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nutrition and digestion > disorders of the upper GI tract 2 W7 > Flashcards

disorders of the upper GI tract 2 W7 Flashcards

1
Q

what is oesophageal sticture

A

narrowing of oesophagus

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2
Q

benign oesophageal stricture causes and features?

A

GORD up to 10%
Barrett’s
extrinsic compression
post-radiotherapy
anastomotic (following surgery)
rings and webs
corrosive

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3
Q

causes of malignant oesophageal stricture?

A

oesophageal cancer

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4
Q

benign oesophageal stricture treatment?

A

proton pump inhibitors eg omeprazole
dilatation (CRE balloon or push dilators)

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5
Q

what is Barrett’s oesophagus?

A

specialised intestinal metaplasia in lower oesophagus

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6
Q

what happens in Barrett’s oesophagus?

A

oesophagus tries to defend itself from GORD. grows stomach-like epithelium - gastric columnar epithelium grows within squamous epithelium of oesophagus (because stomach lining is more robust)
prone to development of dysplastic changes, therefore considered to be premalignant condition (adenocarcinoma
)

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7
Q

what percentage of Barrett’s turns into cancer?

A

0.3%

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8
Q

treatment of Barrett’s?

A

surveillance - give patients regular endoscopies

ablation - burn area to destroy cells and prevent development

long term treatment with proton pump inhibitors

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9
Q

oesophageal cancer types?

A

adenocarcinoma
squamous cell carcinoma

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10
Q

oesophageal adenocarcinoma features?

A

lower third oesophagus
younger
reflux (Barrett’s)
obesity
more common
increasing

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11
Q

oesophageal squamous cell carcinoma features?

A

mid/upper oesophagus
older
smoking
alcohol
less common
declining (in western world)

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12
Q

major risk factors for oesophageal adenocarcinoma?

A

GORD/Barrett’s oesophagus
high BMI (central obesity)
age >50y
male
genetic

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13
Q

investigation of oesophageal cancer?

A

endoscopy
CT and ultrasound

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14
Q

what information does ultrasound give us about oesophageal cancer

A

depth of invasion of tumour

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15
Q

staging of oesophageal cancer

A

TNM:
tumour
nodes
metastases

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16
Q

palliation aims for malignant strictures?

A

to relive the symptoms without necessarily altering the course of the disease or prolonging life if curative treatment not possible. emphasis on improving quality of life.

stent - forces opening of lumen of oesophagus, doesn’t change prognosis by improves quality of life.

17
Q

what is achalasia?

A

failure of the LOS relaxation

18
Q

achalasia features?

A

absence of peristalsis
degenerative lesion of oesophageal innervation
presents with dysphagia to liquids and solids, weight loss, chest pain
endoscopic appearances usually normal
can progress to oesophageal dilatation, resp complications.

19
Q

achalasia manometry?

A

raised LOS pressure
failure of LOS relaxation
absent peristalsis

20
Q

treatment of achalasia?

A

endoscopic pneumatic dilatation
surgical myotomy (weaken sphincter)
botox injection to LOS (elderly)
POEM

21
Q

endoscopic pneumatic dilatation features?

A

balloon stretches, disrupts lower oesophageal sphincter. food drops from oesophagus to stomach.
can create problems - acid reflux.

22
Q

eosinophilic oesophagitis features?

A

eosinophilia only in oesophagus
many eosinophils in biopsy
‘asthma of the oesophagus’

23
Q

eosinophilic oesophagitis treatment?

A

swallowed topical steroid - orodispersible budesonide (Jorvesa) - most important treatment!

PPI therapy may help
6-food elimination diets - children>adults (dairy, eggs, nuts, soya, shellfish, wheat)

24
Q

proton pump inhibitors (PPIs) pharmacology?

A

protonated and unstable in acid pH
enteric coated
ionic trapping by acid pH inside parietal cells
irreversibly bind to proton pump (hydrogen potassium pump)

25
Q

what should PPIs be used with? why?

A

NSAIDs or aspirin
effective prevention of NSAID ulcers and complications

26
Q

adverse effects of PPIs?

A

microscopic colitis (most common reason to stop treatment)
osteoporosis
B12 deficiency proteins
gastric cancer (likely confounding)
iron deficiency
enteric infections

27
Q

peptic ulcer features?

A

can be gastric or duodenal
can be benign or malignant
endoscopy, biopsies
mainly caused by helicobacter pylori.

28
Q

how can helicobacter survive in acidic environments? (the stomach)

A

can utilise urease and produce bicarbonate and ammonia. ammonia buffers acid.

29
Q

first line tests for helicobacter infection?

A

breath test
stool test

30
Q

what increases the risk of ulcers and bleeding in HP-positive patients?

A

aspirin/NSAIDs

31
Q

what does evidence link HP to?

A

unexplained iron deficiency anaemia
I.T.P.
vit B12 deficiency

32
Q

HP eradication therapy?

A

antibiotics:

lansoprazole
clarithromycin
metronidazole

nutrition and digestion (49 decks)

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