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6 Gastroenterology
Food mountains, the pellagra paradox, and the sorrow that weeping
https://t.me/med1917
cannot symbolize
‘The sweet smell is a great sorrow on the land. Men who can graft the trees and
make the seed fertile and big can find no way to let the hungry people eat their
produce. . . The works of the roots of the vines, of the trees, must be destroyed to
keep up the price . . .
There is a crime here that goes beyond denunciation. There is a sorrow here
that weeping cannot symbolize. There is a failure here that topples all our success. The fertile earth, the straight tree rows, the sturdy trunks, and the ripe fruit.
And children dying of pellagra must die because a profit cannot be taken from an
orange. And coroners must fill in the certificates— died of malnutrition— because
the food must rot, must be forced to rot.
The people come with nets to fish for potatoes in the river, and the guards
hold them back; they come in rattling cars to get the dumped oranges, but the
kerosene is sprayed. And they stand still and watch the potatoes float by, listen
to the screaming pigs being killed in a ditch and covered with quicklime, watch
the mountains of oranges slop down to a putrefying ooze; and in the eyes of the
people there is a failure; and in the eyes of the hungry there is a growing wrath. In
the souls of the people the grapes of wrath are filling and growing heavy, growing
heavy for the vintage.’
How do John Steinbeck’s grapes grow in our
J Steinbeck, The Grapes of Wrath.
21
st- century soil? Too well; a
double harvest, it turns out, as not only is much of the world starving, amid plenty
(for those who can pay) but also there is a new ‘sorrow in our land that weeping
cannot symbolize’: pathological ‘voluntary’ self- starvation, again amid plenty, in
pursuit of the body- beautiful according to images laid down by media gods. If
gastroenterologists had one wish it might not be the ending of all their diseases,
but that humankind stand in a right relationship with Steinbeck’s fertile earth, his
straight trees, his sturdy trunks, and his ripe fruit.
241
Fig 6.
2
Petec hiae and pe rifolli cular ha em-
orrhage due to scurvy.
Scurvy; male figure. Wellcome Collection.
Attribution
4.0
International (CC BY 4.0).
Fig 6.
3
Dermatitis caused by chronic pellagra.
Courtesy of the CDC (https:// phil.cdc.gov/ Deta ils.
aspx?pid=
3757
).
6 Gastroenterology
The mouth
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242
The diagnosis will often come out of your patient’s mouth, so open it! So many GI
investigations are indirect... now is your chance for direct observation.
Leucoplakia (fig
6.4
attributable to any other known disease. It is a premalignant lesion, with squamous
cell carcinoma transformation rates ranging from <
riskier). Oral hairy leucoplakia is a shaggy white patch on the side of the tongue seen
HIV
, caused by
in
white lesions (see
EBV,
BOX
Aphthous ulcers (fig
or oral mucosa that heal without scarring.
coeliac disease; Behçet’s (
(herpes simplex, syphilis, Vincent’s angina,
(eg hard toothbrushes) and acidic foods or drinks. Tetracycline or antimicrobial
mouthwashes (eg chlorhexidine) with topical steroids (eg triamcinolone gel) and
topical analgesia. Severe ulcers: consider systemic corticosteroids or thalidomide
(absolutely contraindicated in pregnancy).
to exclude malignancy; refer if uncertain.
Candidiasis (thrush) (fig
cosa. Patches may be hard to remove and bleed if scraped.
DM
; antibiotics; immunosuppression (long- term corticosteroids, including in-
of age;
halers; cytotoxics; malignancy;
6
h). Oral fluconazole for non- responders or oropharyngeal thrush.
swallow/
Cheilitis (angular stomatitis) Fissuring of the mouth’s corners is caused by denture
problems, candidiasis, or deficiency of iron or riboflavin (vitamin
Gingivitis Gum inflammation ± hypertrophy occurs with poor oral hygiene, drugs
(phenytoin, ciclosporin, nifedipine), pregnancy, vitamin
acute myeloid leukaemia (
Microstomia (fig
6.7
the perioral skin after burns or in epidermolysis bullosa (destructive skin and mucous membrane blisters
Oral pigmentation Perioral brown spots characterize Peutz– Jeghers’ (p
Pigmentation anywhere in the mouth suggests Addison’s disease (
(eg antimalarials). Consider malignant melanoma.
osis; Osler– Weber– Rendu syndrome (
at the border of the oral mucosa and the lip vermilion.) Sebaceous cysts, common
and benign. Aspergillus niger colonization may cause a black tongue.
Teeth (fig
6.8
) A blue line at the gum– tooth margin suggests lead poisoning.
Prenatal or childhood tetracycline exposure causes a yellow– brown discolouration.
To ng ue Th is m ay b e fu rred or d ry ( xero sto mia ) in dehy drati on, dru g thera py,3 after
radiotherapy, in Crohn’s disease, Sjögren’s (
Glossitis Means a smooth, red, sore tongue, eg caused by iron, folate, or
fig
8.29
, p
331
ciency (
in colour and size, use the term geographic tongue (harmless migratory glossitis).
Macroglossia The tongue is too big. Causes: myxoedema; acromegaly; amyloid
p
364
). A ranula is a bluish salivary retention cyst to one side of the frenulum,
(
named after the bulging vocal pouch of frogs’ throats (genus Rana).
The most common site for oral cavity
cancer
). If local loss of papillae leads to ulcer- like lesions that change
firm edges. Risk factors: smoking, alcohol.
submental nodes; middle ⅓ to submandibular nodes; posterior ⅓ to deep cervical
nodes. Tre at me nt: radiotherapy or surgery. Surgery is recommended if good functional reconstruction can be achieved.
doubt, refer.
3
Drugs causing xerostomia:
cholinergics; bromocriptine; diuretics; loperamide; nifedipine; opiates; prazosin; prochlorperazine, etc.
4
Betel nut (Areca catechu) chewing, common in South Asia, may be an independent risk factor.
) An oral mucosal white plaque that will not rub o and is not
1
% to 36% (tongue lesions are
and is not premalignant. When in doubt, refer all intra- oral
).
6.5) 20
% of us get these shallow, painful ulcers on the tongue
Causes of severe ulcers Crohn’s and
p
554
); erythema multiforme; lichen planus; infections
p
698
). Minor ulcers: avoid oral trauma
Biopsy ulcers not healing after 3 weeks
6.6
) Causes white patches or erythema of the buccal mu-
Risk factors Extremes
HIV
). Nystatin suspension
p
354
), or Vincent’s angina (p
400 000U (4mL swill and
B
) (fig
8.21
2
C
deficiency (scurvy, p
698
).
, p
327
.)
240
) The mouth is too small, eg from thickening and tightening of
± ankyloglossia) or systemic sclerosis (p
548
).
694
p
220
) or drugs
Telangiectasia Systemic scler-
p
694
). Fordyce glands (Creamy yellow spots
p
548
), and Mikulicz’s syndrome (p
B
12
692
defi-
Tongue
SCC.
Appears as a raised ulcer with
4
Spread: anterior ⅓ of tongue drains to
5
yr survival (early disease): 70%. When in
ACE
- i; antidepressants; antihistamines; antipsychotics; antimuscarinics/ anti-
),
).
).
6 Gastroenterology
White intra- oral lesions
https://t.me/med1917
• Idiopathic keratosis.
• Leucoplakia.
• Lichen planus.
• Poor dental hygiene.
• Candidiasis.
• Squamous papilloma.
Fig 6.
4
Leucoplakia on the underside of the
tongue. It is important to refer leucoplakia because it is premalignant.
• Carcinoma.
• Hairy oral leucoplakia.
• Lupus erythematosus.
• Smoking.
• Aphthous stomatitis.
• Secondary syphilis.
Fig 6.
5
An aphthous ulcer inside the cheek. The
name is tautological: aphtha in Greek means
ulceration.
243
Fig 6.
6
White fur on an erythematous tongue
caused by oral candidiasis. Oropharyngeal candidiasis in an apparently fit patient may suggest
HIV
underlying
Fig 6.
caused by excessive fluoride intake.
infection.
8
White bands on the teeth can be
Fig 6.
7
Microstomia (small, narrow mouth),
eg from hardening of the skin in scleroderma
which narrows the mouth. It is cosmetically and
functionally disabling.
6 Gastroenterology
Endoscopy and biopsy
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244
Consent is needed for all these procedures; see p
Upper GI endoscopy Indications See table
op if possible ( pathology- masking). Nil by mouth for
24
h if sedation is used. Procedure Sedation optional, eg midazolam 1– 5mg slowly
IV
(to remain conscious; if deeper sedation is needed, propofol via an anaesthetist
(narrow therapeutic range)); nasal prong O
imetry). The pharynx may be sprayed with local anaesthetic before the endoscope is
passed. Continuous suction must be available to prevent aspiration.
Sore throat; amnesia from sedation; perforation (<
clopidogrel, warfarin, or
Duodenal biopsy The gold standard test for coeliac disease (p
DOAC
S, these need stopping only if therapeutic procedure).
566
.
6.3
. Pre- procedure Stop
6
h before. Don’t drive for
(eg 2L/ min; monitor respirations & ox-
2
0.1
%); bleeding (if on aspirin,
262
); also useful in un-
usual causes of malabsorption, eg giardiasis, lymphoma, Whipple’s disease.
Sigmoidoscopy Views the rectum + distal colon (to ~splenic flexure). Flexible
sigmoidoscopy has largely displaced rigid sigmoidoscopy for diagnosis of distal
colonic pathology, but
for the rapid assessment of severe ulcerative colitis, and can be used therapeutically, eg for polypectomy or decompression of sigmoid volvulus (
Phosphate enema
~
25
% of cancers are still out of reach. It can also be used
p
PR
1– 2 hours prior. Procedure Learn from an expert; do PR exam
first. Do biopsies— macroscopic appearances may be normal, eg amyloidosis,
microscopic colitis.
Colonoscopy Indications See table
diet on preceding day; split- dose laxative bowel preparation (± simethicone to reduce bubbles).
are given before colonoscope is passed and guided around the colon.
Abdominal discomfort; incomplete examination; haemorrhage after polypectomy (
150
in
Procedure Do PR first. Sedation (see earlier in topic) and analgesia
); perforation (<0.1%). See figs
erating machinery/ driving for
Video capsule endoscopy (
6.4
. Preparation Stop iron 1wk prior; low- fibre
6.9– 6.13
24
h, no flying for 1wk post- polypectomy.
VCE
) 1st line for evaluating obscure GI bleeding (p
. Post- procedure: no alcohol, and no op-
and to detect small bowel pathology. This is a rapidly evolving area; while it is the
gold standard for small bowel visualization, there are now
colonic and upper
endoscopy. Use small bowel imaging (eg contrast) or
patency capsule test ahead of
inal pain or symptoms suggesting small bowel obstruc-
Preparation Clear fluids only the evening before
tion.
then nil by mouth from morning until
swallowed.
lessly to capture device worn by patient. Normal activity can take place for the
Complications Capsule retention in 1% (endoscopic or surgical removal is
day.
needed)— avoid
struction, incomplete exam (eg slow transit, achalasia).
GI
capsule alternatives to traditional
VCE
if patient has abdom-
4
h after capsule
Procedure Capsule is swallowed (fig
MRI
for 2 wks after unless
AXR
Fig 6.
6.14
)— this transmits video wire-
confirms capsule has cleared; ob-
Problems No therapeutic
options; poor localization of lesions; may miss more subtle lesions.
Liver biopsy Route Percutaneous if
Indications 1 Diagnosis— chronic
sions/ cancer, pyrexia of unknown origin, suspected cirrhosis.
gold standard for severity (this indication being replaced by ultrasound- based
elastography).
Give analgesia.
Pre- op Nil by mouth for 8h. Are
Procedure Sedation may be given. The liver borders are percussed
INR
in range else transjugular with
LFT
of unknown aetiology; suspected hepatic le-
INR
<1.5 and platelets >50 ×
2
Staging fibrosis—
and where there is dullness in the mid- axillary line in expiration, lidocaine
filtrated down to the liver capsule. Consider
and a needle biopsy is taken with the breath held in expiration. Afterwards lie on
the right side for
30
min for 2h, then hourly until discharge 4h post- biopsy. Complications Local pain;
pneumothorax; bleeding (<
2
h, then in bed for 4h; check pulse and BP every 15min for 1h, every
0.5
%); death (<0.1%).
US/ CT
guidance. Breathing is rehearsed
PPI
S
2
wks pre-
Complications
603
). Preparation
Complications
14
PillCam®.
2
326
FFP
109/ L?
% is in-
1
)
.
6 Gastroenterology
Table 6.
CI
https://t.me/med1917
3
Indications for upper GI endoscopy
Diagnostic indications Therapeutic indications
Haematemesis/ melaena Treatment of bleeding lesions
Dysphagia Variceal banding and sclerotherapy
Dyspepsia (
55
yrs old + alarm symptoms
or treatment refractory,
p
248
)
Argon plasma coagulation for suspected
vascular abnormality
Duodenal biopsy (?coeliac) Stent insertion, laser therapy
Persistent vomiting and weight loss Stricture dilatation, polyp resection
Iron- deficiency anaemia Treatment of achalasia
Barrett's oesophagus surveillance
Table 6.
4
Indications for colonoscopy
Diagnostic indications Therapeutic indications
Rectal bleeding— when settled, if acute Haemostasis (eg by clipping vessel)
Iron- def. anaemia (/ non- menstruating ) Bleeding angiodysplasia lesion (argon
Persistent diarrhoea of unexplained cause
Positive faecal immunochemical test (
Assessment or suspicion of
IBD
beamer photocoagulation)
Colonic stent deployment (cancer)
FIT
)
Volvulus decompression (flexi sig)
Colon cancer surveillance Pseudo- obstruction
Polypectomy
Fig 6.
9
A big polyp seen on colonoscopy. An
advantage of colonoscopy over barium enema
is the ability to biopsy or intervene at the same
time— in this case, polypectomy.
Image courtesy of Dr Anthony Mee.
Fig 6.
10
Colonoscopic image of an adenocar-
p
608
cinoma—
fig
(
colour, larger, and more aggressive.
. Compared with a colonic polyp
6.9
), the carcinoma is irregular in shape and
Image courtesy of Dr J Simmons.
245
Fig 6.
11
Angiodysplasia lesion seen at colonoscopy. Bleeding may be brisk. : endoscopic obliteration. It is associated with aortic stenosis
(Heyde’s syndrome).
3
Image courtesy of Dr Anthony Mee.
Fig 6.
12
Colonic mucosa in active UC (p
red, inflamed, and friable (bleeds on touching).
Signs of severity: mucopurulent exudate, mucosal ulceration ± spontaneous bleeding. If qui-
escent, there may only be a distorted or absent
mucosal vascular pattern.
Fig 6.
ticulosis (
the colon, avoiding the false lumina of the diverticula, can be a challenge. Don’t go there if
diverticula are inflamed (diverticulitis): perforation is a big risk. Other
last month; ischaemic colitis (Oxford Handbook
of Gastroenterology and Hepatology, Second
Edition (Bloom et al.), p
Image courtesy of Dr J Simmons.
13
Colonoscopic image showing diver-
p
620
). Navigating safely through
to colonoscopy: MI in
165
Image courtesy of Dr J Simmons.
258
); it is
).
6 Gastroenterology
Dysphagia
OHCS
CNS
ABG
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246
Dysphagia is a sensation of dicult swallowing or food sticking after swallowing
and should prompt urgent investigation to exclude malignancy.
Causes Oropharyngeal or oesophageal? Structural or motility related? (See
Five questions to ask to help determine the cause
1 Is the problem initiating a swallow, or a feeling of food sticking seconds later?
Initiating: oropharyngeal, associated coughing/ choking. Sticking: oesophageal.
2
Was there diculty swallowing solids and liquids from the start?
Yes: neuromuscular (motility) disorder of the oesophagus.
No: solids then liquids: structural— suspect a stricture (benign or malignant).
3
Is the dysphagia progressive or intermittent?
Progressive: structural, slowly (peptic) or rapidly (malignant) stricture.
Intermittent: suspect oesophageal spasm.
4
Is swallowing painful (odynophagia)?
Yes: suspect oesophagitis (severe reflux, alcohol, viral infection, Candida in im-
munocompromised or poor steroid inhaler technique, medications) or spasm.
5
Does the neck bulge or gurgle? Yes : suspect a pharyngeal pouch (see
Signs Is the patient cachectic or anaemic? Examine the mouth; feel for supraclavicular
nodes (left supraclavicular node = Virchow’s node— suggests intra- abdominal malignancy); look for signs of systemic disease, eg systemic sclerosis (
Te st s
FBC
(anaemia);
suspicion of pharyngeal pouch consider contrast swallow (±
oscopy may help identify neurogenic causes. Oesophageal manometry for dysmotility.
Specific conditions Oesophagitis See p
intermittent dysphagia ± chest pain. Contrast swallow/ manometry: abnormal con-
5
Achalasia Coordinated peristalsis is lost and the lower oesophageal
tractions.
sphincter fails to relax (due to degeneration of the myenteric plexus), causing dysphagia, regurgitation, and weight. Characteristic findings on manometry or contrast
swallow showing dilated tapering oesophagus. Tr ea tm en t: endoscopic balloon dilatation, or Heller’s cardiomyotomy— then proton pump inhibitors (
toxin injection if a non- invasive procedure is needed (repeat every few months).
Calcium channel blockers and nitrates may also relax the sphincter.
geal stricture
surgery, or radiotherapy. Trea tm en t: endoscopic balloon dilatation.
cancer
Caused by gastro- oesophageal reflux disease (
(p
610
.) Associations: ,
tylosis (palmar hyperkeratosis), Plummer– Vinson syndrome (post- cricoid dysphagia,
upper oesophageal web + iron- deficiency).
and language therapist.
oesophageal disorder. Rule out a structural or motility cause and reassure.
Nausea and vomiting
Consider pregnancy where appropriate! Other causes, p52.
What’s in the vomit?
but represent one of the most over- called signs in clinical medicine— always verify
yourself and look for other evidence of
ognizable food ≈ gastric stasis; feculent ≈ small bowel obstruction.
Timing Morning ≈ pregnancy or
vomiting that relieves pain ≈ peptic ulcer; preceded by loud gurgling ≈
Tests Bloods
alkalosis from loss of gastric contents (pH >
Plain
suspicion of bleed or persistent vomiting. Consider head
Tre at me nt Identify and treat underlying causes. Symptomatic relief: table
emptive, eg pre- op for post- op symptoms. Try oral route first.
emetic, so be prepared to prescribe more than one. Give
severely dehydrated or nil by mouth, and monitor electrolytes and fluid balance.
FBC, U&E, LFT
AXR
If suspected bowel obstruction (p
BOX.
p
420
p
548
),
CNS
U&E
(dehydration). Upper GI endoscopy ± biopsy (fig
252
. Distal oesophageal spasm Causes
ENT
dis ease.
6.15
opi nion). Video fluor-
PPI
S, p
248
). Botulinum
Benign oesopha-
GORD,
p
250
), corrosives,
Oesophageal
GORD
, tobacco, alcohol, Barrett’s oesophagus (p
causes Ask for help from a speech
251
Globus sensation 'I've got a lump in my throat'; functional
Reports of ‘coee grounds’ may indicate upper GI bleeding
GI
bleeding (melaena, anaemia, urea); rec-
ICP
; 1h post food ≈ gastric stasis/ gastroparesis (DM);
2
+
, Ca
, glucose, amylase.
A metabolic (hypochloraemic)
7.45
712
−
, HCO
) indicates severe vomiting.
3
). Upper GI endoscopy (See p
CT
IV
fluid s with K+ replacement if
GI
obs truction .
in case
ICP
.
6.5
30
% need a 2nd- line anti-
244
. Be pre-
)
).
). If
),
). If
6 Gastroenterology
Causes of dysphagia
https://t.me/med1917
Oropharyngeal
Structural:
•
Pharyngeal pouch
• Cervical web
• Cricopharyngeal bar
• Oropharyngeal tumour.
Neuromuscular:
•
Cortical (pseudobulbar palsy (p
• Stroke (p
466
• Multiple sclerosis (p
• Motor neuron disease (p
• Wilson’s or Parkinson’s disease
• Bulbar palsy (p
• Syringobulbia (p
• Motor neuron disease (p
• Peripheral:
• Myasthenia gravis (p
• Poliomyelitis (p
• Guillain– Barré syndrome (p
Fig 6.
15
ture seen at endoscopy. Note the asymmetry and
heaped edges. Benign strictures have a smoother
appearance and tend to be circumferential.
Reproduced from Bloom et al., Oxford Handbook
of Gastroenterology and Hepatology,
)
503
):
512
432
A malignant lower oesophageal stric-
permission from Oxford University Press.
503
)):
492
)
502
)
)
502
)
508
)
)
500
).
2012
Oesophageal
Structural:
•
Benign stricture:
• Malignant stricture (fig
• Extrinsic pressure:
Neuromuscular:
•
Achalasia (see p
• Distal oesophageal spasm
• Systemic sclerosis (p
• Chagas' disease (p
, with
• Oesophageal web or ring
• Peptic stricture
• Oesophagitis
• Oesophageal/ gastric tumour
• Lung cancer
• Mediastinal lymph nodes
• Aortic aneurysm
• Left atrial enlargement
• Retrosternal goitre.
246
)
548
419
).
Remembering your anti- emetics
One way of recalling anti- emetics involves using (simplified) pharmacology.
Table 6.
5
Pharmacology of common anti- emetics
Receptor Antagonist Dose Notes
1
2
HT
3
Cyclizine
Cinnarizine
Metoclopramide
Domperidone
Prochlorperazine
Haloperidol
Ondansetron
hydrobromide
Dexamethasone
Midazolam
50
mg/ 8h PO/ IV/
30
mg/ 8h
PO
10
mg/ 8h
PO/ IV/ IM GI
60
mg/ 12h PR;
20
mg/ 6h
PO
12.5
mg IM;
5
mg/ 8h
PO
1.5
mg/ 12h
PO
4– 8
mg/ 8h IV slowly
200– 600
mcg SC/
6– 10
mg/ d
PO/ SC
2– 4
mg/ d SC
(
syringe driver
IM GI
cause s
Vest ibu lar diso rder s
cause s; also pro kinetic
Also prokinetic
Vest ibu lar/ GI cause s
Chemical causes, eg opioids
Doses can be higher for, eg
emetogenic chemotherapy
Antimuscarinic also an tispas-
IM
modic and antisecretory (don’t
prescribe with a prokinetic)
Unknown mode of action; an
adjuvant
Unknown action; anti- emetic
eect outlasts sedative eect
)
H
D
5
Others Hyoscine
All antidopaminergics can cause dystonias and oculogyric crisis, especially in younger patients.
6.15
)
247
):
4
5
Non- propulsive contractions manifest as tertiary contractions or ‘corkscrew oesophagus’ (fig 16.35, p
and suggest a motility disorder and may lead to acid clearance. Symptoms and radiology may not match.
Nutcracker oesophagus denotes distal peristaltic contractions >
nitrates or sublingual nifedipine.
180
mmHg. It may cause pain, relieved by
727
)
6 Gastroenterology
Dyspepsia and peptic ulcer disease
ALARM S
BNF
https://t.me/med1917
248
War The stomach is a battle ground between the forces of attack (acid, pepsin,
Helicobacter pylori, bile salts) and defence (mucin secretion, cellular mucus, bicarbonate secretion, mucosal blood flow, cell turnover). Gastric antisecretory
agents, eg H
only work if you have optimized cytoprotection (antacids and sucralfate work this
receptor antagonists (
2
way). Success may depend on you being not just a brilliant general, but also a tactician, politician, and diplomat. Plan your strategy carefully
neglecting psychological factors can prove disastrous. The aim is not outright vic-
H2RA
S), and proton pump inhibitors (
5 (fig
6.16
tory but maintaining the balance of power so all may prosper.
Symptoms Epigastric discomfort often related to hunger, specific foods, or time of
day, fullness after meals, heartburn (retrosternal pain); tender epigastrium. Beware
ymptoms: Anaemia (iron deficiency); Loss of weight; Anorexia; Recent
onset/ progressive symptoms;
Melaena/ haematemesis; Swallowing diculty.
H. pylori (See table 6.6.) If 55yrs old ‘Test and treat’ for H. pylori;6 if + ve give
PPI
appropriate
clarithromycin
pression alone.
those
Pepti c ulcer d isease Duodenal (
ulcers (
often malignant). Although there are some distinct features, these usually cannot
be distinguished by the history alone.
NSAID
(
emptying (
burns (Cushing’s or Curling’s ulcers).
immediately (
Nocturnal pain is more common with
Upper
H. pylori. Repeat endoscopy after 6– 8 weeks to confirm healing and exclude malig-
nancy. Measure gastrin concentrations when o
p
267
) is suspected. Non- ulcer dyspepsia; duodenal Crohn’s; TB; lymphoma; pan-
(
creatic cancer (
Gastritis Risk factors Alcohol,
gastritis, granulomas (Crohn’s; sarcoidosis),
Ménétrier’s disease (
Upper GI endoscopy only if suspicious features (fig
and 2- antibiotic combination, eg lansoprazole 30mg/ 12h
250
mg/ 12h PO, and amoxicillin 1g/ 12h PO for 1wk. If –ve give acid sup-
Refer for urgent endoscopy (p
55
yrs with alarm symptoms or with treatment- refractory dyspepsia.
GU
oc cur m ain ly i n the eld erl y, on the l ess er c urve — ulcers elsewhere are more
DU,
fig 6.17) are 4- fold more common than gastric
244
) all with dysphagia, as well as
Major risk factors H. pylori (80– 90%); drugs
S; steroids;
SSRI
). Minor Gastric acid secretion (eg gastrinoma, p
DU
) emptying (GU); blood group O; smoking; stress, eg neurosurgery or
Symptoms Asymptomatic or epigastric pain
GU
) or a few hours (DU) after meals (relieved by antacids) ± weight.
GI
endoscopy with biopsy, and to exclude malignancy (fig
p
612
). Foll ow- up None; if good response to (eg
p
267
& p
DU.
Signs Epigastric tenderness. Diagnosis
PPI
S if Zollinger– Ellison syndrome
NSAID
s, H. pylori, reflux/ hiatus hernia, atrophic
CMV
692
). Symptoms Epigastric pain, vomiting. Tests
, Zollinger– Ellison syndrome &
6.16
PPI
).
Treatment Lifestyle Alcohol and tobacco.
H. pylori eradication Triple therapy is 80– 85% eective at eradication.
Drugs to reduce acid
or
8
(GU) wks. H2 blockers have a place (ranitidine
Drug- induced ulcers Sto p drug if possible .
GI
ulcers and bleeding in patients on
ternative with dierent
reconsider dierential diagnoses (eg gallstones).
Complications Bleeding (p
PPI
S are eective, eg lansoprazole
PPI
S may be best for treating and preventing
NSAID
SE
. If symptoms persist, re- endoscope, retest for H. pylori, and
or antiplatelet drugs. Misoprostol is an al-
Surgery See p
252
), perforation (p
30
300
598
mg/ 24
mg each night PO for 8wks).
614
.
), malignancy, gastric outflow.
Functional (non- ulcer) dyspepsia Common. H. pylori eradication (only after a
PPI
+ ve result) may help. Some evidence favours
psychotherapy. Low- dose amitriptyline (
antispasmodics, H
all have less evidence.
blockers, misoprostol, prokinetic agents, bismuth, or sucralfate
2
S (only short- term courses) and
10– 20
mg each night PO) may help. Antacids,
PPI
S) may
). As in any war,
267
); gastric
6.16
). Test for
).
7
h PO for 4 (DU)
PO,
6
H. pylori is the commonest bacterial pathogen found worldwide (>50% of the world population over 40yrs
has it). It’s a class I carcinogen causing gastritis, duodenal/ gastric ulcers,
p
360
), also associated with coronary artery disease,
7 1
week of therapy sucient; 2 weeks increases eradication rates by ~5% but also increases
infections switch to a
2
nd- line antibiotic combination (see
B
and iron deficiency.
12
).
&
gastric cancer/ lymphoma (
SE.
For resistant
MALT
,
6 Gastroenterology
Table 6.
https://t.me/med1917
6
Tests (other than serology) should be performed after >2wks o
Sensitivity Specificity
Invasive tests
Non- invasive
* The 13C breath test is the most accurate non- invasive Helicobacter test.
CLO
test
Histology
Culture
13
C breath test*
Stool antigen
Serology
95
%
95
%
90
%
95
%
95
%
92
%
Dierential diagnosis of dyspepsia
• Functional dyspepsia
• Oesophagitis/
GORD (15%).
(70%).
• Duodenal/ gastric ulcer
• Gastric malignancy. • Gastritis (p
(15%).
PPI
95
%
95
%
100
%
95
%
94
%
83
%
• Duodenitis.
248
249
).
Fig 6.
16
See
NICE
simply an inflection point in population risk data.
60
. We should not be overly rigid in applying these rules to the patient in front of us— though those
to
who hold the purse strings may at time seek to reduce costs by strict enforcement of such guidelines.
dyspepsia guidelines.
†
Don’t treat + ve cases of H. pylori more than twice. If still + ve refer for specialist opinion.
Fig 6.
17
Endoscopic image of a duodenal ulcer.
5
* Nothing magical happens on the
US
and Canadian guidelines have increased the age
© Dr Jon Simmons.
55
th birthday— this is
6 Gastroenterology
Gastro- oesophageal reflux disease (
GORD
https://t.me/med1917
250
GORD
is common, and caused by reflux of stomach contents (acid ± bile)8 causing
troublesome symptoms and/ or complications. If reflux is prolonged, it may cause
oesophagitis (
and
hiatus hernia (see
fig
6.18
BOX
; it is pre- malignant). Causes Lower oesophageal sphincter hypotension,
), benign oesophageal stricture, or Barrett’s oesophagus (fig
BOX
), oesophageal dysmotility (eg systemic sclerosis), obesity,
)
gastric acid hypersecretion, delayed gastric emptying, smoking, alcohol, pregnancy,
drugs that reduce lower oesophageal sphincter pressure or aect motility (tricyclics,
anticholinergics, nitrates, Ca
2
+
channel blockers), Helicobacter pylori?
Symptoms Oesophageal Heartburn (burning, retrosternal discomfort after meals,
lying, stooping, or straining, relieved by antacids); belching; acid brash (acid or bile
regurgitation); waterbrash (salivation: ‘My mouth fills with saliva’); odynophagia
(painful swallowing, eg from oesophagitis or ulceration).
Nocturnal asthma, chronic cough, laryngitis (hoarseness, throat clearing), sinusitis.
Extra- oesophageal
Complications Oesophagitis, ulcers, benign stricture, iron- deficiency. Metaplasia
GORD
dysplasianeoplasia
Oesophagitis from corrosives,
may lead to Barrett’s oesophagus (fig
NSAID
S, herpes, Candida; duodenal or gastric ul-
cers or cancers; non- ulcer dyspepsia; oesophageal spasm; cardiac disease; functional heartburn/ reflux hypersensitivity.
Te st s Endoscopy if dysphagia, or if ≥55yrs old with alarm symptoms (p
24
treatment- refractory dyspepsia.
GORD
diagnose
whe n endos copy is normal.
h oesophageal pH monitoring ± manometry help
Treatment Lifestyle Weight loss; smoking cessation; small, regular meals; reduce
hot drinks, alcohol, citrus fruits, tomatoes, onions, fizzy drinks, spicy foods, caeine,
chocolate; avoid eating <
3
h before bed. Raise the bed head.
Drugs Antacids, eg magnesium trisilicate mixture (10mL/ 8h), or alginates, eg
10– 20
Gaviscon® (
24
h
PO.
For refractory symptoms, add an H2 blocker and/ or try twice- daily
drugs aecting oesophageal motility (as causes above) or that damage mucosa
NSAID
S,
(
treatment, and use the shortest course possible (discontinue if asymptomatic).
mL/ 8h PO) relieve symptoms. Add a
+
K
salts, bisphosphonates, tetracyclines). Monitor for Mg on long- term
PPI
, eg lansoprazole 30mg/
Surgery (eg laparoscopic Nissen fundoplication, or novel options including lap-
LINX
aroscopic insertion of a
radiofrequency- induced hypertrophy.) These all aim to lower oesophageal
sphincter tone. Consider in
nometry, surgery is superior to medical management
laryngitis) are less likely to improve with surgery than typical symptoms.
® magnetic sphincter prothesis or endoscopic
PPI
- refractory
GORD (
if confirmed by pH monitoring/ ma-
6). Atypical symptoms (cough,
6.19
6.19
9
and
BOX
).
248
) or with
PPI
. Avoid
PPI
Fig 6.
18
Upper GI endoscopy showing longi-
tudinal mucosal breaks in severe oesophagitis.
8
The reflux of duodenal fluid, pancreatic secretions and bile may be as important as acid; it may respond to
similar lifestyle measures, sucralfate (
9
H. pylori association with
predominant gastritis is present.
Fig 6.
19
Barrett’s oesophagus.
© Dr A Mee.
2
g/ 12h PO), domperidone, or metoclopramide.
GORD
controversial, but eradication may help symptoms especially if antral-
© Dr A Mee.
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