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Gastrointestinal RT > Oesophago-Gastric-Duodenal Pathology > Flashcards

Oesophago-Gastric-Duodenal Pathology Flashcards

1
Q

what are the 2 main types of cancer within the oesophagus?

which is most common

A

adenocarcinoma (most common)

squamous cell carcinoma

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2
Q

what is the cause of oesophageal adenocarcinomas?

A

recurrent gastric reflux

squamous epithelium metaplasia into columnar epithelium (which can handle the acid)

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3
Q

what is the cause of oesophageal squamous cell carcinoma?

A

stress (due to smoking or alcohol) turn cells dysplastic

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4
Q

what are the 3 main types of gastric cancer?

A

adenocarcinoma (most common)
Gastrointestinal Stromal Tumours (GIST)
Lymphomas

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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

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6
Q

what gastric cancer are H.pylori associated with?

A

adenocarcinomas

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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)

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8
Q

what type of carcinomas are gastro-oesophageal junction cancers?

A

adenocarcinoma

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9
Q

what is the difference between dysphagia and odynophagia?

A 
dysphagia= hard to swallow
odynophagia= pain on swallowing
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10
Q

what is dysphonia?

A

change in speech

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11
Q

why might an oesophageal cancer cause dysphonia?

A

if it effects the recurrent laryngeal nerve

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12
Q

why might an oeosphageal cancer cause regurgitation?

A

food has been swallowed and stored in oesophagus because it can’t get through

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13
Q

what is dyspepsia?

A

epigastric pain/discomfort

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14
Q

what lymph nodes are likely to be metastasised from oesophageal cancers?

A

supraclavicular

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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
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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

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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
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18
Q

what excludes you from having surgery on an oeosphageal cancer?

A

metastases

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19
Q

what location of oesophageal cancer tends to respond best to radical radiotherapy?

A

cervical oesophagus

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20
Q

what palliative mechanisms for oesophageal cancer are there?

A 
radiotherapy
intubation/stentes
canalisation (ie for laser/alcohol)
photodynamic therapy
terminal care
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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

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22
Q

what is malignant ascites?

A

malignant cells found in fluid in peritoneal cavity

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23
Q

what are the 2 types of surgery used for gastric cancer?

A

total gastrectomy

partial gastrectomy

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24
Q

what type of lesions is a total gastrectomy used for?

A

proximal lesions

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25
Q

what type of surgery is a partial gastrectomy usef for?

A

distal lesions

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26
Q

why is being very young an adverse prognostic feature in gastric cancer? (in addition to being very old)

A

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

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27
Q

what are oesophageal varices?

A

high pressure veins that bulge into your oesophagus due to portal hypertension

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28
Q

what is angiodysplasia?

A

chaotic abnormal blood vessels growing on the surface of the gut

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29
Q

what is Barretts oeosphagus?

A

a premalignant metaplastic change of the squamous cells to columnar cells due to chronic reflux

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30
Q

what is haematemesis?

A

vomiting blood

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31
Q

what is malaena?

A

black tarry stools associated with upper GI bleeding

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32
Q

what techniques can be used to stop varices bleeding or ulcers bleeding?

A 
band ligation
sclerosant
glue
heater (cautery) probe
injection with vasoconstrictors
clip ligation
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33
Q

what is the function of sclerosant?

A

injected into the bleeding blood vessel and causes intense inflammation which stops the bleeding

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34
Q

what are strictures?

A

narrowings that occur throughout the GI tract

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35
Q

how are strictures managed?

A

balloon dilatation

metal/biodegradable stents

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36
Q

what is a polypectomy?

A

band ligation of a polyp

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37
Q

what does acute gastritis tend to be a complication of?

A

major trauma

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38
Q

which is more common- acute or chronic gastritis?

A

chronic gastritis

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39
Q

what are the 3 main types of chronic gastritis?

A

autoimmune
bacterial
chemical

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40
Q

what antibodies are produced in autoimmune chronic gastritis?

A

anti-parietal and anti-intrinsic factor antibodies

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41
Q

what is the result of the autoantibodies produced in autoimmune chronic gastrities?

A

atrophy and intestinal metaplasia
macrocytic pernicious anaemia
increased risk of malignancy

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42
Q

what causes macrocytic pernicious anaemia in autoimmune gastritis?

A

intrinsivc factor autoantibodies result in reduced b12 being absorbed

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43
Q

compare macrocytic anaemia with microcytic anaemia with respect to their causes?

A

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
Q

what supplement must you give to a patient with autoimmune chronis gastritis?

A

vitB12 supplements

45
Q

which bacteria is most associated with chronic gastritis?

A

H. pylori

46
Q

where is H. pylori’s niche in the stomach?

A

between epithelial cell surface and mucous barrier

47
Q

why does H. pylori cause chronic gastrits?

A

excites acute inflammatory repsonse, if not cleared this results in chronic active inflammation

48
Q

what 4 conditions does H. pylori gastritis increase risk of?

A

duodenal ulcer
gastric ulcer
gastric carcinoma
gastric lymphoma

49
Q

how do you test for H. pylori infection?

A

C13 urea breath test

faecal antigen testing

50
Q

what are the 3 main causes of chemical gastritis?

A

NSAIDs
alcohol
bile reflux

51
Q

why does bile reflux cause gastritis?

A

because bile starts to emulsify the lipid bilayer and thus it becomes broken down

52
Q

how do peptic ulcers form?

A

acid and enzymatic (pepsi) attack on the gastrointestinal mucosa causing a breach

53
Q

what is the difference between an intestinal type and diffuse type gastric adenocarcinomas?

A

intestinal type: polypoid mass

diffuse type- infiltrates stomach wall

54
Q

which type- intestinal or diffuse- gastric adenocarcinoma has a greater chance of resection?

A

intestinal gastric adenocarcinoma

55
Q

what happens to the stomach wall in a diffuse type gastric adenocarcinoma?

A

thick, rigid wall that lacks distendability is developed

56
Q

the imbalance of what 2 things predisposes to ulcers?

A
  1. acid + enzymatic attack

2. mucosal barrier

57
Q

what are the 2 subtypes of oesophagitis?

A

acute (rare)

chronic (common)

58
Q

what are the 2 main causes of acute oesophagitis?

A
  • corrosive esophagitis following chemical ingestion

- infective oesophagitis in immunocompromised patients

59
Q

what is the main cause of chronic oesophagitis?

A

reflux oesophagitis

60
Q

what is reflux oesophagitis?

A

inflammation of oesophagus doe to refluxed low pH gastric content

61
Q

why can obesity and pregnancy cause a defective LOS resulting in reflux oesophagitis?

A

they both increase intra-abdominal pressure which puts strain on the sphincter

62
Q

what are the 3 main complications of chronic reflux?

A

ulceration
stricture
barrets oesophagus

63
Q

what is allergic oeosphagitis?

A

a rare chronic condition where allergic causes causes chronic inflammation of the oesophagus- eosinophil mediated

64
Q

what is the treatment for allergic oesophagitis?

A

steroids
chromoglycate
montelukast

65
Q

what is the only benign oesophageal tumour?

A

squamous papilloma (rare)

66
Q

where is an adenocarcinoma of the oeosphagus most common?

A

lower 1/3

this is the area reflux occurs

67
Q

what is the pathogenesis of an adenocarcinoma of the oesophagus?

A
  1. reflux disease
  2. chronic reflux oesophagitis
  3. Barretts Oesophgus
  4. low grade dysplasia
  5. high grade dysplasia
  6. adenocarcinoma
68
Q

what is the Rome III criteria of dyspepsia?

A
  • epigastric pain or burning
  • postprandial fullness
  • early satiety
69
Q

what category do postprandial fullness and early satiety fall under?

A

postprandial distress syndrome

70
Q

what are the structures of the foregut?

A 
oesophagus
stomach
duodenum (1/2)
pancreas (1/2)
gallbladder
71
Q

what are the 4 main causes of dyspepsia?

A

peptic ulcer disease
drugs (NSAIDs)
gastric cancer
idiopathic (‘functional’)

72
Q

what are the examination findings of non-complicated dyspepsia?

A

epigastric tenderness only

73
Q

what are the examination findings of complicated dyspepsia?

A
  • weight loss
  • abdominal mass
  • evidence of gastric -outflow obstruction
  • peritonism
74
Q

what are the signs of gastric outflow obstruction on exmination?

A

distension

succusion splash on auscultation

75
Q

what are the alarm features that need to be checked in a patient who present with dyspepsia?

A 
dysphagia
evidence of GI blood loss
persistent vomiting
unexplained weight loss
upper abdominal mass
76
Q

what is the management of a patient who presents with dyspepsia has no alarm symptoms?

A

‘test and treat’ strategy
check H. pylori status:
-if positive, eradicate + confirm
-if negative, acid inhibition (eg PPI)

77
Q

what is the management of a patient who presents with dyspepsia and has alarm symptoms?

A

refer to hospital specialist

78
Q

what type of dyspepsia do peptic ulcers cause?

A

pain rather than post prandial distress syndrome

79
Q

what are the main 2 causes of peptic ulcer disease?

A

H. pylori

NSAIDs

80
Q

how does H. pylori spread?

A

faecal-oral/-oral oral spread

81
Q

when do G cells secrete gastrin?

A

high pH in stomach

82
Q

what is the pathogenesis of H.pylori causing gastric cancer?

A
  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
Q

what is the pathogenesis of H. pylori causing duodenal ulcers?

A
  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
Q

what happens to the stomach mucosa in an atrophic state?

A

loss of folds, stomach becomes smooth and featureless

85
Q

why must you give PPI’s only after testing for H. pylori?

A

PPIs can give false negatives

86
Q

what enzyme to H. Pylori make which cleaves urea into ammonium bicarbonate?

A

urease

87
Q

what is the treatment for peptic ulcer disease?

A

‘test and treat’ for H pylori
if positive, eradicate and confirm
if negative, antisecretory therapy (PPIs)
withdraw NSAIDs

88
Q

what is the therapy for eradication of H pylori infection?

A

triple therapy for 1 week
PPI + amoxicillin 1g bd + clarithromycin 500mg bd

OR
PPI _ metronidazole 400mg bd + clarithromycin 250mg bg

89
Q

what are the common side effects of triple therapy for H. pylori eradication?

A

nausea diarrhoea

90
Q

after triple therapy for eradication of H pylori what do you do if patient is still symptomatic?

A

retest

91
Q

what are the 4 main complications of peptic ulcer disease?

A

anaemia
bleeding
perforation
gastric outlet/duodenal obstruction

92
Q

what is the post therapy follow up for a duodenal ulcer?

A

uncomplicated duodenal ulcer requires no follow up apart from confirmation of clearance
if symptoms persist then follow up

93
Q

what is the post therapy follow up for a gastric ulcer?

A

follow up endoscopy at 6-8 weeks regardless of clearance of symptoms

94
Q

what determines whether H. pylori is going to cause acid hyposecretion (by reducing number of parietal cells) or acid hypersecretion (by inhibiting somatostatin)?

A

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
Q

what are the 3 main reasons for gastro-oesophageal reflux disease?

A

incompetent LOS
poor oesophageal clearnace (decreased peristalsis)
visceral sensitivity

96
Q

what are the investgations used for GORD suspicion?

A

endoscopy
barium swallow
oeeophageal manometry and pH studies
nuclea studies

97
Q

what are the lifestyle modifications to prevent GORD?

A

stop smoking
lose weight (if obese)
prop up the bed head
avoid provoking factors (alcohol and fatty food etc)

98
Q

what is the management of oeosophageal dysplasia? (pre-malignant)

A 
more frequent surveillance
optimise PPI dose
endoscopic mucosal resection
radiofreq ablation (halo)
argon
99
Q

what is gastroparesis?

A

delayed gastric emptying but with no physical obstruction

100
Q

what are the symptoms of gastroparesis?

A 
post-prandial fullnes
bloating
nausea
vomiting
weight loss
upper abdominal pain
101
Q

what illicit drug is associated with gastroparesis?

A

cannabis

102
Q

what medication is associated with gastroparesis?

A

opiates, anticholinergics

103
Q

how do you investigate suspected gastroparesis?

A

gastric emptying studies

104
Q

what is the management of gastroparesis?

A 
removal of precipitating factors eg drugs
liquid diet
eat little and often
promotility agents
gastric pacemaker
105
Q

what is achalasia?

A

a disorder of the oeosphagus which prevents peristalasis from functioning properly

Gastrointestinal RT (15 decks)

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