulosus.
These cysts are allergens which precipitate a type 1 hypersensitivity reaction
69
Investigations of Hydatid cysts
imaging
1. ultrasound if often used first-line
2. CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts
serology
1. useful for primary diagnosis and for follow-up after treatment
2. wide variety of different antibody/antigen tests available
70
Treatment of Hydatid cysts
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and the contents sterilised first).
71
8 Associations of Pancreatic cancer
increasing age
smoking
diabetes
chronic pancreatitis (alcohol does not appear an independent risk factor though)
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation
72
Investigations of Pancreatic cancer
- ultrasound has a sensitivity of around 60-90%
- high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
- imaging may demonstrate the 'double duct' sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
73
Management of Pancreatic cancer
- less than 20% are suitable for surgery at diagnosis
- a Whipple's resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple's include dumping syndrome and peptic ulcer disease
- adjuvant chemotherapy is usually given following surgery
- ERCP with stenting is often used for palliation
74
drugs tend to cause a hepatocellular picture (10)
1. paracetamol
2. sodium valproate, phenytoin
3. MAOIs
4. halothane
5. anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
6. statins
7. alcohol
8. amiodarone
9. methyldopa
10. nitrofurantoin
75
drugs tend to cause cholestasis (+/- hepatitis):(7)
1. combined oral contraceptive pill
2. antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
3. anabolic steroids, testosterones
4. phenothiazines: chlorpromazine, prochlorperazine
5. sulphonylureas
6. fibrates
7. rare reported causes: nifedipine
76
Drugs causing Liver cirrhosis (3)
1. methotrexate
2. methyldopa
3. amiodarone
77
Inherited causes of jaundice
Unconjugated hyperbilirubinaemia
1. Gilbert's syndrome
2. Crigler-Najjar syndrome
78
Inherited causes of jaundice
conjugated hyperbilirubinaemia
1. Dubin-Johnson syndrome
2. Rotor syndrome
79
Gilbert's syndrome ?
1. autosomal recessive
2. mild deficiency of UDP-glucuronyl transferase
3. benign
80
Crigler-Najjar syndrome?
- type 1
- type 2
Crigler-Najjar syndrome, type 1
- autosomal recessive
- absolute deficiency of UDP-glucuronosyl transferase
- do not survive to adulthood
Crigler-Najjar syndrome, type 2
- slightly more common than type 1 and less severe
- may improve with phenobarbital
81
Dubin-Johnson syndrome
1. autosomal recessive disorder resulting in hyperbilirubinaemia (conjugated, therefore present in urine). Relatively common in Iranian Jews
2. mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin
3. results in a grossly black liver
4. benign
82
Rotor syndrome
1. autosomal recessive
2. defect in the hepatic uptake and storage of bilirubin
3. benign
83
Gilbert's syndrome
- Features
- Investigation
- management
Features
- unconjugated hyperbilirubinaemia (i.e. not in urine)
- jaundice may only be seen during an intercurrent illness, exercise or fasting
- rise in bilirubin following prolonged fasting or IV nicotinic acid
- no treatment required
84
The most common cause of biliary disease in patients with HIV is ....?
sclerosing cholangitis due to infections such as CMV, Cryptosporidium and Microsporidia
85
Cause of Pancreatitis in patients with HIV ....?
may be secondary to anti-retroviral treatment (especially didanosine) or
by opportunistic infections e.g. CMV
86
the main risk factor for cholangiocarcinoma
Primary sclerosing cholangitis
87
Features of Cholangiocarcinoma
1. persistent biliary colic symptoms
2. associated with anorexia, jaundice and weight loss
3. a palpable mass in the right upper quadrant (Courvoisier sign)
4. periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
5. raised CA 19-9 levels
- often used for detecting cholangiocarcinoma in patients with primary sclerosing cholangitis
88
HELLP syndrome
Haemolysis, Elevated Liver enzymes, Low Platelets
89
Acute fatty liver of pregnancy is rare complication which may occur in the ....... trimester or ......
1. Third
2. the period immediately following delivery.
90
Features of Acute fatty liver of pregnancy
abdominal pain
nausea & vomiting
headache
jaundice
hypoglycaemia
severe disease may result in pre-eclampsia
ALT is typically elevated e.g. 500 u/l
91
Management of Acute fatty liver of pregnancy
support care
once stabilised delivery is the definitive management
92
What is the most common liver disease of pregnancy.
Intrahepatic cholestasis of pregnancy (also known as obstetric cholestasis)
93
Features of Intrahepatic cholestasis of pregnancy
pruritus, often in the palms and soles
no rash (although skin changes may be seen due to scratching)
raised bilirubin
94
Management of Intrahepatic cholestasis of pregnancy
1. ursodeoxycholic acid is used for symptomatic relief
2. weekly liver function tests
3. women are typically induced at 37 weeks
95
What is the most common cause of HCC worldwide ?
Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe.
96
The main risk factor for developing HCC
1. liver cirrhosis, for example secondary* to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis.
2. alpha-1 antitrypsin deficiency
3. hereditary tyrosinosis
4. glycogen storage disease
5. aflatoxin
6. drugs: oral contraceptive pill, anabolic steroids
7. porphyria cutanea tarda
8. male sex
9. DM , metabolic syndrome
97
Screening of HCC with ....
ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol
98
Management of HCC
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
99
HBV vs breastfeeding
hepatitis B cannot be transmitted via breastfeeding (in contrast to HIV)
100
Achalasia due to degenerative loss of
ganglia from Auerbach's plexus
101
Treatment of achalasia
- pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients should be a low surgical risk as surgery may be required if complications occur
- surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
- intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
- drug therapy (e.g. nitrates, CCB ) has a role but is limited by side-effects
102
Glasgow-Blatchford score helps clinicians decide ......
whether patient patients can be managed as outpatients or not
103
the Rockall score is used after endoscopy provides a percentage .....?
Risk of rebleeding and mortality
104
Barrett's can be subdivided into ......?
Short if < 3 cm
Long if > 3 cm
105
Risk factors of Barrett's oesophagus
1. GERD
2. MALE
3. SMOKING
4. CENTRAL OBESITY
106
Management of Barrett's oesophagus
- high-dose proton pump inhibitor
- if dysplasia of any grade is identified endoscopic intervention is offered. Options include:
- radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
- endoscopic mucosal resection
107
Barrett's oesophagus
endoscopic surveillance with biopsies
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
108
Risk factors of gastric cancer
1. Helicobacer pylori
- triggers inflammation of the mucosa → atrophy and intestinal metaplasia
2. atrophic gastritis
3. diet
- salt and salt-preserved foods
- nitrates
4. smoking
5. blood group A
109
Management of Gastric cancer
1. surgical options depend on the extent and side but include:
- endoscopic mucosal resection
- partial gastrectomy
- total gastrectomy
2. chemotherapy
110
Gastric MALT lymphoma associated with
H. pylori infection in 95% of cases
good prognosis
111
Indications for upper GI endoscopy in GERD
1. age > 55 years
2. symptoms > 4 weeks or persistent symptoms despite treatment
3. dysphagia
4. relapsing symptoms
5. weight loss
112
In patients with GERD If endoscopy is negative consider .......
24-hr oesophageal pH monitoring (the gold standard test for diagnosis)
113
Drugs causing dyspepsia
NSAIDs
bisphosphonates
steroids
The following drugs may cause reflux
calcium channel blockers*
nitrates*
theophyllines
114
In Eosinophilic oesophagitis , oesophageal biopsy will show
show dense infiltrate of eosinophils in the epithelium
115
Risk factors for developing eosinophilic oesophagitis
1. Allergies/ asthma: suffering from food/ environmental allergies or atopic dermatitis and asthma increases the risk of diagnosis
2. Male sex
3. Family history of eosinophilic oesophagitis or allergies
4. Caucasian race
5. Age between 30-50
6. Coexisting autoimmune disease e.g. coeliac disease
116
eosinophilic oesophagitis
Investigations
Endoscopy: diagnosis can only be made on the histological analysis of an oesophageal biopsy.
Histologically, the diagnosis is made more likely in the presence of epithelial desquamation, eosinophilic microabscesses, and abnormally long papillae
PPI trial: persistence of eosinophilia and no improvement of symptoms after trialling a proton pump inhibitor. This can help the clinician differentiate between eosinophilic oesophagitis and GORD, which can be a tricky task
117
Management of
Dietary modification:
Topical steroids e.g. fluticasone and budesonide are options when dietary modification fails. This requires the patient to swallow
solutions of the steroid to line the oesophagus. This should be done for eight weeks before being reassessed
Oesophageal dilatation: 56% of patients require this at some point in their treatment to reduce the symptoms associated with oesophageal strictures
118
Zollinger-Ellison syndrome are found in which parts of GIT
are found in the first part of the duodenum, with the second most common location being the pancreas.
119
Diagnosis of Zollinger-Ellison syndrome
1. fasting gastrin levels: the single best screen test
2. secretin stimulation test
120
Treatment of Pernicious anaemia
vitamin B12 replacement
no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
more frequent doses are given for patients with neurological features
121
Helicobacter pylori has 2 main mechanisms to survice in the acidic gastric environment:
1. chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
2. secretes urease → urea converted to NH3 → alkalinization of acidic environment → increased bacterial survival
122
pathogenesis mechanism, Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) lead to
disruption of gastric mucosa
123
Urea breath test should not be performed
within ....... of treatment with an antibacterial or
within ........... of PPI
within 4 weeks of treatment with an antibacterial or within 2 weeks of PPI
124
Pyloric stenosis is caused by
It is caused by hypertrophy of the circular muscles of the pylorus.
125
1. projectile' vomiting, typically 30 minutes after a feed
2. constipation and dehydration may also be present
3. a palpable mass may be present in the upper abdomen
4. hypochloraemic, hypokalaemic alkalosis due to persistent vomiting
Features of what?
Pyloric stenosis
126
Pyloric stenosis
Diagnosis is most commonly made by .............
Diagnosis is most commonly made by ultrasound.
127
Management of Pyloric stenosis
Management is with Ramstedt pyloromyotomy.
128
Boerhaave syndrome?
Severe vomiting → oesophageal rupture
129
Adverse effects of Metoclopramide
extrapyramidal effects
acute dystonia e.g. oculogyric crisis
this is particularly a problem in children and young adults
diarrhoea
hyperprolactinaemia
tardive dyskinesia
parkinsonism
130
In Oesophageal cancer
Location of Adenocarcinoma in ....1....
Location of Squamous cell cancer ....2....
1. Lower third - near the gastroesophageal junction
2. Upper two-thirds of the oesophagus
131
Risk factors of Oesophageal Adenocarcinoma
GORD
Barrett's oesophagus
smoking
obesity
132
Risk factors of Oesophageal Squamous cell cancer
smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines
133
Diagnosis of oesophageal cancer
Upper GI endoscopy with biopsy is used for diagnosis
Endoscopic ultrasound is the preferred method for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging
FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.
Laparoscopy is sometimes performed to detect occult peritoneal disease
134
Treatment of oesophageal cancer
Operable disease (T1N0M0) is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy
The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
In addition to surgical resection many patients will be treated with adjuvant chemotherapy
135
The amount of energy that may be derived from 1 gram of food is as follows:
carbohydrates:
protein:
fat:
carbohydrates: 4 kcal
protein: 4 kcal
fat: 9 kcal
136
Patients identified as being malnourished if
1. BMI < 18.5
2. unintentional weight loss of > 10% over 3-6/12
3. BMI < 20 and unintentional weight loss of > 5% over 3-6/12
137
AT RISK of malnutrition
1. Eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
2. Poor absorptive capacity
3. High nutrient losses
4. High metabolism
138
complications of enteral feeding
1. Diarrhoea
2. Aspiration
3. Hyperglycaemia
4. Refeeding syndrome
139
The following brush border enzymes are involved in the breakdown of carbohydrates:
maltase: cleaves disaccharide maltose to ........
sucrase: cleaves sucrose to .......
lactase: cleaves disaccharide lactose to .........
maltase: cleaves disaccharide maltose to glucose + glucose
sucrase: cleaves sucrose to fructose and glucose
lactase: cleaves disaccharide lactose to glucose + galactose
140
In Refeeding syndrome
The metabolic consequences include:
1. hypophosphataemia
this is the hallmark symptom of refeeding syndrome
may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)
2. hypokalaemia
3. hypomagnesaemia: may predispose to torsades de pointes
4. abnormal fluid balance
141
Patients are considered high-risk of Refeeding syndrome if one or more of the following:
1. BMI < 16 kg/m2
2. unintentional weight loss >15% over 3-6 months
3. little nutritional intake > 10 days
4. hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
142
Patients are considered high-risk of Refeeding syndrome if two or more of the following:
1. BMI < 18.5 kg/m2
2. unintentional weight loss > 10% over 3-6 months
3. little nutritional intake > 5 days
4. history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids
143
if a patient hasn't eaten for > 5 days, aim to re-feed at .......
no more than 50% of requirements for the first 2 days.
144
Source of Gastrin
G cells in antrum of the stomach
145
Actions of Gastrin
1. Increases acid secretion by gastric parietal cells, pepsinogen and IF secretion,
2. increases gastric motility,
3. stimulates parietal cell maturation
146
Source of CCK
I cells in upper small intestine
147
Actions of CCK
1. Increases secretion of enzyme-rich fluid from pancreas,
2. contraction of gallbladder and relaxation of sphincter of Oddi,
3. decreases gastric emptying, trophic effect on pancreatic acinar cells, induces satiety
148
Source of Secretin
S cells in upper small intestine
149
Actions of secreting
1. Increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells,
2. decreases gastric acid secretion, trophic effect on pancreatic acinar cells
150
Source of VIP
1. Small intestine,
2. pancreas
151
Actions of VIP
1. Stimulates secretion by pancreas and intestines,
2. inhibits acid secretion
152
Source of Somatostatin
D cells in the pancreas & stomach
153
Actions of Somatostatin
1. Decreases acid and pepsin secretion,
2. decreases gastrin secretion,
3. decreases pancreatic enzyme secretion,
4. decreases insulin and glucagon secretion
5. inhibits trophic effects of gastrin,
6. stimulates gastric mucous production
154
Diagnosis of Angiodysplasia by
1. colonoscopy
2. mesenteric angiography if acutely bleeding
155
Management of Angiodysplasia
endoscopic cautery or argon plasma coagulation
antifibrinolytics e.g. Tranexamic acid
oestrogens may also be used
156
Conditions associated with coeliac disease include
1. dermatitis herpetiformis (a vesicular, pruritic skin eruption)
2. autoimmune disorders (T1DM and autoimmune hepatitis)
157
Which condition is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
Coeliac disease
158
Complications of Coeliac disease
anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies
159
If suspected Codliac disease in patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at .......... prior to testing.
At least 6 weeks
160
Serology of coeliac disease
1. TTG antibodies (IgA) are first-choice according to NICE
2. endomyseal antibody (IgA)
- needed to look for selective IgA deficiency, which would give a false negative coeliac result
3. anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
4. anti-casein antibodies are also found in some patients
161
What is the 'gold standard' for diagnosis - this should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis ?
Endoscopic intestinal biopsy
162
findings supportive of coeliac disease in biopsy
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
163
Complications of diverticulitis include:
abscess formation
peritonitis
obstruction
perforation
164
Management of diverticulitis
mild attacks can be treated with oral antibiotics
more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given
165
In Bile-acid malabsorption the ,test of choice is
SeHCAT
166
Severity of C.diff
Mild: NORMAL WBC
MODERATE: WBC < 15
Severe: WBC > 15 or rise in Creatinine > 50 % above baseline or T > 38.5 or evidence of severe colitis ( abdominal or radiological signs)
Life-threatening : Hypotension, partial or complete ileus toxic megacolon
Or CT evidence of severe disease
167
Treatment of First episode of C. difficile infection
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole
168
Treatment of Recurrent episode c.diff
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
169
Treatment of Life-threatening C. difficile infection
oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered
170
Preventing the spread of C. difficile infection
isolation in side room: the patient should remain isolated until there has been no diarrhoea
171
cause of jejunal villous atrophy
coeliac disease
tropical sprue
hypogammaglobulinaemia
gastrointestinal lymphoma
Whipple's disease
cow's milk intolerance
172
In Melanosis coli, Histology demonstrates ........
pigment-laden macrophages.
173
Melanosis coli is associated with
laxative abuse, especially anthraquinone compounds such as senna
174
In IBS, First-line pharmacological treatment - according to predominant symptom
pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line
175
Diagnosis of Small bowel bacterial overgrowth syndrome by
Hydrogen breath test
176
Treatment of Small bowel bacterial overgrowth syndrome
1. correction of the underlying disorder
2. antibiotic therapy:
rifaximin is now the treatment of choice due to relatively low resistance. Co-amoxiclav or metronidazole are also effective in the majority of patients.
177
Peutz-Jeghers syndrome is an autosomal ....... condition
dominant
178
Peutz-Jeghers syndrome is also associated
associated with numerous hamartomatous polyps in the gastrointestinal tract, pigmented freckles on the lips, face, palms and soles.
179
In Peutz-Jeghers syndrome, responsible gene encodes .......
serine threonine kinase LKB1 or STK11
180
Management of Peutz-Jeghers syndrome
conservative unless complications develop
181
Whipple's disease is a rare multi-system disorder caused by........
Tropheryma whippelii infection.
182
Whipple's disease is more common in those who are .........
HLA-B27 positive and in middle-aged men.
183
Whipple's disease, jejunal biopsy shows .....
jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules
184
Management of Whipple's disease
oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin
185
Intestinal causes of malabsorption
coeliac disease
Crohn's disease
tropical sprue
Whipple's disease
Giardiasis
brush border enzyme deficiencies (e.g. lactase insufficiency)
186
Pancreatic causes of malabsorption
chronic pancreatitis
cystic fibrosis
pancreatic cancer
187
Biliary causes of malabsorption
biliary obstruction
primary biliary cirrhosis
188
Deep ulcers, skip lesions - 'cobble-stone' appearance
Seen in ?
Crohn's disease
189
appearance of pseudopolyps seen in
Ulcerative colitis
190
Hirschsprung's disease is associated with
Down's syndrome
191
Investigations of carcinoid syndrome
urinary 5-HIAA
plasma chromogranin A y
192
Management of carcinoid syndrome
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help
193
Risk factors of anal cancer
1. human papillomavirus (HPV)
2. Anal intercourse
3. Smoking
4. Those with HIV and those taking immunosuppressive medication
5. Immunosuppressive drugs used in transplant recipients
6. Women with a history of cervical cancer or cervical intraepithelial neoplasia
194
familial adenomatous polyposis, It is due to a mutation in a tumour suppressor gene called .................
adenomatous polyposis coli gene (APC), located on chromosome 5.
195
hereditary non-polyposis colorectal carcinoma (Lynch syndrome),
The most common genes involved are:
MSH2 (60% of cases)
MLH1 (30%)
196
Colorectal cancer: screening
With
Faecal Immunochemical Test (FIT) screening to older adults
patients with abnormal results are offered a colonoscopy
197
Crohn's disease commonly affects ........
the terminal ileum and colon
198
Crohn's disease: management
Inducing remission
1. glucocorticoids (oral, topical or intravenous) are generally used to induce remission
2. 5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
3. azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy. Methotrexate is an alternative to azathioprine
4. infliximab is useful in refractory disease and fistulating Crohn's. Patients typically continue on azathioprine or methotrexate
5. metronidazole is often used for isolated peri-anal disease
199
Maintaining remission, Crohn's disease
1.lmazathioprine or mercaptopurine is used first-line to maintain remission
2. methotrexate is used second-line
200
TPMT activity should be assessed before offering methotrexate, azathioprine or mercaptopurine therapy in
* thiopurine methyltransferase (TPMT) activity
Crohn's disease
201
patients with symptomatic perianal fistulae are usually given oral
metronidazole
202
the investigation of choice for suspected perianal fistulae
MRI
203
Factors may trigger an ulcerative colitis flare
1. stress
2. medications (NSAIDs & antibiotics)
3. cessation of smoking
204
Mild ulcerative colitis
4 < stools daily with or without blood
205
Moderate ulcerative colitis
4- 6 stools daily with minimal systemic disturbance
206
Severe ulcerative colitis
1. > 6 stools a day, containing blood
2. Evidence of systemic disturbance, e.g.
fever
tachycardia
abdominal tenderness, distension or reduced bowel sounds
anaemia
hypoalbuminaemia
207
In ulcerative colitis, Factors increasing risk of cancer
disease duration > 10 years
patients with pancolitis
onset before 15 years old
unremitting disease
poor compliance to treatment
208
Colonoscopy surveillance in inflammatory bowel disease patients should be decided following risk stratification.
By follow up colonoscopy
1. Low risk: 5 years
2. Intermediate risk: 3 years
3. High risk: 1 year
209
Adverse effects of Cholestyramine
constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides
210
Treatment of diarrhea following bowel resection in crohn's disease
Cholestyramine
211
Treating mild-to-moderate ulcerative colitis
proctitis
1. topical (rectal) aminosalicylate
If no improvement after 4 weeks then
2. Oral aminosalicylate
If no improvement then
3. Oral or topical steroids
212
Treating mild-to-moderate ulcerative colitis
proctosigmoiditis and left-sided ulcerative colitis
1. topical (rectal) aminosalicylate
If no improvement after 4 weeks then
2. high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
If no improvement after 4 weeks then
3. oral aminosalicylate and an oral corticosteroid
213
Treating mild-to-moderate ulcerative colitis
extensive disease
1. topical and a high-dose oral aminosalicylate
if remission is not achieved within 4 weeks
2. stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid
214
Treatment of Severe ulcerative colitis
1. Iv steroids are usually given first-line
* iv ciclosporin may be used if steroid are contraindicated
2. if after 72 hours there has been no improvement, consider adding iv ciclosporin to iv corticosteroids or consider surgery
215
Maintaining remission
Following a mild-to-moderate ulcerative colitis flare
proctitis and proctosigmoiditis
1. Topical aminosalicylate
Or
2. Topical and oral aminosalicylate
Or
3. Oral aminosalicylate
216
Maintaining remission
Following a mild-to-moderate ulcerative colitis flare
Following a severe relapse or >=2 exacerbations in the past year
oral azathioprine or oral mercaptopurine
217
Associated factors of NAFLD
1. Obesity
2. T2DM
3. hyperlipidaemia
4. jejunoileal bypass
5. sudden weight loss/starvation
218
In patients with non-alcoholic fatty liver disease, ........ testing is recommended to aid diagnosis of liver fibrosis
enhanced liver fibrosis (ELF) testing
219
Side effects of Sulphasalazine
1.rashes,
2. oligospermia
3. headache
4. Heinz body anaemia, megaloblastic anaemia
5. lung fibrosis
220
Side effects of Mesalazine
1. GI upset
2. headache
3. agranulocytosis,
4. pancreatitis,
5. interstitial nephritis
221
What can stimulate the release of gastrin from G-cells?
Distension of stomach,
vagus nerves (mediated by gastrin-releasing peptide),
luminal peptides/amino acids
222
The combination of deranged LFTs combined with secondary amenorrhoea in a young female strongly suggest ......
autoimmune hepatitis
223
What is the strongest risk factor for anal cancer
HPV infection
224
non-specific lower gastrointestinal symptoms
secretory diarrhoea may occur
microcytic anaemia
hypokalaemia
Features of
Villous adenomas
225
Perianal itching in children, possibly affecting other family members →
Enterobius vermicularis (threadworms)
226
what percentage of patients with a positive faecal occult blood test have colorectal cancer
5 - 15 %
227
What percentage of patients with Peutz-Jeghers syndrome will have died from a related cancer by the age of 60 years?
50 %
228
Hepatorenal syndrome is primarily caused by ........ vasodilation
splanchnic vasodilat
229
What is the function of MSH2 gene.
DNA mismatch repair
230
biospy shows pigment laden macrophages =
laxative abuse
231
Which one of laxatives is shown to have to carcinogenic potential?
Co-danthramer
232
Non-caseating granulomas is features of ....
Crohn's disease
233
SeHCAT is the investigation of choice for .....
bile acid malabsorption
234
1. increased goblet cells in .....
2. depletion of goblet cells and mucin from gland epithelium in ......
1. CD
2. UC
235
Screening for haemochromatosis
general population: .........
family members: .........
Screening for haemochromatosis
general population: transferrin saturation > ferritin
family members: HFE genetic testing
236
familial adenomatous polyposis (FAP) is Autosomal .......
Autosomal dominant.
237
- anti-mitochondrial antibodies
- smooth muscle antibodies
- Raise serum IgM
PBC
238
Treatment of Small bowel bacterial overgrowth syndrome
rifaximin
* Tetracyclines are no longer commonly used due to widespread bacterial resistance.
MRCP Part 1
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