Oesophago-Gastric-Duodenal Pathology Flashcards
(105 cards)
1
Q
what are the 2 main types of cancer within the oesophagus?
which is most common
A
adenocarcinoma (most common)
squamous cell carcinoma
2
Q
what is the cause of oesophageal adenocarcinomas?
A
recurrent gastric reflux
squamous epithelium metaplasia into columnar epithelium (which can handle the acid)
3
Q
what is the cause of oesophageal squamous cell carcinoma?
A
stress (due to smoking or alcohol) turn cells dysplastic
4
Q
what are the 3 main types of gastric cancer?
A
adenocarcinoma (most common)
Gastrointestinal Stromal Tumours (GIST)
Lymphomas
5
Q
where do gastrointestinal stromal tumours develop?
A
in the wall of the GI tract and not the epithelium like 90% of GI cancers
6
Q
what gastric cancer are H.pylori associated with?
A
adenocarcinomas
7
Q
what are the 3 types of gastro-oesophageal junction cancer?
A
type 1: oesophageal (just above junction growing distally)
type 2: true junctions
type 3: gastric (occus in cardia and grow proximally)
8
Q
what type of carcinomas are gastro-oesophageal junction cancers?
A
adenocarcinoma
9
Q
what is the difference between dysphagia and odynophagia?
A
dysphagia= hard to swallow odynophagia= pain on swallowing
10
Q
what is dysphonia?
A
change in speech
11
Q
why might an oesophageal cancer cause dysphonia?
A
if it effects the recurrent laryngeal nerve
12
Q
why might an oeosphageal cancer cause regurgitation?
A
food has been swallowed and stored in oesophagus because it can’t get through
13
Q
what is dyspepsia?
A
epigastric pain/discomfort
14
Q
what lymph nodes are likely to be metastasised from oesophageal cancers?
A
supraclavicular
15
Q
how do you diagnose an oesophageal or gastric cancer?
A
upper GI endoscopy+ biopsy barium meal CT scan of chest and abdomen PET scan bronchscopies
16
Q
why are fitness studies needed to be under taken before an operation of the oeosphagus can take place?
A
operation is severe and only fit patients can undertake it
17
Q
what are the 7 alarm features which might suggest oesophageal/gastric cancer?
A
>55 years of age dysphagia GI blood loss persistent vomiting unexplained weight loss upper abdominal mass anaemia
18
Q
what excludes you from having surgery on an oeosphageal cancer?
A
metastases
19
Q
what location of oesophageal cancer tends to respond best to radical radiotherapy?
A
cervical oesophagus
20
Q
what palliative mechanisms for oesophageal cancer are there?
A
radiotherapy intubation/stentes canalisation (ie for laser/alcohol) photodynamic therapy terminal care
21
Q
what are the 3 main contraindications of having surgery to remove a gastric cancer?
A
widely metastatic disease
malignant ascites
brief life expectency
22
Q
what is malignant ascites?
A
malignant cells found in fluid in peritoneal cavity
23
Q
what are the 2 types of surgery used for gastric cancer?
A
total gastrectomy
partial gastrectomy
24
Q
what type of lesions is a total gastrectomy used for?
A
proximal lesions
25
what type of surgery is a partial gastrectomy usef for?
distal lesions
26
why is being very young an adverse prognostic feature in gastric cancer? (in addition to being very old)
because gastric cancer is very aggressive in the young
young females who develop gastric cancer below 40 all die within a year whether they have surgery or not- tumour is very aggressive and feeds off female hormones
27
what are oesophageal varices?
high pressure veins that bulge into your oesophagus due to portal hypertension
28
what is angiodysplasia?
chaotic abnormal blood vessels growing on the surface of the gut
29
what is Barretts oeosphagus?
a premalignant metaplastic change of the squamous cells to columnar cells due to chronic reflux
30
what is haematemesis?
vomiting blood
31
what is malaena?
black tarry stools associated with upper GI bleeding
32
what techniques can be used to stop varices bleeding or ulcers bleeding?
```
band ligation
sclerosant
glue
heater (cautery) probe
injection with vasoconstrictors
clip ligation
```
33
what is the function of sclerosant?
injected into the bleeding blood vessel and causes intense inflammation which stops the bleeding
34
what are strictures?
narrowings that occur throughout the GI tract
35
how are strictures managed?
balloon dilatation
| metal/biodegradable stents
36
what is a polypectomy?
band ligation of a polyp
37
what does acute gastritis tend to be a complication of?
major trauma
38
which is more common- acute or chronic gastritis?
chronic gastritis
39
what are the 3 main types of chronic gastritis?
autoimmune
bacterial
chemical
40
what antibodies are produced in autoimmune chronic gastritis?
anti-parietal and anti-intrinsic factor antibodies
41
what is the result of the autoantibodies produced in autoimmune chronic gastrities?
atrophy and intestinal metaplasia
macrocytic pernicious anaemia
increased risk of malignancy
42
what causes macrocytic pernicious anaemia in autoimmune gastritis?
intrinsivc factor autoantibodies result in reduced b12 being absorbed
43
compare macrocytic anaemia with microcytic anaemia with respect to their causes?
macrocytic anaemia is to with a problem with the production of RBCs (eg vit B12 deficiency)
microcytic anamia is to do with a problem with the production of haemoglobin (eg iron deficiency)
44
what supplement must you give to a patient with autoimmune chronis gastritis?
vitB12 supplements
45
which bacteria is most associated with chronic gastritis?
H. pylori
46
where is H. pylori's niche in the stomach?
between epithelial cell surface and mucous barrier
47
why does H. pylori cause chronic gastrits?
excites acute inflammatory repsonse, if not cleared this results in chronic active inflammation
48
what 4 conditions does H. pylori gastritis increase risk of?
duodenal ulcer
gastric ulcer
gastric carcinoma
gastric lymphoma
49
how do you test for H. pylori infection?
C13 urea breath test
| faecal antigen testing
50
what are the 3 main causes of chemical gastritis?
NSAIDs
alcohol
bile reflux
51
why does bile reflux cause gastritis?
because bile starts to emulsify the lipid bilayer and thus it becomes broken down
52
how do peptic ulcers form?
acid and enzymatic (pepsi) attack on the gastrointestinal mucosa causing a breach
53
what is the difference between an intestinal type and diffuse type gastric adenocarcinomas?
intestinal type: polypoid mass
| diffuse type- infiltrates stomach wall
54
which type- intestinal or diffuse- gastric adenocarcinoma has a greater chance of resection?
intestinal gastric adenocarcinoma
55
what happens to the stomach wall in a diffuse type gastric adenocarcinoma?
thick, rigid wall that lacks distendability is developed
56
the imbalance of what 2 things predisposes to ulcers?
1. acid + enzymatic attack
| 2. mucosal barrier
57
what are the 2 subtypes of oesophagitis?
acute (rare)
| chronic (common)
58
what are the 2 main causes of acute oesophagitis?
- corrosive esophagitis following chemical ingestion
| - infective oesophagitis in immunocompromised patients
59
what is the main cause of chronic oesophagitis?
reflux oesophagitis
60
what is reflux oesophagitis?
inflammation of oesophagus doe to refluxed low pH gastric content
61
why can obesity and pregnancy cause a defective LOS resulting in reflux oesophagitis?
they both increase intra-abdominal pressure which puts strain on the sphincter
62
what are the 3 main complications of chronic reflux?
ulceration
stricture
barrets oesophagus
63
what is allergic oeosphagitis?
a rare chronic condition where allergic causes causes chronic inflammation of the oesophagus- eosinophil mediated
64
what is the treatment for allergic oesophagitis?
steroids
chromoglycate
montelukast
65
what is the only benign oesophageal tumour?
squamous papilloma (rare)
66
where is an adenocarcinoma of the oeosphagus most common?
lower 1/3
| this is the area reflux occurs
67
what is the pathogenesis of an adenocarcinoma of the oesophagus?
1. reflux disease
2. chronic reflux oesophagitis
3. Barretts Oesophgus
4. low grade dysplasia
5. high grade dysplasia
6. adenocarcinoma
68
what is the Rome III criteria of dyspepsia?
- epigastric pain or burning
- postprandial fullness
- early satiety
69
what category do postprandial fullness and early satiety fall under?
postprandial distress syndrome
70
what are the structures of the foregut?
```
oesophagus
stomach
duodenum (1/2)
pancreas (1/2)
gallbladder
```
71
what are the 4 main causes of dyspepsia?
peptic ulcer disease
drugs (NSAIDs)
gastric cancer
idiopathic ('functional')
72
what are the examination findings of non-complicated dyspepsia?
epigastric tenderness only
73
what are the examination findings of complicated dyspepsia?
- weight loss
- abdominal mass
- evidence of gastric -outflow obstruction
- peritonism
74
what are the signs of gastric outflow obstruction on exmination?
distension
| succusion splash on auscultation
75
what are the alarm features that need to be checked in a patient who present with dyspepsia?
```
dysphagia
evidence of GI blood loss
persistent vomiting
unexplained weight loss
upper abdominal mass
```
76
what is the management of a patient who presents with dyspepsia has no alarm symptoms?
'test and treat' strategy
check H. pylori status:
-if positive, eradicate + confirm
-if negative, acid inhibition (eg PPI)
77
what is the management of a patient who presents with dyspepsia and has alarm symptoms?
refer to hospital specialist
78
what type of dyspepsia do peptic ulcers cause?
pain rather than post prandial distress syndrome
79
what are the main 2 causes of peptic ulcer disease?
H. pylori
| NSAIDs
80
how does H. pylori spread?
faecal-oral/-oral oral spread
81
when do G cells secrete gastrin?
high pH in stomach
82
what is the pathogenesis of H.pylori causing gastric cancer?
1. H. pylori reduces number of parietal cells and therefore reduces HCl
2. G cells are stimulated to produce gastrin
3. hypergastraemia occurs- more gastrin released than parietal cell receptors present
4. this causes atrophy
5. dysplasia
(LOW ACID)
83
what is the pathogenesis of H. pylori causing duodenal ulcers?
1. H. pylori inhibits somatostatin
2. increased gastric secretion
3. increased HCl secretion
4. this is released into the duodenum causing ulcers
(HIGH ACID)
84
what happens to the stomach mucosa in an atrophic state?
loss of folds, stomach becomes smooth and featureless
85
why must you give PPI's only after testing for H. pylori?
PPIs can give false negatives
86
what enzyme to H. Pylori make which cleaves urea into ammonium bicarbonate?
urease
87
what is the treatment for peptic ulcer disease?
'test and treat' for H pylori
if positive, eradicate and confirm
if negative, antisecretory therapy (PPIs)
withdraw NSAIDs
88
what is the therapy for eradication of H pylori infection?
triple therapy for 1 week
PPI + amoxicillin 1g bd + clarithromycin 500mg bd
OR
PPI _ metronidazole 400mg bd + clarithromycin 250mg bg
89
what are the common side effects of triple therapy for H. pylori eradication?
nausea diarrhoea
90
after triple therapy for eradication of H pylori what do you do if patient is still symptomatic?
retest
91
what are the 4 main complications of peptic ulcer disease?
anaemia
bleeding
perforation
gastric outlet/duodenal obstruction
92
what is the post therapy follow up for a duodenal ulcer?
uncomplicated duodenal ulcer requires no follow up apart from confirmation of clearance
if symptoms persist then follow up
93
what is the post therapy follow up for a gastric ulcer?
follow up endoscopy at 6-8 weeks regardless of clearance of symptoms
94
what determines whether H. pylori is going to cause acid hyposecretion (by reducing number of parietal cells) or acid hypersecretion (by inhibiting somatostatin)?
pro-inflammatory host genotype (host response)
IL-1B genotype is more likely to go onto acid hyposecretion (gastric cancer causing)
no IL-1b genotype is more likely to go onto acid hypersecretion (duodenal ulcer causing)
95
what are the 3 main reasons for gastro-oesophageal reflux disease?
incompetent LOS
poor oesophageal clearnace (decreased peristalsis)
visceral sensitivity
96
what are the investgations used for GORD suspicion?
endoscopy
barium swallow
oeeophageal manometry and pH studies
nuclea studies
97
what are the lifestyle modifications to prevent GORD?
stop smoking
lose weight (if obese)
prop up the bed head
avoid provoking factors (alcohol and fatty food etc)
98
what is the management of oeosophageal dysplasia? (pre-malignant)
```
more frequent surveillance
optimise PPI dose
endoscopic mucosal resection
radiofreq ablation (halo)
argon
```
99
what is gastroparesis?
delayed gastric emptying but with no physical obstruction
100
what are the symptoms of gastroparesis?
```
post-prandial fullnes
bloating
nausea
vomiting
weight loss
upper abdominal pain
```
101
what illicit drug is associated with gastroparesis?
cannabis
102
what medication is associated with gastroparesis?
opiates, anticholinergics
103
how do you investigate suspected gastroparesis?
gastric emptying studies
104
what is the management of gastroparesis?
```
removal of precipitating factors eg drugs
liquid diet
eat little and often
promotility agents
gastric pacemaker
```
105
what is achalasia?
a disorder of the oeosphagus which prevents peristalasis from functioning properly
