Gastrointestinal Flashcards
(256 cards)
1
Q
What are the two inflammatory bowel diseases?
A
Crohn’s disease
Ulcerative colitis
2
Q
What is the pattern of inflammation in Crohn’s disease?
A
Patchy inflammation anywhere from the mouth to the anus (skip lesions).
It is transmural (goes through the whole thickness of the bowel wall)
3
Q
What cells / features are present in the bowel wall in Crohn’s disease?
A
White aphthous ulcers
Deep aggregates of lymphocytes in the bowel wall
Granulomas (collection of epithelioid macrophages surrounded by lymphocytes)
4
Q
What is the typical appearance of the bowel mucosa in Crohn’s disease?
A
Cobblestone
Fibrosis and strictures
5
Q
What are the layers of the bowel wall?
A
mucosa
submucosa
muscularis propria
fat
6
Q
What is the aetiology of Crohn’s Disease?
A
Inappropriate immune response against the gut flora in a genetically susceptible individual
7
Q
What age does Crohn’s disease typically present?
A
20-40 years old
8
Q
What are the symptoms of Crohn’s disease?
A
**Diarrhoea May be bloody May become chronic (more than 6 weeks at a time) **Abdominal Pain **Weight loss Failure to thrive Fatigue Fever Malaise Anorexia
9
Q
How may children present in Crohn’s disease?
A
Poor growth
Delayed puberty
Malnutrition
Bone demineralisation
10
Q
What is the typical course or presentation of Crohn’s
A
Typically there are periods of acute exacerbation interspersed with remissions or less active disease
11
Q
What are the signs of Crohn’s disease?
A
Bowel ulceration Abdominal tenderness/palpable mass Perianal abscess/fistulae/skin tags (characteristic) Anal strictures Beyond the gut - Clubbing - Skin, joint and eye problems - Mouth ulcers
12
Q
Name 1 systemic complication of Crohn’s disease?
A
Amyloidosis
13
Q
Name 5 complications that occur in the bowel as a result of Crohn’s disease?
A
Malabsorption - caused by damage to the mucosal surface in the small bowel.
Obstruction - acute swelling, chronic fibrosis.
Perforation due to deep fissuring ulcers
Fistula formation caused by deep fissuring ulcers
Anal (skin tags, fissure, fistula)
Neoplasia - there is an increased risk on developing colorectal cancer but the risk depends on the duration and severity of the Crohn’s
14
Q
What is toxic dilation classed as ?
A
When the colonic diameter exceeds 6cm
15
Q
What tests do you do in a patient with suspected Crohn’s disease?
A
Blood tests
- FBC
- CRP
- U&Es
- LFTs
- Ferritin
- B12
- Folate
Stool sample
Faecal calprotectin
Colonoscopy and biopsy
16
Q
Why is CRP a useful indicator in Crohn’s diease?
A
Useful for assessing a patient’s risk of relapse as high levels are indicative of active disease or a bacterial complication
17
Q
Why do you do a stool sample in patients with Crohn’s?
A
MC&S to exclude C.diff, campylobacter, E.coli
18
Q
Why is faecal calprotectin a good test to do in Crohn’s patients?
A
The concentration of calprotectin in faeces has been shown to correlate well with the severity of intestinal inflammation
19
Q
What are the three kinds of treatment options you can offer a patient with Crohn’s disease to induce remission?
A
Monotherapy
Add on therapy
Biologics
20
Q
What monotherapy can you offer to Crohn’s patients to induce remission?
A
Prednisolone or methylprednisolone
If CI or isn’t tolerated : budesonide
21
Q
What add on therapy can you offer to patients with Crohn’s patients that have had 2 or more inflammatory exacerbations in the last 12 months?
And if these cannot be tolerated?
A
azathioprine or mercaptopurine
Methotrexate
22
Q
What biologic drugs are there that can help to induce remission in Crohn’s patients?
Name an example of a drug in each class?
A
Anti-TNF-alphas : Infliximab / adalimumab
Anti-integrin :Vendolizumab
Anti-IL-12/23 : Ustekinumab
23
Q
How do anti-TNF-alpha drugs help in Crohn’s disease?
A
These block the action of the cytokine tumour necrosis factor alpha which mediates inflammation in Crohn’s
Severe active disease
24
Q
How do anti-integrin drugs help in Crohn’s disease?
A
Monoclonal antibodies that target adhesion molecules involved in gut lymphocyte trafficking
Reduces disease activity
25
What treatments are there to maintain remission in Crohn's patients?
Stop smoking
Azathioprine
6-mercaptopurine
Methotrexate
26
What are the side effects of the drug treatments used to maintain remission in Crohn's disease?
abdominal pain, nausea, pancreatitis, leucopenia
27
What non-pharmacological treatment is used in Crohn's disease? When is it indicated?
```
Surgery
To resect the affected areas
Indications
Drug failure
GI obstruction from stricture
Perforation
Fistulae
Abscess
```
Psychological support and nutritional advice.
28
What nutrition advice can be given to Crohn's patients?
No evidence to suggest that dietary modification can prevent flares or induce remission. A healthy, balanced diet including a variety from all food groups is recommended.
A low-FODMAP diet can be used in patients who report IBS symptoms during remission periods of IBD
Calcium and vitamin D supplementation should be considered in particular during flare ups.
29
What is the pattern of inflammation in ulcerative colitis?
Relapsing and remitting inflammation of the colonic mucosa
Inflammation is all mucosal (i.e does not extend deeper into the bowel). It starts in the rectum and is continuous but is only confined to the colon.
30
Can there be inflammation of the terminal ileum in ulcerative colitis?
Yes, but this is only caused due to backwash of inflammatory cells caused by an incompetent ileocaecal valve.
31
Aetiology of ulcerative colitis?
Inappropriate immune response against potentially abnormal colonic flora in genetically susceptible individuals
32
What genetic association is there in ulcerative colitis?
HLA-B27
33
Symptoms of ulcerative colitis?
- Episodic or chronic diarrhoea + blood (blood may be brighter/fresher than in Crohn’s as it is colonic inflammation only)
- Crampy (colicky) abdominal discomfort
- Bowel frequency (relates to severity)
- Urgency
- Tenesmus (a feeling of incomplete defecation with an inability or difficulty to empty bowel at defecation
Systemic symptoms during attacks
- Fever
- Malaise
- Anorexia
- Weight loss
34
Signs of ulcerative colitis
Depends on disease severity
Patient may be clearly unwell, pale, febrile, dehydrated
May have tachycardia or hypotension
Abdominal examination may reveal tenderness, distension or palpable mass (toxic megacolon)
35
What extra-intestinal disease may present in patients with ulcerative colitis?
Liver
- Fatty change
- Sclerosing cholangitis - fibrosis of bile ducts
Colorectal cancer
Joints
- Ankylosing spondylitis
- Arthritis
Eyes
- Iritis
- Uveitis
- Episcleritis
Skin
- Erythema nodosum
- Pyoderma gangrenosum
36
What is an acute complication of ulcerative colitis?
Toxic dilatation of colon with risk of perforation
| Venous thromboembolism
37
What is a chronic complication of ulcerative colitis?
Colonic cancer. Risk is related to duration and severity of the disease
38
What investigations do you do in ulcerative colitis?
Limited flexible sigmoidoscopy if acute to assess and biopsy, full colonoscopy once controlled to define disease extent
Bloods
FBC, renal function, LFTs, ESR, CRP, iron studies, vitamin B12, folate
Stool microscopy culture and sensitivity
Exclude campylobacter, C.diff
Faecal calprotectin
Abdominal X-ray
39
What may an abdominal x-ray show/be used to show in a patient with ulcerative colitis?
To exclude colonic dilatation
May also help assess disease extent in UC
Mucosal thickening / islands
No faecal shadows
40
What drug treatment is used in patients with mild-moderate ulcerative colitis?
Topical mesalazine 5-aminosalicylic acid
Oral aminosalicylate e.g mesalazine
Oral/topical corticosteroid
41
What is the treatment for patients with severe ulcerative colitis?
Unwell + 6 or more motions a day
IV hydration
IV steroids
Rectal steroids
42
What other treatment options are there if the patient has not responded to conventional drug therapy used in ulcerative colitis?
Immunomodulation
Biologic agents
Surgery
43
When is immunomodulation therapy indicated in ulcerative colitis patients?
Name a drug used
Immunomodulation is indicated if the patients flare on steroids or require 2 or more courses of steroids in a year
Azathioprine
44
What biologic agents can be used to treat ulcerative colitis?
Infliximab
| Adalimumab
45
What surgery may be needed in patients with ulcerative colitis?
May need emergency treatment for severe UC that does not respond to drug treatment
46
What is the pathology of irritable bowel syndrome
Seems to involved abnormal smooth muscle activity +/- visceral hypersensitivity and abnormal central processing of painful stimuli
47
What is the aetiology of irritable bowel syndrome?
No organic cause
48
What is the age of onset of irritable bowel syndrome?
less than 40 years old
49
What are the symptoms of irritable bowel syndrome?
How long must they have had these symptoms to be able to diagnose IBS?
6 month history of either
Abdominal discomfort/pain
Bloating
Change in bowel habit
Plus the recurrent abdominal pain is associated with at least 2 of
Relief by defecation
Altered stool form
Altered bowel frequency (constipation and diarrhoea may alternate)
```
AND at least 2 of the following
Altered passage of stool
Abdominal bloating, distension or hardness
Symptoms are aggravated by eating
Passage of mucus rectally
```
```
Other symptoms
Lethargy
Nausea
Backache
Bladder symptoms
```
50
What can make IBS symptoms worse?
exacerbated by stress, menstruation or gastroenteritis
51
Signs of IBS?
Examination may be normal but general abdominal tenderness is common
52
How do you diagnose IBS?
Diagnosis should be made positively on symptom based criteria
53
What tests do you when investigation IBS?
FBC
ESR
CRP
Coeliac screen
CA 125 (for women with symptoms that could be ovarian cancer)
Faecal calprotectin (in patients with symptoms that could be IBD)
54
Female patient presents with IBS type symptoms but they say that their pain is cyclical - what may this suggest?
Endometriosis
55
What advice would you give to a patient with IBS who has
1. constipation
2. diarrhoea
1. adequate water and fibre intake. Physical activity, avoid insoluble fibre like bran. If this fails then can try simple laxatives
2. avoid sorbitol sweetners, alcohol and caffeine. Reduce dietary fibre content
56
What medication can you give to a patient with IBS who experiences colic or bloating?
Oral antispasmodics
| medbevrine
57
how is surface area in the intestine increased?
mucosal folds
villi
brush border of microvilli
58
what are the role of crypts in the intestine?
proliferative cells that replace higher up epithelial cells as they come to the end of their lifespan
59
What are the 5 main reasons why malabsorption may occur?
1. Defective intraluminal digestion
2. Insufficient absorptive area
3. lack of digestive enzymes
4. defective epithelial transport
5. lymphatic obstruction
60
Name 3 things that can cause malapsorption by causing defective intraluminal digestion.
1. Pancreatic insufficiency
2. Defective bile secretion
3. Bacterial overgrowth
61
Name 2 diseases that cause pancreatic insufficiency leading to malabsorption? Why?
Chronic pancreatitis
- repeated bouts of inflammation leads to insufficient pancreatic tissue to produce digestive enzymes
Cystic Fibrosis
- viscous secretions block the duct, the pancreas atrophies and there are insufficient enzymes for digestion
62
Why can defective bile secretion cause malabsorption?
In what conditions may this occur?
Bile salts are needed for fat absorption. If there are not enough of these bile salts then fats cannot be absorbed.
```
Biliary obstruction (gallstones)
Ileal resection - because the ileum absorbs and recirculates the bile salts
```
63
where are bile salts absorbed?
ileum
64
Name 4 conditions that may cause malabsorption by insufficient absorptive area
1. Coeliac disease
2. Crohn's disease
3. Extensive surface parasitisation
4. Small intestinal resection or bypass
65
Why may extensive parasitusation cause malabsorption?
Giardia lamblia
| When you have a large infestation they carpet the villi and digested food cannot be absorbed
66
Why can Crohn's cause malabsoprtion?
Cobblestone mucosa and inflammation reduce the surface area for absorption
67
What is a common digestive enzyme deficiency that can cause some degree of malabsorption ?
Disaccharidase deficiency (lactose intolerance)
68
Why do symptoms of lactose intolerance manifest?
Lactose arrives at the colon undigested where there are lots of microbes that use lactose as energy. When they digest the lactose they produce gas, causing distension, wind and bloating
69
Name two conditions that cause defective epithelial transport leading to malabsorption and why?
1. Abetalipoproteinemia
- genetic mutations that cause a particular protein to not be produced so a particular nutrient cannot be absorbed
2. Primary bile acid malabsorption
70
What can cause lymphatic obstruction leading to malabsoption and why?
Lymphoma
TB
Cannot get transported from the lacteal to the rest of the body
71
Name 5 symptoms of malabsorption?
Diarrhoea Weight loss (despite maintaining a normal calorie intake/diet)
Lethargy
Steatorrhoea
Bloating
72
What are the features of steatorrhoea?
Unpleasant faeces
Fat isn’t being absorbed
Stools may be bulky and difficult to flush, have a pale and oily appearance and can be especially foul-smelling
73
What are the signs of malabsorption?
```
Anaemia
- Decreased iron
- Decreased B12
- Decreased folate
Bleeding disorders
- Due to decreased vitamin K
Oedema
- Due to decreased protein
Metabolic bone disease
- Due to decreased vitamin D
Neurological features
```
74
What tests do you do in malabsorption?
```
FBC
Decreased or increased MCV
Decreased calcium
Decreased iron
Decreased B12 and folate
Increased INR
Lipid profile
Coeliac serology
Stool
Breath hydrogen analysis
Endoscopy and small bowel biopsy
```
75
What stain would you use on a stool sample to look for fat globules?
Sudan stain
76
What does breath hydrogen analysis show?
For bacterial overgrowth
77
Name 2 causes of infective malabsorption?
Giardia
Cryptosporidium
Tropical sprue
78
How many people does coeliac disease affect?
1% of the adult population
79
When does coeliac disease often develop?
Commonly presents between the 4th and 6th decade
80
What is the pathology of coeliac disease?
1. Gluten peptides in the intestinal lumen cross the lumen and reach the lamina propria
2. They activate innate and adaptive immunity
3. IL-15 promotes lymphocyte growth and can play a role in intestinal damage
4. Tissue transglutaminase is involved in the cross linking of collagen and tissue
5. tTG operates a deamidation process to gluten peptides.
6. These peptides become negatively charged and have a high affinity to binding to the HLA-DQ2 / HLA-DQ8 molecules that are expressed on antigen presenting cells.
7. The HLA-DQ2 and HLA-DQ8 molecules are able to present these gluten peptides to CD4+ cells and trigger an immune response
81
What genetic molecules are associated with coeliac disease?
HLA-DQ2/DQ8 molecules
HLA-DQ2 molecules are expressed in 95% of patients and HLA-DQ8 molecules are expressed in 5%.
82
If a person has the genetic molecules that are seen in coeliac does that mean they will have coeliac disease?
No, they are necessary for development of the disease but are not definitive for getting the disease
83
What is the negative predictive value of HLA-DQ2 and HLA-DQ8 when diagnosing coeliac?
Have a negative predictive value of 100%
i.e if you do not have them then you will not get the disease
84
What is the aetiology of coeliac disease?
```
Gluten
Glidans
Glutenins
Individual factors
Genetic predisposition
- HLA-DQ2 and HLA-DQ8
- Tissue transglutaminase
```
85
What immune response do the coeliac antigens cause?
TH1- natural killed cells release cytokines leading to mucosal inflammation and cause villous atrophy
TH2 - B cells, antibodies are formed (anti-gliadin, anti-endomysial and anti-tissue transglutaminase). This causes autoimmunity and presents with intestinal and extraintestinal symptoms.
86
What antibodies are formed in coeliac disease?
anti-gliadin,
anti-endomysial and
anti-tissue transglutaminase
87
Name a risk factor that increases your risk of developing coeliac?
Relative risk in first degree relatives is 6 fold
88
What are the symptoms of coeliac disease?
Steatorrhoea
Diarrhoea
Weight loss
Failure to thrive in children
```
Abdominal pain
Bloating
Nausea + vomiting
Aphthous ulcers
Angular stomatitis
Fatigue
Weakness
```
Or patient can be asymptomatic
89
What complications can arise from coeliac?
```
Anaemia
Dermatitis herpetiformis
Osteopenia/osteoporosis
Hyposplenism
GI T cell lymphoma
Increased risk of malignancies
-Lymphoma
-Gastric
-Oesophageal
```
90
What investigations do you do in coeliac disease?
Serology
Positive IgA tissue transglutaminase
IgA anti- endomysial antibody
```
Upper GI endoscopy and duodenal biopsy
Villous atrophy
Crypt hyperplasia
Flat mucosa
Increased intraepithelial lymphocyte count
```
91
What are the histological features of the intestine in a person with coeliac?
Villous atrophy
Crypt hyperplasia
Flat mucosa
Increased intraepithelial lymphocyte count
92
What important thing do patients need to do before they are tested for coeliac disease?
Before testing patients NEED to keep gluten in their diet! Need to eat some gluten in their diet in more than 1 meal every day for at least 6 weeks before testing.
93
What is the treatment for coeliac disease?
Gluten-free diet lifelong
94
What foods do patients with coeliac have to avoid?
Avoid bread, cakes, pasta, cereals, wheat flour, meat pies, sausages, fish fingers, wheat, rye, barley
95
What is the pathology of GORD?
Backflow of gastric acid from the stomach into the oesophagus due to incompetent oesophageal sphincter
96
What is the normal histology of the oesophagus?
stratified muscle
| non-keratinized squamous epithelium
97
Name 5 causes of GORD?
Most causes are due to an increase in intra-abdominal pressure
-Lower esophageal sphincter hypotension
-Inadequate cardiac sphincter for anatomical reasons or factors that reduce tone and also poor esophageal peristalsis
-Hiatus hernia
-Esophageal dysmotility
-Obesity
-Gastric acid hypersecretion
-Delayed gastric emptying
-Smoking
-Alcohol
-Pregnancy
-Fatty meals
Relaxes the tone of the cardiac sphincter
-Drugs
98
Why can smoking cause GORD?
reduces the tone of the cardiac sphincter
99
What drugs relax the tone of the cardiac sphincter and can cause GORD?
Tricyclic antidepressants
Anticholinergics
Nitrates
100
What are the oesophageal symptoms of GORD?
```
Heartburn
- Burning, retrosternal discomfort after meals, lying, stooping or straining
Belching
Acid brash
- Acid or bile regurgitation
Waterbrash
- Increased salivation
Odynophagia
- Painful swallowing
```
101
When can heartburn be felt?
Burning, retrosternal discomfort after meals, lying, stooping or straining
102
What are the extra-oesophageal symptoms of GORD?
Nocturnal asthma
Chronic cough
Laryngitis
Sinusitis
103
Name three differential diagnoses from GORD?
```
Oesophagitis
NSAIDs
Herpes
Candida
Duodenal or gastric ulcers
Non-ulcer dyspepsia
Oesophageal spasm
Cardiac causes
```
104
How can you differentiate GORD from angina?
In GORD there is no relationship with exercise and pain
105
Name three complications of GORD?
```
Oesophagitis
Ulcers
Benign stricture
Iron-deficiency
Metaplasia → dysplasia → neoplasia
GORD may lead to Barrett’s oesophagus
```
106
What investigations do you do in GORD?
Endoscopy
FBC - to exclude significant anaemia
Esophageal 24 hour pH monitoring to assess if symptoms coincide with acid in the oesophagus
- Used if the endoscopy is normal
107
What are the different grades of GORD based on the endoscopy?
Grade 1
Single or multiple erosions on a single fold
Grade 2
Multiple erosions on multiple folds
Grade 3
Multiple circumferential erosions
Grade 4
Ulcer, stenosis or esophageal shortening
Grade 5
Barrett’s epithelium. Columnar metaplasia in the form of circular or non-circular extensions
108
What lifestyle advice would you give to someone with GORD?
```
Weight loss
Stop smoking
Small, regular meals
Reduce
-Hot drinks
-Alcohol
-Citrus fruits
-Tomatoes
-Onions
-Fizzy drinks
-Spicy foods
-Caffeine
-Chocolate
Avoid eating less than 3 hours before bed
Raised the bed head
Avoid drugs that affect oesophageal motility or damage the mucosa
```
109
What are the pharmacological treatment options used in GORD?
Antacids to reduce symptoms
- Magnesium trisilicate mixture
Proton pump inhibitor
Avoid drugs that affect esophageal motility or damage the mucosa (e.g NSAIDs)
110
Name 2 examples of a proton pump inhibitor?
Lansoprazole
| Omeprazole
111
Mechanism of action of PPIs?
Inhibit the proton pump on the parietal cells decreasing the concentration of HCl in the stomach, increasing pH
112
Mechanism of action of NSAIDs?
COX-1 enzyme inhibitor inhibiting prostaglandin synthesis decreasing inflammation
113
What surgical treatment options are there for GORD patients?
How do they work?
Laparoscopic fundoplication surgery
- Narrowing the hiatus where the oesophagus enters the stomach
- Wrapping the upper part of the stomach around the lower oesophagus to recreate the valve at the lower end of the oesophagus
Magnetic bead band
- Encircles the distal oesophagus at the gastro-oesophageal junction
- Ring of interlinked titaniumbeads, each with a weak magnetic force which holds the beads together to keep the distal oesophagus closed
- When patient swallows the magnetic force is overcome allowing the ring to open
114
What are the red flag symptoms for cancer?
```
unexplained weight loss
anaemia
evidence of GI bleed
Dysphagia
Upper abdominal mass
Persistent vomiting
```
115
define Barrett's oesophagus?
A premalignant condition.
Oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium.
116
Pathology of Barrett's oesophagus?
Long-standing reflux of acid causes the normal squamous epithelium that lines the oesophagus to die.
There then may be gaps in the epithelial lining leading to ulceration which can cause pain and indigestion.
If reflux continues then the oesophagus has intestinal metaplasia and consists of columnar epithelium with goblet cells and tall intervening mucus-producing cells that secrete intestinal-type mucins.
117
What is the oesophageal lining seen in Barrett's oesophagus?
columnar epithelium with goblet cells and tall intervening mucus-producing cells
118
What are the risk factors for Barrett's oesophagus?
```
Chronic GORD
- Risk increases with longer duration and increased frequency of gastro-oesophageal symptoms
Hiatus hernia
Obesity
Alcohol
Smoking
```
119
What are the symptoms of Barrett's oesophagus?
May be asymptomatic
Dysphagia
Weight loss
Retrosternal chest pain
120
What are the signs of Barrett's Oesophagus?
Hoarseness
| Cough
121
What investigation do you do in Barrett's oesophagus?
Endoscopy and biopsy
122
What will the biopsy show in a patient with Barrett's oesophagus?
Columnar epithelium with goblet cells and mucus producing cells in the oesophagus
Red islands
123
What are the management options for patients with Barrett's oesophagus who have dysplasia?
Endoscopic mucosal resection
- Removal of small polyps or growths from the lining of the oesophagus
Radiofrequency
- Burn away the abnormal cells
Surgery
- Oesophagectomy is recommended when there is severe dysplasia
124
What is the first line treatment for a patient with dysplasia in Barrett's oesophagus?
Radiofrequency
| Burn away the abnormal cells
125
What is the management for patients with Barrett's oesophagus and no dysplasia?
```
Lifestyle
Weight loss
Reduced alcohol intake
Stop smoking
Reduce portion sizes
Avoid eating within 3 hours of going to bed
```
Medications
Long term PPI
126
What does Barrett's oesophagus increase the risk for?
What should you look for that may indicate they could be developing this?
oesophageal adenocarcinoma
```
Persistence of reflux
Difficulting swallowing
Unexplained weight loss
Bringing up blood
Hoarse voice
```
127
What are the two main types of oesophageal cancers?
Squamous carcinoma
| Adenocarcinoma
128
What is the pathology of squamous carcinoma (oesophagus)
Develops from squamous epithelium and may come before any dysplastic changes.
129
What is dysplastic squamous epithelium characterised by?
lack of maturation of cells towards the surface and immature cells are seen close to the surface. Degree of dysplasia can be low or high grade
130
Where are squamous carcinoma tumours usually found?
usually found in the middle and upper third of the oesophagus
Can have a superficial cancer, a polypoid into the lumen or it can become invasive going through the mucosa.
131
What are the risk factors for developing squamous carcinoma of the oesophagus?
Heavy smoking
Alcohol
Achalasia - oesophagus has a reduced/no ability to do peristalsis
Vitamin deficiencies
Repeated therapy injury due to hot beverages
132
What are the symptoms of squamous carcinoma of the oesophagus?
Usually asymptomatic until advanced disease stage.
Dysphagia (at first with solids then liquids)
Weight loss
133
What type of dysphagia is seen in squamous carcinoma of the oesophagus?
at first with solids then liquids)
134
What is the investigations in squamous carcinoma of the oesophagus?
Endoscopy and biopsy
CT for staging
Identifies primary tumour in most cases as well as any spread to the lymph nodes or other organs such as the live, lungs and bone
135
What is the radical treatment for squamous carcinoma of the oesophagus?
Nutritional assessment and support
Offer people with resectable non-metastatic squamous cell carcinoma of the oesophagus the choice of…
- Radical chemotherapy
- Chemoradiotherapy before surgical resection (only a low number of cases can be offered surgical resection)
136
What is the palliative care for squamous carcinoma of the oesophagus?
Chemotherapy
| Local tumour treatment including stenting or palliative radiotherapy
137
what is the difference in location of squamous carcinoma of the oesophagus and adenocarcinoma of the oesophagus?
squamous carcinoma: occurs in the upper 2/3
adenocarcinoma: occurs in the lower 1/3
138
What is the difference in presenting dysphagia between malignant and benign disease
benign : dysphagia to solids and liquids from the start
malignant: dysphagia starts with solids then moves onto liquids
139
What cells does adenocarcinoma of the oesophagus primarily arise frrom?
columnar-lined epithelium in the lower oesophagus
140
What are 3 risk factors that increases the likelihood of developing adenocarcinoma of the oesophagus?
Barrett’s oesophagus
GORD
Smoking
Obesity
141
What is the clinical presentation of adenocarcinoma of the oesophagus?
Usually there are no physical signs and the cancer is typically extremely advanced when it is found
Dysphagia
Starting with solids and moving onto liquids
Weight loss
Lymphadenopathy
Anorexia
Pain due to impaction of food or infiltration of cancer into adjacent structures
142
What investigations are used in adenocarcinoma of the oesophagus?
Oesophagoscopy with biopsy
Histological proof of the carcinoma
Barium swallow - to see strictures
CT for staging
143
What are the treatment options for adenocarcinoma of the oesophagus?
Surgical resection
Best chance of cure if the tumour has not infiltrated outside the oesophageal wall
Combined with chemotherapy before surgery
If locally incurable or metastatic - systemic chemotherapy
Treatment of dysphagia
Endoscopic insertion of expanding metal stent across tumour to ensure oesophageal patency
Palliative care may be the only option
70% of patients have widespread local disease or metastatic disease at presentation and cannot be cured by surgical resection
May receive palliative chemotherapy, chemoradiation or treated with a stent to improve dysphagia
144
how do malignant tumours of the stomach arise
The change from normal gastric mucosa to intestinal metaplasia and then dysplasia.
Can be early or locally advanced
Normal gastric mucosa → intestinal metaplasia → dysplasia → intramucosal carcinoma → invasive carcinoma
145
What are the two different pathologies of malignant cancers of the stomach?
What are their differences
Intestinal
Well formed and differentiated glandular structures
More likely to involve distal stomach
```
2. Diffuse
Poorly cohesive undifferentiated cells
Tend to infiltrate the gastric wall
Can involve any part of the stomach
Worse prognosis that intestinal
```
146
Aetiology of malignant tumours of the stomach?
Helicobacter pylori infection Dietary - high salts and nitrates
Smoking
Obesity
Previous gastric surgery for benign disease
Hereditary diffuse gastric cancer
Presence of a CDH1 germline mutation
Deletion of tumour suppressor gene p53
147
Why does H.pylori infection have a role in early stages of gastric cancer?
Can lead to atrophic gastritis and pre-malignant intestinal metaplasia
Appears to have a role in the early stages of gastric cancer development as it binds to the surface of the normal gastric epithelial cell
Given the high prevalence of H.pylori infection and the comparative rarity of gastric cancer it is highly unlikely that the organism or its products are directly acting mutagens
148
What are the risk factors for malignant tumours of the stomach?
```
Pernicious anaemia
H. pylori infection
Atrophic gastritis
Adenomatous polyps
Lower social class
Smoking
Diet
```
149
What are the symptoms of stomach cancer?
Usually non-specific.
Most patients that have gastric carcinoma have advanced disease at the time of presentation.
```
Dyspepsia
Weight loss
Vomiting
- Frequent and can be severe if the tumour encroaches on the pylorus
Dysphagia
Anaemia
```
150
What is pernicious anaemia?
Large immature nucleated cells circulate in the blood and do not function as RBC.
This is caused by the impaired uptake of vitamin B12 due to lack of intrinsic factor in the gastric mucosa.
151
What are the signs of an incurable gastric mass?
```
Epigastric mass
Virchow’s node
Hepatomegaly
Jaundice (liver mets)
Ascites
```
152
What is Virchow's node?
Lies near to the junction of the thoracic duct and the left subclavian vein.
Tumour embolisation of the GI cancers via the thoracic duct usually leads to the enlargement of this node
153
What investigations are used for malignant tumours of the stomach?
Gastroscopy and biopsy multiple ulcers
Aim to biopsy all ulcers
Endoscopic ultrasound can evaluate the depth of the invasion of the carcinoma
Staging laparoscopy is recommended for locally advanced tumours
154
What are the different stages of gastric cancer?
In situ intramucosal : likely to develop into invasive but currently is unlikely to have spread
Early gastric cancer: limited to the mucosa or submucosa
Locally advanced gastric cancer: spreads into the muscular wall of the stomach
If it has spread into the peritoneal cavity then it cannot be cured
155
Treatment of early stomach cancer?
Surgical resection is likely
Chemotherapy before
Nutritional support
156
Treatment / management of more advanced stomach cancer?
Partial gastrectomy for more advanced distal tumours
Surgery and combination chemotherapy
Just chemotherapy can increase quality of life survival
Surgical palliation is often needed for obstruction, pain or haemorrhage
Nutritional support
157
What are the two types of small intestine tumours?
Adenocarcinoma
| Lymphomas
158
What are the risk factors for developing small intestine tumours?
Coeliac
| Crohn’s
159
Are small intestine tumours common?
No, they are relatively resistant to the development of neoplasia
160
What are the symptoms of small intestinal tumours?
```
Pain
Diarrhoea
Anorexia
Weight loss
Anaemia
```
161
Sign of a small intestinal tumour?
May be a palable mass
162
What investigations do you do for a small intestinal tumour?
Ultrasound
Endoscopic biopsy to histologically confirm a diagnosis
CT scan
163
What may the CT scan show a small intestinal tumour?
May show small bowel wall thickening and lymph node involvement
164
What is the treatment for a small intestinal tumour
Surgical resection
Radiotherapy
165
What are polyps
abnormal growth of tissue projecting from the colonic musoca. Most are asymptomatic and found by chance.
Can be epithelial or mesenchymal
166
What type of cancer do colorectal cancers tend to be?
adenocarcinoma
167
What is the usual progression for colorectal cancer development?
Usually progresses from :
| Normal epithelium → adenoma → colorectal carcinoma
168
What are colonic adenomas?
benign dysplastic tumour of columnar cells or glandular tissue
169
What causes adenomas to progress to carcinomas?
Activation of oncogenes
Loss or mutations of tumour suppressor genes
Defects in DNA repair
170
Aetiology of colorectal cancer?
Diet
Inherited genetic factors
Long standing ulcerative colitis
171
What inherited genetic factors can cause colorectal cancer?
What is the pattern of inheritance?
How do they increase likelihood of developing colorectal cancer?
Familial adenomatous polyposis
Autosomal dominant pattern of inheritance that causes mutations in the APC tumour suppressor gene
Numerous adenomas develop at an early age mainly in the large intestine and subsequently undergo malignant change
172
What impact does diet have on the colon?
affects the flora of the large bowel, the bowel transit time and the amount of cellulose, amino acids and bile acids in bowel contents
173
What type of diet is associated with colorectal cancer? Why?
High fat, high protein, low fibre diet is linked to colorectal cancer
High fat increases bile salt production leading to a higher load of faecal bile acids
High protein leads to transformation of amino acids by bacteria
Low fibre reduces the number of volatile fatty acids which prolongs intestinal transit time leading to more time for bacterial action on the content. There is prolonged contact between any carcinogen generated and the mucosa
174
Name three predisposing factors that can increase risk of developing colorectal carcinoma?
```
Neoplastic polyps
IBD
Increased alcohol consumption
Smoking
Family history
Previous cancer
```
175
Where do the majority of colorectal cancers present?
rectum
176
What features are more visible the closer the cancer is to the outside?
The closer the cancer is to the outside the more visible the blood and mucus will be
177
What is the clinical presentation of left sided colorectal cancer?
```
Stenosing type
Obstruction
Bleeding/mucus in the stools
Altered bowel habit
Tenesmus
Mass PR
Diarrhoea or alteration constipation and diarrhoea
Colicky abdominal pain
Less advanced disease at presentation
```
178
What is the clinical presentation of right sided colorectal cancer?
Iron deficiency anaemia
Weight loss
Decreased haemoglobin
Abdominal pain
Occult bleeding (not visible to the patient or doctor)
Disease is more likely to be advanced at presentation
179
What can be a feature of either right or left sided colorectal cancer?
```
Abdominal mass
Perforation
Haemorrhage
Fistula
Jaundice and hepatomegaly indicate advanced disease with extensive liver metastases
```
180
What investigations do you do in colorectal cancer?
Colonoscopy is the gold standard investigation
Biopsy
Removal of polyps
FBC - microcytic anaemia
Faecal occult blood
It checks blood in the faeces
Home kit is used for screening
181
When would you do a barium enema in a patient with suspected colorectal cancer?
If patient cannot tolerate a colonoscopy or if the colonoscopy fails to visualise the caecum can do a barium enema
Avoids perforation risk
More limited in detecting small lesions
182
How can you help to prevent colorectal cancer?
increase the fibre in the diet
- wholegrain bread and oats
- wholewheat pasta
- berries, pears, melon
- broccoli, carrots, sweetcorn
- peas, beans and pulses
- potatoes with skin
183
What is the treatment options of colorectal cancer?
Surgery
Radiotherapy
Chemotherapy
184
What surgery can you do to treat colorectal cancer?
Aims to cure or relieve symptoms
Laparoscopic surgery to
(hemi) colectomy
185
When would you use radiotherapy in the treatment of colorectal cancer?
Locally advanced rectal cancer
Palliation of colonic cancer
Post-op radiotherapy is used in patients with rectal tumours that are at high risk of local recurrence
186
What type of colorectal cancer do you use chemotherapy?
Adjuvant chemotherapy in stage 3 disease (cancer is invading the subserosa and beyond but not other organs)
187
What is more common duodenal or gastric ulcer?
Duodenal ulcer is 4 x more common
188
What is a peptic ulcer?
a localised defect extending at least into the submucosa.
189
What is the pathophysiology behind a H. pylori infection causing a peptic ulcer?
A bacteria that lives in the mucin layer of the stomach
Causes a decrease in duodenal HCO3-. This increases the acidity of the stomach as there is less alkali to buffer the acid
Bacteria secretes urease splitting urea into CO2 and ammonia
Also secrete proteases which attack the gastric epithelium
Increases gastrin released from G cells, increasing acid secretion
Decreases somatostatin leading to increased acid secretion
Inflammatory response
Increased acidity overwhelms the protective mucin resulting in mucosal damage.
190
What is the pathophysiology of NSAIDs causing a peptic ulcer?
Mucus secretion by mucosal cells is stimulated by prostaglandins
Cyclo-oxygenase 1 is needed for prostaglandin synthesis
NSAIDs inhibit COX-1 enzyme
Reduced mucosal defence
Cells are not protected from the HCl of the stomach which can cause cell death and can develop a micro ulcer
Acid can then get into the micro ulcer and damage the adjacent cells
191
Causes of a duodenal ulcer?
```
H.pylori infection
NSAIDs
Smoking
Steroids
Increased gastric acid secretion
```
192
Causes of a gastric ulcer?
```
H.pylori infection
Smoking
NSAIDs
Reflux or duodenal contents
Delayed gastric emptying
Stress
Alcohol - usually only spirits
```
193
Symptoms of a duodenal ulcer?
May be asymptomatic
Epigastric pain relieved by antacids
Pain usually presents 1-3 hours after food
Can wake patients at night
Pain is worse when the patient is hungry
May present with weight loss
Nausea
194
sign of a duodenal ulcer?
Epigastric tenderness
195
Symptoms of a gastric ulcer?
May be asymptomatic
Epigastric pain relieved by antacids
May present with weight loss
Nausea
196
What type of bacteria is H.pylori?
Gram negative spiral bacillus
197
Where is H.pylori most prevalent?
In poor socioeconomic and overcrowded areas
198
How is H.pylori infection acquired?
Faecal-oral or oral-oral route
199
Investigations in peptic ulcers?
C-urea breath test for H.pylori
Stool antigen test for H.pylori
Endoscopy
200
What is the treatment for a H.pylori infection?.
Lansoprazole (PPI)
Amoxicillin
Metronidazole
201
What lifestyle advice can you offer to a patient with a peptic ulcer?
Reduce alcohol intake
| Reduce tobacco consumption
202
What drugs can reduce stomach acid where the cause of the peptic ulcer is not H.pylori?
PPI
| H2 blockers e.g ranitidine
203
Name an example of a H2 blocker drug?
ranitidine
| cimetidine
204
How do H2 receptor blocking drugs work?
Block the H2 receptor on the parietal cell
Histamine cannot bind to the receptor
Decreasing the proton pump activity
Decreasing the concentration of HCl in the stomach
205
When do acute ulcers tend to develop?
Develop as part of acute gastritis as a complication of a severe stress response due to mucosal ischaemia or as a result of extreme hyperacidity
206
Where do chronic ulcers most frequently develop?
Mucosal junctions
207
What are 2 complications of peptic ulcers?
- Haemorrhage - ulcer erodes deeper, can erode into a large blood vessel (most commonly the gastroduodenal artery)
- Perforation - causes an acute abdomen with epigastric pain
Peritonitis - as acid enters the peritoneum
- Scarring of the duodenum may lead to pyloric stenosis
- Malignancy
- Reduced gastric outflow
208
Pathology of appendicitis?
Sudden inflammation of the appendix, usually initiated by the obstruction of the lumen of the appendix
Lumen of the appendix becomes obstructed resulting in the invasion of gut organisms into the appendix wall
Leads to oedema, ischaemia, necrosis and inflammation
209
Name 3 causes of appendicitis?
```
Faecolith
Lymphoid hyperplasia
Filarial worms
Normal stool blocking the lumen
Infective agents
```
210
Symptoms of appendicitis?
Pain in the umbilical region that migrates to the right iliac fossa
- Early inflammation irritates the structure and walls of the appendix so a colicky pain is referred to the mid-abdomen around the umbilical area
- As the inflammation continues it irritates the parietal peritoneum and the pain settles at McBurney’s point
Anorexia
Nausea and vomiting
Constipation is usual but may also have diarrhoea
211
What are 3 signs of appendicitis?
Tenderness in the right iliac fossa with guarding due to localised peritonitis
May be a tender mass in the right iliac fossa
Low grade pyrexia
212
Name 2 complications that can arise from appendicitis?
Perforation
Wound infection
Appendix mass
- Omentum and small bowel adhere to the appendix
- Usually presents with a fever and palable mass
Appendix abscess
213
What investigations do you do for appendicitis? What is the gold standard?
Essentially a clinical diagnosis
Blood tests
Raised WCC
Neutrophil leukocytosis
Elevated ESR and CRP
Ultrasound can detect an inflamed appendix
CT is the gold standard for diagnosis and will show an enlarged appendix
214
Treatment for appendicitis?
Laparoscopic appendectomy
| IV prophylaxis antibiotics
215
What is gastritis?
Lining of the stomach becomes inflamed after mucosal damage
216
How does H.pylori infection cause gastritis?
Bacteria that live in the mucin layer of the stomach and are ingested
Bacteria produce chemicals which attract acute inflammatory cells to the mucin which damage cells
217
How does an autoimmune reaction cause gastritis?
What does it lead to?
Affects the fundus and body
| Atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia
218
How do NSAIDs cause gastritis?
Inhibit prostaglandin synthesis via the inhibition of COX enzyme leading to less mucus production and therefore gastritis
219
Name 3 causes of gastritis?
```
H.pylori infection
Autoimmune
NSAIDs
Viruses (CMV, herpes simplex)
Duodenogastric reflux - bile salts enter the stomach and damage mucin protection
Mucosal ischaemia
Increased acid
Alcohol
```
220
How does gastritis present?
Epigastric pain
Vomiting
Abdominal bloating
Indigestion
221
Investigation for gastritis?
Upper GI endoscopy
222
Treatment for gastritis?
Remove any causative agents e.g alcohol
Reduce stress
H.pylori eradication therapy
PPI
Amoxicillin
Metronidazole
H2 antagonist e.g ranitidine or cimetidine
Antacids
223
What is a consequence of bowel obstruction?
If you have an obstruction food will begin to accumulate which causes bacterial growth
224
What are the three different types of bowel obstruction?
Intraluminal - material inside the lumen
Intramural - something in the wall of the bowel that is causing bowel to constrict causing obstruction
Extraluminal - something on the outside of the intestinal wall pushing down on the bowel and decreasing it’s size
225
Name three causes of intraluminal bowel obstruction?
Tumour (carcinoma or lymphoma)
Meconium ileus
- SI obstruction resulting from thickening and desiccation of the vicious meconium. Commonly seen in cystic fibrosis
Gallstone ileus
- caused by impaction of a gallstone within the lumen of the small intestine. Commonly caused by a fistula
226
What is the difference in presentation between a RHS and LHS intraluminal tumour causing obstruction?
If on the RHS the material inside the bowel is more liquid so will cause less of an obstruction
If on the LHS the faecal material is more solid
227
Name three causes of intramural intestinal obstruction?
Inflammatory - Crohn's, diverticulitis
Tumours
Neural - Hirschsprung's disease
228
What is Hirschsprung's disease
Congenital aganglionic megacolon.
Failure of neuroblasts to migrate into the developing gut leading to failure of intramural parasympathetic nerve plexuses to develop.
There is no contraction or circular muscle in the gut wall leading to small bowel obstruction
229
What is the histologocal diagnosis of Hirschsprung's disease?
there are no ganglion cells in the submucosal and myenteric plexuses
230
Name 3 causes of extraluminal intestinal obstruction?
Adhesions
Fibrous adhesions between loops of bowel
Volvulus
360 degrees twist in the bowel that occludes it’s lumen
SI or sigmoid (occurs at the part of bowel with mesentery)
Tumour
Mainly ovarian cancer
231
Where do volvulus usually occur?
SI or sigmoid (occurs at the part of bowel with mesentery)
232
What are the symptoms of a small bowel obstruction?
```
Vomiting presents early
Pain is colicky to constant (diffuse)
Constipation presents late
Distension, will probably be less marked
Tenderness
Progress is faster
```
233
What are the symptoms of large bowel obstruction?
```
Abdominal discomfort
Fullness/bloating/nausea
Vomiting
Late presentation
Faeculent
Constipation presents early
There may be a history of progressive constipation of change in bowel habits
Abdominal pain
```
234
What is the presentation of a volvulus?
Sudden
Pain
Localised tenderness and distension
235
What are the signs of intestinal obstruction?
Distension (more marked the lower the obstruction)
Tympany (hollow sound) due to an air filled stomach
High pitched and irregular bowel sounds
Look for signs of dehydration
If there is strangulation or perforation there will be features of an acute abdomen
236
What are three complications of an intestinal obstruction?
Bowel ischaemia
Perforation
Sepsis
237
What investigations do you do in a patient that has an intestinal obstruction?
```
Fluid charts
Abdominal X-ray
Bloods
FBC
U&Es
Creatinine
Glucose may be high due to stress
```
CT scan of abdomen
Ultrasound
238
What is the conservative treatment for intestinal obstruction?
Fluid resuscitation
Electrolyte replacement
Bowel rest
Intestinal decompression
239
What is the surgical treatment for patients with intestinal obstruction?
Laparotomy required without a clear diagnosis
Bowel resection
Prophylactic antibiotics
240
What is a non-surgical treatment of intestinal obstruction?
Endoscopic stenting (usually palliative)
241
How do you treat a volvulus?
Decompression
242
what is pseudo-obstruction of the intestine?
A false obstruction of the intestine
condition characterized by impairment of the muscle contractions that move food through the digestive trac
243
What can cause a pseudo-obstruction of the intestine?
Myopathy - there is no peristaltic contractions
Neuropathy
- Hirschsprung's disease
- no innervation so abnormal movement of muscle
244
What can pseudo-obstruction lead to?
Sepsis
245
What is a diverticulum?
Outpouching of the gut wall
| Usually at the sites of perforating arteries
246
What is diverticulitis?
Diverticulitis is evidence of diverticular inflammation
247
Where does diverticulitis most commonly occur?
Most commonly seen in the sigmoid colon in the taenia coli
248
What is the pathology of diverticulitis?
1. Diverticular form at gaps in the wall of the gut where blood vessels penetrate
2. Sigmoid motility is sensitive to the bulk of colonic contents - if this is low then abnormally high intraluminal pressures are generated to help move faeces along
3. Pressure pushes the mucosa into and out of the wall leading to pouches of mucosa being formed
4. Faeces can become stuck and obstruct these diverticular causing stagnation and allowing the bacteria to multiply producing inflammation
249
What are the causes of diverticulitis?
Low fibre diet
Obesity in the young
Smoking
NSAIDs
250
What are the symptoms of diverticulitis?
```
Left iliac fossa pain
Pain may be intermittent or constant and may be associated with a change in bowel habits
Fever
Tachycardia
Anorexia
Nausea
Vomiting
```
251
What are the signs of diverticulitis?
Hypotension
Localised tenderness
Guarding and rigidity on the left side of the abdomen
A palpable mass can be occasionally felt
Reduced bowel sounds
Rectal examination may reveal tenderness or a mass
252
Name three complications of diverticulitis?
Abscess
Perforation
Fistula
Hemorrhage
253
What investigations do you do in diverticulitis?
Blood tests
Polymorphonuclear leukocytosis
ESR raised
CRP raised
CT colonography
Shows colonic wall thickening and diverticula
Abdominal erect X-ray - may identify obstruction of free air
254
What is the treatment for mild attacks of diverticulitis?
ciprofloxacin
| Paracetamol
255
What is the treatment for diverticulitis and signs of systemic disease?
Bowel rest
IV fluids
IV antibiotics
Paracetamol
256
What surgery may be needed for patients with diverticulitis and when is it indicated?
```
Surgery - bowel resection
Faecal peritonitis
Uncontrolled sepsis
Fistula
Obstruction
```
