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Risk factors of
age Fatty meal
≥3months ofbothersome postprandial fullness,
satiety, or epigastricpainor burning
onsetat least 6 months before diagnosisin the
✢The pathophysiology ofdyspepsia notwellunderstood so
the researchersarefocused onseveralkeyfactors :
Pathophysiology of functional dyspepsia
Motility and nonmotility
the diseases that can affect the motility of GIT like : GERD (
decrease th lower esophageal sphincter tone ), Impaired gastric
fundus relaxation after eating…
visceral afferent hypersensitivity (These individuals with functional
heartburn are believed to have heightened perception of
normal esophageal pH and volume)
With motility disorders there is little correlation between symptoms
and severity of duodenitis , and no relation between treatment and
improvement of mucosal appearance on endoscopy .
Dr. Robin Warren, a pathologist from
Perth, Australia, observed small
curved bacteria colonizing the lower
part of the stomach in about 50% of
patients who had their stomachs
biopsied. He observed that signs of
inflammation were always present in
the gastric mucosa close to where he
saw the bacteria.
Barry Marshall, a colleague, became interested in
Warren’s findings and together they initiated a study of
biopsies from 100 patients. Marshall succeeded in
cultivating a previously unknown bacterial species – later
named Helicobacter pylori – from several of these
biopsies. They found that the organism was present in
almost all patients with gastric inflammation, duodenal
ulcer, or gastric ulcer. Based on these results, they
proposed that this newly identified bacterium caused
Until that time, so entrenched was the belief that lifestyle
caused ulcers that, even with their evidence, it was
difficult for these two researchers to convince the world
of H. pylori’s role in ulcer disease.” To provide even more
conclusive evidence, in 1985 Marshall deliberately
infected himself with the bacterium and established his
own stomach illness. Eradication therapy was then
employed with mixed success, but both received the
Nobel Prize for Medicine and Physiology in 2005..
a gram-negative bacillus that has
naturally colonized humans for at least 100,000 year
and probably throughout human evolution.
It lives in gastric mucus, with a small proportion
of the bacteria adherent to the mucosa and possibly
avery small number of the organisms entering cells
or penetrating the mucosa
Its spiral shape and flagella render H. pylori motile in
the mucus environment. The
organism has several acid-resistance mechanisms, most notably a
highly expressed urease that catalyzes urea hydrolysis to produce
buffering ammonia. H. pylori is microaerophilic (i.e., requires low
levels of oxygen), is slow-growing, and requires complex growth
media in vitro
Prevalence and Risk Factors
• Theprevalenceof H.pyloriamong
✢ adultsis<30% inmostpartsoftheUnitedStatesandin
• >80% inmostdeveloping countries.
• IntheUnitedStates,prevalence varieswithage: up
• ~20% of 30-year-oldpersons,
• andfewerthan10% ofchildrenarecolonized. H
✢ Humansarethe onlyimportant reservoir of H.pylori.
oftenthe primarycaregiver) orfrom other children
✢ Whether transmissiontakes place more often
✢ by thefecal-oral or theoral-oral route is unknown,
✢ but H.pyloriiseasilycultured from vomitus and
gastroesophageal refluxate andis lesseasilycultured from
✢ Most H.pylori–colonizedpersonsdo notdevelop
✢ Thatsome persons develop overt diseasewhereas
others do notis related to acombination of factors:
1. bacterial straindifferences,
2. hostsusceptibility to disease,
3. and environmentalfactors
Peptic Ulcer Disease
Worldwide, >80% of duodenal ulcers
and>60% of gastric ulcers are related to H. pylori colonization
However, in particular, the proportion of gastric
ulcers caused by aspirin and nonsteroidal anti-inflammatory drugs
(NSAIDs) is increasing,
and in many developed countries these drugs
have overtaken H. pylori as a cause of gastric ulceration. The main lines
of evidence supporting an ulcer-promoting role for H. pylori are that
(1) the presence of the organism is a risk factor for the development of
(2) non-NSAID-induced ulcers rarely develop in the absence of H. pylori,
(3) eradication of H. pylori virtually abolishes long-term ulcer relapse, and
(4) experimental H. pylori infection of gerbils can cause gastric ulceration.
Pathogenesis of duodenal ulceration
Gastric colonization causes
duodenal ulceration is now
becoming more clear. H. pylori–
induced inflammation of the
gastric antrum diminishes the
number of somatostatin producing
D cells. Because somatostatin
inhibits gastrin release, gastrin
levels are higher than in H. pylori–
ve , and these higher levels lead
to increased meal-stimulated acid
secretion from the relatively
spared gastric corpus.
How this situation increases
duodenal ulcer risk remains
controversial, but the increased
acid secretion may contribute to
the formation of the potentially
protective gastric metaplasia
found in the duodenum of
patients. Gastric metaplasia in
the duodenum may become
colonized by H. pylori and
subsequently inflamed and
Gastric Adenocarcinoma and Lymphoma
Prospective nested case-control
studies have shown that H. pylori colonization is a risk factor for
adenocarcinomas of the distal (noncardia) stomach .
Long-term experimental infection of gerbils also may result in
gastric adenocarcinoma. Moreover, H. pylori may induce primary
gastric lymphoma, although this condition is much less common.
Many low-grade gastric B-cell lymphomas are dependent on H.
pylori for continuing growth and proliferation, and these tumors
may regress either fully or partially after H. pylori eradication.
However, they require careful short- and long-term monitoring,
and some necessitate
additional treatment with chemotherapeutic agents.
Pathogenesis of gastric ulceration and gastric
The pathogenesis of these conditions is less well understood, although both arise in
association with pan- or corpus predominant gastritis.
The inflammation in the gastric corpus means that it produces less acid
(hypochlorhydria) despite hypergastrinemia. Gastric ulcers usually occur at the
junction of antral and corpus-type mucosa, an area that is often particularly inflamed.
Gastric cancer probably stems from progressive DNA damage and the survival of
abnormal epithelial cell clones. The DNA damage is thought to be due principally to
reactive oxygen and nitrogen species arising from inflammatory cells, perhaps in
relation to other bacteria that survive in a hypochlorhydric stomach. Longitudinal
analyses of gastric biopsy specimens taken years apart from the same patient show
that the common intestinal type of gastric adenocarcinoma follows stepwise changes
from simple gastritis to gastric atrophy, intestinal metaplasia, and dysplasia. A
second, diffuse type of gastric adenocarcinoma found more commonly in younger
adults may arise from chronic gastritis without atrophic changes.
Many patients have upper gastrointestinal symptoms
but have normal results on upper gastrointestinal endoscopy
(so-called functional or nonulcer dyspepsia).
H. pylori is common, some of these patients will be colonized with the
organism. H. pylori eradication leads to symptom resolution a little
more commonly (from 0 to 7% in different studies) than does placebo
✢ FIRST LINE THERAPY
✢ PPI takensimultaneouslywithtwoantibiotics(from amoxicillin, clarithromycin
✢ Successisachievedin80–90% ofpatients
✢ SECOND LINE THERAPY
✢ quadrupletherapyregimen, consisting
✢ recommended. In areasof clarithromycinresistanceANDsecond-line therapyto
✢ THIRD LINE THERAPY
✢ antimicrobial sensitivity testing,
✢ rescuetherapy(levofloxacin,PPIand clarithromycin)or
✢ Eradication of the infectionhas provenbenefitsin several
✢ extragastric disorders, includingunexplainedB12 deficiency and
✢ iron deficiency anaemia, once sourcesofgastrointestinal bleeding
✢ have beenlooked forand excluded. Platelet countsimprove
✢ andmay normalise after eradication therapyinpatientswith
✢ idiopathic thrombocytopenic purpura
✢ Themechanism for this isunclear
Use of Tests to Assess Treatment Success
be usedto assessthe successof treatment
However,becausethesetestsare dependent on H. pylori load,
their use<4 weeksaftertreatment mayyield falsenegativeresults.
Furthermore, thesetests are unreliable if performed
within 4 weeksof intercurrenttreatment with antibiotics orbismuth
compounds or within 2 weeksof the discontinuation ofproton pump
inhibitor (PPI)treatment. Inthe assessmentoftreatment success,
•However, after gastric ulceration,endoscopy should be
repeated to ensure healing and to exclude gastric carcinoma
by further histologic sampling.
•Serologic tests are not used to monitor treatment success,
as the gradual drop in titer of H. pylori specific antibodies is
too slow to be of practical use.
✢ Theprevalence of peptic ulcer (0.1–0.2%)
✢ The male-to female ratio for DU varies from 5 : 1
to 2 : 1, GU is2 : 1 or less.
✢ Chronic GU is usually single; 90% are situated on
the lesser curve within the antrum or at the
junction between body andantral mucosa.
✢ Chronic DU usually occurs in the first part of the
duodenum and50% areon the anterior wall.
✢ NSAIDs: Treatment with NSAIDs is associated
with peptic ulcers due to impairment of mucosal
✢ Smoking: Smoking confers an increased risk of
gastric ulcer and, to alesserextent, duodenal ulcer.
✢ This is defined as chronic dyspepsia in the absence of organic
✢ Other commonly reported symptoms include early satiety, fullness,
bloating and nausea.
✢ ‘Ulcer-like’ and ‘dysmotility-type’ subgroups are often reported,
but there is overlap between these and with irritable bowel
✢ The cause is poorly understood but probably covers a spectrum of
mucosal, motility and psychiatric disorders.
✢ Pt. are usually young (< 40 years) and women are affected as twice as
✢ Abdominal discomfort is associated with other ‘dyspeptic’
symptoms (nausea,early satiety and bloating after meals).
✢ Morning symptoms arecharacteristic andpain or nauseamay occur
✢ Directenquiry may elicit symptoms suggestiveof IBS.
✢ Peptic ulcer disease must be considered, whilst in older subjects
intra-abdominal malignancyisa prime concern.
✢ There are no diagnostic signs, apart perhaps from
inappropriate tendernesson abdominal palpation.
✢ Symptoms may appear disproportionate to clinical well-
being andthere is no weight loss.
✢ Patients often appear anxious.
✢ A drug history should be taken and the possibility of a
depressive illnessshould be considered.
✢ Pregnancy should be ruled out in young women before
radiological studies areundertaken.
✢ Alcohol misuse should be suspected when early morning
nauseaand retching areprominent
✢ All patients should be checked for H. pylori infection.
✢ patients over the age of 55 years should undergo
endoscopy to exclude mucosal disease.
✢ The most important elements are explanation and
reassurance, Possible psychological factors should be
✢ restrictive diets are of little benefit, but smaller portions
And fat restriction may help.
✢ Up to 10%of patients benefitfrom H. pylori eradication
✢ therapy also removes a major risk factor for gastric
✢ but at the cost of a small risk of side effects and
worsening symptoms of underlying gastrooesophageal
✢ Antacids, suchas hydrotalcite, are sometimes helpful.
✢ Prokinetic drugs, such as metoclopramide (10 mg 3
times daily) or domperidone (10–20 mg 3 times daily),
may be given before meals if nausea, vomiting or
✢ H2-receptor antagonist drugs may be tried if night
painor heartburn is troublesome.
✢ Low-dose tricyclic agents, such as amitriptyline, are of
value inup to two-thirds.
✢ Some patients need behavioural or other formal
✢ Two-thirds of patients with advanced cancers have
✢ 50% have ulcer-likepain.
✢ Anorexia and nauseaoccur inone-third.
✢ Early satiety, haematemesis, melaena and dyspepsia
aloneare less common
✢ Weight loss
✢ Palpable epigastric mass
✢ Jaundice or ascites
✢ tumour spread occurs to the supraclavicular lymph
nodes (Troisier’s sign), umbilicus (Sister Joseph’s
nodule) or ovaries (Krukenbergtumour).
✢ Paraneoplastic phenomena, such as acanthosis
nigricans, thrombophlebitis (Trousseau’s sign) and
dermatomyositis, occur rarely
✢ Is characterised by recurrent abdominal pain in
association with abnormal defecation in the
absenceof astructural abnormality of the gut.
✢ About 10–15% of the population are affected at
some time but only 10% of these consult their
doctors because of symptoms.
✢ Young women are affected 2–3 times more often
✢ Coexisting conditions, such as non-ulcer dyspepsia,
chronic fatigue syndrome, dysmenorrhoea and
✢ The cause of IBS is incompletely understood but
biopsychosocial factors are thought to play an
important role, along with luminal factors, such as
diet andthe gutmicrobiota.
✢ Behavioural and psychosocial factors About 50% of
patients referred to hospital have a psychiatric
illness, such as anxiety,depression, somatisation
✢ Acute psychological stress and overt psychiatric
disease are known to alter visceral perception and
✢ These factors contribute to but do not causeIBS.
✢ The most common presentationisthat:
Recurrent abdominal discomfort , colicky or
cramping in nature,felt in the lower abdomen
relieved by defecation.
Abdominal bloating worsens throughout theday
✢ The cause is unknown but it is not due to excessive
✢ Most patients alternate between episodes of diarrhoea
and constipation, but it is useful to classify patients as
having predominantly constipation or predominantly
✢ Those with constipation tend to pass infrequent
pellety stools, usually in association with abdominal
✢ Those with diarrhoea have frequent defecation but
produce low-volume stools and rarely have nocturnal
✢ Passage of mucus is common but rectal bleeding does
✢ Patients do not lose weight and are constitutionally
✢ The diagnosis isclinical innature.
✢ Full blood count and faecal calprotectin, with or
without sigmoidoscopy,are usually done and are
normal in IBS.
✢ Colonoscopy should be undertaken in;
(over 40 yearsof age)to exclude colorectal cancer.
report rectal bleeding to exclude colon cancer and
Those who present atypically require investigations to
exclude other gastrointestinal diseases. Diarrhoea
predominant patientsjustify investigations to exclude:
✢ coeliac disease
✢ microscopic colitis
✢ lactose intolerance ,
✢ bile acid malabsorption,
✢ parasitic infection.
Rome IIIcriteria for diagnosis of irritable bowel syndrome
Recurrent abdominal pain ordiscomfort at least3days/mth inthe
last 3months, associated withtwo ormore of the following:
• Improvement withdefecation
• Onsetassociated witha changeinfrequencyofdefecation
• Onsetassociated witha changeinform (appearance)ofstool
Features supportingadiagnosis ofIBS
• Symptoms >6mths
• Frequent consultationsfor
• Previous medically
• Stress worsenssymptoms
• Age>50 yrs;male gender
• Family history of colon
• Rectal bleeding
✢ 80% of casesin Westfrom alcohol misuse.
✢ severe chronic calcific pancreatitis occurs in non-
alcoholics, possibly as a result of malnutrition and
✢ Abdominal pain, in 50%, this occurs as episodes of
✢ Slowly progressive chronic pain without acute
exacerbations affects 35% of patients, whilst the
remainder have nopainbut presentwith diarrhoea.
✢ Pain may be relieved by leaning forwards or by
✢ Steatorrhoea :> 90% of theexocrinetissue isdestroyed
✢ 30% of patients are diabetic, 70% in those with chronic
✢ erythema ab igne
✢ 90% areadenocarcinomas from the ducts.
✢ Manypt. areasympt. until an advanced stage.
✢ They present with central abdominal pain, weight loss and
✢ The pain results from invasion of the coeliac plexus and is
✢ It often radiates from the upper abdomen through to the back and
may be eased a little by bending forwards.
✢ Almost all patientslose weightand manyare cachectic.
✢ 60% of tumours in head of the pancreas, and involvement of the
CBD resultsin obstructive jaundice, with severe pruritus.
✢ A few patients present with diarrhoea, vomiting from duodenal
obstruction, diabetes mellitus, recurrent venous thrombosis, acute
pancreatitis or depression.
✢ Weight loss, An abdominal mass, a palpable gallbladder or hepatic
metastasis, A palpable gallbladder in a jaundiced patient is usually
the consequence of distal biliary obstruction by a pancreatic cancer
✢ Headache, myalgia, arthralgia, nausea and anorexia usually
precedes the development of jaundiceby a fewdays to 2 weeks.
✢ Vomiting and diarrhoea may follow, and abdominal discomfort is
✢ Darkurineandpale stools may precede jaundice.
✢ Theliver isoften tender but only minimally enlarged.
✢ Occasionally, mild splenomegaly and cervical lymphadenopathy
✢ Only 10% of individualswithgallstonesdevelop
clinical evidence of gallstonedisease.
✢ Symptomatic stones within the gallbladder
manifest as either biliary pain (‘biliary colic’) or
✢ The term ‘biliary colic’ is a misnomer because
the pain does not rhythmically increase and
decrease in intensitylikeother forms of colic.
✢ Combinations of fatty food intolerance,
dyspepsia and flatulence‘gallstonedyspepsia’.
✢ Pain is usually felt in the epigastrium (70% of
patients) or rightupper quadrant (20%).
✢ Radiates to the interscapular region or the tip
of the right scapula,the left upper quadrant and
the lower chest.
✢ It occurs suddenly and persists for about 2
✢ Left colon: freshrectal bleeding iscommon with earlyobstruction.
✢ Right colon: anaemia from occult bleeding or with altered bowel
habit, but obstruction is a late feature.
✢ Colicky lower abdominal pain is present in twothirds of patients
andrectal bleeding occurs in50%.
✢ Some present with either obstruction or perforation, leading to
peritonitis, localised abscess or fistula formation.
✢ Ca. of the rectum usually causes early bleeding, mucus discharge or
afeelingof incomplete emptying.
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