GASTROENTEROLOGY Flashcards
(214 cards)
1
Q
What are the features of Wernicke’s encephalopathy?
A
CAN OPEN: Confusion Ataxia Nystagmus Ophthamoplegia PEripheral Neuropathy
2
Q
What is the antibiotic management of C.diff infection?
A
- Oral vancomycin
- Oral fidaxomicin
- Oral vancomycin + IV metronidazole
Life-threatening = oral vancomycin AND IV metronidazole
Recurrent = oral fidaxomicin (<12 weeks) + oral vancomycin (>12 weeks)
3
Q
Which antibiotics are associated with c.diff infection?
A
Second & third gen cephalosporins (ceftriaxone)
Clindamycin
+ PPIs
4
Q
Which marker is used to determine the severity of c.diff infection?
A
WCC
<15 = moderate
>15 = severe
Hypotension/toxic megacolon = life-threatening
5
Q
How is C.diff infection diagnosed?
A
CDT (C.diff toxin) in the stool
6
Q
Name 5 causes of hepatitis?
A
• Alcoholic hepatitis • Non alcoholic fatty liver disease • Viral hepatitis • Autoimmune hepatitis - Drug induced hepatitis (e.g. paracetamol overdose)
7
Q
How does hepatitis present?
A
• Abdominal pain • Fatigue • Pruritis (itching) • Muscle and joint aches • Nausea and vomiting • Jaundice Fever (viral hepatitis)
8
Q
What is found on liver function tests in hepatitis?
A
^AST/ALT
^ALP (but less rise)
Bilirubin^
9
Q
What is the most common viral hepatitis worldwide?
A
A
10
Q
Which viral hepatitis’ can you receive vaccinations for?
A
A, B (notifiable diseases PHE)
11
Q
How is hepatitis A transmitted?
A
Faecal oral (contaminated warer/food)
12
Q
How does hepatitis A present?
A
Nausea Vomiting Anorexia Jaundice Cholestasis - pale stools, dark urine
13
Q
What is the management of hepatitis A?
A
Analgesia
Resolves without treatment 1-3 months
Notify PHE
14
Q
What causes hepatitis B?
A
DNA virus
15
Q
How is hepatitis B transmitted?
A
Sex
IVDU
Tattoos
Vertical transmission
16
Q
How long is recovery from hepatitis B?
A
2-3 months
Some people are carriers for life
17
Q
What is implied by E antigen on hepatitis serology (HBeAg)?
A
High infectivity
18
Q
What is HBV DNA?
A
Direct count of viral load of hepatitis B
19
Q
How can you confirm a response to the hepatitis B vaccine?
A
HBsAg (surface antigen)
20
Q
What is the management of hepatitis B?
A
Refer to gastroenterology for specialist management Education about reducing transmission Antivirals Liver transplantation (end stage) Notify PHE
21
Q
What causes hepatitis C?
A
RNA virus
22
Q
What is the transmission of hepatitis C?
A
Blood/bodily fluids
23
Q
What is the prognosis for hepatitis C?
A
1/4 full recovery
3/4 chronic disease –> liver cirrhosis –> hepatocellular carcinoma
24
Q
How can you test for hepatitis C?
A
Hepatitis C RNA testing
25
What is the management for hepatitis C?
```
Refer to gastroenterology for specialist management
Education about reducing transmission
Direct acting antivirals (curative)
Liver transplantation (end stage)
Notify PHE
```
26
What causes hepatitis D?
RNA virus
| Can only be concomitant with hepatitis B
27
What is the management of hepatitis D?
No specific treatment
| Notify PHE
28
What causes hepatitis E?
RNA virus
29
How is hepatitis E transmitted?
Faecal oral route
30
How does hepatitis E present?
Mild illness
No treatment required
Cleared within a month
Rarely causes chronic hepatitis in immunocompromised patients
31
What are the two types of autoimmune hepatitis?
Type 1: occurs in adults
| Type 2: occurs in children
32
How does type 1 autoimmune hepatitis present?
Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.
33
How does type 2 autoimmune hepatitis present?
In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.
34
Which antibodies are found in type 1 autoimmune hepatitis?
• Anti-nuclear antibodies (ANA)
• Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)
35
Which antibodies are found in type 2 autoimmune hepatitis?
• Anti-liver kidney microsomes-1 (anti-LKM1)
| Anti-liver cytosol antigen type 1 (anti-LC1)
36
How is autoimmune hepatitis diagnosed?
Liver biopsy
37
What is the management of autoimmune hepatitis?
1. High dose steroids (prednisolone)
| 2. Introduce immunosuppressants - azathioprine
38
How do you screen for harmful alcohol use?
CAGE questionnaire
C - cut down?
A - annoyed about other people saying you should cut down
G - guilty about your drinking?
E - eye opener
OR
AUDIT questionnaire (10 questions)
39
What are the complications of harmful alcohol use?
```
• Alcoholic Liver Disease
• Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
• Alcohol Dependence and Withdrawal
• Wernicke-Korsakoff Syndrome (WKS)
• Pancreatitis
Alcoholic Cardiomyopathy
```
40
What are the features of Wernicke's encephalopathy?
1. Confusion
2. Oculomotor disturbances (disturbances of eye movements)
3. Ataxia (difficulties with coordinated movements)
41
What are the features of Korsakoff's syndrome?
```
Memory impairment (retrograde and anterograde)
Behavioural changes
```
42
What is the management of Wernicke's encephalopathy?
Pabrinex (high dose vitamin B - thiamine)
43
Name 4 causes of Wernicke's encephalopathy?
Alcohol excess
Persistent vomiting
Stomach cancer
Dietary deficiency
44
What are the symptoms of alcohol withdrawal?
6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”
45
What is the mortality of DTs?
35%
46
What is the first-line treatment of DTs?
Lorazepam PO
IV lorazepam or haloperidol
If DT develops during detox, review regimen
47
What scoring system is used to assess alcohol withdrawal?
The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.
48
What is the first-line treatment for alcohol withdrawal?
Chlordiazepoxide (librium)
49
What is the management of alcohol withdrawal?
Chlordiazepoxide
| IV high dose vitamin B (pabrinex) (followed by regular dose thiamine)
50
What is used to detox from alcohol?
Chlordiazepoxide - either fixed or variable dose depending on symptoms
Preferably done as an inpatient to manage side effects and precent DTs
51
What medications can be used to prevent relapse in alcohol addiction?
```
• Group therapy or self-help (e.g. AA)
• Naltrexone - decrease the amount and frequency of drinking (DO NOT use with opioids = may precipitate withdrawal)
• Baclofen: ↓ cravings
• Acamprosate: ↓ cravings
Disulfiram: aversion therapy
```
52
What are the three steps in the progression of alcoholic liver disease?
1. Alcohol related fatty liver disease
2. Alcoholic hepatitis
Cirrhosis
53
What are the signs of liver disease?
```
• Jaundice
• Hepatomegaly
• Spider Naevi
• Palmar Erythema
• Gynaecomastia
• Bruising – due to abnormal clotting
• Ascites
• Caput Medusae – engorged superficial epigastric veins
Asterixis – “flapping tremor” in decompensated liver disease
```
54
What bloods should be checked in alcoholic liver disease?
```
FBC = MCV
LFT = AST>ALT, gamma-GT^
Clotting = PT^
U&Es = hepatorenal syndrome
```
55
What is the treatment of alcoholic hepatitis?
Steroids improve short term outcomes (over 1 month)
56
Which score is used to determine the need for steroid therapy and severity of alcoholic hepatitis? What is the cut off score?
Maddrey Discriminant Function
| Score >32 = steroid therapy
57
Which score predicts mortality in alcoholic hepatitis?
Glasgow alcoholic hepatitis score
58
What is the management of alcoholic cirrhosis?
Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
59
What is the definitive treatment of alcoholic cirrhosis?
Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
60
Which score is used to determine the severity of liver cirrhosis? Which values are used to calculate this score?
MELD - uses a combination of INR, BR and creatinine to determine survival and severity of cirrhosis.
61
Which scoring systems is used for the prognosis of chronic liver disease?
Child-Pugh score
62
Which score is used in ED and primary care to determine the need for further alcohol screening?
FAST
63
How does alcoholic ketoacidosis present?
Abdominal pain
| Vomiting
64
What might be seen on an ABG in alcoholic ketoacidosis?
Normal glucose
^Ketones
Metabolic acidosis
65
Who is at risk of developing alcoholic ketoacidosis?
Chronic binge drinkers, especially if not eating
66
What is the treatment of alcohol ketoacidosis?
IV fluids
| Thiamine (vit B1)
67
What is PBC?
immune system attacks the small bile ducts within the liver
Causes obstruction of bile --> cholestasis --> fibrosis --> cirrhosis
68
Which part of the liver is affected first in PBC?
Intralobar ducts, also known as the Canals of Hering.
69
Which three liver products build up in the blood due to PBC and cause symptoms?
Bile acids - pruritis
Bilirubin - jaundice
Cholesterol - xanthelasma (+ increase risk of cardiovascular disease)
70
What is the role of bile acids?
Digestion of fats
71
What are the risk factors for PBC?
- Middle aged women
- Other autoimmune diseases (e.g. thyroid, coeliac)
- Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)
72
How does PBC present?
```
• Fatigue
• Pruritus
• GI disturbance and abdominal pain
• Jaundice
• Pale stools
• Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
```
73
How is PBC diagnosed and staged?
Liver biopsy
74
Which liver enzyme is raised first in PBC and PSC?
ALP
75
Which autoantibodies are found in PBC? Which is most specific?
AMA - most specific (part of the diagnostic criteria)
| ANA
76
Which blood tests are done in suspected PBC?
LFTs
Antibodies - ANA, AMA
ESR - raised
IgM - raised
77
What is the treatment of PBC? (4)
• Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
• Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
• Liver transplant in end stage liver disease
Immunosuppression (e.g. with steroids) is considered in some patients
78
What is the action of ursodeoxycholic acid?
reduces the intestinal absorption of cholesterol
79
What is the action of colesyramine?
bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
80
What is the definitive management of PBC?
Liver transplant in end stage liver disease
81
What is PSC?
intrahepatic or extrahepatic ducts become strictured and fibrotic
82
What is the cause of PSC?
Unclear
Genetic
Autoimmune
Ulcerative colitis (70%)
83
What are the risk factors for PSC?
• Male
• Aged 30-40
• Ulcerative Colitis
Family History
84
How does PSC present?
```
• Jaundice
• Chronic right upper quadrant pain
• Pruritus
• Fatigue
Hepatomegaly
```
85
What is the role of autoantibody testing in PSC?
Limited
Antibodies are non-specific
Might indicate whether there will be a response to immunosuppressants
86
Which autoantibodies are associated with PSC?
• Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
• Antinuclear antibodies (ANA) in up to 77%
Anticardiolipin antibodies (aCL) in up to 63%
87
What is the gold standard diagnostic investigation in PSC?
MRCP
88
What is the management of PSC?
Liver transplant (80% 5 year survival)
ERCP - dilate & stent
Colestyramine - bile acid sequestrate
Monitoring for complications
89
What are the complications of PSC?
```
• Acute bacterial cholangitis
• Cholangiocarcinoma develops in 10-20% of cases
• Colorectal cancer
• Cirrhosis and liver failure
• Biliary strictures
Fat soluble vitamin deficiencies
```
90
What are the four most common causes of cirrhosis?
• Alcoholic liver disease
• Non Alcoholic Fatty Liver Disease
• Hepatitis B
Hepatitis C
91
Give some signs of cirrhosis.
• Jaundice – caused by raised bilirubin
• Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
• Splenomegaly – due to portal hypertension
• Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
• Palmar Erythema – caused by hyperdynamic circulation
• Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
• Bruising – due to abnormal clotting
• Ascites
• Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
92
Why do you get gynaecomastia in liver cirrhosis?
Endocrine dysfunction:
increased production of androstenedione by the adrenal glands
increased aromatisation of androstenedione to oestrogen loss of clearance of adrenal androgens by the liver
93
What is seen on LFTs in cirrhosis?
May be normal
| Decompensated = all markers deranged
94
What is first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease?
Enhanced Liver Fibrosis (ELF) blood test
95
How is the ELF blood test interpreted?
```
• Nodularity of the surface of the liver
• A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
• Enlarged portal vein with reduced flow
• Ascites
Splenomegaly
```
96
When should you screen for hepatocellular carcinoma in cirrhosis? What does screening involve?
US and alpha-fetoprotein
| Every 6 months
97
What is a Fibroscan?
Checks the elasticity of the liver
| Assesses the degree of cirrhosis
98
Which patients should receive a Fibroscan?
Every 2 years in patients at risk of cirrhosis:
• Hepatitis C
• Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
• Diagnosed alcoholic liver disease
• Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
Chronic hep B (every year)
99
Which three markers are measured by ELF blood test?
HA, PIIINP and TIMP-1
100
Which scoring systems can be used to assess prognosis of cirrhosis?
Child-Pugh Score
| MELD score
101
Which markers are used in the MELD score? (5)
```
Bilirubin
Creatinine
INR
Sodium
Dialysis
```
102
How is the MELD score used?
gives a percentage estimated 3 month mortality and helps guide referral for liver transplant
103
When should patients with cirrhosis get a MELD score?
Every 6 months
104
What is the general management of cirrhosis?
* Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
* Endoscopy every 3 years in patients without known varices
* High protein, low sodium diet
* MELD score every 6 months
* Consideration of a liver transplant
105
What is the 5 year survival of cirrhosis?
50%
106
Name 6 complications of cirrhosis.
```
Malnutrition
Portal hypertension & varices
Ascites & SBP
Hepatic encephalopathy
Hepatorenal syndrome
HCC
```
107
How does cirrhosis lead to muscle wasting?
increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth
108
What advice can you give to avoid malnutrition in cirrhosis?
• Regular meals (every 2-3 hours)
• Low sodium (to minimise fluid retention)
• High protein and high calorie (particularly if underweight)
Avoid alcohol
109
How does cirrhosis lead to portal hypertension?
Scarring of the liver increases resistance to blood flow
| Pressure builds in portal system
110
Where do varices most commonly occur?
- Gastro oesophageal junction
- Ileocaecal junction
- Rectum
- Anterior abdominal wall via the umbilical vein (caput medusae)
111
How do you treat stable varices?
• Propranolol reduces portal hypertension by acting as a non-selective beta blocker
• Elastic band ligation of varices
- Injection of sclerosant (less effective than band ligation)
112
What can be done if the medical and endoscopic treatment of varices fails?
TIPS procedure
113
What is ascites?
Fluid accumulation within the abdomen.
114
What is the pathophysiology of ascites?
Portal HTN causes leaking of fluid from capillaries in the liver/bowel into the peritoneal cavity.
Loss of circulating volume causes the kidneys to produce renin --> aldosterone.
Aldosterone leads to increased reabsorption of fluid and sodium.
115
What type of ascites is caused by cirrhosis?
Transudative (low protein) - HIGH SAAG
116
What is SAAG? How is it used and how is it calculated?
SAAG = serum-ascites albumin gradient
It is used to determined the cause of ascites.
SAAG = (serum albumin concentration) - (ascitic albumin concentration)
117
How can the causes of ascites be grouped?
```
High SAAG (>11g/L)
Low SAAG (<11g/L)
```
118
What are the high SAAG causes of ascites?
Liver disease - acute liver failure, cirrhosis, liver metastases = PORTAL HTN
Cardiac - RHF, constrictive pericarditis
Other - Budd-Chiari syndrome, portal vein thrombosis
119
What are the low SAAG causes of ascites?
Nephrotic syndrome
Peritoneal carcinoma
Infection - TB
120
How is ascites managed?
1. Reduce dietary sodium
2. Aldosterone antagonist - Spironactalone
3. Drain - needs PT and albumin cover
4. Prophylactic Abx (prevent SBP)
5. TIPS - last line, high risk
121
What is paracentesis induced circulatory dysfunction?
Can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate.
122
When should you give prophylactic Abx in ascities? Which abx is used?
Ascitic albumin concentration <15g/L (found on paracentesis)
| Ciprofloxacin PO
123
What is another name for paracentesis?
Ascitic tap/drain
124
What is the gold standard diagnostic investigation for SBP?
Paracentesis
| Neutrophil count >250 cells/ul
125
What percentage of patients with ascites secondary to cirrhosis will develop SBP?
10%
126
What is the mortality of SBP?
10-20%
127
How does SBP present?
• Can be asymptomatic so have a low threshold for ascitic fluid culture
• Fever
• Abdominal pain
• Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
• Ileus
- Hypotension
128
What are the most common organisms that cause SBP?
• Escherichia coli
• Klebsiella pnuemoniae
- Gram positive cocci (such as staphylococcus and enterococcus)
129
What is the management of SBP?
- Take an ascitic culture prior to giving antibiotics
| - Usually treated with an IV cephalosporin such as cefotaxime
130
What is the pathophysiology of hepatorenal syndrome?
Loss of circulating blood volume (portal vessel dilatation, ascites)
Activation of RAAS
Vasoconstriction of renal blood vessels
Deteriorating kidney function
131
What is the prognosis of hepatorenal syndrome?
Fatal within a week
| Needs liver transplant
132
What is the management of hepatorenal syndrome?
Liver transplant
133
What is another name for hepatic encephalopathy?
Portosystemic encephalopathy
134
Which toxin causes hepatic encephalopathy?
Ammonia
135
Why does ammonia build up in the blood of patients with liver cirrhosis?
- Functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products.
- Collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.
136
How does hepatic encephalopathy present?
Reduced consciousness
Confusion
Changes to personality, memory and mood
137
What factors can precipitate hepatic encephalopathy?
```
• Constipation
• Electrolyte disturbance
• Infection
• GI bleed
• High protein diet
- Medications (particularly sedative medications)
```
138
What is the management of hepatic encephalopathy?
• Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
• Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
- Nutritional support. They may need nasogastric feeding.
139
Which autoimmune conditions are commonly associated with coeliac disease?
```
Diabetes type I - all new presentations are tested for coeliac
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
```
140
What are the genetic associations with coeliac disease?
• HLA-DQ2 gene (90%)
| HLA-DQ8 gene
141
When does coeliac present?
Biomodal - infancy & 50-60 years
142
How is the spleen affected by coeliac disease?
Hyposplenism
143
How does coeliac disease present?
• Failure to thrive in young children
• Diarrhoea
• Fatigue
• Weight loss
• Mouth ulcers
• Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
144
What neurological symptoms can be caused by coeliac disease?
• Peripheral neuropathy
• Cerebellar ataxia
Epilepsy
145
What is the gold standard investigation for diagnosing coeliac disease?
Jejunal biopsy
146
How is a biopsy taken in suspected coeliac disease?
From the jejunum via a Crosby capsule
147
What features are seen on biopsy for coeliac disease?
Villous atrophy
Crypt hyperplasia/hypertrophy
Increase in intraepithelial lymphocytes
Lamina propria infiltration with lymphocytes
148
Which three auto-antibodies are associated with coeliac disease? Which is most specific?
IgA tissue transglutaminase (TTG) antibodies - specific
Anti-endomysial (anti-EMA)
Deaminated gliadin peptides antibodies (anti-DGPs)
149
Why should you test for IgA levels as well as specific autoantibodies?
Some patients have an IgA deficiency. if total IgA is low then the coeliac test will be negative even when they have coeliacs
150
What are the complications of untreated coeliac disease?
```
• Vitamin deficiency
• Anaemia
• Osteoporosis
• Ulcerative jejunitis
• Enteropathy-associated T-cell lymphoma (EATL) of the intestine
• Non-Hodgkin lymphoma (NHL)
• Small bowel adenocarcinoma (rare)
Dermatitis herpetiformis
```
151
What is the management of coeliac disease?
Life-long gluten free diet
152
Name two dermatological complications of coeliac disease?
Dermatitis herpetiformis
| Aphthous ulcers
153
Which foods should be avoided in coeliac?
Barley
Rye
Oats
Wheat
154
Which foods are okay to eat in coeliac disease?
Maise, soya, rice
155
Which vaccination should people with coeliac receive?
Pneumococcal (due to hyposplenism)
156
How is the oesophagus anatomically divided?
Divided into 3rds: reflects change in musculature from striated → mixed → smooth.
157
Which epithelium lines the oesophagus?
• Lined by non-keratinising squamous epithelium.
| Z-line: transition from squamous → gastric columnar
158
How can the causes of dysphagia be grouped?
Inflammatory
Neurological
Mechanical obstruction
159
Name 4 inflammatory causes of dysphagia.
• Tonsillitis, pharyngitis
• Oesophagitis: GORD, candida
• Oral candidiasis
- Aphthous ulcers
160
Name 4 local neurological causes of dysphagia.
- Achalasia
- Diffuse oesophageal spasm
- Nutcracker oesophagus
- Bulbar / pseudobulbar palsy (CVA, MND)
161
Name 2 systemic neurological causes of dysphagia.
MG
| Systemic sclerosis/CREST syndrome
162
How can the mechanical obstructive causes of dysphagia be grouped?
Luminal - FB, food bolus
Mural - stricture, malignancy
Extra-mural - retrosternal goitre, lung ca, mediastinal lymphoma, TAA
163
What is Boerhaave's syndrome?
Oesophageal tear
164
Give some features of an oesophageal tear.
- Odonophagia (painful swallowing)
- Mediastinitis: tachypnoea, dyspnoea, fever, shock
- Surgical emphysema
165
What investigations should be done in dysphagia?
Upper GI endoscopy
| Ba swallow
166
What is indicated by a corkscrew oesophagus on barium swallow?
Diffuse oesophageal spasm
167
Why is the incidence of oesophageal cancer increasing?
Barret's oesophagus
168
What is the median age of presentation in oesophageal cancer?
50-70 years
169
What are the risk factors for oesophageal cancer?
```
• EtOH
• Smoking
• Achalasia
• GORD → Barrett’s
• Plummer-Vinson
• Fatty diet
• ↓ vit A+C
Nitrosamine exposure
```
170
Which type of cancer is found in the upper and middle thirds of the oesophagus?
Squamous cell carcinoma - associated with alcohol, smoking
171
Which type of cancer is found in the lower third of the oesophagus?
Adenocarcinoma - associated with Barret's oesophagus
172
Which type of oesophageal cancer is most common?
Adenocarcinoma (65%)
173
How does oesophageal cancer present?
Progressive dysphagia (solids --> liquids)
Weight loss
Retrosternal chest pain
Lymphadenopathy
174
How might a malignant mass in the upper third of the oesophagus present?
Hoarseness: recurrent laryngeal nerve invasion
| Cough --> aspiration pneumonia
175
Where might oesophageal cancer metastasise to?
Direct
Lymphatics
Blood
75% of patients have mets at presentation
176
How is oesophageal cancer staged?
TNM
CT, US
177
How is oesophageal cancer diagnosed?
Upper GI endoscopy + biopsy
178
What is the treatment of oesophageal cancer?
MDT
Oesophagectomy (25-30% resectable)
Neo-adjuvant chemo - cisplatin
179
What is the 5 year survival for oesophageal cancer?
<5%
180
Name some palliative approaches to oesophageal cancer.
Stenting
Radiotherapy
Analgesia
Macmillan nurses & palliative care referral
181
What is achalasia?
Degeneration of myenteric plexus (Auerbach’s)
↓ peristalsis
LOS fails to relax
182
What are the two causes of achalasia?
1O / idiopathic: commonest
| 2O: Chagas’ disease (T. cruzii)
183
How does a patient present with achalasia?
Dysphagia: liquids --> solids
Regurgitation
Weight loss
Substernal cramps
184
Give a complication of achalasia.
SCC of the oesophagus (3-5%)
185
What is seen on barium swallow in achalasia?
dilated tapering oesophagus - Bird’s beak
186
What can be seen on CXR in achalasia?
widened mediastinum, double RH border
187
How is achalasia managed?
- Medical - CCBs, nitrates
- Interventions: botox injection, endoscopic balloon dilatation
- Surgical: Heller's cardiomyotomy
188
What is a pharyngeal pouch?
Outpouching between crico- and thyro-pharyngeal components of the inf. pharyngeal constrictor.
Area of weakness - Killan's dehiscence
189
What might be seen on examination on someone with a pharyngeal pouch?
Bulge on left side of the neck
190
How might someone present with a pharyngeal pouch?
Regurgitation, halitosis, gurgling sounds
191
What is the treatment for a pharyngeal pouch?
Excision
| Endoscopic stapling
192
How does GORD present?
```
• Heartburn
• Acid regurgitation
• Retrosternal or epigastric pain
• Bloating
• Nocturnal cough
Hoarse voice
```
193
Which patients should be admitted for an urgent endoscopy?
Signs of GI bleed:
- Melaena
- Coffee ground vomiting
194
When should patients have a 2WWW for endoscopy?
* Dysphagia (difficulty swallowing) at any age gets a two week wait referral
* Aged over 55 (this is generally the cut off for urgent versus routine referrals)
* Weight loss
* Upper abdominal pain / reflux
* Treatment resistant dyspepsia
* Nausea and vomiting
* Low haemoglobin
* Raised platelet count
OR if symptoms >4 weeks with treatment
195
What is the gold standard test for diagnosing GORD?
24-hr oesophageal pH monitoring
196
What advice should be given to patients with GORD?
```
• Reduce tea, coffee and alcohol
• Weight loss
• Avoid smoking
• Smaller, lighter meals
• Avoid heavy meals before bed time
Stay upright after meals rather than lying flat
```
197
What is the surgical treatment of GORD?
Laparoscopic fundoplication
198
What is the treatment of endoscopically proven oesophagitis?
• full dose proton pump inhibitor (PPI) for 1-2 months
• if response then low dose treatment as required
- if no response then double-dose PPI for 1 month
199
What is the treatment of endoscopically negative reflux disease?
• full dose PPI for 1 month
• if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
if no response then H2RA or prokinetic for one month
200
What is H.Pylori?
gram negative aerobic bacteria
201
How does H.Pylori cause dyspepsia?
exposes the epithelial cells underneath to acid
| also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells
202
Name four associated conditions of H.Pylori.
```
• peptic ulcer disease
○ 95% of duodenal ulcers
○ 75% of gastric ulcers
• gastric cancer
• B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
- atrophic gastritis
```
203
Who should be offered H.Pylori testing?
Anyone with dyspepsia
204
Which three tests are used for H.Pylori?
• Urea breath test using radiolabelled carbon 13
• Stool antigen test
- Rapid urease test can be performed during endoscopy.
205
How long do patients need to be off PPIs before testing for H.Pylori?
2 weeks
206
When can you take a urea breath test?
off abs 4 weeks
| off PPIs 2 weeks
207
How is H.Pylori treated?
Triple therapy:
| a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.
208
What is used to test for eradication?
urea breath test
209
What is Barrett's oesophagus?
metaplasia of the lower oesophageal mucosa
| Squamous cell --> columnar
210
Which condition is associated with Barrett's oesophagus?
Adenocarcinoma
211
What are the two types of Barrett's oesophagus?
Short <3cm
| Long >3cm
212
When should patients with metaplasia receive endoscopic surveillance?
every 3-5 years
213
What is the management of dysplasia?
• endoscopic mucosal resection
| - radiofrequency ablation
214
Laxative abuse can result in which bowel condition?
Melanosis coli
